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		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=161303</id>
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		<updated>2014-10-29T01:15:28Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Lab Attendance */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
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==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 10===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:08, 15 October 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 11===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:07, 22 October 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 12===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:14, 29 October 2014 (EST)&lt;br /&gt;
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== Online Assignment 1 ==&lt;br /&gt;
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Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
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The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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[[File: Hypothyroidism.jpg|300px|right|thumb|This image compares the anatomy and histology of a normal thyroid gland and a hypothyroid thyroid gland]]&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;br /&gt;
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Project 7: Neural &lt;br /&gt;
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This project has a great introduction and overview of the brain and spinal cord anatomy. The first image is eye catching however I find it hard to follow and it seems like there is too much information on it. Perhaps it would be better positioned further down in the report after more neural developmental stages have been explained. The timeline section is clear and to the point. There is an excellent use of images to support the information. The fluorescent stained images make the ventricular, subventricular and other cortical layers clear and easy to understand. The information under the brain development section is simple and effective. However there are some terms mentioned that are not explained in enough detail like the specific layering of the cortex. It is a complicated migration process that deserves some more research. It is good that the student has explained gyration and sulcation in this section. &lt;br /&gt;
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This project is clearly still in progress however the information in the first section of the wiki page indicates a very promising final product. The spinal cord and meninges development section still needs to be written up. If it follows along the course of the brain development section, it will be flawless. The current research models and finding section reveals an in-depth understanding of complex ideas. However for a student embryology wiki page, there is too much detail. If the student wants to illustrate a complicated research finding, images or tables of the results found from this research would help convey the message to the student. A table would help summarise the results in the first current research description, particularly for the results gathered from the different parts of the brain. &lt;br /&gt;
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The final part of this report on abnormalities is unfinished however the bulk of the information presented already is very good. The images supporting the abnormality are excellent and important for keeping the student reading this page engaged. However there are a few spelling and grammar errors in the neural tube defects section: “which affect the either the brain”, “the openings remain which leas”. There is still room for more research and information on other neural development abnormalities and the subheadings the student has incorporated indicates their intention of adding more information. This report has excellent reference formatting and citation throughout the page. The tables and images are referenced correctly and the long list at the end is very neat. &lt;br /&gt;
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Project 8: musculoskeletal &lt;br /&gt;
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This project is still in its early days but the layout and plan is very good. With additional information added to the subheadings, it will be a very interesting student wiki page. Reviewing what has already been completed on this page, it is too content heavy. There are a lot of large chunks of text indicating the student has gone to a lot of effort to find complex research papers. This is further supported by the huge amount of references at the end of the page. However as this is to be a student embryology wiki page, it would help if the passages of text were broken up into bullet points and tables. Furthermore there are no images or student drawn diagrams. These would also help convey the main messages of musculoskeletal development. The sections after tendon development are unfinished and very brief. Furthermore the only in text referencing present is in the first two sections. Citations should be carried through the entire page. &lt;br /&gt;
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The second trimester muscular development section is particularly clear and to the point. However the information present doesn’t stretch much further than what was covered in the lecture material. By adding diagrams of the pharyngeal arch origins and including further research into this section, its quality will be greatly improved.&lt;br /&gt;
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==Online Assessment 9==&lt;br /&gt;
'''&amp;lt;sup&amp;gt;Sensory System Development - The Eye&amp;lt;/sup&amp;gt;'''&lt;br /&gt;
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Embryological eye development is an area of sensory embryology that has recently been the subject of various research papers. A paper that has particular relevance to eye development is by Yao Chen et al, titled Effects of High Salt-Exposure on the Development of Retina and Lens in 5.5-Day Chick Embryo. It was published on the 20th August 2014 making it very current research. Although they used Chick embryos instead of human embryos, the Chick model is very useful for looking at eye development because that sensory system is relatively large in the early stage embryo, hence making it easier to study. &lt;br /&gt;
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This paper investigates the effect of high salt exposure to the developing embryo particularly on eye, lens and retina shape and development. It compares a control eye that had normal salt exposure with two variations: exposure to 280mosm/l Sodium Chloride (NaCl) solution and 300mosm/l NaCl solution. Once the fertilised chick embryos were treated with these solutions, they were incubated and then H&amp;amp;E stained for analysis of transverse sections. The eye diameter and retina thickness were measured using Image-Pro Plus 6.0, a photography program. The proliferation of cells in the retina were measured using Phospho-Histone P3 immunostaining to measure the expression of the Pax6 gene which is vital in normal retina development. &lt;br /&gt;
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This report also explains early vertebrate eye development in the embryo. The eye has three main embryonic origins: the optic vesicle, the surrounding mesenchyme and the overlying surface ectoderm. In response to signals from the optic vesicle, the surface ectoderm thickens to form the lens placode and around week 4 disassociates from the surface of the embryo to form a lens vesicle. This lens vesicle will form the actual lens. The optic vesicle invaginates to form an optic cup where the internal layer forms the neuroretina and the outter layer forms the pigmented retinal epithelium.  There is also neural crest cell contribution to the development of retinal ganglion cells, cone photoreceptors, rod photoreceptors, bipolar cells and Muller glia cells. The Paired Box 6 gene (Pax6) is also very important for proper development of the eye, eye size, neuronal differentiation and retina development. &lt;br /&gt;
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The results gathered form this investigation highlighted the detrimental effect high salt intake can have on a developing embryo, in particular eye development. The level of eye deformity increased with increased level of NaCl exposure. The size of the eye decreased significantly, the diameter of the lens decreased and the lens was thinner. These results were gathered by looking at the images after H&amp;amp;E staining. Furthermore, using immunostaining, it was evident that there was decreased expression of the Pax6 gene in high-NaCl embryos.  This is very important since it has been found that this gene is expressed during optic vesicle and integration of the surface ectoderm into development of eye structures in the early embryo. If this gene is not expressed due to high salt levels, the embryo will have abnormal eye development. This can be observed in humans who suffer from pan-ocular disorders and in mice models where an under expression of Pax6 leads to the eyeless phenotype. Pax6 is also important during neural crest cell migration specifically the periocular mesenchyme cells that contribution to eye structures. Hence it is clear that this report shows how high levels of salt intake can have detrimental effects on eye development. &amp;lt;ref name=&amp;quot;PMID10.1159/000363044&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1159/000363044&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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{{Vision Links}}&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=158960</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=158960"/>
		<updated>2014-10-24T01:53:24Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid */&lt;/p&gt;
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&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
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==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
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===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
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===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
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===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
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===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
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===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
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===Lab 10===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:08, 15 October 2014 (EST)&lt;br /&gt;
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===Lab 11===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:07, 22 October 2014 (EST)&lt;br /&gt;
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== Online Assignment 1 ==&lt;br /&gt;
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Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
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The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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[[File: Hypothyroidism.jpg|300px|right|thumb|This image compares the anatomy and histology of a normal thyroid gland and a hypothyroid thyroid gland]]&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;br /&gt;
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Project 7: Neural &lt;br /&gt;
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This project has a great introduction and overview of the brain and spinal cord anatomy. The first image is eye catching however I find it hard to follow and it seems like there is too much information on it. Perhaps it would be better positioned further down in the report after more neural developmental stages have been explained. The timeline section is clear and to the point. There is an excellent use of images to support the information. The fluorescent stained images make the ventricular, subventricular and other cortical layers clear and easy to understand. The information under the brain development section is simple and effective. However there are some terms mentioned that are not explained in enough detail like the specific layering of the cortex. It is a complicated migration process that deserves some more research. It is good that the student has explained gyration and sulcation in this section. &lt;br /&gt;
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This project is clearly still in progress however the information in the first section of the wiki page indicates a very promising final product. The spinal cord and meninges development section still needs to be written up. If it follows along the course of the brain development section, it will be flawless. The current research models and finding section reveals an in-depth understanding of complex ideas. However for a student embryology wiki page, there is too much detail. If the student wants to illustrate a complicated research finding, images or tables of the results found from this research would help convey the message to the student. A table would help summarise the results in the first current research description, particularly for the results gathered from the different parts of the brain. &lt;br /&gt;
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The final part of this report on abnormalities is unfinished however the bulk of the information presented already is very good. The images supporting the abnormality are excellent and important for keeping the student reading this page engaged. However there are a few spelling and grammar errors in the neural tube defects section: “which affect the either the brain”, “the openings remain which leas”. There is still room for more research and information on other neural development abnormalities and the subheadings the student has incorporated indicates their intention of adding more information. This report has excellent reference formatting and citation throughout the page. The tables and images are referenced correctly and the long list at the end is very neat. &lt;br /&gt;
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Project 8: musculoskeletal &lt;br /&gt;
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This project is still in its early days but the layout and plan is very good. With additional information added to the subheadings, it will be a very interesting student wiki page. Reviewing what has already been completed on this page, it is too content heavy. There are a lot of large chunks of text indicating the student has gone to a lot of effort to find complex research papers. This is further supported by the huge amount of references at the end of the page. However as this is to be a student embryology wiki page, it would help if the passages of text were broken up into bullet points and tables. Furthermore there are no images or student drawn diagrams. These would also help convey the main messages of musculoskeletal development. The sections after tendon development are unfinished and very brief. Furthermore the only in text referencing present is in the first two sections. Citations should be carried through the entire page. &lt;br /&gt;
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The second trimester muscular development section is particularly clear and to the point. However the information present doesn’t stretch much further than what was covered in the lecture material. By adding diagrams of the pharyngeal arch origins and including further research into this section, its quality will be greatly improved.&lt;br /&gt;
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==Online Assessment 9==&lt;br /&gt;
'''&amp;lt;sup&amp;gt;Sensory System Development - The Eye&amp;lt;/sup&amp;gt;'''&lt;br /&gt;
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Embryological eye development is an area of sensory embryology that has recently been the subject of various research papers. A paper that has particular relevance to eye development is by Yao Chen et al, titled Effects of High Salt-Exposure on the Development of Retina and Lens in 5.5-Day Chick Embryo. It was published on the 20th August 2014 making it very current research. Although they used Chick embryos instead of human embryos, the Chick model is very useful for looking at eye development because that sensory system is relatively large in the early stage embryo, hence making it easier to study. &lt;br /&gt;
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This paper investigates the effect of high salt exposure to the developing embryo particularly on eye, lens and retina shape and development. It compares a control eye that had normal salt exposure with two variations: exposure to 280mosm/l Sodium Chloride (NaCl) solution and 300mosm/l NaCl solution. Once the fertilised chick embryos were treated with these solutions, they were incubated and then H&amp;amp;E stained for analysis of transverse sections. The eye diameter and retina thickness were measured using Image-Pro Plus 6.0, a photography program. The proliferation of cells in the retina were measured using Phospho-Histone P3 immunostaining to measure the expression of the Pax6 gene which is vital in normal retina development. &lt;br /&gt;
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This report also explains early vertebrate eye development in the embryo. The eye has three main embryonic origins: the optic vesicle, the surrounding mesenchyme and the overlying surface ectoderm. In response to signals from the optic vesicle, the surface ectoderm thickens to form the lens placode and around week 4 disassociates from the surface of the embryo to form a lens vesicle. This lens vesicle will form the actual lens. The optic vesicle invaginates to form an optic cup where the internal layer forms the neuroretina and the outter layer forms the pigmented retinal epithelium.  There is also neural crest cell contribution to the development of retinal ganglion cells, cone photoreceptors, rod photoreceptors, bipolar cells and Muller glia cells. The Paired Box 6 gene (Pax6) is also very important for proper development of the eye, eye size, neuronal differentiation and retina development. &lt;br /&gt;
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The results gathered form this investigation highlighted the detrimental effect high salt intake can have on a developing embryo, in particular eye development. The level of eye deformity increased with increased level of NaCl exposure. The size of the eye decreased significantly, the diameter of the lens decreased and the lens was thinner. These results were gathered by looking at the images after H&amp;amp;E staining. Furthermore, using immunostaining, it was evident that there was decreased expression of the Pax6 gene in high-NaCl embryos.  This is very important since it has been found that this gene is expressed during optic vesicle and integration of the surface ectoderm into development of eye structures in the early embryo. If this gene is not expressed due to high salt levels, the embryo will have abnormal eye development. This can be observed in humans who suffer from pan-ocular disorders and in mice models where an under expression of Pax6 leads to the eyeless phenotype. Pax6 is also important during neural crest cell migration specifically the periocular mesenchyme cells that contribution to eye structures. Hence it is clear that this report shows how high levels of salt intake can have detrimental effects on eye development. &amp;lt;ref name=&amp;quot;PMID10.1159/000363044&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1159/000363044&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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{{Vision Links}}&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
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	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=File:Hypothyroidism.jpg&amp;diff=158420</id>
		<title>File:Hypothyroidism.jpg</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=File:Hypothyroidism.jpg&amp;diff=158420"/>
		<updated>2014-10-23T23:18:28Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: This image compares a normal thyroid gland (a) anatomy with a hypothyroidism thyroid gland (b). The histology images reveal in the abnormal thyroid gland, there is less thyroid hormone produced due to irregular epithelium on the surface of the follicle...&lt;/p&gt;
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&lt;div&gt;This image compares a normal thyroid gland (a) anatomy with a hypothyroidism thyroid gland (b). The histology images reveal in the abnormal thyroid gland, there is less thyroid hormone produced due to irregular epithelium on the surface of the follicles. The researchers in this report found that once thyroid stimulating hormone was added to the hypothyroid follicles, the epithelium became more columnar and the lumens became smaller, similar to healthy thyroid follicles. &amp;lt;ref name =Endo T, Kobayashi T&amp;gt;Endo T, Kobayashi T, 2012, '&amp;quot;Dominant Negative Effect of Mutated Thyroid Stimulating Hormone Receptor (P556L) Causes Hypothyroidism in C.RF-Tshrhyt/wild Mice&amp;quot;', PLoS ONE: 7(8); e42358, http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042358&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0042358 &lt;br /&gt;
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© Endo, Kobayashi. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.&lt;br /&gt;
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		<author><name>Z3414648</name></author>
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	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=158375</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=158375"/>
		<updated>2014-10-23T22:58:01Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid */&lt;/p&gt;
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&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
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==Introduction==&lt;br /&gt;
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The endocrine system is awesome!&lt;br /&gt;
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==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
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[[File:Keith1902 fig167.jpg|200px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg|170px|thumb|right|Image 2: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
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The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.  The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth. &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || Pinealocytes || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
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'''Timeline''':&lt;br /&gt;
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[[File:Primary brain vesicles.jpg|150px|left|thumb|Image 3: Primary brain vesicles]]&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Week 6 embryonic development of CNS.jpg|150px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
[[File:Week 11 fetal development of CNS.jpg|150px|right|thumb|Image 5: Week 11 fetal development of CNS]]&lt;br /&gt;
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*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). &lt;br /&gt;
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[[File:Fetal pineal gland 01.jpg|150px|thumb|right|Image 6: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
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&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
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*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)&lt;br /&gt;
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*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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* '''Pineal tumors'''&lt;br /&gt;
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Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|150px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
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*'''Pineal hypoplasia'''&lt;br /&gt;
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Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Hypothalamus==&lt;br /&gt;
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===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signalling pathways, the Hyothalamus-Pituitary-Adrenal (HPA) and the Hypothalamus-Pituitary-Gonad (HPG) and exerts most of it's influence on the body through these two axes.&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
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''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || (also known as antidiuretic hormone) Controls the body's water balance electrolyte concentration and blood pressure by increasing water permeability in distal convoluted tubules and in the collecting duct of nephrons in the kidney. Results in higher reabsorption of water in kidneys and thus higher blood volume and pressure. &lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Stimulates lactation, hormone release during labor causes the muscles of the uterus contract&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Releases thyroid-stimulating hormone (TSH) as well as limited prolactin from anterior pituitary &lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Inhibits release of prolactin from anterior pituitary&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Stimulates release of growth hormone from anterior pituitary&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Releases adrenocorticotropic hormone (ACTH) from anterior pituitary&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Stimulates release of follicle-stimulating hormone (FSH) as well as luteinizing hormone (LH) from anterior pituitary.&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Stimulates release of growth hormone (GH) from anterior pituitary and also has inhibitory effect on release of thyroid-stimulating hormone (TSH) from the anterior pituitary&lt;br /&gt;
|}&lt;br /&gt;
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[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
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The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in fetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Fetal oxytocin may initiate or accelerate the course of labor whereas vasopressin plays a role in the adaptation to stress caused by the birth process by redistribution of fetal blood flow. &lt;br /&gt;
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'''Timeline'''&lt;br /&gt;
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[[File:Development of hypothalamus.jpg|900px|right|thumb|Image 3: Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]] &lt;br /&gt;
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'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
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* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
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* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
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'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
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* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
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* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
[[File:Stage 22 image 057.jpg|200x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
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* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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*'''Congenital Hypothalamic Hamartoma'''&lt;br /&gt;
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A hypothalamic hamartoma arises from the region of the tuber cinereum and is commonly associated with isosexual precocious puberty, i.e. puberty that develops unusually early in infants. It involves the alteration of pathways that modulate gonadotropins and contain releasing hormones within the floor of the third ventricle. .&amp;lt;ref name=Booth&amp;gt;T. Booth, C. Timmons, K. Shapiro, N.K. Rollins, ‘Pre- and Postnatal MR Imaging of Hypothalamic Hamartomas Associated with Arachnoid Cysts’, Americal Jounral of Neuroradiology:2004, http://www.ajnr.org/content/25/7/1283.full&amp;lt;/ref&amp;gt; Precocious puberty may either result from a physical manipulation of inhibitory pathways by the hamartoma or a direct neurosecretory process of the hamartoma itself. Seizures are also another common clinical presentation in children with a hypothalamic hamartoma. MR imaging is typically used to identify and monitor the growth of a hypothalamic hamartoma during embryonic and fetal development. Research has shown a trend of congenital hamartomas forming in the embryo within a period of 26 weeks. Because of the known association with other congenital anomalies of the central nervous system, hypothalamic hamartoma is thought to form as early as 4 weeks and may in fact be part of a developmental abnormality spectrum.&amp;lt;ref name=Booth&amp;gt;T. Booth, C. Timmons, K. Shapiro, N.K. Rollins, ‘Pre- and Postnatal MR Imaging of Hypothalamic Hamartomas Associated with Arachnoid Cysts’, Americal Jounral of Neuroradiology:2004, http://www.ajnr.org/content/25/7/1283.full&amp;lt;/ref&amp;gt;. Treatment options are currently limited to post-natal deliver of leuprolide acetate to the infant and in general it is relatively effective in managing and treating the condition. &lt;br /&gt;
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==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Anterior pituitary &lt;br /&gt;
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[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
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By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
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* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
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'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
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The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
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'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
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The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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==Thyroid==&lt;br /&gt;
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===Fetal development===&lt;br /&gt;
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The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
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The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
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Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
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'''How far has the thyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of Thyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis&amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Week 16 - 18 is when fetal thyroid hormone synthesis occurs&lt;br /&gt;
** Prior to this, the fetus receives vital maternal thyroid hormones via the placenta&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Thyroid Hormone Action'''&lt;br /&gt;
The following table explains the ontogenic action of thyroid hormone on the developing fetus. Thyroid hormones are essential in brain and central nervous system development in the fetus. A lot of neurological disorders are associated with insufficient thyroid hormone synthesis:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Types !! Ontogenic Action&lt;br /&gt;
|-&lt;br /&gt;
| Thyroid Hormone || &lt;br /&gt;
* T3 -  triiodothyronine&lt;br /&gt;
* T4 - thyroxine&lt;br /&gt;
|| Brain development: &lt;br /&gt;
* Central Nervous System development and maturation &amp;lt;ref name =J Patel, K Landers, H Li, R H Mortimer and K Richard&amp;gt;J Patel, K Landers, H Li, R H Mortimer and K Richard, 2011, '''Thyroid hormones and fetal neurological development''', Journal of Endocrinology:209;1-8, http://joe.endocrinology-journals.org.wwwproxy0.library.unsw.edu.au/content/209/1/1.full.pdf+html&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Glial cell proliferation&lt;br /&gt;
*Neural myelination&lt;br /&gt;
*Axon and dendrite sprouting&lt;br /&gt;
*Synapse formation&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Hypothyroidism'''&lt;br /&gt;
&lt;br /&gt;
Hypothyroidism is an abnormality that can occur in fetal development were there is insufficient thyroid hormone action. This can be due to mutations in the thyroid-stimulating hormone receptor on the thyroid gland, hence the hypothalmic-pituitary-thyroid axis communication is lost. This then results in distinct decrease in T3 and T4 levels in the fetus. Follow on effects of this deficiency include abnormal brain and central nervous system development due to lack of neuron branching and myelination. Postnatally, this can cause learning difficulties, issues with olfactory and optic systems and impaired reflex actions. &amp;lt;ref name =Jung-Yu C. Hsu, Stuart A. Stein and Xiao-Ming Xu&amp;gt;Jung-Yu C. Hsu, Stuart A. Stein and Xiao-Ming Xu, 2008, '''Abnormal Growth of the Corticospinal Axons Into the Lumbar Spinal Cord of the hyt/hyt Mouse With Congenital Hypothyroidism''', Journal of Neuroscience Research: 86; 3126-3139, http://onlinelibrary.wiley.com.wwwproxy0.library.unsw.edu.au/store/10.1002/jnr.21750/asset/21750_ftp.pdfv=1&amp;amp;t=i1lzkkit&amp;amp;s=8b2bb85677790b58b7415f9376e06a5c4329578b&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone || Secreted by || Function || Image&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine. || [[File:Active parathyroid hormone assay cartoon.png|200px|thumb|This images shows an active parathyroid hormone and its chemical structure.]]&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Thymic aplasia'''&lt;br /&gt;
&lt;br /&gt;
Thymic aplasia is a condition that has a strong correlation to DiGeorge syndrome. This syndrome is a congenital birth defect which occurs when the fetus either inherits an abnormal chromosome 22 or has a mutation of the same chromosome.  In particularly, the mutation is a deletion of the genomic information packaged in the chromosomes and normally occurs when there isn’t proper recombination of chromosomal material during fertilisation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;4166528&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result of this deletion, the third and fourth pharyngeal pouches fail to develop in the twelfth gestational week, thereby leading to the absence or partial absence of the thymus and parathyroid glands. Other associated abnormalities with thymic aplasia as a result of the deletion of chromosome 22 genetic material are severe cardiac defects, low immunity, hypocalcaemia and facial abnormalities. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;5057550&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Statistics suggest that the thymic aplasia may occur in 1:4000 to 1:6395 of fetuses.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 10861201&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Treatment is normally difficult for fetuses that exhibit thymic aplasia, however calcium levels can be monitored and regulated and heart problems can be resolved though surgery. Immunity defects can be managed from controlling phosphorus levels in the fetus and protecting them from sources of infection.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;1454183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Histopathology of the thymus with hyperplasia.jpg|250px|thumb|right|This image shows the histopathology of the thymus with hyperplasia and thymoma]]&lt;br /&gt;
&lt;br /&gt;
'''Thymoma'''&lt;br /&gt;
&lt;br /&gt;
Thymoma is the term given to the neoplasms of the thymus gland. These tumours emerge from the thymic epithelium cells of the thymus gland and do not normally show cytologic characteristics of malignancy, however are considered malignant as they are likely to undergo invasion. Thymomas are classified into different types based on the content and structure of the cells. If the tumour has spindle cell conformation, it is known as type A thymoma and constitutes to 4% to 7% of all thymomas. The tumor is made up of neoplastic thymic epithelial cells that exhibit a spindle oval shape conformation, lack nuclear atypia and have low levels of non-neoplastic lymphocytes. Mixed thymoma, also known as type AB thymoma are similar to a type A thymoma except that the foci is enriched with non-neoplastic lymphocytes. It makes up approximately 28% to 34% of all thymomas.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25143131&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Type B1 thymoma also termed as lymphocytic thymoma is similar to a healthy functional thymus as it contains a large proportion of cells exhibiting features indistinguishable from a healthy thymic cortex with areas similar to thymic medulla. It makes up for approximately 9% to 20% of all thymomas.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24672784&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Cortical thymoma, also known as type B2 thymoma contains neoplastic epithelial cells which appear scattered with vesicular nuclei and distinct nucleoli located in a dense population of non-neoplastic lymphocytes.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2698424&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It is similar to type B1 thymoma but the foci of medullary differentiation are less visible. It makes up for approximately 20% to 36% of all thymomas. Epithelial thymoma, also known as type B3 thymoma is formed mainly from polygonal shaped epithelial cells that show no atypia.  The mixture of non-neoplastic lymphocytes gives the tumour a sheet-like appearance. This makes up for approximately 10% to 14% of all thymomas.  Since some of these are hard to differentiate from normal thymus tissues, there is poor prognosis.&lt;br /&gt;
&lt;br /&gt;
Thymomas have been closely linked with another disease called myasthenia gravis. It is caused when nerve impulses are disrupted at the neuromuscular junction of skeletal muscles from the lack of binding of acetylcholine (neurotransmitter) to acetylcholine receptors needed to generate muscle contraction. Antibodies produced from the thymus gland destroy the acetylcholine receptors and hence have a strong correlation to myasthenia gravis. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21747138&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Since thymomas contain more cells than normal and are malignant, it is more likely to generate antibodies which target acetylcholine receptors.  The formation of these antibodies in B cells is T cell dependent. The T cells involved in this mechanism are generated in the thymus via nontolerogenic thymopoiesis through an abnormal function of thymic epithelial cells.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 20402580&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Overall, incorrect signalling messages could be sent out and hence cause an autoimmune attack.&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
*'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Congenital Adrenal Hyperplasia (CAH)'''&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more.[[File:Cushing's syndrome.jpg|150px|right|thumb|This image shows a  3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]] Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Cushing's Syndrome'''&lt;br /&gt;
&lt;br /&gt;
Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24656295&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
'''How far has the ovary developed by week 8 of gestation?'''&lt;br /&gt;
*Week 5- Thickening of mesothelium forms on the mesonephros. Formation of the gonadal ridge results from proliferation of the mesothelium and mesenchymal tissue beneath it &amp;lt;ref name= PMID&amp;gt;17237341&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Projection of finger-like gonadal (epithelial) cords into the mesenchyme. Indifferent gonad segmented medulla )regresses) and cortex (differentiates to form the ovary)&lt;br /&gt;
*PGCs migrate through the primitive streak in gastrulation and then reside at the junctional region of the hindgut yolk sac. Migration of the PGCs to the gonadal ridge along the hindgut’s dorsal mesentery &amp;lt;ref name= PMID&amp;gt;17237341&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Week 6- PGCs incorporated into the gonadal cords and are called oogonia, having entered underlying mesenchyme.&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of ovarian development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
[[File:Fetal ovary morphogenesis (mouse).jpg|300px|right|thumb|Diagramatic representation of fetal mouse ovary morphogenesis]]&lt;br /&gt;
*Weeks 8 to 9- Gonad is identifiable as an ovary now due to change in internal structure. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. Inner ovary; disintegrating blastema surrounded by a thick blastemal layer. Tissue has a cortical region (encloses PGCs) and a central medullary region (reticulum of somatic cells) &amp;lt;ref name= PMID&amp;gt;7158813&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10 to 12- Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue &amp;lt;ref name= PMID&amp;gt;22106406&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. Medulla contains less densely-packed globules, mainly oogonia &amp;lt;ref name= PMID&amp;gt;7158813&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 14 to 28- In mid-gestation; depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth &amp;lt;ref name= PMID&amp;gt;22106406&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium. Primordial follicle formation is the result of active mitosis of oogonia &amp;lt;ref name= PMID&amp;gt;7158813&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Congenital gonadal dysgenesis – Turner Syndrome&lt;br /&gt;
&lt;br /&gt;
Female congenital gonadal dysgenesis syndrome refers to a condition where the fetus undergoes abnormal gonadal development with a presentation of streaks of connective tissue on the developing ovary, also referred to as &amp;quot;streak gonads&amp;quot;. Streak ovaries extend from the lateral pelvic wall to the attachment of the utero-ovarian ligaments and are essentially sections of functionless tissue. They vary considerably in size but are usually approximately 4 cm in length and 2–3 mm in width. Dysgenetic ovaries are characterized by also absence of follicular structures and oocytes. In women, the most common cause of congenital gonadal dysgenesis is Turner syndrome, 45X which has a prevalence of approximately 1 in 2500 new born girls worldwide&amp;lt;ref name= PMID15475933&amp;gt;&amp;lt;pubmed&amp;gt;15475933&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Turner syndrome is a genetic abnormality due to an incomplete or completely missing X chromosome in females. Growth hormones treatments such as estrogen replacement therapy may be used after the child has reached 12-13 years of age to help treat the symptoms&amp;lt;ref name= PMID0001417&amp;gt;&amp;lt;pubmed&amp;gt;0001417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''How far has the testis developed by week 8 of gestation?'''&lt;br /&gt;
*By week 8, masculine differentiation is induced in the mesonephric duct and external genitalia. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1769902&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1769902&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of testicular development - from week 8 of gestation onwards'''&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
*Week 9- Yellowish elongated tube with mesonephros laterally and urinary bladder inferomedially &lt;br /&gt;
*Week 13- Testes have acquired the ellipsoidal shape found in the adult and are located above the inguinal canal in the groin region. Convexly curved across all but posterior surface &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Week 16- Located above deep inguinal ring, convexly curved anterior border and flat posterior border covered by epididymis&lt;br /&gt;
*Week 17- Migration of testes begins &lt;br /&gt;
*Week 24- Testes grow in size and still located about the deep inguinal ring or inside inguinal canal. The testicular poles seem more prominent. Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26 &amp;lt;ref name= Subhalakshmi&amp;gt;Subhalakshmi Wahengbam, S. Arunchandra Singh, Ningthoujam Damayanti '''Development and Morphogenesis of Testis in Human Fetuses'''. Journal of Anatomical Society of India: 2011, 60(2); 160-167, http://www.sciencedirect.com/science/article/pii/S0003277811800171&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum &amp;lt;ref name= Subhalakshmi&amp;gt;Subhalakshmi Wahengbam, S. Arunchandra Singh, Ningthoujam Damayanti '''Development and Morphogenesis of Testis in Human Fetuses'''. Journal of Anatomical Society of India: 2011, 60(2); 160-167, http://www.sciencedirect.com/science/article/pii/S0003277811800171&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Week 30- Testes sinus is towards lower portion of testes and epididymis tail continuous with vas deferens. Testes are located in the scrotum having passed through the superficial inguinal ring &lt;br /&gt;
*Week 36- Testes located within scrotal sac, they enlarge in size and are maximally convex &amp;lt;ref name= Subhalakshmi&amp;gt;Subhalakshmi Wahengbam, S. Arunchandra Singh, Ningthoujam Damayanti '''Development and Morphogenesis of Testis in Human Fetuses'''. Journal of Anatomical Society of India: 2011, 60(2); 160-167, http://www.sciencedirect.com/science/article/pii/S0003277811800171&amp;lt;/ref&amp;gt;&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Klinefelter’s syndrome'''&lt;br /&gt;
&lt;br /&gt;
Klinefelter’s syndrome is the common form of congenital primary hypogonadism with a prevalence of an estimated 1 in 1000 men. Male hypogonadism is defined as a testicular dysfunction resulting in decreased sperm and testosterone production&amp;lt;ref name=Sexson&amp;gt;E. Sexson, J. Knezevich, ‘Male Hypogonadism: A Review of the Disease and Its Treatment’, U.S. Pharmacist:2010, http://www.uspharmacist.com/content/d/health%20systems/c/21150/&amp;lt;/ref&amp;gt;.. This genetic disorder occurs when a male is born with an additional X chromosome causing complications and a general underdevelopment of structures such as the seminiferous tubules and Leydig cells within the testis. As a consequence, the size of the testis is abnormally small and the patient has a low sperm count and testosterone levels. In addition to infertility caused by testosterone deficiency, men born with this disorder frequently have increased length of their long bones, including those in the arms, legs, and hands. Many other complications exist independent of the testosterone deficiency seen with these patients&amp;lt;ref name=Sexson&amp;gt;E. Sexson, J. Knezevich, ‘Male Hypogonadism: A Review of the Disease and Its Treatment’, U.S. Pharmacist:2010, http://www.uspharmacist.com/content/d/health%20systems/c/21150/&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*'''Placenta accreta'''&lt;br /&gt;
&lt;br /&gt;
[[File:Placenta accreta.jpg|150px|right|thumb|This image shows an area of profuse bleeding in the human placenta, with a region of placenta accreta indicated by the arrow]]&lt;br /&gt;
&lt;br /&gt;
Placenta accreta (PA )is a rare obstetric abnormality characterised by abnormal insertion of the placenta to the myometrium of the uterus. The 3 types of PA are classified based on the depth of invasion; placenta accreta (superficial- chorionic villi attach to myometrium rather than just decidua basalis), placenta increta (middle layer) or placenta perceta (deep) being the most dire with 1 in 7000 incidence. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has an incidence of 1 in 2500 deliveries and is associated with grand-scale haemorrhage and requires hysterectomy and blood transfusion. &amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The condition normally occurs in the lower segment of the uterus which is prone to bleeding  being poorly contractile and a site of angiogenesis. Prenatal diagnosis of PA is based on second and third trimester ulstrasound findings indicating; retroplacental zone loss, many lucanue in the vasculature and a very thin (&amp;lt;1mm) retroplacental thickness of the myometrium.&amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has a 40% likelihood in women aged over 35 who have had Caesarian section with placenta previa in their uterine scars. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
| &lt;br /&gt;
'''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''Jennifer R Gardiner, Abigail L Jackson, Julie Gordon, Heiko Lickert, Nancy R Manley, M Albert Basson '''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''. Development: 2012, 139(18);3456-66 PMID: 22912418''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
|'''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''Stéphanie Migrenne, Evelyne Moreau, Pirjo Pakarinen, Andrée Dierich, Jorge Merlet, René Habert, Chrystèle Racine '''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''. PLoS ONE: 2012, 7(12);e53257 PMID: 23300903''&lt;br /&gt;
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This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
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Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
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The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
|}&lt;br /&gt;
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{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
|'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24757681&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''Morten Møller, Pansiri Phansuwan-Pujito, Corin Badiu '''Neuropeptide Y in the adult and fetal human pineal gland'''. Biomed Res Int: 2014, 2014;868567 PMID: 24757681''&lt;br /&gt;
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Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland. Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&lt;br /&gt;
|}&lt;br /&gt;
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{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
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A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, '''Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation.’'' Neuroscience Letters. 556; pp 124–128 http://www.sciencedirect.com/science/article/pii/S0304394013009300&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This study investigates the expression of the voltage operated calcium channels subunits α1A and α1D in the male and female bovine hypothalamus during four embryonic stages of development. The expression of both these subunits have been identified in the brain of adult mammals, however, their distribution and expression during fetal neuronal differentiation has not yet been determined&amp;lt;ref name=Peruffoa&amp;gt;A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, ‘Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation.’ Neuroscience Letters. 556; pp 124–128 http://www.sciencedirect.com/science/article/pii/S0304394013009300&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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The results suggest that expressions of α1A and α1D are correlated with the stage of development, with an increase only in males that peaks on the last period of gestation. Bovine male hypothalami showed significantly higher α1A and α1D expression values in comparison to female ones during the whole developmental period. Additionally immunohistological studies confirmed the presence of the α1A and α1D protein subunits in fetal hypothalamic neurons starting from the third fetal stage. &lt;br /&gt;
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These calcium channels may have a role in modulating physiological responses of surrounding neural structures during the second trimester of gestation while the hypothalamus is defined and networks start to develop. Due to the long duration of the pregnancy like humans, fetal bovine tissues may represent an important model for translational studies on the human hypothalamic development. In contrast with rodent models, in long gestation species such as the bovine, the critical period for hypothalamic sexual differentiation occurs in earlier gestation phases and thus presents a more relevant model to correlate to human embryonic sexual development&amp;lt;ref name=Peruffoa&amp;gt;A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, ‘Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation.’ Neuroscience Letters. 556; pp 124–128 http://www.sciencedirect.com/science/article/pii/S0304394013009300&amp;lt;/ref&amp;gt;.  &lt;br /&gt;
|}&lt;br /&gt;
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=References=&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157223</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157223"/>
		<updated>2014-10-23T10:55:05Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid */&lt;/p&gt;
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&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
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==Introduction==&lt;br /&gt;
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==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
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[[File:Keith1902 fig167.jpg|200px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg|170px|thumb|right|Image 2: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
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The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.  The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth. &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || Pinealocytes || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
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'''Timeline''':&lt;br /&gt;
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[[File:Primary brain vesicles.jpg|150px|left|thumb|Image 3: Primary brain vesicles]]&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Week 6 embryonic development of CNS.jpg|150px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
[[File:Week 11 fetal development of CNS.jpg|150px|right|thumb|Image 5: Week 11 fetal development of CNS]]&lt;br /&gt;
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*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). &lt;br /&gt;
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[[File:Fetal pineal gland 01.jpg|150px|thumb|right|Image 6: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
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&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
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*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)&lt;br /&gt;
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*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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* '''Pineal tumors'''&lt;br /&gt;
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Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|150px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
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*'''Pineal hypoplasia'''&lt;br /&gt;
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Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Hypothalamus==&lt;br /&gt;
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===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signalling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
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*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
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The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
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[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
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'''Timeline'''&lt;br /&gt;
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'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
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* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
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* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
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'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
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* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
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* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
[[File:Stage 22 image 057.jpg|200x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
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* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
[[File:Development of hypothalamus.jpg|900px|left|thumb|Image 3: Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]] &lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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*'''Congenital Hypothalamic Hamartoma'''&lt;br /&gt;
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A hypothalamic hamartoma arises from the region of the tuber cinereum and is commonly associated with isosexual precocious puberty, i.e. puberty that develops unusually early in infants. It involves the alteration of pathways that modulate gonadotropins and contain releasing hormones within the floor of the third ventricle. .&amp;lt;ref name=Booth&amp;gt;T. Booth, C. Timmons, K. Shapiro, N.K. Rollins, ‘Pre- and Postnatal MR Imaging of Hypothalamic Hamartomas Associated with Arachnoid Cysts’, Americal Jounral of Neuroradiology:2004, http://www.ajnr.org/content/25/7/1283.full&amp;lt;/ref&amp;gt; Precocious puberty may either result from a physical pertubation of inhibitory pathways by the hamartoma or a direct neurosecretory process of the hamartoma itself. Seizures are also another common clinical presentation in children with a hypothalamic hamartoma. MR imaging is typically used to identify and monitor the growth of a hypothalamic hamartoma during embryonic and fetal development. Research has shown a trend of congenital hamartomas forming in the utero within a period of 26 weeks. Because of the known association with other congenital anomalies of the central nervous system, hypothalamic hamartoma is thought to form as early as 4 weeks and may in fact be part of a developmental abnormality spectrum.&amp;lt;ref name=Booth&amp;gt;T. Booth, C. Timmons, K. Shapiro, N.K. Rollins, ‘Pre- and Postnatal MR Imaging of Hypothalamic Hamartomas Associated with Arachnoid Cysts’, Americal Jounral of Neuroradiology:2004, http://www.ajnr.org/content/25/7/1283.full&amp;lt;/ref&amp;gt;. Treatment options are currently limited to post-natal deliver of leuprolide acetate to the infant and in general it is relatively effective in managing and treating the condition. &lt;br /&gt;
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'''Recent Findings'''&lt;br /&gt;
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A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
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E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
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'''References'''&lt;br /&gt;
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Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
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[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Anterior pituitary &lt;br /&gt;
&lt;br /&gt;
[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''How far has the thyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of Thyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis&amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Week 16 - 18 is when fetal thyroid hormone synthesis occurs&lt;br /&gt;
** Prior to this, the fetus receives vital maternal thyroid hormones via the placenta&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Thyroid Hormone Action'''&lt;br /&gt;
The following table explains the ontogenic action of thyroid hormone on the developing fetus. Thyroid hormones are essential in brain and central nervous system development in the fetus. A lot of neurological disorders are associated with insufficient thyroid hormone synthesis:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Types !! Ontogenic Action&lt;br /&gt;
|-&lt;br /&gt;
| Thyroid Hormone || &lt;br /&gt;
* T3 -  triiodothyronine&lt;br /&gt;
* T4 - thyroxine&lt;br /&gt;
|| Brain development: &lt;br /&gt;
* Central Nervous System development and maturation &amp;lt;ref name =J Patel, K Landers, H Li, R H Mortimer and K Richard&amp;gt;J Patel, K Landers, H Li, R H Mortimer and K Richard, 2011, '''Thyroid hormones and fetal neurological development''', Journal of Endocrinology:209;1-8, http://joe.endocrinology-journals.org.wwwproxy0.library.unsw.edu.au/content/209/1/1.full.pdf+html&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Glial cell proliferation&lt;br /&gt;
*Neural myelination&lt;br /&gt;
*Axon and dendrite sprouting&lt;br /&gt;
*Synapse formation&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Header text !! Header text !! Header text&lt;br /&gt;
|-&lt;br /&gt;
| Example || Example || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone || Secreted by || Function || Image&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine. || [[File:Active parathyroid hormone assay cartoon.png|200px|thumb|This images shows an active parathyroid hormone and its chemical structure.]]&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Thymic aplasia'''&lt;br /&gt;
&lt;br /&gt;
Thymic aplasia is a condition that has a strong correlation to DiGeorge syndrome. This syndrome is a congenital birth defect which occurs when the fetus either inherits an abnormal chromosome 22 or has a mutation of the same chromosome.  In particularly, the mutation is a deletion of the genomic information packaged in the chromosomes and normally occurs when there isn’t proper recombination of chromosomal material during fertilisation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;4166528&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result of this deletion, the third and fourth pharyngeal pouches fail to develop in the twelfth gestational week, thereby leading to the absence or partial absence of the thymus and parathyroid glands. Other associated abnormalities with thymic aplasia as a result of the deletion of chromosome 22 genetic material are severe cardiac defects, low immunity, hypocalcaemia and facial abnormalities. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;5057550&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Statistics suggest that the thymic aplasia may occur in 1:4000 to 1:6395 of fetuses.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 10861201&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Treatment is normally difficult for fetuses that exhibit thymic aplasia, however calcium levels can be monitored and regulated and heart problems can be resolved though surgery. Immunity defects can be managed from controlling phosphorus levels in the fetus and protecting them from sources of infection.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;1454183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
*'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Congenital Adrenal Hyperplasia (CAH)'''&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more.[[File:Cushing's syndrome.jpg|150px|right|thumb|This image shows a  3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]] Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Cushing's Syndrome'''&lt;br /&gt;
&lt;br /&gt;
Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24656295&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*'''Placenta accreta'''&lt;br /&gt;
&lt;br /&gt;
[[File:Placenta accreta.jpg|150px|right|thumb|This image shows an area of profuse bleeding in the human placenta, with a region of placenta accreta indicated by the arrow]]&lt;br /&gt;
&lt;br /&gt;
Placenta accreta (PA )is a rare obstetric abnormality characterised by abnormal insertion of the placenta to the myometrium of the uterus. The 3 types of PA are classified based on the depth of invasion; placenta accreta (superficial- chorionic villi attach to myometrium rather than just decidua basalis), placenta increta (middle layer) or placenta perceta (deep) being the most dire with 1 in 7000 incidence. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has an incidence of 1 in 2500 deliveries and is associated with grand-scale haemorrhage and requires hysterectomy and blood transfusion. &amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The condition normally occurs in the lower segment of the uterus which is prone to bleeding  being poorly contractile and a site of angiogenesis. Prenatal diagnosis of PA is based on second and third trimester ulstrasound findings indicating; retroplacental zone loss, many lucanue in the vasculature and a very thin (&amp;lt;1mm) retroplacental thickness of the myometrium.&amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has a 40% likelihood in women aged over 35 who have had Caesarian section with placenta previa in their uterine scars. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
| &lt;br /&gt;
'''''*Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''Jennifer R Gardiner, Abigail L Jackson, Julie Gordon, Heiko Lickert, Nancy R Manley, M Albert Basson Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis. Development: 2012, 139(18);3456-66 PMID: 22912418''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
|'''''*Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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''Stéphanie Migrenne, Evelyne Moreau, Pirjo Pakarinen, Andrée Dierich, Jorge Merlet, René Habert, Chrystèle Racine Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life. PLoS ONE: 2012, 7(12);e53257 PMID: 23300903&lt;br /&gt;
''&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
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The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
|}&lt;br /&gt;
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{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
|''''*Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24757681&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''Morten Møller, Pansiri Phansuwan-Pujito, Corin Badiu Neuropeptide Y in the adult and fetal human pineal gland. Biomed Res Int: 2014, 2014;868567 PMID: 24757681&lt;br /&gt;
''&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland. Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&lt;br /&gt;
|}&lt;br /&gt;
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=References=&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157214</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157214"/>
		<updated>2014-10-23T10:52:46Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid */&lt;/p&gt;
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&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
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==Introduction==&lt;br /&gt;
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==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
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[[File:Keith1902 fig167.jpg|200px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg|170px|thumb|right|Image 2: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
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The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.  The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth. &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || Pinealocytes || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
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'''Timeline''':&lt;br /&gt;
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[[File:Primary brain vesicles.jpg|150px|left|thumb|Image 3: Primary brain vesicles]]&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Week 6 embryonic development of CNS.jpg|150px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
[[File:Week 11 fetal development of CNS.jpg|150px|right|thumb|Image 5: Week 11 fetal development of CNS]]&lt;br /&gt;
&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). &lt;br /&gt;
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[[File:Fetal pineal gland 01.jpg|150px|thumb|right|Image 6: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
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&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
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*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)&lt;br /&gt;
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*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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* '''Pineal tumors'''&lt;br /&gt;
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Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|150px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
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*'''Pineal hypoplasia'''&lt;br /&gt;
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Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signalling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
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*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
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The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
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[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
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'''Timeline'''&lt;br /&gt;
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'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
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* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
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'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
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* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
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* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
[[File:Stage 22 image 057.jpg|200x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
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* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
[[File:Development of hypothalamus.jpg|900px|left|thumb|Image 3: Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]] &lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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*'''Congenital Hypothalamic Hamartoma'''&lt;br /&gt;
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A hypothalamic hamartoma arises from the region of the tuber cinereum and is commonly associated with isosexual precocious puberty, i.e. puberty that develops unusually early in infants. It involves the alteration of pathways that modulate gonadotropins and contain releasing hormones within the floor of the third ventricle. .&amp;lt;ref name=Booth&amp;gt;T. Booth, C. Timmons, K. Shapiro, N.K. Rollins, ‘Pre- and Postnatal MR Imaging of Hypothalamic Hamartomas Associated with Arachnoid Cysts’, Americal Jounral of Neuroradiology:2004, http://www.ajnr.org/content/25/7/1283.full&amp;lt;/ref&amp;gt; Precocious puberty may either result from a physical pertubation of inhibitory pathways by the hamartoma or a direct neurosecretory process of the hamartoma itself. Seizures are also another common clinical presentation in children with a hypothalamic hamartoma. MR imaging is typically used to identify and monitor the growth of a hypothalamic hamartoma during embryonic and fetal development. Research has shown a trend of congenital hamartomas forming in the utero within a period of 26 weeks. Because of the known association with other congenital anomalies of the central nervous system, hypothalamic hamartoma is thought to form as early as 4 weeks and may in fact be part of a developmental abnormality spectrum.&amp;lt;ref name=Booth&amp;gt;T. Booth, C. Timmons, K. Shapiro, N.K. Rollins, ‘Pre- and Postnatal MR Imaging of Hypothalamic Hamartomas Associated with Arachnoid Cysts’, Americal Jounral of Neuroradiology:2004, http://www.ajnr.org/content/25/7/1283.full&amp;lt;/ref&amp;gt;. Treatment options are currently limited to post-natal deliver of leuprolide acetate to the infant and in general it is relatively effective in managing and treating the condition. &lt;br /&gt;
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'''Recent Findings'''&lt;br /&gt;
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A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
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E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
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'''References'''&lt;br /&gt;
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Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
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[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
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==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Anterior pituitary &lt;br /&gt;
&lt;br /&gt;
[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''How far has the thyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of Thyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis&amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Week 16 - 18 is when fetal thyroid hormone synthesis occurs&lt;br /&gt;
** Prior to this, the fetus receives vital maternal thyroid hormones via the placenta&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Thyroid Hormone Action'''&lt;br /&gt;
The following table explains the ontogenic action of thyroid hormone on the developing fetus. Thyroid hormones are essential in brain and central nervous system development in the fetus. A lot of neurological disorders are associated with insufficient thyroid hormone synthesis:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Types !! Ontogenic Action&lt;br /&gt;
|-&lt;br /&gt;
| Thyroid Hormone || &lt;br /&gt;
* T3 -  triiodothyronine&lt;br /&gt;
* T4 - thyroxine&lt;br /&gt;
|| Brain development: &lt;br /&gt;
* Central Nervous System development and maturation &amp;lt;ref name =J Patel, K Landers, H Li, R H Mortimer and K Richard&amp;gt;J Patel, K Landers, H Li, R H Mortimer and K Richard, 2011, '''Thyroid hormones and fetal neurological development''', Journal of Endocrinology:209;1-8, http://joe.endocrinology-journals.org.wwwproxy0.library.unsw.edu.au/content/209/1/1.full.pdf+html&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Glial cell proliferation&lt;br /&gt;
*Neural myelination&lt;br /&gt;
*Axon and dendrite sprouting&lt;br /&gt;
*Synapse formation&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Header text !! Header text !! Header text&lt;br /&gt;
|-&lt;br /&gt;
| Example || Example || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone || Secreted by || Function || Image&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine. || [[File:Active parathyroid hormone assay cartoon.png|200px|thumb|This images shows an active parathyroid hormone and its chemical structure.]]&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Thymic aplasia'''&lt;br /&gt;
&lt;br /&gt;
Thymic aplasia is a condition that has a strong correlation to DiGeorge syndrome. This syndrome is a congenital birth defect which occurs when the fetus either inherits an abnormal chromosome 22 or has a mutation of the same chromosome.  In particularly, the mutation is a deletion of the genomic information packaged in the chromosomes and normally occurs when there isn’t proper recombination of chromosomal material during fertilisation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;4166528&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result of this deletion, the third and fourth pharyngeal pouches fail to develop in the twelfth gestational week, thereby leading to the absence or partial absence of the thymus and parathyroid glands. Other associated abnormalities with thymic aplasia as a result of the deletion of chromosome 22 genetic material are severe cardiac defects, low immunity, hypocalcaemia and facial abnormalities. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;5057550&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Statistics suggest that the thymic aplasia may occur in 1:4000 to 1:6395 of fetuses.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 10861201&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Treatment is normally difficult for fetuses that exhibit thymic aplasia, however calcium levels can be monitored and regulated and heart problems can be resolved though surgery. Immunity defects can be managed from controlling phosphorus levels in the fetus and protecting them from sources of infection.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;1454183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
*'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Congenital Adrenal Hyperplasia (CAH)'''&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more.[[File:Cushing's syndrome.jpg|150px|right|thumb|This image shows a  3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]] Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Cushing's Syndrome'''&lt;br /&gt;
&lt;br /&gt;
Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24656295&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*'''Placenta accreta'''&lt;br /&gt;
&lt;br /&gt;
[[File:Placenta accreta.jpg|150px|right|thumb|This image shows an area of profuse bleeding in the human placenta, with a region of placenta accreta indicated by the arrow]]&lt;br /&gt;
&lt;br /&gt;
Placenta accreta (PA )is a rare obstetric abnormality characterised by abnormal insertion of the placenta to the myometrium of the uterus. The 3 types of PA are classified based on the depth of invasion; placenta accreta (superficial- chorionic villi attach to myometrium rather than just decidua basalis), placenta increta (middle layer) or placenta perceta (deep) being the most dire with 1 in 7000 incidence. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has an incidence of 1 in 2500 deliveries and is associated with grand-scale haemorrhage and requires hysterectomy and blood transfusion. &amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The condition normally occurs in the lower segment of the uterus which is prone to bleeding  being poorly contractile and a site of angiogenesis. Prenatal diagnosis of PA is based on second and third trimester ulstrasound findings indicating; retroplacental zone loss, many lucanue in the vasculature and a very thin (&amp;lt;1mm) retroplacental thickness of the myometrium.&amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has a 40% likelihood in women aged over 35 who have had Caesarian section with placenta previa in their uterine scars. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
| &lt;br /&gt;
'''''*Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
|'''''*Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
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The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
{|&lt;br /&gt;
|-bgcolor=&amp;quot;F5FFFA&amp;quot;&lt;br /&gt;
|''''*Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24757681&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland. Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&lt;br /&gt;
|}&lt;br /&gt;
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=References=&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157103</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157103"/>
		<updated>2014-10-23T10:10:15Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid */&lt;/p&gt;
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&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
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==Introduction==&lt;br /&gt;
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==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
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[[File:Keith1902 fig167.jpg|200px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg|170px|thumb|right|Image 2: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
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The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.  The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth. &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || Pinealocytes || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
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'''Timeline''':&lt;br /&gt;
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[[File:Primary brain vesicles.jpg|150px|left|thumb|Image 3: Primary brain vesicles]]&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Week 6 embryonic development of CNS.jpg|150px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
[[File:Week 11 fetal development of CNS.jpg|150px|right|thumb|Image 5: Week 11 fetal development of CNS]]&lt;br /&gt;
&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). &lt;br /&gt;
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[[File:Fetal pineal gland 01.jpg|150px|thumb|right|Image 6: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
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&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
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*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)&lt;br /&gt;
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*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
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Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|150px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
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*'''Pineal hypoplasia'''&lt;br /&gt;
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Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
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===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
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[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
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*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
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[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
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[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
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The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
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[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
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'''Timeline'''&lt;br /&gt;
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'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
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* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
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* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
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'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
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* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
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* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
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* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
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* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
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[[File:Development of hypothalamus.jpg|560px|left|thumb|Image 3: Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]] &lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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*'''Congenital Hypothalamic Hamartoma'''&lt;br /&gt;
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A hypothalamic hamartoma arises from the region of the tuber cinereum and is commonly associated with isosexual precocious puberty, i.e. puberty that develops unusually early in infants. It involves the alteration of pathways that modulate gonadotropins and contain releasing hormones within the floor of the third ventricle. .&amp;lt;ref name=Booth&amp;gt;T. Booth, C. Timmons, K. Shapiro, N.K. Rollins, ‘Pre- and Postnatal MR Imaging of Hypothalamic Hamartomas Associated with Arachnoid Cysts’, Americal Jounral of Neuroradiology:2004, http://www.ajnr.org/content/25/7/1283.full&amp;lt;/ref&amp;gt; Precocious puberty may either result from a physical pertubation of inhibitory pathways by the hamartoma or a direct neurosecretory process of the hamartoma itself. Seizures are also another common clinical presentation in children with a hypothalamic hamartoma. MR imaging is typically used to identify and monitor the growth of a hypothalamic hamartoma during embryonic and fetal development. Research has shown a trend of congenital hamartomas forming in the utero within a period of 26 weeks. Because of the known association with other congenital anomalies of the central nervous system, hypothalamic hamartoma is thought to form as early as 4 weeks and may in fact be part of a developmental abnormality spectrum.&amp;lt;ref name=Booth&amp;gt;T. Booth, C. Timmons, K. Shapiro, N.K. Rollins, ‘Pre- and Postnatal MR Imaging of Hypothalamic Hamartomas Associated with Arachnoid Cysts’, Americal Jounral of Neuroradiology:2004, http://www.ajnr.org/content/25/7/1283.full&amp;lt;/ref&amp;gt;. Treatment options are currently limited to post-natal deliver of leuprolide acetate to the infant and in general it is relatively effective in managing and treating the condition. &lt;br /&gt;
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'''Recent Findings'''&lt;br /&gt;
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A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
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E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
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'''References'''&lt;br /&gt;
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Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
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[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
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==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Anterior pituitary &lt;br /&gt;
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[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
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By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
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* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
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'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
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The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''How far has the thyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of Thyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis&amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Week 16 - 18 is when fetal thyroid hormone synthesis occurs&lt;br /&gt;
** Prior to this, the fetus receives vital maternal thyroid hormones via the placenta&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Thyroid Hormone Action'''&lt;br /&gt;
The following table explains the ontogenic action of thyroid hormone on the developing fetus. Thyroid hormones are essential in brain and central nervous system development in the fetus. A lot of neurological disorders are associated with insufficient thyroid hormone synthesis:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Types !! Ontogenic Action&lt;br /&gt;
|-&lt;br /&gt;
| Thyroid Hormone || &lt;br /&gt;
* T3 -  triiodothyronine&lt;br /&gt;
* T4 - thyroxine&lt;br /&gt;
|| Brain development: &lt;br /&gt;
* Central Nervous System development and maturation &amp;lt;ref name =J Patel, K Landers, H Li, R H Mortimer and K Richard&amp;gt;J Patel, K Landers, H Li, R H Mortimer and K Richard, 2011, '''Thyroid hormones and fetal neurological development''', Journal of Endocrinology:209;1-8, http://joe.endocrinology-journals.org.wwwproxy0.library.unsw.edu.au/content/209/1/1.full.pdf+html&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Glial cell proliferation&lt;br /&gt;
*Neural myelination&lt;br /&gt;
*Axon and dendrite sprouting&lt;br /&gt;
*Synapse formation&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Header text !! Header text !! Header text&lt;br /&gt;
|-&lt;br /&gt;
| Example || Example || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone || Secreted by || Function || Image&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine. || [[File:Active parathyroid hormone assay cartoon.png|200px|thumb|This images shows an active parathyroid hormone and its chemical structure.]]&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Thymic aplasia'''&lt;br /&gt;
&lt;br /&gt;
Thymic aplasia is a condition that has a strong correlation to DiGeorge syndrome. This syndrome is a congenital birth defect which occurs when the fetus either inherits an abnormal chromosome 22 or has a mutation of the same chromosome.  In particularly, the mutation is a deletion of the genomic information packaged in the chromosomes and normally occurs when there isn’t proper recombination of chromosomal material during fertilisation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;4166528&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result of this deletion, the third and fourth pharyngeal pouches fail to develop in the twelfth gestational week, thereby leading to the absence or partial absence of the thymus and parathyroid glands. Other associated abnormalities with thymic aplasia as a result of the deletion of chromosome 22 genetic material are severe cardiac defects, low immunity, hypocalcaemia and facial abnormalities. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;5057550&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Statistics suggest that the thymic aplasia may occur in 1:4000 to 1:6395 of fetuses.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 10861201&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Treatment is normally difficult for fetuses that exhibit thymic aplasia, however calcium levels can be monitored and regulated and heart problems can be resolved though surgery. Immunity defects can be managed from controlling phosphorus levels in the fetus and protecting them from sources of infection.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;1454183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
*'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Congenital Adrenal Hyperplasia (CAH)'''&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more.[[File:Cushing's syndrome.jpg|150px|right|thumb|This image shows a  3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]] Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Cushing's Syndrome'''&lt;br /&gt;
&lt;br /&gt;
Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24656295&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*'''Placenta accreta'''&lt;br /&gt;
&lt;br /&gt;
[[File:Placenta accreta.jpg|150px|right|thumb|This image shows an area of profuse bleeding in the human placenta, with a region of placenta accreta indicated by the arrow]]&lt;br /&gt;
&lt;br /&gt;
Placenta accreta (PA )is a rare obstetric abnormality characterised by abnormal insertion of the placenta to the myometrium of the uterus. The 3 types of PA are classified based on the depth of invasion; placenta accreta (superficial- chorionic villi attach to myometrium rather than just decidua basalis), placenta increta (middle layer) or placenta perceta (deep) being the most dire with 1 in 7000 incidence. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has an incidence of 1 in 2500 deliveries and is associated with grand-scale haemorrhage and requires hysterectomy and blood transfusion. &amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The condition normally occurs in the lower segment of the uterus which is prone to bleeding  being poorly contractile and a site of angiogenesis. Prenatal diagnosis of PA is based on second and third trimester ulstrasound findings indicating; retroplacental zone loss, many lucanue in the vasculature and a very thin (&amp;lt;1mm) retroplacental thickness of the myometrium.&amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has a 40% likelihood in women aged over 35 who have had Caesarian section with placenta previa in their uterine scars. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland. Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24757681&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157088</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157088"/>
		<updated>2014-10-23T10:02:53Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
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[[File:Keith1902 fig167.jpg|200px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg|170px|thumb|right|Image 2: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
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The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.  The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth. &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
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{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || Pinealocytes || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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'''Timeline''':&lt;br /&gt;
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[[File:Primary brain vesicles.jpg|150px|left|thumb|Image 3: Primary brain vesicles]]&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Week 6 embryonic development of CNS.jpg|150px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
[[File:Week 11 fetal development of CNS.jpg|150px|right|thumb|Image 5: Week 11 fetal development of CNS]]&lt;br /&gt;
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*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). &lt;br /&gt;
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[[File:Fetal pineal gland 01.jpg|150px|thumb|right|Image 6: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
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&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
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*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
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*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)&lt;br /&gt;
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*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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* '''Pineal tumors'''&lt;br /&gt;
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Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|150px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
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*'''Pineal hypoplasia'''&lt;br /&gt;
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Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Hypothalamus==&lt;br /&gt;
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===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
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[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
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*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
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{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
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! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
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| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
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[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
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[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
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The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
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[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
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'''Timeline'''&lt;br /&gt;
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'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
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* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
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* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
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'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
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* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
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* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
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* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
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* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
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[[File:Development of hypothalamus.jpg|340px|thumb|Image 3: Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]] &lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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*Hypothalamus&lt;br /&gt;
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'''Recent Findings'''&lt;br /&gt;
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A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
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E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
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'''References'''&lt;br /&gt;
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Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
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[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
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==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Anterior pituitary &lt;br /&gt;
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[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
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By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
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* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
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'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
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The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
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! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
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| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
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'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
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The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
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! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
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| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
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==Thyroid==&lt;br /&gt;
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===Fetal development===&lt;br /&gt;
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The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
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The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
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Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
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'''How far has the thyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of Thyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis&amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Week 16 - 18 is when fetal thyroid hormone synthesis occurs&lt;br /&gt;
** Prior to this, the fetus receives vital maternal thyroid hormones via the placenta&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Thyroid Hormone Action'''&lt;br /&gt;
The following table explains the ontogenic action of thyroid hormone on the developing fetus. Thyroid hormones are essential in brain and central nervous system development in the fetus. A lot of neurological disorders are associated with insufficient thyroid hormone synthesis:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Types !! Ontogenic Action&lt;br /&gt;
|-&lt;br /&gt;
| Thyroid Hormone || &lt;br /&gt;
* T3 -  triiodothyronine&lt;br /&gt;
* T4 - thyroxine || Brain development: &lt;br /&gt;
* Central Nervous System development and maturation &amp;lt;ref name =J Patel, K Landers, H Li, R H Mortimer and K Richard&amp;gt;J Patel, K Landers, H Li, R H Mortimer and K Richard, 2011, '''Thyroid hormones and fetal neurological development''', Journal of Endocrinology:209;1-8, http://joe.endocrinology-journals.org.wwwproxy0.library.unsw.edu.au/content/209/1/1.full.pdf+html&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Glial cell proliferation&lt;br /&gt;
*Neural myelination&lt;br /&gt;
*Axon and dendrite sprouting&lt;br /&gt;
*Synapse formation&lt;br /&gt;
|-&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone || Secreted by || Function || Image&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine. || [[File:Active parathyroid hormone assay cartoon.png|200px|thumb|This images shows an active parathyroid hormone and its chemical structure.]]&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Thymic aplasia'''&lt;br /&gt;
&lt;br /&gt;
Thymic aplasia is a condition that has a strong correlation to DiGeorge syndrome. This syndrome is a congenital birth defect which occurs when the fetus either inherits an abnormal chromosome 22 or has a mutation of the same chromosome.  In particularly, the mutation is a deletion of the genomic information packaged in the chromosomes and normally occurs when there isn’t proper recombination of chromosomal material during fertilisation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;4166528&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result of this deletion, the third and fourth pharyngeal pouches fail to develop in the twelfth gestational week, thereby leading to the absence or partial absence of the thymus and parathyroid glands. Other associated abnormalities with thymic aplasia as a result of the deletion of chromosome 22 genetic material are severe cardiac defects, low immunity, hypocalcaemia and facial abnormalities. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;5057550&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Statistics suggest that the thymic aplasia may occur in 1:4000 to 1:6395 of fetuses.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 10861201&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Treatment is normally difficult for fetuses that exhibit thymic aplasia, however calcium levels can be monitored and regulated and heart problems can be resolved though surgery. Immunity defects can be managed from controlling phosphorus levels in the fetus and protecting them from sources of infection.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;1454183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
*'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Congenital Adrenal Hyperplasia (CAH)'''&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more.[[File:Cushing's syndrome.jpg|150px|right|thumb|This image shows a  3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]] Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Cushing's Syndrome'''&lt;br /&gt;
&lt;br /&gt;
Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24656295&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*'''Placenta accreta'''&lt;br /&gt;
&lt;br /&gt;
[[File:Placenta accreta.jpg|150px|right|thumb|This image shows an area of profuse bleeding in the human placenta, with a region of placenta accreta indicated by the arrow]]&lt;br /&gt;
&lt;br /&gt;
Placenta accreta (PA )is a rare obstetric abnormality characterised by abnormal insertion of the placenta to the myometrium of the uterus. The 3 types of PA are classified based on the depth of invasion; placenta accreta (superficial- chorionic villi attach to myometrium rather than just decidua basalis), placenta increta (middle layer) or placenta perceta (deep) being the most dire with 1 in 7000 incidence. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has an incidence of 1 in 2500 deliveries and is associated with grand-scale haemorrhage and requires hysterectomy and blood transfusion. &amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The condition normally occurs in the lower segment of the uterus which is prone to bleeding  being poorly contractile and a site of angiogenesis. Prenatal diagnosis of PA is based on second and third trimester ulstrasound findings indicating; retroplacental zone loss, many lucanue in the vasculature and a very thin (&amp;lt;1mm) retroplacental thickness of the myometrium.&amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has a 40% likelihood in women aged over 35 who have had Caesarian section with placenta previa in their uterine scars. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland. Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24757681&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157067</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157067"/>
		<updated>2014-10-23T09:54:11Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|200px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg|170px|thumb|right|Image 2: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.  The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || Pinealocytes || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Primary brain vesicles.jpg|150px|left|thumb|Image 3: Primary brain vesicles]]&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Week 6 embryonic development of CNS.jpg|150px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
[[File:Week 11 fetal development of CNS.jpg|150px|right|thumb|Image 5: Week 11 fetal development of CNS]]&lt;br /&gt;
&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). &lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|150px|thumb|right|Image 6: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)&lt;br /&gt;
&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&lt;br /&gt;
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&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|150px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
&lt;br /&gt;
* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
&lt;br /&gt;
[[File:Development of hypothalamus.jpg|340px|thumb|Image 3: Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]] &lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Hypothalamus&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Anterior pituitary &lt;br /&gt;
&lt;br /&gt;
[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''How far has the thyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of Thyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis&amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Week 16 - 18 is when fetal thyroid hormone synthesis occurs&lt;br /&gt;
** Prior to this, the fetus receives vital maternal thyroid hormones via the placenta&lt;br /&gt;
&lt;br /&gt;
'''Thyroid Hormone Action'''&lt;br /&gt;
The following table explains the ontogenic action of thyroid hormone on the developing fetus. Thyroid hormones are essential in brain and central nervous system development in the fetus. A lot of neurological disorders are associated with insufficient thyroid hormone synthesis:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Types !! Ontogenic Action&lt;br /&gt;
|-&lt;br /&gt;
| Thyroid Hormone || &lt;br /&gt;
* T3 -  triiodothyronine&lt;br /&gt;
* T4 - thyroxine || Brain development: &lt;br /&gt;
* Central Nervous System development and maturation &amp;lt;ref name =J Patel, K Landers, H Li, R H Mortimer and K Richard&amp;gt;J Patel, K Landers, H Li, R H Mortimer and K Richard, 2011, '''Thyroid hormones and fetal neurological development''', Journal of Endocrinology:209;1-8, http://joe.endocrinology-journals.org.wwwproxy0.library.unsw.edu.au/content/209/1/1.full.pdf+html&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
**Glial cell proliferation&lt;br /&gt;
**Neural myelination&lt;br /&gt;
**Axon and dendrite sprouting&lt;br /&gt;
**Synapse formation&lt;br /&gt;
|-&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone || Secreted by || Function || Image&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine. || [[File:Active parathyroid hormone assay cartoon.png|200px|thumb|This images shows an active parathyroid hormone and its chemical structure.]]&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Thymic aplasia'''&lt;br /&gt;
&lt;br /&gt;
Thymic aplasia is a condition that has a strong correlation to DiGeorge syndrome. This syndrome is a congenital birth defect which occurs when the fetus either inherits an abnormal chromosome 22 or has a mutation of the same chromosome.  In particularly, the mutation is a deletion of the genomic information packaged in the chromosomes and normally occurs when there isn’t proper recombination of chromosomal material during fertilisation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;4166528&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result of this deletion, the third and fourth pharyngeal pouches fail to develop in the twelfth gestational week, thereby leading to the absence or partial absence of the thymus and parathyroid glands. Other associated abnormalities with thymic aplasia as a result of the deletion of chromosome 22 genetic material are severe cardiac defects, low immunity, hypocalcaemia and facial abnormalities. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;5057550&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Statistics suggest that the thymic aplasia may occur in 1:4000 to 1:6395 of fetuses.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 10861201&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Treatment is normally difficult for fetuses that exhibit thymic aplasia, however calcium levels can be monitored and regulated and heart problems can be resolved though surgery. Immunity defects can be managed from controlling phosphorus levels in the fetus and protecting them from sources of infection.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;1454183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
*'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Congenital Adrenal Hyperplasia (CAH)'''&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more.[[File:Cushing's syndrome.jpg|150px|right|thumb|This image shows a  3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]] Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Cushing's Syndrome'''&lt;br /&gt;
&lt;br /&gt;
Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24656295&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*'''Placenta accreta'''&lt;br /&gt;
&lt;br /&gt;
[[File:Placenta accreta.jpg|150px|right|thumb|This image shows an area of profuse bleeding in the human placenta, with a region of placenta accreta indicated by the arrow]]&lt;br /&gt;
&lt;br /&gt;
Placenta accreta (PA )is a rare obstetric abnormality characterised by abnormal insertion of the placenta to the myometrium of the uterus. The 3 types of PA are classified based on the depth of invasion; placenta accreta (superficial- chorionic villi attach to myometrium rather than just decidua basalis), placenta increta (middle layer) or placenta perceta (deep) being the most dire with 1 in 7000 incidence. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has an incidence of 1 in 2500 deliveries and is associated with grand-scale haemorrhage and requires hysterectomy and blood transfusion. &amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The condition normally occurs in the lower segment of the uterus which is prone to bleeding  being poorly contractile and a site of angiogenesis. Prenatal diagnosis of PA is based on second and third trimester ulstrasound findings indicating; retroplacental zone loss, many lucanue in the vasculature and a very thin (&amp;lt;1mm) retroplacental thickness of the myometrium.&amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has a 40% likelihood in women aged over 35 who have had Caesarian section with placenta previa in their uterine scars. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland. Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24757681&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157058</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=157058"/>
		<updated>2014-10-23T09:49:38Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|200px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]] [[File:Pineal-body.jpg|170px|thumb|right|Image 2: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin. The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon reproductive hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.  The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;. &lt;br /&gt;
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Melatonin plays an important role during fetal development. Both pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammalian fetus, intrinsic circadian rhythms are already established prior to birth. &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || Pinealocytes || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
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&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Primary brain vesicles.jpg|150px|left|thumb|Image 3: Primary brain vesicles]]&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Week 6 embryonic development of CNS.jpg|150px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
[[File:Week 11 fetal development of CNS.jpg|150px|right|thumb|Image 5: Week 11 fetal development of CNS]]&lt;br /&gt;
&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). &lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|150px|thumb|right|Image 6: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis (shown in Image 5)&lt;br /&gt;
&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|150px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
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&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
&lt;br /&gt;
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*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
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[[File: diagram &lt;br /&gt;
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''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
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[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
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[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
&lt;br /&gt;
* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
&lt;br /&gt;
[[File:Development of hypothalamus.jpg|340px|thumb|Image 3: Stages of hypothalamus development: a) Week 6 b) Week 9 c) Week 18 d) Weeks 19-28]] &lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Hypothalamus&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Anterior pituitary &lt;br /&gt;
&lt;br /&gt;
[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''How far has the thyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of Thyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis&amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Week 16 - 18 is when fetal thyroid hormone synthesis occurs&lt;br /&gt;
** Prior to this, the fetus receives vital maternal thyroid hormones via the placenta&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The following table explains the ontogenic action of thyroid hormone on the developing fetus. Thyroid hormones are essential in brain and central nervous system development in the fetus. A lot of neurological disorders are associated with insufficient thyroid hormone synthesis:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Types !! Ontogenic Action&lt;br /&gt;
|-&lt;br /&gt;
| Thyroid Hormone || &lt;br /&gt;
* T3 -  triiodothyronine&lt;br /&gt;
* T4 - thyroxine || Brain development: &lt;br /&gt;
* Central Nervous System development and maturation &amp;lt;ref name =J Patel, K Landers, H Li, R H Mortimer and K Richard&amp;gt;J Patel, K Landers, H Li, R H Mortimer and K Richard, 2011, '''Thyroid hormones and fetal neurological development''', Journal of Endocrinology:209;1-8, http://joe.endocrinology-journals.org.wwwproxy0.library.unsw.edu.au/content/209/1/1.full.pdf+html&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
**Glial cell proliferation&lt;br /&gt;
**Neural myelination&lt;br /&gt;
**Axon and dendrite sprouting&lt;br /&gt;
**Synapse formation&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone || Secreted by || Function || Image&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine. || [[File:Active parathyroid hormone assay cartoon.png|200px|thumb|This images shows an active parathyroid hormone and its chemical structure.]]&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Thymic aplasia'''&lt;br /&gt;
&lt;br /&gt;
Thymic aplasia is a condition that has a strong correlation to DiGeorge syndrome. This syndrome is a congenital birth defect which occurs when the fetus either inherits an abnormal chromosome 22 or has a mutation of the same chromosome.  In particularly, the mutation is a deletion of the genomic information packaged in the chromosomes and normally occurs when there isn’t proper recombination of chromosomal material during fertilisation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;4166528&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result of this deletion, the third and fourth pharyngeal pouches fail to develop in the twelfth gestational week, thereby leading to the absence or partial absence of the thymus and parathyroid glands. Other associated abnormalities with thymic aplasia as a result of the deletion of chromosome 22 genetic material are severe cardiac defects, low immunity, hypocalcaemia and facial abnormalities. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;5057550&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Statistics suggest that the thymic aplasia may occur in 1:4000 to 1:6395 of fetuses.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 10861201&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Treatment is normally difficult for fetuses that exhibit thymic aplasia, however calcium levels can be monitored and regulated and heart problems can be resolved though surgery. Immunity defects can be managed from controlling phosphorus levels in the fetus and protecting them from sources of infection.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;1454183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
*'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*'''Congenital Adrenal Hyperplasia (CAH)'''&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more.[[File:Cushing's syndrome.jpg|150px|right|thumb|This image shows a  3-month old child with classic signs of Cushing’s syndrome; central obesity, chubby cheeks and moon facies]] Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Cushing's Syndrome'''&lt;br /&gt;
&lt;br /&gt;
Cushing’s Syndrome (CS) is a metabolic disorder characterised by abnormally high production of endogenous cortisol or exogenous levels of corticosteroids, which disrupts the metabolism of macromolecules such as lipids and carbohydrates. It is most common in obese adults aged 20-50 and the most common cause is the therapeutic administration of exogenous ACTH &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24656295&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Cushing’s Syndrome’s two forms are either ACTH-dependent CS (80-85% of patients) or ACTH independent. The etiology of the dependent form is adrenal gland hyperplasia and excessive ACTH secretion by adenomas in the pituitary, however other causes include; small cell lung carcinoma ACTH production ectopically, or medullary thyroid carcinomas. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The independent form is however caused by neoplastic growths in the adrenal gland such as carcinomas, adenomas and macronodular hyperplasia. Clinical manifestations of this disorder include; moon facies, cataracts, hyperglycaemia, abnormal fat distribution, poor wounding of the skin, obesity in the central body and muscle wasting in 60% of patients. &amp;lt;ref name= PMID24365350&amp;gt;&amp;lt;pubmed&amp;gt;24365350&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*'''Placenta accreta'''&lt;br /&gt;
&lt;br /&gt;
[[File:Placenta accreta.jpg|150px|right|thumb|This image shows an area of profuse bleeding in the human placenta, with a region of placenta accreta indicated by the arrow]]&lt;br /&gt;
&lt;br /&gt;
Placenta accreta (PA )is a rare obstetric abnormality characterised by abnormal insertion of the placenta to the myometrium of the uterus. The 3 types of PA are classified based on the depth of invasion; placenta accreta (superficial- chorionic villi attach to myometrium rather than just decidua basalis), placenta increta (middle layer) or placenta perceta (deep) being the most dire with 1 in 7000 incidence. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has an incidence of 1 in 2500 deliveries and is associated with grand-scale haemorrhage and requires hysterectomy and blood transfusion. &amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The condition normally occurs in the lower segment of the uterus which is prone to bleeding  being poorly contractile and a site of angiogenesis. Prenatal diagnosis of PA is based on second and third trimester ulstrasound findings indicating; retroplacental zone loss, many lucanue in the vasculature and a very thin (&amp;lt;1mm) retroplacental thickness of the myometrium.&amp;lt;ref name= PMID21280984&amp;gt;&amp;lt;pubmed&amp;gt;21280984&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; PA has a 40% likelihood in women aged over 35 who have had Caesarian section with placenta previa in their uterine scars. &amp;lt;ref name= PMID23127895&amp;gt;&amp;lt;pubmed&amp;gt;23127895&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland. Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24757681&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156554</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156554"/>
		<updated>2014-10-23T04:03:05Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|250px|thumb|right|Image 2: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin.&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;[[File:Primary brain vesicles.jpg|250px|left|thumb|Image 3: Primary brain vesicles]]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). [[File:Week 6 embryonic development of CNS.jpg|250px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb|right|Image 6: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|180px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
&lt;br /&gt;
* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
* Anterior pituitary &lt;br /&gt;
&lt;br /&gt;
[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Secreted by ||Function&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Congenital Adrenal Hyperplasia (CAH)&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more. Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt; Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156536</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156536"/>
		<updated>2014-10-23T03:54:53Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin.&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|250px|thumb|right|Image 2: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;[[File:Primary brain vesicles.jpg|250px|left|thumb|Image 3: Primary brain vesicles]]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). [[File:Week 6 embryonic development of CNS.jpg|250px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb|right|Image 6: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|180px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
&lt;br /&gt;
* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Secreted by ||Function&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Congenital Adrenal Hyperplasia (CAH)&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more. Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt; Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156527</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156527"/>
		<updated>2014-10-23T03:51:53Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin.&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|250px|thumb|right|Image 2: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle (Image 3).&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;[[File:Primary brain vesicles.jpg|250px|left|thumb|Image 3: Primary brain vesicles]]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement and an evagination of the pineal gland is visible (shown in image 4). [[File:Week 6 embryonic development of CNS.jpg|250px|left|thumb|Image 4: Week 6 embryonic development of CNS]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb|right|Image 6: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|180px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
&lt;br /&gt;
* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
[[File:Anterior Pituitary Hormones.jpg|300px|right|thumb|Timeline of anterior pituitary hormone expression and synthesis]]&lt;br /&gt;
&lt;br /&gt;
'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Secreted by ||Function&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Congenital Adrenal Hyperplasia (CAH)&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more. Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
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===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt; Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
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		<updated>2014-10-23T03:49:38Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
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&lt;div&gt;This student-drawn diagram is adapted from a diagram found in the research report Gonadotrope and thyrotrope development in the human and mouse anterior pituitary gland published in the Developmental Biology journal. It illustrates the fetal timeline of anterior pituitary hormone precursor cells and synthesis. It shows that by week 14 there are Gonadotroph Secreting Unit (GSC) precursor cells for Luteinizing hormone (LH), follicle-stimulating hormone (FSH) and other GSU production which proliferate and are not fully differentiated. By week 19 the LH, FSH and thyroid-stimulating hormone (TSH) secreting cells exist independently and do not proliferate. The diagram also shows how these cells migrate within the anterior pituitary gland in a rostro-caudal fashion. &amp;lt;ref name =Caroline Pope, Judy R. McNeilly, Shiona Coutts, Mike Millar, Richard A. Anderson, Alan S. McNeilly&amp;gt;Caroline Pope, Judy R. McNeilly, Shiona Coutts, Mike Millar, Richard A. Anderson, Alan S. McNeilly, 2006, &amp;quot;'Gonadotrope and thyrotrope development in the human and mouse anterior pituitary gland&amp;quot;', Developmental Biology: 297(1); 172-181, http://www.sciencedirect.com/science/article/pii/S0012160606007755&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
http://www.sciencedirect.com/science/article/pii/S0012160606007755&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=File:Anterior_Pituitary_Hormones.jpg&amp;diff=156503</id>
		<title>File:Anterior Pituitary Hormones.jpg</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=File:Anterior_Pituitary_Hormones.jpg&amp;diff=156503"/>
		<updated>2014-10-23T03:48:52Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: This student-drawn diagram is adapted from a diagram found in the research report Gonadotrope and thyrotrope development in the human and mouse anterior pituitary gland published in the Developmental Biology journal. It illustrates the fetal timeline o...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;This student-drawn diagram is adapted from a diagram found in the research report Gonadotrope and thyrotrope development in the human and mouse anterior pituitary gland published in the Developmental Biology journal. It illustrates the fetal timeline of anterior pituitary hormone precursor cells and synthesis. It shows that by week 14 there are Gonadotroph Secreting Unit (GSC) precursor cells for Luteinizing hormone (LH), follicle-stimulating hormone (FSH) and other GSU production which proliferate and are not fully differentiated. By week 19 the LH, FSH and thyroid-stimulating hormone (TSH) secreting cells exist independently and do not proliferate. The diagram also shows how these cells migrate within the anterior pituitary gland in a rostro-caudal fashion. &amp;lt;ref name =Caroline Pope, Judy R. McNeilly, Shiona Coutts, Mike Millar, Richard A. Anderson, Alan S. McNeilly&amp;gt;Caroline Pope, Judy R. McNeilly, Shiona Coutts, Mike Millar, Richard A. Anderson, Alan S. McNeilly, 2006, &amp;quot;'Gonadotrope and thyrotrope development in the human and mouse anterior pituitary gland&amp;quot;', Developmental Biology: 297(1); 172-181, http://www.sciencedirect.com/science/article/pii/S0012160606007755&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
http://www.sciencedirect.com/science/article/pii/S0012160606007755&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156458</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156458"/>
		<updated>2014-10-23T03:33:59Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin.&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|250px|thumb|right|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb|right|Image 6: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|180px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
&lt;br /&gt;
* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 10 - Growth Hormone and ACTH detectable &lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
'''Anterior Pituitary - Adenohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
'''Posterior Pituitary - Neurohypophysis'''&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Secreted by ||Function&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Congenital Adrenal Hyperplasia (CAH)&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more. Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt; Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156368</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156368"/>
		<updated>2014-10-23T02:56:35Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin.&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|250px|thumb|right|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb|right|Image 6: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|180px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
&lt;br /&gt;
* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By week 8 of embryological development, the pituitary gland is fully formed and begins functioning as a control centre for release of hormones that are vital for subsequent organ development. &lt;br /&gt;
&lt;br /&gt;
* Week 21 - Vasopressin hormone synthesis established &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://www.sciencedirect.com/science/article/pii/S030100820900046X#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Cardiomyogenesis&lt;br /&gt;
* Protective action of fetal neurons during brain development &lt;br /&gt;
* Neuronal development and plasticity &amp;lt;ref name =Yuzo Murata, Ming-Zi Li, Sadahiko Masuko&amp;gt;Yuzo Murata, Ming-Zi Li, Sadahiko Masuko, 2011, '''Developmental expression of oxytocin receptors in the neonatal medulla&lt;br /&gt;
oblongata and pons''', Neuroscience Letters; 502 (2011), pp157-161, http://www.sciencedirect.com/science/article/pii/S0304394011010949#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://www.sciencedirect.com/science/article/pii/016701159390207O#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Secreted by ||Function&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Congenital Adrenal Hyperplasia (CAH)&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more. Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt; Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156308</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=156308"/>
		<updated>2014-10-23T02:26:28Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb|right| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin.&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and fetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|250px|thumb|right|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&amp;lt;ref name=Bruce&amp;gt;J.N. Bruce, E.M. Housepian, ‘Pineal Tumors’, Medscape:2013, http://emedicine.medscape.com/article/249945-overview&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb|right|Image 6: Shows the location of the pineal gland in the adult brain.]]&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
 &lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus.&amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|180px|thumb|right|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life.&amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process&amp;lt;ref name= PMID7643957&amp;gt;&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally&amp;lt;ref name= PMID11954031&amp;gt;&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.&lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode (shown in pink in Image 3.a) forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold.&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch (shown in Image 3.b).&lt;br /&gt;
&lt;br /&gt;
* Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch with lumean (shown in Image 3.c). &lt;br /&gt;
&lt;br /&gt;
* Weeks 19-27 Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus (shown in Image 3.d)&amp;lt;ref name=Rizzoti&amp;gt;K. Rizzoti, R. Lovell-Badge, ‘Regenerative Medicine: organ recital in a dish’, Nature:2011, http://www.nature.com/nature/journal/v480/n7375/full/480044a.html&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
=== Fetal development ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || No function in fetal development. All postnatal action.&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|-&lt;br /&gt;
| Example || Example || Example || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://ac.els-cdn.com/S030100820900046X/1-s2.0-S030100820900046X-main.pdf?_tid=42bc9e94-59ac-11e4-acd8-00000aacb361&amp;amp;acdnat=1413955891_77158b95d9eb4f3e4942d81440455daa&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Neurophysin || Example || Hypothalamic paraventricular and supraoptic nuclei  || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || Cardiomyogenesis&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || &lt;br /&gt;
* Regulates fetal renal function&lt;br /&gt;
* Regulates amniotic fluid content and concentration &lt;br /&gt;
* Regulates blood pressure, heart rate, cardiac output and placental blood flow &amp;lt;ref name =M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher &amp;gt;M. Gore Ervin, Linda K. Kullama, Michael G. Ross, Rosemary D. Leake and Delbert A. Fisher , 1993, '''Vasopressin receptors and effects during fetal development''', Regulatory Peptides; 45, pp203-208, http://ac.els-cdn.com/016701159390207O/1-s2.0-016701159390207O-main.pdf?_tid=eb365656-5a5a-11e4-8006-00000aacb35f&amp;amp;acdnat=1414030906_06a28e810ea051ec2c0d03e203e6368d&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |420px|thumb|right|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the Parathyroid gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Secreted by ||Function&lt;br /&gt;
|-&lt;br /&gt;
| Parathyroid hormone || Chief cells || Regulates calcium levels in the blood by bone resorption releasing calcium in the blood when calcium levels are low. It also increases the ability to absorb calcium from food sources as well as aid the kidney in retaining calcium that would otherwise be lost in the urine.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Fetal hyperparathyroidism'''&lt;br /&gt;
&lt;br /&gt;
Fetal hyperparathyroidism is a condition that is caused when an excess of parathyroid hormone (PTH) is present the bloodstream.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 1745971&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This may be due to an overstimulated maternal parathyroid gland out of all the four which transfers the over accumulated PTH to the fetus. Normal fetal development requires 25–30 gms of calcium for bone mineralization and around 80% of this calcium accretion is observed in the third trimester of pregnancy. However the calcium gradient of 1.0:1.4 is no longer maintained when there is hyperparathyroidism present.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 12140371&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Instead the gradient is elevated causing fetal parathyroid gland suppression thereby leading to Hypocalcemia. Calcium mobilisation then becomes difficult and hence fetal tetany may occur followed by miscarriage.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25327435&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; In the event that the fetus survives, postnatal problems such as the baby having weak bones will be likely and would require calcium treatment throughout most of their lives.&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
[[File:Thymic Epithelial Cell Development and Function.png|300px|thumb|right|This image shows thymic epithelial cell development and function]]&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the thymus gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Thymosin || Transforms white blood cells (lymphocytes) that pass through the thymus gland into T cells.&lt;br /&gt;
|-&lt;br /&gt;
| Thymopoietin hormones || Belongs to the polypeptide hormone family and is secreted by thymic epithelial cells. These cause differentiation of precursor lymphocytes into thymocytes.&lt;br /&gt;
|-&lt;br /&gt;
| Thymic humoral factors || Increase the number of T-cells which enhances cell-mediated immunity.&lt;br /&gt;
|-&lt;br /&gt;
| Thymostimulin || Stimulates T cell proliferation and differentiation&lt;br /&gt;
|-&lt;br /&gt;
| Factor thymic serum || Involved in T-cell differentiation.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Development of the pancreas during fetal development.jpg|250px|thumb|right|This images shows normal pancreatic development of the fetus.]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|350px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the pancreas:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
'''Annular Pancreas'''&lt;br /&gt;
[[File:Annular pancreas.jpg|200px|thumb|right|This image shows annular pancreas where a ring of the pancreatic tissue encircles the growing duodenum.]]&lt;br /&gt;
Annular pancreas is a rare abnormality that can occur during fetal development in which a ring of the pancreatic tissue encircles the growing duodenum.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25124266&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; It occurs in 1 out of 7000 birth and is commonly associated with other abnormalities such as esophageal atresia and malrotation of the midgut. It is assumed that annular pancreas occurs when the tip of right ventral bud sticks to the duodenal wall which then forms a ring from the continuous stretching of the wall during rotation.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 25165593&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This part of the pancreas can constrict the duodenum thereby restricting the flow of food to the intestines of the gastrointestinal tract.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24890427&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Furthermore, annular pancreas is divided into two forms. Complete annular pancreas is when the pancreatic parenchyma wraps around the 2nd part of the duodenum completely whereas in incomplete annular pancreas, the tissue only surrounds the duodenum partially.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt; 24741860&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;Treatment for annular pancreas mainly involves surgery to bypass the constricted portion of the duodenum.&lt;br /&gt;
&lt;br /&gt;
'''Gestational diabetes mellitus'''&lt;br /&gt;
&lt;br /&gt;
Gestational diabetes mellitus (GDM) is a disorder in which women without any history of diabetes show elevated blood glucose levels during pregnancy normally around the third trimester. It is caused when insulin receptors fail to respond correctly due to interference from signalling molecules related to pregnancy such as the interaction between human placental lactogen, prolactin and estradiol with the insulin receptors.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;2141655&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; As a result, high blood glucose levels are observed. Patients with GDM have high levels of insulin resistance with increased β-cells production of the pancreas since the high levels of blood glucose are not interacting with the abnormal insulin receptors. Glucose is known to diffuse through the placenta via GLUT1 carrier situated in the syncytiotrophoblast of both the microvillus and basal membranes. With GDM, the number of GLUT1 molecules increase and hence placing high levels of glucose to the fetus since insulin itself cannot diffuse across the placenta and counteract this extremity.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25333246&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  This mechanism is known to lead to excessive growth at birth with a low glucose environment as it declines and high insulin production overall leading to hypoglycaemia.&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25315294&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;It can also lead to jaundice and seizures in the new born with mothers having high susceptibility to type 2 diabetes mellitus. GDM can be controlled by monitoring blood sugar levels and controlling levels of glucose and insulin through pharmaceutical drugs.&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &amp;lt;ref name= PMID7011178&amp;gt;&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table of hormones produced by the adrenal gland:''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
*Congenital Adrenal Hyperplasia (CAH)&lt;br /&gt;
&lt;br /&gt;
Congenital Adrenal Hyperplasia (CAH) is the collective term for several autosomal recessive endocrine disorders caused by impaired adrenal steroidogenesis due to mutated steroidogenic enzymes. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;.These mutations inhibit proper synthesis of cortisol from cholesterol, which in turn leads to excess adrenal growth and hyperplasia due to adrenocorticotropic hormone (ACTH) hypersecretion by the pituitary gland. The most commonly affected enzyme (90% of cases) is a 21-hydroxylase deficiency (21-OHD) which clinically presents as cortisol and aldosterone production deficiency. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;10748766&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;  CAH has both a classic (severe) and non-classic (mild) forms with the classic form affecting 1 in 10 000 and non-classic form affecting many more. Females affected by the classic form undergo pre-natal virilisation and have genital ambiguity at birth, whereas virilisation does not occur in the mild form. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;15838095&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Males tend to appear asymptomatic but can exhibit oligozoospermia. &amp;lt;ref name= PMID25227725&amp;gt;&amp;lt;pubmed&amp;gt;25227725&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Ovary==&lt;br /&gt;
&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells &lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium &lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Testis==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemoral nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone). &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28- Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. &amp;lt;ref name= PMID1260417&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12. &amp;lt;ref name= PMID10510117&amp;gt;&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the fallopian tubes and uterus in the developing male. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. &amp;lt;ref name= PMID1769902&amp;gt;&amp;lt;pubmed&amp;gt;1260417&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct.&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
===Fetal development===&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
&lt;br /&gt;
[[File:Placenta schematic.jpg|300px|right|thumb|This schematic shows the different components of the mature human placenta]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
===Abnormalities===&lt;br /&gt;
&lt;br /&gt;
* '''Pre-eclampsia'''&lt;br /&gt;
Pre-eclampsia is a common abnormality of human pregnancy characterised by significant proteinuria (presence of protein in the urine) and systemic hypertension. There occurs significantly reduced uteroplacental blood flow due to; angiogenic and antiangiogenic factors, hypoxia and inflammation. &amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;25071761&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. Its incidence is about 2-8% of pregnancies, usually in women after gestational week 20 and it contributes to high maternal morbidity rates worldwide, with 50 000 deaths each year. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt; There is evidence that the cause of pre-eclampsia is a combination of an abnormal inflammatory response cascade, damage to endothelial cells and impaired immune function of the maternal placenta. Soluble factors are released into the maternal placenta from the ischemic placenta, leading to significant endothelial dysfunction. It has also been suggested that abnormal differentiation and invasion of cytotrophoblasts into the uterus have an aetiological role, as does failure of arterial remodelling in the uterus. &amp;lt;ref name= Evain-Brion&amp;gt;&amp;lt;Danielle Evain-Brion, Malassine Andre '’’Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Recent Findings==&lt;br /&gt;
&lt;br /&gt;
'''''Localised inhibition of FGF signalling in the third pharyngeal pouch is required for normal thymus and parathyroid organogenesis'''''&lt;br /&gt;
&lt;br /&gt;
The third pharyngeal pouch endoderm is the origin of development for both the thymus and parathyroid glands. After the formation of the third pouch, there is are two noticeable domains by embryonic day 10.5 of mouse development. The parathyroid domain is located in the anterior-dorsal aspect of the pouch and is further recognised by lack of glial cells (Gcm2) expression needed for parathyroid organogenesis. On the posterior-ventral aspect of the pouch is the domain for the thymus where Bmp4 and Foxn1 expression characterise thymic differentiation and survival. Once these subdivisions are established, separation occurs between the two organs from the pharynx and migration towards to the anterior-ventral mediastinum occurs through apoptosis. Although, apoptotic signals Pax1, Pax9 and Hoxa3 have been shown to cause this separation, it is not fully understood how this separation actually occurs.&lt;br /&gt;
&lt;br /&gt;
There has been research showing that fibroblast growth factor (FGF) signalling controls the organogenesis processes of the pharyngeal region. Mutations in FGF signalling are known to impact the thymus and parathyroid organs by causing aplasia or hypoplasia.  FGF feedback antagonists of the sprouty gene family are key regulators in the formation of the mentioned organs. Localised inhibition of FGF signalling by sprouty proteins has shown a favourable result in the organogenesis of the thymus and parathyroid organs by inducing differentiating factors Gcm2, Bmp4 and Foxn1 expression in the third pouch as well as apoptosis.&lt;br /&gt;
&lt;br /&gt;
In this study, mouse embryos are used to show how FGF feedback antagonists that inhibit FGF can result in proper organogenesis of the thymus and parathyroid organs. Mouse embryos that contained the two FGF feedback antagonists, Spry1 and Spry2 and those that lacked them were studied. Data revealed that there was increased FGF signalling when Spry1 and Spry2 were not present, thereby leading to lack of Gcm2 expression and hence parathyroid hypoplasia. Similarly, levels of Bmp4 expression was also decreased in the thymus domain when Spry1 and Spry2 were absent, leading to thymus hypoplasia. It was also found that FGF Ligands were upregulated in the third pouch which resulted in the deletion of the sprouty gene. Consequently, the markers needed for thymus and parathyroid organogenesis was altered and apoptosis was inhibited leaving the organs still attached to the pharynx. Therefore, it is established that localised inhibition of FGF signalling present in the third pharyngeal pouch is vital for the organogenesis of the thymus and parathyroid organs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;22912418&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''''Mouse testis development and function are differently regulated by follicle-stimulating hormone receptors signaling during fetal and prepubertal life'''''&lt;br /&gt;
&lt;br /&gt;
This article investigates the role of Follicle Stimulating Hormone (FSH) on Sertoli cell development in the fetal and post-natal period  using a mouse model. Although the role of FSH is clear in the rat, there remains a lack of understanding in the mouse. They confirm the current understanding that  Sertoli cell formation occurs during fetal life at 11.5-12.5 days post conception (dpc) in the mouse and proliferation is fully established at day 17. In Rathke’s pouch, detection of the alpha-gycoprotein subunit occurs 11.5dpc and the number of Sertoli cells reduces between 18.5dpc and birth in hypogonadal mice.&lt;br /&gt;
&lt;br /&gt;
Through performing morphometric studies on FSH+/+, FSH+/- and FSH-/- mice, at days 0, 6, 8 and 10, the study found that FSH-/- mice contained 22% less fetal Sertoli cells than wild-type mice. Assessment of the transcription factor GATA-6 was performed to establish the expression of Sertoli cell specific markers and the study concluded that GATA-6 was expressed less than wild-type mice by 30% compared to FSH-R-/- mice. Also, a molecule involved in testis organogenesis, Claudin 11, was found to be expressed at significantly less levels in FSH-/- testes.The expression of testicular steroidogenesis genes such as P450scc and StAR revealed that these molecules had greater expression in FSH-/- mice than control ones.&lt;br /&gt;
&lt;br /&gt;
The study thus provides light on the fact that Sertoli cells have a paracrine mechanism of action to regulate FSH-R function of Leydig cells in the fetal period and that FSH controls Sertoli cell development in both the mouse and rat.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref&amp;gt;&amp;lt;pubmed&amp;gt;23300903&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
''''Neuropeptide Y in the Adult and Fetal Human Pineal Gland''''&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt; Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself.&amp;lt;ref name =Moller&amp;gt;M. Moller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland.’ BioMed Research International:2014, http://www.hindawi.com/journals/bmri/2014/868567/&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=155171</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=155171"/>
		<updated>2014-10-22T05:35:42Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5) &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
C.P. Maurizi, '''Could exogenous melatonin prevent sudden infant death syndrome?''', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || Example&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|-&lt;br /&gt;
| Example || Example || Example || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://ac.els-cdn.com/S030100820900046X/1-s2.0-S030100820900046X-main.pdf?_tid=42bc9e94-59ac-11e4-acd8-00000aacb361&amp;amp;acdnat=1413955891_77158b95d9eb4f3e4942d81440455daa&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Neurophysin || Example || Hypothalamic paraventricular and supraoptic nuclei  || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || Example&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=155162</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=155162"/>
		<updated>2014-10-22T05:32:37Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5) &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
C.P. Maurizi, '''Could exogenous melatonin prevent sudden infant death syndrome?''', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || Example&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|-&lt;br /&gt;
| Example || Example || Example || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by cells of the posterior pituitary which is also known as the neurohypophysis. These hormones contribute to proper brain and central nervous system development. Their neuronal origin are from the hypothalamus and run into the pituitary gland where they are released to take action on various systems and organs. &amp;lt;ref name =Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd&amp;gt;Heon-Jin Lee, Abbe H. Macbeth, Jerome H. Pagani, W. Scott Young 3rd, 2009, '''Oxytocin: The great facilitator of life''', Progress in Neurobiology; 88, pp127-151, http://ac.els-cdn.com/S030100820900046X/1-s2.0-S030100820900046X-main.pdf?_tid=42bc9e94-59ac-11e4-acd8-00000aacb361&amp;amp;acdnat=1413955891_77158b95d9eb4f3e4942d81440455daa&amp;gt;&amp;lt;ref/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Neuronal Origin !! Header text&lt;br /&gt;
|-&lt;br /&gt;
| Neurophysin || Example || Hypothalamic paraventricular and supraoptic nuclei  || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || Example || Hypothalamic paraventricular and supraoptic nuclei || Example&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || Example || Hypothalamic paraventricular and supraoptic nuclei || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI and cross-sectional anatomy of the fetal adrenal gland at gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion, Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst. The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*After week 8- Syncytiotrophoblast production of placental progesterone is enough to maintain pregnancy in spite of ovariectomy&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10.  Peak levels of hCG are produced in maternal serum. &amp;lt;ref name= Evain-Brion&amp;gt;Danielle Evain-Brion , Malassine Andre '''Human placenta as an endocrine organ'''. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: 2003, 13;S37-S37, http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;. &lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Neil M Gude, Claire T Roberts, Bill Kalionis, Roger G King '''Growth and function of the normal human placenta'''. Thrombosis Research: 2004, 114(5-6); 397-407, http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=155123</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=155123"/>
		<updated>2014-10-22T04:45:45Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5) &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
C.P. Maurizi, '''Could exogenous melatonin prevent sudden infant death syndrome?''', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || Example&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|-&lt;br /&gt;
| Example || Example || Example || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI of the fetal adrenal gland as gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst &lt;br /&gt;
*The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10 &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=155117</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=155117"/>
		<updated>2014-10-22T04:39:30Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;. Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5) &amp;lt;ref name=Maurizi&amp;gt;C.P. Maurizi, 'Could exogenous melatonin prevent sudden infant death syndrome?', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
C.P. Maurizi, '''Could exogenous melatonin prevent sudden infant death syndrome?''', Medical Hypotheses:1997, 49(5); 425-427, http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref name =Nussey S, Whitehead S&amp;gt;&amp;lt; Nussey S, Whitehead S, Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The following table summarises the hormones secreted by particular cells of the anterior pituitary during the fetal period. The cell types that are present are somatotrophs and gonadotrophs which secrete hormones that cause cell proliferation and activation of gonadal cells respectively. &amp;lt;ref name =M A Japón, M Rubinstein and M J Low&amp;gt;&amp;lt;M A Japón, M Rubinstein and M J Low, 1994, '''In situ hybridization analysis of anterior pituitary hormone gene expression during fetal mouse development''', Journal of Histochemistry and Cytochemistry; 8(42), 1117-1125, http://jhc.sagepub.com/content/42/8/1117.long&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Cell Type !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Growth Hormone || GH || Somatotroph || Example&lt;br /&gt;
|-&lt;br /&gt;
| Luteinizing Hormone || LH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Leydig cells to produce testosterone&lt;br /&gt;
* Females: stimulates ovary to produce estrogen&lt;br /&gt;
|-&lt;br /&gt;
| Follicle Stimulating Hormone || FSH || Gonadotroph || &lt;br /&gt;
* Males: stimulates Sertoli cells to produce androgen-binding protein --&amp;gt; in turn stimulating spermatogenesis&lt;br /&gt;
* Females: stimulates ovary to produce progesterone during luteal phase and estradiol during follicular phase&lt;br /&gt;
|-&lt;br /&gt;
| Example || Example || Example || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI of the fetal adrenal gland as gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst &lt;br /&gt;
*The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10 &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154880</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154880"/>
		<updated>2014-10-22T01:47:46Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth (2). Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref&amp;gt;Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI of the fetal adrenal gland as gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst &lt;br /&gt;
*The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10 &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154874</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154874"/>
		<updated>2014-10-22T01:44:56Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Timeline */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth (2). Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref&amp;gt;Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI of the fetal adrenal gland as gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst &lt;br /&gt;
*The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10 &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154859</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154859"/>
		<updated>2014-10-22T01:42:37Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Pituitary gland */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth (2). Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref&amp;gt;Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pituitary Development.jpg|300px|right|thumb|Anatomy of Human Pituitary Gland]]&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI of the fetal adrenal gland as gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst &lt;br /&gt;
*The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10 &amp;lt;ref name= Evain-Brion&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref name=PMID17624715&amp;gt;&amp;lt;pubmed&amp;gt;17624715&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=File:Pituitary_Development.jpg&amp;diff=154838</id>
		<title>File:Pituitary Development.jpg</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=File:Pituitary_Development.jpg&amp;diff=154838"/>
		<updated>2014-10-22T01:38:25Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;A cartoon image of the human pituitary gland anatomy showing the Anterior Pituitary (AP) and Posterior Pituitary (NP) separated by the Marginal Zone (MZ). The MZ is surrounded by dilated Rathke's remnant's cysts in orange and labelled RC on the H&amp;amp;E staining image. &amp;lt;ref name=Garcia-Lavandeira M, Quereda V, Flores I, Saez C, Diaz-Rodriguez E, et al&amp;gt;&amp;lt;Garcia-Lavandeira M, Quereda V, Flores I, Saez C, Diaz-Rodriguez E, et al. (2009) A GRFa2/Prop1/Stem (GPS) Cell Niche in the Pituitary. PLoS ONE 4(3): e4815. doi:10.1371/journal.pone.0004815 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004815&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004815 &lt;br /&gt;
&lt;br /&gt;
© 2009 Garcia-Lavandeira et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=File:Pituitary_Development.jpg&amp;diff=154820</id>
		<title>File:Pituitary Development.jpg</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=File:Pituitary_Development.jpg&amp;diff=154820"/>
		<updated>2014-10-22T01:37:23Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: A cartoon image of the human pituitary gland anatomy showing the Anterior Pituitary (AP) and Posterior Pituitary (NP) separated by the Marginal Zone (MZ). The MZ is surrounded by dilated Rathke's remnant's cysts in orange and labelled RC on the H&amp;amp;E sta...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;A cartoon image of the human pituitary gland anatomy showing the Anterior Pituitary (AP) and Posterior Pituitary (NP) separated by the Marginal Zone (MZ). The MZ is surrounded by dilated Rathke's remnant's cysts in orange and labelled RC on the H&amp;amp;E staining image. &lt;br /&gt;
&lt;br /&gt;
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004815 &lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=Garcia-Lavandeira M, Quereda V, Flores I, Saez C, Diaz-Rodriguez E, et al&amp;gt;&amp;lt;Garcia-Lavandeira M, Quereda V, Flores I, Saez C, Diaz-Rodriguez E, et al. (2009) A GRFa2/Prop1/Stem (GPS) Cell Niche in the Pituitary. PLoS ONE 4(3): e4815. doi:10.1371/journal.pone.0004815 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004815&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
© 2009 Garcia-Lavandeira et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154604</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154604"/>
		<updated>2014-10-22T00:57:28Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth (2). Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref&amp;gt;Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI of the fetal adrenal gland as gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst &lt;br /&gt;
*The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref&amp;gt;Myren M, Mose T, Mathiesen L, Knudsen L 2007, ‘The human placenta – An alternative for studying foetal exposure’. Toxicology in Vitro, Volume 21, Issue 7, Obtober 2007, accessed September 28, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0887233307001701&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154562</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154562"/>
		<updated>2014-10-22T00:53:14Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Thyroid Development */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth (2). Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref&amp;gt;Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File.ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI of the fetal adrenal gland as gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst &lt;br /&gt;
*The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref&amp;gt;Myren M, Mose T, Mathiesen L, Knudsen L 2007, ‘The human placenta – An alternative for studying foetal exposure’. Toxicology in Vitro, Volume 21, Issue 7, Obtober 2007, accessed September 28, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0887233307001701&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154529</id>
		<title>2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=2014_Group_Project_6&amp;diff=154529"/>
		<updated>2014-10-22T00:49:06Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014header}}&lt;br /&gt;
=The Endocrine System=&lt;br /&gt;
&lt;br /&gt;
==Introduction==&lt;br /&gt;
&lt;br /&gt;
==Pineal gland==&lt;br /&gt;
&lt;br /&gt;
The pineal gland is part of the epithalamus, located in the diencephalon. Like the other neurosecretory glands, it is formed by the neuroectoderm of the neural plate. Its primary function is to regulate circadian cycles postnatally through its secretion of melatonin.  however it also has a role in reproductive development. Recent findings have shown that the pineal gland does play an important role during fetal development through the production of it's primary hormone, melatonin. &lt;br /&gt;
&lt;br /&gt;
[[File:Keith1902 fig167.jpg|300px|thumb| Image 1: schematic of a developing pineal gland in week 6 of gestation]]&lt;br /&gt;
&lt;br /&gt;
Pineal and placental melatonin have a regulatory effect on maintaining homeostasis in the uterus as well as fetal maturation and reproductive development. The suprachiasmatic nuclei in the hypothalamus acts as the central pacemaker for melatonin production. As the two circuits are already interconnected in the mammilian fetus, intrinsic circadian rhythms are already established prior to birth. However it is not until after birth that the infant produces significant levels of melatonin to sustain cyclic rhythms associated with day/night and light exposure. During early fetal development before the pineal gland is developed, it is the maternal melatonin that exerts its effect on development after crossing the placental barrier. &lt;br /&gt;
&lt;br /&gt;
In adults, the pineal gland converts sympathetic input into hormonal output by producing melatonin, which has regulatory effects upon hormones such as luteinizing hormone (LH) and follicle-stimulating (FSH) hormone.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human pineal gland and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Melatonin || pinealocytes;  The synthesis of melatonin is regulated by a dense network of sympathetic nerve fibers located in the autonomic superior cervical ganglia. The activity of the pineal gland is inhibited by stimulation from the photoreceptors of the retina. This light sensitivity causes melatonin to be produced only in low light or darkness and thus the pineal gland is active most at night.   || Contributes to the development of gametes and also helps in maintaining uterine homeostasis through its antioxidant properties. &lt;br /&gt;
Melatonin also inhibits the secretion of gonadotrophin releasing hormone (GnRH) until puberty. This mechanism is in place to protect premature initiation of pubertal pubertal activation of reproductive functions that are dependent on plasma gonadotropin levels. &amp;lt;ref name= PMID15119946&lt;br /&gt;
&amp;gt;&amp;lt;pubmed&amp;gt;15119946&lt;br /&gt;
&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
|}	&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline''':&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''How far has the pineal gland developed by week 8 of gestation?'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
*Week 5 - The pineal gland primarily begins its development after the diencephalon is differentiated from the prosenecephalon and forms on the diencephalic roof of the third ventricle. [1]&lt;br /&gt;
*Week 6 - A number of hollow diverticula begin formation in a clustered arrangement. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;'''Fetal Stage of Pineal Development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
*Week 8 - Proliferation of cells begins and these cells form the walls of the diverticulum&lt;br /&gt;
*Week 9-11 - On the caudal roof of the hollow diverticulum, cells continue proliferation and begin to differentiate into pinealoctyes to form the solid epiphysis&lt;br /&gt;
*Week 15-17 - By the second trimester small amounts of melatonin production by the fetal pinealocytes has begun, however the pineal gland is not fully functional till post-natally.&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal pineal gland 01.jpg|300px|thumb|Image 5: shows a fetal pineal gland at the end of the first trimester of development.]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities&lt;br /&gt;
'''&lt;br /&gt;
&lt;br /&gt;
* '''Pineal tumors'''&lt;br /&gt;
Tumors of the pineal region during fetal development are generally a result of displaced embryonic tissue or chromosomal abnormalities. Fetal pineal tumors are characterized by pigmented (melanin) epithelial cells, small undifferentiated cells, and a fibrovascular stroma. &amp;lt;ref name= PMID851944&amp;gt;&amp;lt;pubmed&amp;gt;851944&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the size and type of tumor the fetus may survive till birth however infants with pineal gland tumor experience abnormal puberty development and have a high probability of developing hydrocephalus. As the pineal gland sits just superior to the cerebral aqueduct (shown in image 7 below), pineal tumors can compress this aqueduct, resulting a build up of pressure of CSF in the brain, a condition known as obstructive congenital hydrocephalus. &amp;lt;ref name= PMID1652883&amp;gt;&amp;lt;pubmed&amp;gt;1652883&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
[[File:Pineal-body.jpg|250px|thumb| Image 6: Shows the location of the pineal gland in the adult brain.]] &lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
[[File:Congenital hydrocephalus MRI02.jpg|250px|thumb|Image 7: Infant with obstructive congenital hydrocephalus]]&lt;br /&gt;
''&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*'''Pineal hypoplasia'''&lt;br /&gt;
&lt;br /&gt;
Pineal gland hypoplasia is the underdevelopment of the pineal gland resulting in the production of an insufficient level of melatonin. As discussed, fetal melatonin plays a crucial role in the growth and development of important organs and functions so a lack of melatonin particularly during the second and third trimesters of gestation may have detrimental results on the health of the fetus. Studies have suggested a possible link between neonatal pineal gland hypoplasia and sudden infant death syndrome (SIDS) with almost 95% of deaths occurring within 6 months of birth (2). Oxidative stress of the brain, as melatonin's hydroxyl radical reducing ability is lost is suggested as a possible cause of SIDS. Additionally, the loss of melatonin's antioxidant activity during the fetal period is proposed as another factor to consider in development of atherosclerotic vascular disease later on in adult life. (3)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;small&amp;gt;*'''Neuropeptide Y in the Adult and Fetal Human Pineal Gland'''&lt;br /&gt;
&amp;lt;/small&amp;gt;&lt;br /&gt;
&lt;br /&gt;
M. Møller, P. Phansuwan-Pujito &amp;amp; C. Badiu, Neuropeptide Y in the Adult and Fetal Human Pineal Gland, 2014, BioMed Research International, http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
Neuropeptide Y was isolated from the porcine brain in 1982 and shown to be closely linked to noradrenaline in sympathetic nerve terminals. In a number of studies over the years the peptide has been detected in sympathetic nerve fibers innervating the pineal gland in many mammalian species. The investigation sets out to identify the presence of neuropeptide Y in the adult and fetal human pineal gland. Neuropeptide Y-containing nerve fibers were confirmed as being present in the adult pineal and could be also be detected as early as in the pineal of four- to five-month-old fetuses. This early innervation of the human pineal is markedly different from studies of rodents models, where the innervation starts postnatally which is an important factor to consider when applying animal models to research of the human pineal gland.[4] Another variation from rodent models were the numerous NPY-immunoreactive nerve fibers endowed with large boutons en passage (shown in image 8) that were present in a perifollicular position unlike in rodents where immunoreactive nerve fibers penetrate and densely innervate the follicle itself. (5)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[IMAGE 8 http://www.hindawi.com/journals/bmri/2014/868567/fig2/]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[1] http://emedicine.medscape.com/article/249945-overview&lt;br /&gt;
&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/1652883&lt;br /&gt;
&lt;br /&gt;
(2) http://www.sciencedirect.com/science/article/pii/S0306987797900918&lt;br /&gt;
&lt;br /&gt;
(3) http://ac.els-cdn.com/S0306987798900123/1-s2.0-S0306987798900123-main.pdf?_tid=45519798-571f-11e4-9b0b-00000aab0f6c&amp;amp;acdnat=1413675434_b030429cee80326aee288b111c3c9c76&lt;br /&gt;
&lt;br /&gt;
[4]http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
[5] http://www.hindawi.com/journals/bmri/2014/868567/&lt;br /&gt;
&lt;br /&gt;
==Hypothalamus==&lt;br /&gt;
&lt;br /&gt;
The hypothalamus is part of the diencephalon and plays an important role in the maintenance of homeostasis and the driving of motivated behaviours. Distinct nuclei in the hypothalamus secrete specific hormones that function to regulate thirst, hunger, thermoregulation, circadian rhythms, reproduction and defensive behaviour. The hypothalamus is involved in two main signaling pathways or &amp;quot;axes&amp;quot;:&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus small.gif|thumb|location of hypothalamus in the adult brain]]&lt;br /&gt;
&lt;br /&gt;
*HPA (Hyothalamus-Pituitary-Adrenal) &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
*HPG (Hypothalamus-Pituitary-Gonad). &lt;br /&gt;
&lt;br /&gt;
[[File: diagram &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
''Table 1. Summarises the hormones released by the human hypothalamus and their role in embryonic and foetal development&lt;br /&gt;
''&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Abbreviation !! Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Vasopressin || ADH || Paraventricular and Magnocellullar neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Oxytocin || || Magnocellular neurosecretory cells || Example&lt;br /&gt;
|-&lt;br /&gt;
| Thyrotropin-releasing hormone (Prolactin-releasing hormone) || TRH, TRF, or PRH || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|-&lt;br /&gt;
| Dopamine (Prolactin-inhibiting hormone) || DA or PIH || Dopamine neurons of the arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Growth hormone-releasing hormone || GHRH || Neuroendocrine neurons of the Arcuate nucleus || Example&lt;br /&gt;
|-&lt;br /&gt;
| Corticotropin-releasing hormone || CRH or CRF || Parvocellular neurosecretory neurons || Example&lt;br /&gt;
|- &lt;br /&gt;
| Gonadotropin-releasing hormone || GnRH or LHRH || Neuroendocrine cells of the Preoptic area || Example&lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin (growth hormone-inhibiting hormone) || SS, GHIH, or SRIF || Neuroendocrine cells of the Periventricular nucleus || Example&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Adult human hypothalamus 04.jpg|250x|thumb|Figure 1. illustrates the location of nuclei in the hypothalamus]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Stage 22 image 057.jpg|250x|thumb|Image 1. Histological cross-section of stage 22 embryo]]&lt;br /&gt;
&lt;br /&gt;
The sexually dimorphic nucleus (SDN, intermediate nucleus) is twice as large in young male adults as in young females. Immediately after birth, only 20% of the SDN cell number is present. During the post-natal period up till two to four years of age cell numbers continue to increase rapidly and equally in both sexes. Past this age, cell numbers start to decrease in girls and this is the point of physiological differentiation in sex. &lt;br /&gt;
&lt;br /&gt;
Neurosecretory cells of the supraoptic (SON) and paraventricular nucleus (PVN) project to the neurohypophysis, where they release vasopressin and oxytocin into the blood circulation. These hormones play an important role in foetal development up till and including the birth process. Foetal oxytocin may initiate or accelerate the course of labor whereas foetal vasopressin plays a role in the adaptation to stress caused by the birth process, by redistribution of the foetal blood flow. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Hypothalamus histology 001.jpg|250x|thumb|Image 2. Histological cross-section of adult monkey hypothalamus depicting two major nuclei]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;How far has the hypothalamus gland developed by week 8 of gestation?&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 5: The development of the CNS has reached the five vesicle stage, where the prosencephalon divides into the diencephalon which is more caudal and in which the hypothalamus is formed, and the telencephalon located more rostrally. &lt;br /&gt;
&lt;br /&gt;
* Week 6: During pre-foetal phase when the head folds begin to take shape, a thickening called the hypophyseal placode forms at the midline of the rostral ectoderm, adjacent to the area where the hypothalamus will form on the neural fold. &lt;br /&gt;
&lt;br /&gt;
'''&amp;lt;small&amp;gt;Fetal Stage of hypothalamus development - from week 8 of gestation onwards:&lt;br /&gt;
&amp;lt;/small&amp;gt;'''&lt;br /&gt;
&lt;br /&gt;
* Week 9: The hypophyseal placode changes shape as it is pulled upwards, towards the overlying neuroepithelium, to form Rathke's pouch.&lt;br /&gt;
&lt;br /&gt;
*  Week 18: By mid-gestation, this simple epithelial invagination separates from the underlying ectoderm to form the definitive Rathke's pouch. Subsequent cell proliferation and differentiation of the intermediate zone allows for the formation of the primordial hypothalamus. The posterior lobe and the pituitary stalk connects the gland to the hypothalamus.&lt;br /&gt;
&lt;br /&gt;
* Week 28: Sexual differentiation of hypothalamus is complete [2]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Abnormalities'''&lt;br /&gt;
&lt;br /&gt;
Complications in development of these nuclei regions lead to disorders characteristic to those regions affected.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Recent Findings'''&lt;br /&gt;
&lt;br /&gt;
A. Peruffoa, M. Giacomellob, S. Montellia, M. Panina, B. Cozzia, 2013, Expression profile of the pore-forming subunits α1A and α1D in the foetal bovine hypothalamus: A mammal with a long gestation. ''Neuroscience Letters.'' Vol. 556, pp 124–128http://www.sciencedirect.com/science/article/pii/S0304394013009300&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
E. Muraa, M. Sumana, S. Montellia, A. Peruffoa, B. Cozzia, V. Farinab, 2013, Characterization of an established endothelial cell line from primary cultures of fetal sheep hypothalamus. ''Research in Veterinary Science''. Vol. 94:3, pp 388–393http://www.sciencedirect.com/science/article/pii/S0034528812003256&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
Rizzoti, K.	&amp;amp; Lovell-Badge, R. Development of the pituitary and hypothalamus, Regenerative Medicine: Organ recital in a dish. ''Nature'' Vol. 480, pp 44–46http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
[2] http://www.nature.com/nature/journal/v480/n7375/box/480044a_BX1.html&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;11954031&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7643957&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Y. Koutcherov, J.K, Mai, G. Paxinos Hypothalamus of the human fetus, Journal of Chemical Neuroanatomy, 26:4, pp 253–270&lt;br /&gt;
&lt;br /&gt;
==Pituitary gland==&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=== Timeline ===&lt;br /&gt;
Pre-fetal stage of pituitary gland development:&lt;br /&gt;
*Formation of Rathke's Pouch by week 4-5 of gestation &lt;br /&gt;
** At the point of the oropharynx in the primitive gut there is an invagination of the ectoderm and this is the origin of the anterior pituitary lobe&lt;br /&gt;
** Eventually Rathke's pouch is pinched off and separates from the oral cavity. All the Rathke cells need to migrate down to sit in the sphenoid bone of the skull. Any cells left behind can becomes tumours. &lt;br /&gt;
* The posterior pituitary is formed from the downward outgrowth of the third ventricle forming a median eminence&lt;br /&gt;
* Together with cells from the mammillary body, a neural stalk forms giving the neurohypophysis &amp;lt;ref&amp;gt;Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 7, The pituitary gland&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thyroid==&lt;br /&gt;
&lt;br /&gt;
===Thyroid Development===&lt;br /&gt;
&lt;br /&gt;
The functional unit of the thyroid gland is the follicle hence it is necessary to understand how the follicle develops in order to understand the important function of this gland. There are progenitor cells in the anterior endoderm that are specified thyroid progenitor cells and contribute to thyroid organogenesis. The proliferation of these cells results in the formation of a placode along the midline of the pharyngeal floor, just below the future tongue. The left and right lobes of the thyroid gland start off as single structures: buds of endoderm surrounded by mesoderm. &lt;br /&gt;
&lt;br /&gt;
The mammalian thyroid gland is unique in the sense that there is a second endocrine cell called the parafollicular C cell. The progenitor cell for this enters the gland at the stage where there is a fusion between the thyroid progenitor proper and the ultimobranchial bodies. The ultimobranchial bodies arise bilaterally in the most inferior pharyngeal arches and are important in the final organ. &lt;br /&gt;
&lt;br /&gt;
Eventually the midline primordium stretches laterally to reach the ultimobranchial bodies and there is a bilobation event resulting in the recognisable bilobed thyroid gland. &amp;lt;ref name=&amp;quot;PMID24290349&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24290349&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[ThyroidDevelopment.png|300px|right|thumb|This image summarises the endodermal and mesodermal cellular contribution to the formation of the thyroid gland]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Timeline===&lt;br /&gt;
How far has the thyroid gland developed by week 8 of gestation?&lt;br /&gt;
* Formation of medial anlage (foregut endoderm origin) and 2 lateral anlages (neuroectodermal origin and derivatives of the 4th pharyngeal pouch)&lt;br /&gt;
* Budding of ventral pharynx to form thryoid primoridum&lt;br /&gt;
* Fusion event of the median anlage with the lateral angales (ultimobranchial bodies) followed by migration of median anlage to it's final pretracheal location&lt;br /&gt;
* Sonic hedgehog plays a role in directing correct lobulation of the median anlage into two lobes connected by an isthmus &lt;br /&gt;
&lt;br /&gt;
Fetal Stage of Thyroid Development - from week 8 of gestation onwards:&lt;br /&gt;
* Terminal differentiation of thyroid gland occurs from week 7 to 8 of embryo gestation and involves the onset of the gland function&lt;br /&gt;
* '''Pre-colloid''' stage is week 7-9 and is where the thyroid gland contains strands of compact unpolarised Thyroid Follicular Cell (TFC) precursors &lt;br /&gt;
* '''The beginning colloid''' stage is week 10-11 and involves the polarisation of the TFC precursors. &lt;br /&gt;
**This gives the first appearance of small thyroid follicles (the eventual functional unit of the gland)&lt;br /&gt;
* '''Progressive follicular''' growth occurs in week 12&lt;br /&gt;
** At this point the fetal thyroid gland gains the ability to accumulate iodine and begin thyroid hormone synthesis &amp;lt;ref name=&amp;quot;PMID10.1016/j.beem.2013.08.005&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Parathyroid gland==&lt;br /&gt;
&lt;br /&gt;
[[File:Parathyroid position in mouse embryo.jpg |400px|thumb|left|This image shows the position of the parathyroid in the embryo]]&lt;br /&gt;
&lt;br /&gt;
The parathyroid gland is an important endocrine organ that plays an essential role in regulating extracellular calcium homeostasis and hence serves many physiological processes that involve muscle contraction, blood coagulation, and synaptic activity. They detect changes fluctuations of calcium levels in blood which is detected by the calcium-sensing receptor (CasR). This process then stimulates the secretion of parathyroid hormone (PTH) which releases calcium from internal stores such as bone in order to counterbalance any extremities.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the parathyroid gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 5 - the Parathyroid glands arise from the endodermal third and fourth pharyngeal pouches in cranial portions.&lt;br /&gt;
* Cranial third pharyngeal pouches form inferior parathyroids and cranial fourth pharyngeal pouches forms superior parathyroids.&lt;br /&gt;
* Pouches are bilateral and hence form four parathyroids&lt;br /&gt;
* Parathyroid gland development cannot occur without the transcription factor encoded by Gcm-2.&lt;br /&gt;
* Week 6 - diverticulum extends from the pouch which is hollow at first and then solidifies with dorsal cell proliferation&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of parathyroid Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Active transport regulates high fetal calcium concentrations levels (11-12 mg/dl) from maternal serum via an ATP-dependent calcium pump situated across the syncytiotrophoblast. &lt;br /&gt;
* The middle portion of the parathormone related peptide (PTHrP) is secreted via the fetal parathyroid and activates the placental calcium pump.&lt;br /&gt;
* Sections 1-34 of the Parathormone (PTH) or PTHrP stimulate PTH/PTHrP receptors causing a fetal skeletal calcium flux. This subsequently leads to the excretion of calcium via the fetal renal 1, 25 (OH) 2 D production also occurs which serves to increase the calcium transport occurring in carrying mothers. Calcium reabsorption from amniotic fluid also takes place through this action.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808183&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22649358&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21881196&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21904825&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7344740&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7835276&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Thymus==&lt;br /&gt;
&lt;br /&gt;
The thymus gland is an organ that belongs to two systems of the human body which are the endocrine and immune system. It consists of two distinct but identical lobes which are both encased  by a tough and fibrous capsule. Within each lobe are two layers which is the cortex that is superficial to the deep medullary layer in the tissue. Epithelial tissues and lymphatic tissues including macrophages make up majority of the thymus.&lt;br /&gt;
In terms of its role in the endocrine system, it is responsible for the development of hormone called thymosin. This hormone is needed to tranform white blood cells (lymphocytes) that pass through the thymus gland into T cells, thereby forming the link to aid the immune system. This important gland is located in the upper anterior chest straight behind the sternum and in between the lungs.  Other associated hormones of the thymus gland include thymopoietin hormones, thymic humoral factors , thymostimulin and Factor thymic serum.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the thymus gland developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* It originates primarily from the third pharyngeal pouch.&lt;br /&gt;
* The primordia is initially divided into the thymic and parathyroid domains which are both encased in a neural crest-derived mesenchymal capsule.&lt;br /&gt;
* Week 7 - mid week 8,  the thymic part of the primordium migrates ventrally and attach at the pericardium&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of thymus Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 8 -  the thymic primordium contains undifferentiated epithelial cells&lt;br /&gt;
* Week 8-9, intrathymic cell types such as mesenchymal, vascular and lymphoid cells begin to develop&lt;br /&gt;
* Weeks 8-16 -  Medullary development occurs from week 8 and distinct cortical and medullary compartments are formed by week 16&lt;br /&gt;
*Weeks 14- 16, mature lymphocytes begin to migrate from the thymus to seed the peripheral immune system &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21733645&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20836742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21263742&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;512270&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Pancreas==&lt;br /&gt;
&lt;br /&gt;
[[File:Ratio of alpha &amp;amp; beta cells at different phases of fetal development.png|400px|thumb|right|This image shows the ratio of alpha &amp;amp; beta cells at different phases of fetal development]]&lt;br /&gt;
&lt;br /&gt;
The pancreas is an endocrine organ situated well into the abdomen. It has a dual role and is responsible for digestion via its exocrine function and regulating blood sugar levels through its endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Timeline'''&lt;br /&gt;
&lt;br /&gt;
'''How far has the pancreas developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
* Week 4 – Pancreatic development begin at the septum transversum as dorsal and ventral endodermic buds forms. Dorsal and ventral mesentery are formed by splanchnic mesoderm.&lt;br /&gt;
* Dorsal buds normally develop first and form majority of the pancreas whereas the ventral bud only forms a portion of the head and uncinated process of the pancreas.&lt;br /&gt;
* Week 6-8 – These buds migrate and fuse from duodenum growth and rotation. In order to make space for the pancreas, the duodenum rotates in to C-shaped conformation. The ventral bud also situates itself dorsally behind the dorsal bud.&lt;br /&gt;
* Pancreatic bud endoderm in particularly the ventral bud duct and distal part of dorsal bud differentiates into islet cell clusters which form acini and exocrine ducts needed for exocrine function. At the periphery of these exocrine clusters form the pancreatic islets which serve endocrine function.&lt;br /&gt;
&lt;br /&gt;
'''Fetal Stage of pancreas Development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
* Week 7 to 20 – Maternal insulin increases exponentially as fetus grows.&lt;br /&gt;
* Week 10 – The first cells to differentiate are  glucagon (alpha) cells followed by somatostatin (delta), and insulin (beta) cells. Fetus begins to secrete insulin&lt;br /&gt;
* Week 15 – Levels of glucagon become noticeable in fetal plasma&lt;br /&gt;
&lt;br /&gt;
Hormones:&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !!  Produced by !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Glucagon ||  Alpha cells of the islets of Langerhans || Elevates blood sugar levels when blood sugar levels are low.&lt;br /&gt;
|-&lt;br /&gt;
| Insulin || Beta cells of the islets of Langerhans || Reduces blood sugar levels when blood sugar levels are too high. It also converts glucose into glycogen to store in the liver for future source of energy. &lt;br /&gt;
|-&lt;br /&gt;
| Somatostatin ||  Delta cells of pancreas || Inhibits the secretion of other pancreatic hormones such as insulin and glucagon.&lt;br /&gt;
|-&lt;br /&gt;
| Pancreatic Polypeptide ||  Pancreatic polypeptide cells || Prevents secretion of somatostatin from the pancreas.&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22761699&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24496309&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22968764&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;3743355&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19893748&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Adrenal gland==&lt;br /&gt;
&lt;br /&gt;
The characteristic zonation of the adult adrenal gland is absent in the fetal gland which is instead arranged in an inner fetal zone and an outer definitive (adult) zone. The inner zone atrophies following birth and contains steroid-secreting cell characteristics while the adult zone contains cells that resemble those present in the adult zona glomerulosa. The adrenal medulla is not a distinct, recogniseable zone during gestation, except for scattered chromaffin cells present throughout the cortex in small clusters. &lt;br /&gt;
&lt;br /&gt;
'''Development overview:''&lt;br /&gt;
&lt;br /&gt;
[[File:Fetal adrenal gland.png|300px|right|thumb|This image shows a transverse MRI of the fetal adrenal gland as gestational weeks 24 (A) and 36 (B)]]&lt;br /&gt;
&lt;br /&gt;
*Week 6: Adrenal gland is present at the cranial side of the mesonephric kidney as a condensed mass of coelomic epithelium, appearing as large cells like those of older fetus fetal zones. &lt;br /&gt;
*Week 8: The definitive or adult zone is formed by a second round of epithelial cell proliferation, where a cap is formed by a narrow rim of cells over the fetal zone. Around the central part of the gland can be seen clumps of medullary cells and neural elements infiltrate it through the vascular pole. &lt;br /&gt;
*Weeks 10-20: Rapid growth of the adrenal gland by increased size of the fetal and definitive zones from about 100mg in week 10 to 2g at week 20. Appearance of vasculature and sinusoidal plexuses and increase of medullary cells. &lt;br /&gt;
*Weeks 20-30: Gland size doubles with adult-type zonation appearing in the definitive zone around week 30. The zona glomerulosa is delineated by connective tissue stroma and cells appear arranged in a columnar fashion in the developing zona fasciculata. &lt;br /&gt;
*Week 30-term: Weight of fetal adrenal gland doubles and 80% of the gland’s volume is made up of the fetal zone. &lt;br /&gt;
&lt;br /&gt;
The zona reticularis develops post-natally in year 3 of development, unlike the two other cortical zones.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the adrenal gland:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Aldosterone ||  Mineralocorticoid  || Zona glomerulosa || Works on the kidneys, sweat and salivary glands to maintain normal extracellular concentrations of Na+ and K+ and so extracellular volume &lt;br /&gt;
|-&lt;br /&gt;
| Cortisol || Glucocorticoid || Zona fasciculata || Restoration of homeostasis following stress; suppresses immune system, increases blood sugar by gluconeogenesis, helps metabolise protein, carbohydrates and fat, activates the CNS. In the foetus/neonate, causes organ development and maturation e.g. lungs. There are high levels of cortisol at childbirth&lt;br /&gt;
|-&lt;br /&gt;
| Adrenaline and noradrenaline  || Catecholamine || Adrenal medulla || Increase; heart rate contractility, vasoconstriction, ventilation, lipolysis, glycogenolysis and decrease gut motility. Work with the sympathetic nervous system to regulate 'flight or fight' response. &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7011178&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24116052&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC3365797&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;15635500&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Gonad development==&lt;br /&gt;
&lt;br /&gt;
===Ovary===&lt;br /&gt;
&lt;br /&gt;
'''Development overview:'''&lt;br /&gt;
&lt;br /&gt;
*Weeks 8 and 9: &lt;br /&gt;
**Week 8- Change to the gonad’s internal structure; it can be identified as an ovary now. Cortical differentiation occurs from the cranial pole to the lower pole. The dense central core spans the mesovarian into the mesonephric organ in a caudal direction, resembling the ‘rete blastema’ which differentiates. &lt;br /&gt;
**Inner ovary is composed of the indifferent gonad’s disintegrating blastema, surrounded by a thick blastemal layer, giving the ovary a non-uniform crenated surface&lt;br /&gt;
**Ovarian tissue has a cortical region and a central medullary region with an irregular demarcation. The cortex encloses primordial germ cells (PGCs) between somatic cells and medulla has a reticulum of somatic cells&lt;br /&gt;
*Weeks 10 to 12:&lt;br /&gt;
**Growth and lobulation of the cortex. Supporting cells grow peripherally and segment the cortex into irregular globules containing rapidly multiplying germ cells and light and dark somatic supporting cells, interspersed with connective tissue. &lt;br /&gt;
**Week 12- Cortex is penetrated by dark supporting cells, giving the superficial epithelium a ‘dark’ appearance, amongst the original ‘light’ cells of the coelomic epithelium. &lt;br /&gt;
**Oogonia appear in clusters, primordial cells still dominate and oocytes in the premeiotic period exist in small groups. &lt;br /&gt;
**Medulla contains less densely-packed globules, mainly oogonia&lt;br /&gt;
*Weeks 14 to 28:&lt;br /&gt;
**In mid-gestation- Depletion of the germ cells by apoptosis, highest from weeks 14-28 and decreasing closer to birth&lt;br /&gt;
**Week 16- Cortical cords break up into primordial follicles (cell clusters) housing an oogonium each from a PGC. Follicles enclosed by monolayer of flat follicular cells from surface epithelium&lt;br /&gt;
**Primordial follicle formation is the result of active mitosis of oogonia&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17237341&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7623307&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7158813&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22106406&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
===Testis===&lt;br /&gt;
&lt;br /&gt;
'''Testis migration'''&lt;br /&gt;
&lt;br /&gt;
The human testes early in fetal development begins at the abdominal cavity and migrates progressively towards the scrotum. This migration is caused by both mechanical determinants (genitofemroal nerve development, cremasteric muscle and epipdydmis development and gubernaculum development) and hormonal regulators (influences of gonadotropin and androgens such as testosterone).&lt;br /&gt;
&lt;br /&gt;
*Gestational week 17- Migration begins&lt;br /&gt;
*By Week 23- Approximately 90% of testes still remain in the abdomen, with migration accelerating in weeks 24-26.&lt;br /&gt;
*Weeks 26-28: Arrival of testes in the inguinal canal within a couple of days through the deep inguinal ring, helped by the gubernaculum&lt;br /&gt;
*Week 28- Passing of testes through superficial inguinal ring to scrotum. Is usually completed in 3-4 weeks but can occasionally take up to 12 weeks post-natally. &lt;br /&gt;
&lt;br /&gt;
By 22 weeks, 10% of testes are descending and this changes to 50% by 25 weeks, 75% by 26 weeks and 80% by 32 weeks. &lt;br /&gt;
&lt;br /&gt;
'''Testes development''' &lt;br /&gt;
&lt;br /&gt;
By week 8, masculine differentiation is induced in the mesonephric duct and external genitalis. This is caused by the interstitial cells (Leydig cells) in the mesenchymal tissue surrounding seminiferous tubules beginning secretion of the androgens androstenedione and testosterone, which is stimulated by human chorionic gonadotropin, peaking in weeks 8-12.  &lt;br /&gt;
&lt;br /&gt;
Antimulleran hormone, AMH (or mullerian-inhibiting substance, MIS), a glycoprotein, is produced by sustentacular (Sertoli) cells. This causes mesonephric duct suppression to prevent formation of the falltopian tubes and uterus in the developing male.  &lt;br /&gt;
&lt;br /&gt;
The majority of the seminiferous epithelium of the fetal testes is composed of Sertoli cells and this epithelium later flattens forming external mesothelium. 15-20 mesonephric tubules are continuous with the rete testes later form efferent ductules, connected to the mesonephric duct to form the epididymis duct. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''References'''&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;PMC1260417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;6846859&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8292535&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10510117&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
[http://www.mdconsult.com.wwwproxy0.library.unsw.edu.au/books/page.do?eid=4-u1.0-B978-1-4377-2002-0..00012-6--s0095&amp;amp;isbn=978-1-4377-2002-0&amp;amp;uniqId=466385578-2 Moore: The Developing Human, 9th ed. Chapter 12]&lt;br /&gt;
&lt;br /&gt;
==Placenta==&lt;br /&gt;
&lt;br /&gt;
The placenta is a highly specialised, transient and autonomous organ of pregnancy that plays an essential role in normal fetal development. Its functions include; the transfer of nutrients and oxygen to the developing fetus, removal of carbon dioxide, release of hormones into the materno-fetal circulation, and exchange of metabolic products to protect the fetus from infection, maternal diseases and xenobiotic molecules &amp;lt;ref&amp;gt;Evain-Brion D, Malassine A 2003, ‘Human placenta as an endocrine organ’. Proceedings of the 34th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism, Volume 13, August 2003, accessed October 6, &amp;lt;http://www.sciencedirect.com/science/article/pii/S1096637403000534#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''How far has the placenta developed by week 8 of gestation?'''&lt;br /&gt;
&lt;br /&gt;
*Days 6-7- Placental development starts with invasion of the endometrium by the blastocyst &lt;br /&gt;
*The outer cover of the blastocyst (trophectoderm) and vascular components are allantois-derived. The trophoblast differentiates into the syncytiotrophoblast following invasion of the uterine mucosa. &amp;lt;ref&amp;gt;Myren M, Mose T, Mathiesen L, Knudsen L 2007, ‘The human placenta – An alternative for studying foetal exposure’. Toxicology in Vitro, Volume 21, Issue 7, Obtober 2007, accessed September 28, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0887233307001701&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
*Days 8-13- The chorionic villi are developed, arising in the syncytiotrophoblast and composed of trabeculae and lacunae. The primary chorionic plate surrounds this system &lt;br /&gt;
*From day 12- Establishment of the primitive maternal circulation from trophoblastic shell cels. Mesenchymal cells invade the primary villi to form secondary villi. &lt;br /&gt;
*By the end of week 5- The intra-placental fetal circulation is fully established. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Fetal stage of placental development - from week 8 of gestation onwards:'''&lt;br /&gt;
&lt;br /&gt;
*Until beginning of week 8- Chorionic villi cover the whole chorionic sac&lt;br /&gt;
*By about week 10- The fetal-placental maternal circulation is fully established. Exchange of blood to the embryo occurs via diffusion until week 10&lt;br /&gt;
*Until week 18- Rapid growth in the size and thickness of the placenta. Fully mature placenta comprises one sixth of the fetal weight. &lt;br /&gt;
*Week 22-24- Decidua capillaris degenerates due to lack of blood supply. There is fusion of the chorionic sac with the decidua parietalis &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
Both fetal tissue from the chorionic sac and endometrium-derived maternal tissue contribute to form the utero-placental unit.The two parts of the mature placenta are; the chorionic plate (fetal part) containing chorionic blood vessels and the basal plate (maternal part) formed by the decidua basalis. In between these two parts is the intervillous space containing the villous structures of fetal blood vessels. Maternal-fetal exchange occurs at the terminal regions of these chorionic villi. &amp;lt;ref&amp;gt;Gude NM, Roberts CT, Kalionis B, King RG 2004, ‘Growth and function of the normal human placenta’. Thrombosis Research, Volume 114, Issues 5-6, 2004, pages 397-407, accessed October 5, &amp;lt;http://www.sciencedirect.com/science/article/pii/S0049384804003421#&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''Table of hormones produced by the placenta:'''&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Hormone !! Type !! Produced in !! Function&lt;br /&gt;
|-&lt;br /&gt;
| Human chorionic gonadotropin (hCG) || Glycoprotein || Trophectoderm || Maintenance of the corpus luteum in first 8 weeks of pregnancy, enhancement of spontaneous cytotrophoblast differentiation into syncytiotrophoblasts  &lt;br /&gt;
|-&lt;br /&gt;
| Placental Growth Hormone (PGH) || Trophoblast hormone || Syncytiotrophoblast layer || Controls levels of maternal insulin-like growth factor I (IGF-I), prevents variations in maternal blood glucose and allows maternal pregnancy metabolic adaptation&lt;br /&gt;
|-&lt;br /&gt;
| Progesterone and estrogens  || Steroid hormones || Syncytiotrophoblast || Maintenance of pregnancy even after ovary removal &lt;br /&gt;
|-&lt;br /&gt;
&lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10419690&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7673080&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Associated Abnormalities==&lt;br /&gt;
&lt;br /&gt;
{| class=&amp;quot;wikitable&amp;quot;&lt;br /&gt;
|-&lt;br /&gt;
! Disease !! Description&lt;br /&gt;
|-&lt;br /&gt;
| Diabetes Mellitus ||&lt;br /&gt;
|-&lt;br /&gt;
| Congenital Hypothyroidism || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|-&lt;br /&gt;
| Example || &lt;br /&gt;
|}&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22808198&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22893718&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24595965&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
=References=&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=154343</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=154343"/>
		<updated>2014-10-22T00:07:36Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
&lt;br /&gt;
[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
&lt;br /&gt;
==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
&lt;br /&gt;
===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
&lt;br /&gt;
===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 10===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:08, 15 October 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 11===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:07, 22 October 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 1 ==&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Article 1&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
&lt;br /&gt;
The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
&lt;br /&gt;
These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Article 2&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
&lt;br /&gt;
These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
&lt;br /&gt;
The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 2 ==&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;br /&gt;
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Project 7: Neural &lt;br /&gt;
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This project has a great introduction and overview of the brain and spinal cord anatomy. The first image is eye catching however I find it hard to follow and it seems like there is too much information on it. Perhaps it would be better positioned further down in the report after more neural developmental stages have been explained. The timeline section is clear and to the point. There is an excellent use of images to support the information. The fluorescent stained images make the ventricular, subventricular and other cortical layers clear and easy to understand. The information under the brain development section is simple and effective. However there are some terms mentioned that are not explained in enough detail like the specific layering of the cortex. It is a complicated migration process that deserves some more research. It is good that the student has explained gyration and sulcation in this section. &lt;br /&gt;
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This project is clearly still in progress however the information in the first section of the wiki page indicates a very promising final product. The spinal cord and meninges development section still needs to be written up. If it follows along the course of the brain development section, it will be flawless. The current research models and finding section reveals an in-depth understanding of complex ideas. However for a student embryology wiki page, there is too much detail. If the student wants to illustrate a complicated research finding, images or tables of the results found from this research would help convey the message to the student. A table would help summarise the results in the first current research description, particularly for the results gathered from the different parts of the brain. &lt;br /&gt;
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The final part of this report on abnormalities is unfinished however the bulk of the information presented already is very good. The images supporting the abnormality are excellent and important for keeping the student reading this page engaged. However there are a few spelling and grammar errors in the neural tube defects section: “which affect the either the brain”, “the openings remain which leas”. There is still room for more research and information on other neural development abnormalities and the subheadings the student has incorporated indicates their intention of adding more information. This report has excellent reference formatting and citation throughout the page. The tables and images are referenced correctly and the long list at the end is very neat. &lt;br /&gt;
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Project 8: musculoskeletal &lt;br /&gt;
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This project is still in its early days but the layout and plan is very good. With additional information added to the subheadings, it will be a very interesting student wiki page. Reviewing what has already been completed on this page, it is too content heavy. There are a lot of large chunks of text indicating the student has gone to a lot of effort to find complex research papers. This is further supported by the huge amount of references at the end of the page. However as this is to be a student embryology wiki page, it would help if the passages of text were broken up into bullet points and tables. Furthermore there are no images or student drawn diagrams. These would also help convey the main messages of musculoskeletal development. The sections after tendon development are unfinished and very brief. Furthermore the only in text referencing present is in the first two sections. Citations should be carried through the entire page. &lt;br /&gt;
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The second trimester muscular development section is particularly clear and to the point. However the information present doesn’t stretch much further than what was covered in the lecture material. By adding diagrams of the pharyngeal arch origins and including further research into this section, its quality will be greatly improved.&lt;br /&gt;
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==Online Assessment 9==&lt;br /&gt;
'''&amp;lt;sup&amp;gt;Sensory System Development - The Eye&amp;lt;/sup&amp;gt;'''&lt;br /&gt;
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Embryological eye development is an area of sensory embryology that has recently been the subject of various research papers. A paper that has particular relevance to eye development is by Yao Chen et al, titled Effects of High Salt-Exposure on the Development of Retina and Lens in 5.5-Day Chick Embryo. It was published on the 20th August 2014 making it very current research. Although they used Chick embryos instead of human embryos, the Chick model is very useful for looking at eye development because that sensory system is relatively large in the early stage embryo, hence making it easier to study. &lt;br /&gt;
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This paper investigates the effect of high salt exposure to the developing embryo particularly on eye, lens and retina shape and development. It compares a control eye that had normal salt exposure with two variations: exposure to 280mosm/l Sodium Chloride (NaCl) solution and 300mosm/l NaCl solution. Once the fertilised chick embryos were treated with these solutions, they were incubated and then H&amp;amp;E stained for analysis of transverse sections. The eye diameter and retina thickness were measured using Image-Pro Plus 6.0, a photography program. The proliferation of cells in the retina were measured using Phospho-Histone P3 immunostaining to measure the expression of the Pax6 gene which is vital in normal retina development. &lt;br /&gt;
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This report also explains early vertebrate eye development in the embryo. The eye has three main embryonic origins: the optic vesicle, the surrounding mesenchyme and the overlying surface ectoderm. In response to signals from the optic vesicle, the surface ectoderm thickens to form the lens placode and around week 4 disassociates from the surface of the embryo to form a lens vesicle. This lens vesicle will form the actual lens. The optic vesicle invaginates to form an optic cup where the internal layer forms the neuroretina and the outter layer forms the pigmented retinal epithelium.  There is also neural crest cell contribution to the development of retinal ganglion cells, cone photoreceptors, rod photoreceptors, bipolar cells and Muller glia cells. The Paired Box 6 gene (Pax6) is also very important for proper development of the eye, eye size, neuronal differentiation and retina development. &lt;br /&gt;
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The results gathered form this investigation highlighted the detrimental effect high salt intake can have on a developing embryo, in particular eye development. The level of eye deformity increased with increased level of NaCl exposure. The size of the eye decreased significantly, the diameter of the lens decreased and the lens was thinner. These results were gathered by looking at the images after H&amp;amp;E staining. Furthermore, using immunostaining, it was evident that there was decreased expression of the Pax6 gene in high-NaCl embryos.  This is very important since it has been found that this gene is expressed during optic vesicle and integration of the surface ectoderm into development of eye structures in the early embryo. If this gene is not expressed due to high salt levels, the embryo will have abnormal eye development. This can be observed in humans who suffer from pan-ocular disorders and in mice models where an under expression of Pax6 leads to the eyeless phenotype. Pax6 is also important during neural crest cell migration specifically the periocular mesenchyme cells that contribution to eye structures. Hence it is clear that this report shows how high levels of salt intake can have detrimental effects on eye development. &amp;lt;ref name=&amp;quot;PMID10.1159/000363044&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1159/000363044&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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{{Vision Links}}&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=154295</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=154295"/>
		<updated>2014-10-21T23:48:58Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Online Assessment 9 */&lt;/p&gt;
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&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
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==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
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===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
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===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
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===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
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===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
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===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
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===Lab 10===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:08, 15 October 2014 (EST)&lt;br /&gt;
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== Online Assignment 1 ==&lt;br /&gt;
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Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
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The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;br /&gt;
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Project 7: Neural &lt;br /&gt;
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This project has a great introduction and overview of the brain and spinal cord anatomy. The first image is eye catching however I find it hard to follow and it seems like there is too much information on it. Perhaps it would be better positioned further down in the report after more neural developmental stages have been explained. The timeline section is clear and to the point. There is an excellent use of images to support the information. The fluorescent stained images make the ventricular, subventricular and other cortical layers clear and easy to understand. The information under the brain development section is simple and effective. However there are some terms mentioned that are not explained in enough detail like the specific layering of the cortex. It is a complicated migration process that deserves some more research. It is good that the student has explained gyration and sulcation in this section. &lt;br /&gt;
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This project is clearly still in progress however the information in the first section of the wiki page indicates a very promising final product. The spinal cord and meninges development section still needs to be written up. If it follows along the course of the brain development section, it will be flawless. The current research models and finding section reveals an in-depth understanding of complex ideas. However for a student embryology wiki page, there is too much detail. If the student wants to illustrate a complicated research finding, images or tables of the results found from this research would help convey the message to the student. A table would help summarise the results in the first current research description, particularly for the results gathered from the different parts of the brain. &lt;br /&gt;
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The final part of this report on abnormalities is unfinished however the bulk of the information presented already is very good. The images supporting the abnormality are excellent and important for keeping the student reading this page engaged. However there are a few spelling and grammar errors in the neural tube defects section: “which affect the either the brain”, “the openings remain which leas”. There is still room for more research and information on other neural development abnormalities and the subheadings the student has incorporated indicates their intention of adding more information. This report has excellent reference formatting and citation throughout the page. The tables and images are referenced correctly and the long list at the end is very neat. &lt;br /&gt;
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Project 8: musculoskeletal &lt;br /&gt;
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This project is still in its early days but the layout and plan is very good. With additional information added to the subheadings, it will be a very interesting student wiki page. Reviewing what has already been completed on this page, it is too content heavy. There are a lot of large chunks of text indicating the student has gone to a lot of effort to find complex research papers. This is further supported by the huge amount of references at the end of the page. However as this is to be a student embryology wiki page, it would help if the passages of text were broken up into bullet points and tables. Furthermore there are no images or student drawn diagrams. These would also help convey the main messages of musculoskeletal development. The sections after tendon development are unfinished and very brief. Furthermore the only in text referencing present is in the first two sections. Citations should be carried through the entire page. &lt;br /&gt;
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The second trimester muscular development section is particularly clear and to the point. However the information present doesn’t stretch much further than what was covered in the lecture material. By adding diagrams of the pharyngeal arch origins and including further research into this section, its quality will be greatly improved.&lt;br /&gt;
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==Online Assessment 9==&lt;br /&gt;
'''&amp;lt;sup&amp;gt;Sensory System Development - The Eye&amp;lt;/sup&amp;gt;'''&lt;br /&gt;
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Embryological eye development is an area of sensory embryology that has recently been the subject of various research papers. A paper that has particular relevance to eye development is by Yao Chen et al, titled Effects of High Salt-Exposure on the Development of Retina and Lens in 5.5-Day Chick Embryo. It was published on the 20th August 2014 making it very current research. Although they used Chick embryos instead of human embryos, the Chick model is very useful for looking at eye development because that sensory system is relatively large in the early stage embryo, hence making it easier to study. &lt;br /&gt;
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This paper investigates the effect of high salt exposure to the developing embryo particularly on eye, lens and retina shape and development. It compares a control eye that had normal salt exposure with two variations: exposure to 280mosm/l Sodium Chloride (NaCl) solution and 300mosm/l NaCl solution. Once the fertilised chick embryos were treated with these solutions, they were incubated and then H&amp;amp;E stained for analysis of transverse sections. The eye diameter and retina thickness were measured using Image-Pro Plus 6.0, a photography program. The proliferation of cells in the retina were measured using Phospho-Histone P3 immunostaining to measure the expression of the Pax6 gene which is vital in normal retina development. &lt;br /&gt;
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This report also explains early vertebrate eye development in the embryo. The eye has three main embryonic origins: the optic vesicle, the surrounding mesenchyme and the overlying surface ectoderm. In response to signals from the optic vesicle, the surface ectoderm thickens to form the lens placode and around week 4 disassociates from the surface of the embryo to form a lens vesicle. This lens vesicle will form the actual lens. The optic vesicle invaginates to form an optic cup where the internal layer forms the neuroretina and the outter layer forms the pigmented retinal epithelium.  There is also neural crest cell contribution to the development of retinal ganglion cells, cone photoreceptors, rod photoreceptors, bipolar cells and Muller glia cells. The Paired Box 6 gene (Pax6) is also very important for proper development of the eye, eye size, neuronal differentiation and retina development. &lt;br /&gt;
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The results gathered form this investigation highlighted the detrimental effect high salt intake can have on a developing embryo, in particular eye development. The level of eye deformity increased with increased level of NaCl exposure. The size of the eye decreased significantly, the diameter of the lens decreased and the lens was thinner. These results were gathered by looking at the images after H&amp;amp;E staining. Furthermore, using immunostaining, it was evident that there was decreased expression of the Pax6 gene in high-NaCl embryos.  This is very important since it has been found that this gene is expressed during optic vesicle and integration of the surface ectoderm into development of eye structures in the early embryo. If this gene is not expressed due to high salt levels, the embryo will have abnormal eye development. This can be observed in humans who suffer from pan-ocular disorders and in mice models where an under expression of Pax6 leads to the eyeless phenotype. Pax6 is also important during neural crest cell migration specifically the periocular mesenchyme cells that contribution to eye structures. Hence it is clear that this report shows how high levels of salt intake can have detrimental effects on eye development. &amp;lt;ref name=&amp;quot;PMID10.1159/000363044&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1159/000363044&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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{{Vision Links}}&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=154292</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=154292"/>
		<updated>2014-10-21T23:45:49Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
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&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
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==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
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===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
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===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
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===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
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===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
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===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
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===Lab 10===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:08, 15 October 2014 (EST)&lt;br /&gt;
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== Online Assignment 1 ==&lt;br /&gt;
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Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
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The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;br /&gt;
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Project 7: Neural &lt;br /&gt;
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This project has a great introduction and overview of the brain and spinal cord anatomy. The first image is eye catching however I find it hard to follow and it seems like there is too much information on it. Perhaps it would be better positioned further down in the report after more neural developmental stages have been explained. The timeline section is clear and to the point. There is an excellent use of images to support the information. The fluorescent stained images make the ventricular, subventricular and other cortical layers clear and easy to understand. The information under the brain development section is simple and effective. However there are some terms mentioned that are not explained in enough detail like the specific layering of the cortex. It is a complicated migration process that deserves some more research. It is good that the student has explained gyration and sulcation in this section. &lt;br /&gt;
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This project is clearly still in progress however the information in the first section of the wiki page indicates a very promising final product. The spinal cord and meninges development section still needs to be written up. If it follows along the course of the brain development section, it will be flawless. The current research models and finding section reveals an in-depth understanding of complex ideas. However for a student embryology wiki page, there is too much detail. If the student wants to illustrate a complicated research finding, images or tables of the results found from this research would help convey the message to the student. A table would help summarise the results in the first current research description, particularly for the results gathered from the different parts of the brain. &lt;br /&gt;
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The final part of this report on abnormalities is unfinished however the bulk of the information presented already is very good. The images supporting the abnormality are excellent and important for keeping the student reading this page engaged. However there are a few spelling and grammar errors in the neural tube defects section: “which affect the either the brain”, “the openings remain which leas”. There is still room for more research and information on other neural development abnormalities and the subheadings the student has incorporated indicates their intention of adding more information. This report has excellent reference formatting and citation throughout the page. The tables and images are referenced correctly and the long list at the end is very neat. &lt;br /&gt;
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Project 8: musculoskeletal &lt;br /&gt;
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This project is still in its early days but the layout and plan is very good. With additional information added to the subheadings, it will be a very interesting student wiki page. Reviewing what has already been completed on this page, it is too content heavy. There are a lot of large chunks of text indicating the student has gone to a lot of effort to find complex research papers. This is further supported by the huge amount of references at the end of the page. However as this is to be a student embryology wiki page, it would help if the passages of text were broken up into bullet points and tables. Furthermore there are no images or student drawn diagrams. These would also help convey the main messages of musculoskeletal development. The sections after tendon development are unfinished and very brief. Furthermore the only in text referencing present is in the first two sections. Citations should be carried through the entire page. &lt;br /&gt;
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The second trimester muscular development section is particularly clear and to the point. However the information present doesn’t stretch much further than what was covered in the lecture material. By adding diagrams of the pharyngeal arch origins and including further research into this section, its quality will be greatly improved.&lt;br /&gt;
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==Online Assessment 9==&lt;br /&gt;
Sensory System Development - The Eye&lt;br /&gt;
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Embryological eye development is an area of sensory embryology that has recently been the subject of various research papers. A paper that has particular relevance to eye development is by Yao Chen et al, titled Effects of High Salt-Exposure on the Development of Retina and Lens in 5.5-Day Chick Embryo. It was published on the 20th August 2014 making it very current research. Although they used Chick embryos instead of human embryos, the Chick model is very useful for looking at eye development because that sensory system is relatively large in the early stage embryo, hence making it easier to study. &lt;br /&gt;
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This paper investigates the effect of high salt exposure to the developing embryo particularly on eye, lens and retina shape and development. It compares a control eye that had normal salt exposure with two variations: exposure to 280mosm/l Sodium Chloride (NaCl) solution and 300mosm/l NaCl solution. Once the fertilised chick embryos were treated with these solutions, they were incubated and then H&amp;amp;E stained for analysis of transverse sections. The eye diameter and retina thickness were measured using Image-Pro Plus 6.0, a photography program. The proliferation of cells in the retina were measured using Phospho-Histone P3 immunostaining to measure the expression of the Pax6 gene which is vital in normal retina development. &lt;br /&gt;
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This report also explains early vertebrate eye development in the embryo. The eye has three main embryonic origins: the optic vesicle, the surrounding mesenchyme and the overlying surface ectoderm. In response to signals from the optic vesicle, the surface ectoderm thickens to form the lens placode and around week 4 disassociates from the surface of the embryo to form a lens vesicle. This lens vesicle will form the actual lens. The optic vesicle invaginates to form an optic cup where the internal layer forms the neuroretina and the outter layer forms the pigmented retinal epithelium.  There is also neural crest cell contribution to the development of retinal ganglion cells, cone photoreceptors, rod photoreceptors, bipolar cells and Muller glia cells. The Paired Box 6 gene (Pax6) is also very important for proper development of the eye, eye size, neuronal differentiation and retina development. &lt;br /&gt;
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The results gathered form this investigation highlighted the detrimental effect high salt intake can have on a developing embryo, in particular eye development. The level of eye deformity increased with increased level of NaCl exposure. The size of the eye decreased significantly, the diameter of the lens decreased and the lens was thinner. These results were gathered by looking at the images after H&amp;amp;E staining. Furthermore, using immunostaining, it was evident that there was decreased expression of the Pax6 gene in high-NaCl embryos.  This is very important since it has been found that this gene is expressed during optic vesicle and integration of the surface ectoderm into development of eye structures in the early embryo. If this gene is not expressed due to high salt levels, the embryo will have abnormal eye development. This can be observed in humans who suffer from pan-ocular disorders and in mice models where an under expression of Pax6 leads to the eyeless phenotype. Pax6 is also important during neural crest cell migration specifically the periocular mesenchyme cells that contribution to eye structures. Hence it is clear that this report shows how high levels of salt intake can have detrimental effects on eye development. &amp;lt;ref name=&amp;quot;PMID10.1159/000363044&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1159/000363044&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_6&amp;diff=150599</id>
		<title>Talk:2014 Group Project 6</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_6&amp;diff=150599"/>
		<updated>2014-10-15T01:16:02Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Group Project Topic - Endocrine */&lt;/p&gt;
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==Peer Reviews==&lt;br /&gt;
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Great work, it looks like your group has a clear mindset and direction to where your group project is going, even if it is not there yet. One of the images next to the timeline section was too small to be view without actually opening up the actual image. There are a few images on your page, and also a few tables, perhaps uploading a few more images that correspond to the text.&lt;br /&gt;
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Under the heading of Pineal gland, there is a sub-section labelled 'timeline', however there are only three points under this and no time course, or time frame included. The timeline needs to be further developed. &lt;br /&gt;
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There is not information for Abnormalities. Only an uncompleted table and references exist. This information needs to be filled out the sooner the better. There seems to be a sub-section about abnormalities for each endocrine organ, but this does not contain much information-see Pineal gland and Hypothalamus sections. Perhaps your group would consider, just having one section in your project for all the abnormalities associated with the endocrine system. &lt;br /&gt;
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There are several reference lists within your group project page that need to be put together to create just one reference list, I understand why this is at the moment, just remember to change before your final group submission. &lt;br /&gt;
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Introduction is missing in the project. It would be great to include the functions of endocrine system and the contents that will be covered including system development, abnormalities, current research, etc.&lt;br /&gt;
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There is a lot to cover in endocrine system, it is a great way to separate timeline and recent findings under each individual organ. Using table to illustrate the function of hormone is good, however, I think it would be better to have a summary of hormone in a table form at the top/the end of all individual organs. The parathyroid gland and pancreas are well-researched with the use of images. More information has to be included in other sections.&lt;br /&gt;
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More work has to be done on abnormalities. Actually, they could be separated under each organ, just like current findings. It would also be good to see historic findings under each organ.&lt;br /&gt;
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In terms of referencing, there is no in-text reference and the reference list at the bottom is empty at this moment. This project overall has a good structure, but more information and images are needed.&lt;br /&gt;
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An introduction has not yet been added, however when doing so aim to mention the gist of the project and the manner in which is has been divided so that the reader/marker can effectively understand what is in this project. The wikipage is separated into the numerous endocrine organs, which is great as a future student can easily navigate to the organ of interest. &lt;br /&gt;
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As it is only a draft copy it is assumed that improvement and adding of information will take place leading to the submission of the final as there are subheadings such as “Recent findings” that have been left blank. With what is currently present, each organ contains well researched information. In the beginning two organs, the pineal gland and hypothalamus, there is a subheading for abnormalities, however there is also a section towards the end of the wikipage solely for abnormalities, so refrain from doubling up on the information and either place all the abnormalities in one section or separate the malformations in terms of their respective structure. References are also seen at the end of each section or subsection and no in-text citation has been used yet, so it might be easier to cite the dot points or information as you go so you can remember where you got that from instead of trying to find that piece in the numerous research articles you have. Once that has been done, it will be best to relocate all the references at the end of the page, where you have already made the heading.&lt;br /&gt;
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The structure is consistent throughout the page with each organ having a timeline and most containing an image and a table. This makes the project appealing and easy to read and understand. All the images uploaded contain comprehensive information and thus I am able to decipher the image and as a result enriches the learning aims of this assignment. The creation of a timeline for each organ is clever as each exhibits its own developmental process. The separation into many smaller timelines allows for specific events to be included that would otherwise overload a collective timeline. The setup of a table under the organisation of hormone, cells and function further simplifies an extremely complicated developmental system. As a student learning about the endocrine system I would be relieved to discover tables and content of this standard and structure. &lt;br /&gt;
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The introduction section is blank so I suggest you start on it as soon as possible.&lt;br /&gt;
I like how you have organised the sections in terms of each gland.&lt;br /&gt;
Pineal gland section requires in text citations and more information with the aid of an image. Spelling error for abnormalities.&lt;br /&gt;
Hypothalamus section needs more information and images. Good idea to use a table but it is incomplete. In text citations are needed throughout.&lt;br /&gt;
Pituitary gland section only has the timeline and references. It needs much more information and images with in text citations.&lt;br /&gt;
Thyroid section is a bit better but still is missing little information.&lt;br /&gt;
Parathyroid gland has a very good image and the information is well presented. Once again in text citations are needed.&lt;br /&gt;
Thymus section only has little information so work more on this.&lt;br /&gt;
Pancreas by far is a much better section compared to others as it consists of an image, table and a timeline. In text citation are missing.&lt;br /&gt;
Adrenal gland section is missing a little information and an image that’s all. Also in text citation is missing.&lt;br /&gt;
Gonad development section is well presented just add images to it.&lt;br /&gt;
Placenta section just has references. You need to start researching information on this.&lt;br /&gt;
Associated abnormalities section just has an incomplete table.&lt;br /&gt;
The page could use a bit more uniformity. Throughout the page, two different spellings are used for fetal (fetal and foetal). Try keeping the context consistent.&lt;br /&gt;
Overall I suggest you start researching more for your project as A LOT of work may be needed to be done. In text citation is crucial as you have noticed by my constant repetition for it. Recent findings and historic sections are missing. I suggest researching on pubmed under “(gland name) historic/research findings”. All the references will look better and more professional if it was in the end of the page in a bulk. There are some really good information and images on your page. If possible try adding hand drawn images too. You may only have 1-2 weeks to complete this project but I believe you can do it so good luck!&lt;br /&gt;
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This project would greatly benefit from an introduction, to present the contents of the project. The content is broken up into individual organs, of all the systems endocrine definitely one of the most varied in location so this approach does have some merit for initial data gathering. It does present the problem for viewers in navigation and resulting in continual repletion of timelines. Each organ is subdivided into timeline, introduction, structure, function, development and abnormalities. The content presented is solid and obviously well referenced. Placenta section should be added, because of its significant endocrine organ during fetal development. The references are mostly placed at the bottom of each organs section, these should be moved to bottom of the whole project in combination with in text citation. This will make the body of the project less cluttered and more fluid.&lt;br /&gt;
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The table for hypothalamus hormones and associated abnormalities are mostly incomplete with “Example” filling many of the boxes. I would advise completion of hypothalamus hormone table and removal of associated abnormalities. In total there were only 3 images, addition of 2+ more images would help readers visualize the developmental organs. With at least one image per organ and preferably an additional image for an abnormality. Sufficient content is presented in this project though significant formatting changes are needed to create a completed project, additional images would be preferable.&lt;br /&gt;
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Overall, this is quite a good project considering the complexity of the system. I think that generally, this project would benefit from some restructuring, so as to improve the cohesiveness of your work. I think that an introduction is a good idea to organize your ideas and give the reader a good background when trying to understand some of the more difficult concepts. I think that the choice of sub headings should be advised. It is interesting that you have chosen to deviate from the given subheadings, and I understand for your system that that may be necessary- however I think that some structure or regular subheadings for each part may be a bit easier to control. Also I think an overall timeline is always a great idea as it provides a visual representation and puts things into perspective.&lt;br /&gt;
I also think that some areas could use a bit more research, for example a large part of the pineal gland and hypothalamus appears to be missing and there are kind of “insert text here” sections- which I’m sure you’ll work on by the submission date.&lt;br /&gt;
I also think its important to remember that your referencing needs to be carefully done and consistent. Currently it seems quite poorly organized, and I think overall could use with a few more resources for every section.  I think because you are already deviating from the normal structure of things, it would be a good idea to leave your references until last, just so your work isn’t broken up even further.  The abnormalities section is severely lacking- the table is a good idea, but make sure you fill it!&lt;br /&gt;
Overall a good start, some places need some serious content others just need a tidy up.&lt;br /&gt;
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Great job on doing the endocrine system! There are lots of content for each organ of this system, which is good. I can see that this system was broken down into organs and allocated to different members. The only problem I see with this format is that presentation could be incoherent. I suggest try to follow the outline Dr. Hill gave us like development, current findings, etc. and just break each section into sub-sections for each organ. If that’s too much, then maybe just a single timeline of the development of the whole system. Also try to have a uniform layout for the tables about the hormones secreted by each gland.&lt;br /&gt;
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There aren’t many images used in the page so maybe try to add more images. They really help with getting the readers to understand the information. In terms of referencing and citations, good job on choosing the research articles. All of them seem to be relevant to the the project. Don’t forget to use in-text citations. Not only is it important but it will make the page look a lot cleaner. Also, try to get all the references into one bulk at the bottom of the page. Overall, there aren’t a lot of problems in terms of the content but mainly about organising the page, making it coherent, and cleaning it up. I think the thyroid, parathyroid, pancreas, and adrenal sections were remarkable. Well done!&lt;br /&gt;
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Group Project 6 – Endocrine Development&lt;br /&gt;
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An introduction could be very useful to summarise what the page is going to discuss. Sections 1.2-1.11 could all be subheadings under the main heading ‘System Development’, and then each of these subheading could be further divided into smaller subheadings with timeline, introduction detailing structure/ function of the endocrine organ. It is however very well done how the headings of each organ are then further subdivided into ‘abnormalities’, ‘research findings’ and ‘timeline’. However, the fact that each section has its own references and is subdivided as such, shows that even though the page may appear more ordered, there appears to be little communication between group members at this stage. So perhaps a goal could be to make the page look like one flowing work piece as opposed to sections that each person has done. &lt;br /&gt;
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I think the content is very well researched and I like the way each organ of the endocrine system is discussed, as all are important in fetal development. The use of images is appropriate and very well done as they are referenced correctly and when you click on an image it takes you to a new page showing the student image template, copyright information as well as extra information regarding the image. There are no student-drawn images however, so perhaps it could be possible to draw a flow chart perhaps of gonadal fetal development. The use of tables is also done very well and is frequent throughout the page, with some being used to illustrate the anatomical development of certain organs, for example, the adrenal gland and pancreas. The graphs are also useful in portraying information from research findings.&lt;br /&gt;
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The project page is missing information regarding historic findings, and I think that if this page is going to have a main heading for Abnormalities, then the group should put all their information regarding abnormalities under this section. Although it is not an endocrine organ that grows within the developing foetus, but is an important part of the mother, there is not much information on the page regarding the placenta. This section needs to be completed as the placenta is an important source of hormones and acts as an endocrine organ during the pregnancy, sustaining the foetus.&lt;br /&gt;
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It is good that there are many references, indicating thorough research into the endocrine system with each organ heading have its own sources, however I think these references need to be ordered better. The actual referencing is done correctly, however in-text referencing is absent, so it may be best to fix this. Most images are referenced correctly as well.&lt;br /&gt;
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Overall, keep up the good work, but just edit the page to make it look neater and finish the sections you need to.&lt;br /&gt;
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At first glance, a lot of sections seem to be incomplete. On second glance, I’ve noticed that you have added all the headings used by other groups (timeline, current findings, abnormalities) as subheadings for your own project, which I think it a really smart idea. Because you have so many glands that need to be covered, writing these sections separately can be confusing with the information quickly becoming muddled up. Doing it this way eliminates that confusion. &lt;br /&gt;
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Make sure the use of tables is appropriate, using a table for one row of info is kind of pointless (pineal gland). The timelines used should also start with the week number, otherwise it can be quite confusing trying to work out the time (e.g. try not to say times such as ‘by the second trimester’). The information presented was concise and to the point, no long-winded explanations or slabs of text which was good. The images used were relevant and captioned.&lt;br /&gt;
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Concerning the work completed, overall it was done well. A lot more work still needs to be completed however. References should also be made in text. If you are unsure how to do this, just go into edit mode in another group’s project and see how they have done it, instead of listing all the references at the bottom of the corresponding section. Make sure all the references are also presented at the bottom of the page, not separated into sections. It would also be nice if more images are used, if not one image for every gland then at least one for every second gland mentioned (it just needs more images).&lt;br /&gt;
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There seems to be no introduction on the page, don’t forget to add content to this section before the final submission. The overall page looks disjointed by the choice of sub-headings. I think an overall timeline is needed to know which glands/organs develop when and originate from where.  It would look much neater and would be easier to follow. &lt;br /&gt;
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The parathyroid gland and pancreas seems to be the only sections that are properly completed. Both sections have good use of images and the tables provide easy readability. The images are all properly cited, good job. &lt;br /&gt;
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The overall referencing of the page is all over the place and lacks in-text citations. I suggest you go through the contents and add these where necessary. If you are unsure how to do this, just look at the handout Mark gave out in week 2 for further reference. Or, alternatively you could look at some of the other project pages in edit mode. I would also suggest you leave all the references to the end of the page by simply putting &amp;lt;/references&amp;gt; at the bottom of the page, as it looks neater to have them all in one place, rather than at the bottom of each sub-heading.&lt;br /&gt;
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The abnormalities section is lacking content and there is only 2 diseases listed, with no description. &lt;br /&gt;
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Overall, the page has good content, just needs to be edited to put in-text referencing. Some sections need contents such as the placenta and adding images to the page will also improve its presentation.&lt;br /&gt;
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So far you have made a good start. The introduction is a really important part of the project so it’s important that you get that down.  The pineal gland part has made a good start but it would be good if some more hormones could be added.  I think it would be good maybe if you all combined all of your times line and put them at the top of the page. You could maybe do this in a table form, but it’s certainly something that would make the project more succinct. Also instead of having references spread all over the page it would be a good idea to put the all of them at the page to make the page look more neat and tidy. &lt;br /&gt;
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The hypothalamus part also needs to add extra information on the hormone part and add their illustration. I think it may be a good idea to add a student image because this makes the page more interesting and people looking at the page will be instantly attracted to this. Something that is really important and goes for the whole page is that you need to do in text referencing, as having the references at the end of the writing is tough because we don’t know which parts came from where. &lt;br /&gt;
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Its good that there is recent findings in the hypothalamus part but I think this probably highlights the biggest issue with your project, being that It probably doesn’t link with all parts that well. I think it would be good if you could link all parts of the endocrine system together to make it easier to understand. For example, if you put the recent findings as a whole new part then everyone puts their recent findings in there it will make it easier to understand and look more collaborative. Also there is an imbalance in written information to pictures which tips in favor of the information. While it’s great to have a lot of information it becomes a bit boring just reading all the time so I think adding more images, particularly student drawn images would be something that would definitely improve the page. &lt;br /&gt;
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Overall it has been a good start but the main points that need to be focused on are to finish off the information, make sure you correctly reference with in text citations and putting the references at the end of the page, and adding more images to make it more interesting. Good luck with the rest of the project.&lt;br /&gt;
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There is no introduction! You should definitely add one! &lt;br /&gt;
The graph in the pineal gland only has one rows; I suppose you are planning on adding more rows and hormones secreted by the pineal gland? If not, maybe just scrap the graph in general cause there’s really not much point.  The graph in the hypothalamus section doesn’t have any examples yet, I presume that you’ll be adding stuff soon?&lt;br /&gt;
The overall project having been divided according to  the each endocrine organs is really nice. &lt;br /&gt;
Hardly any work has been done yet on the pituitary gland yet, you might want to get started. &lt;br /&gt;
Beautiful work on the thyroid, parathyroid and pancreas; easy to understand the paragraphs, and they are visually aided with pictures.  For the development of the adrenal glands, and the testis and ovaries, I think you should find a picture.&lt;br /&gt;
Historic findings, placental development and abnormalities are basically non-existent, which are vital components to this project. &lt;br /&gt;
Overall, the project is very very informative and very well done! The page has good content, just add the in-text referencing, and maybe try to improve the aesthetics to make it more appealing to your readers. Good luck group 6!&lt;br /&gt;
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The page is set out really well especially since the endocrine development covers so many organs. It’s a nice clear and concise way of structuring the page.  Each particular organ is addressed really well. There is good consistency with each one on the page that is great. The page contains a sufficient about of content and detail in the info for each section of an organ addressed. It is good to see the use of tables and some dot point formatting which always helps to keep the content clear.  There are parts in each section that are missing info these include the abnormalities and tables.  The use of images with captions containing well detailed descriptions are also constant under each section. Some suggestions to consider include adding more info to the abnormalities would be great. Focusing on discussing what each abnormality is, how it’s contracted, statistics and then treatment. Throughout the whole page in text citations have not been used at all which should be included, especially when research studies are mentioned. A way to assist with this is to use the following format; for pubmed  &amp;lt;ref name=PMIDnumber&amp;gt;&amp;lt;pubmed&amp;gt;pubmedIDnumber&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; and then for other references &amp;lt;ref&amp;gt;insert source&amp;lt;/ref&amp;gt; . Then after those are inserted, add an additional referencing heading and under it write &amp;lt;references/&amp;gt; .&lt;br /&gt;
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Overall the page does not need too many changes, just a few adjustments mostly with formatting and references. Then some sections need a little bit more info to be completed. An introduction would also be a great way to provide an overview of the content that will be covered since there is a lot discussed.  So far it can be seen that a great deal of research has been conducted. It’s also understandable that not all sections are completed just yet as this is a pretty lengthy system. Try to also incorporate some graphs, drawings and even video’s, they are a great visual aids. Keep up the good and the page will be really great, good luck :).&lt;br /&gt;
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Just must say, this must be one of the hardest topics to cover! Excellent work overall and continue to work hard in completing and finalising this page. But please don’t forget to add an introduction which clearly lists the outcomes that the page will hope to address&lt;br /&gt;
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I really believe that this page would greatly benefit by re-structuring the entire layout by the headings suggested to us- ie. Development timeline, recent findings, current research and abnormalities. Seems a bit disjointed and is hard to follow.&lt;br /&gt;
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Due to the manner in which you guys have subdivided the sections via organs, it is hard to comment and critique via the headings suggested. Some organs have been excellently covered (pancreas, thyroid, parathyroid), however, some organs do need a bit more development (eg. Pineal gland). Also, due to the way you guys have decided to approach this page, the writing styles and presentation of information does have notable differences amongst the oragans.&lt;br /&gt;
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Overall, there is an excellent choice of headings and subheadings though. There is also excellent and correct citing in most of the sections. However, this page could be greatly benefited by re-structuring the entire page to follow the suggested headings.  I really believe that the information and research included in this (hard) topic is excellent and demonstrates significant scientific research, however, the overall structure makes it hard to follow and understand! I believe re-structuring will address a lot of the issues mentioned. But again, excellent work so far in this very hard topic!&lt;br /&gt;
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In this review I intend to highlight the merits of your project and suggest some areas for improvement in light of the marking criterial provided. &lt;br /&gt;
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I believe that an organ-by-organ approach to this section is great. This really helps organise the information. This layout also makes the page easy to navigate allowing students to directly refer to the section that they want to learn about. However by doing so I think you may have neglected some of the areas. &lt;br /&gt;
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Each endocrine organ has a great introduction describing the structural features and nature of the organ. I suggest including an image or a hand-drawn diagram of each gland and location, as this would really aid understanding The time line is a great way to summaries the major stages in development, I feel that this section has been completed with sufficient research and detail.&lt;br /&gt;
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The section on abnormalities needs to be completed, even if only one abnormality is addressed make sure you include information on the following areas. Epidemiology; Description; Cause and Treatment. Furthermore ensure that the section on current research and historical findings is researched and addressed addressed.&lt;br /&gt;
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I feel that your project is incredibly cohesive and attempts to provide a through summary of all the main endocrine organs. However a number of sections are yet to be completed. You have a great template right now. If all these areas are completed the project will be a success. In addition; I suggest placing all the references at the end of your project page, under one heading. Good Luck!&lt;br /&gt;
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The endocrine system is made up of different glands and there is so much information that could be provided regarding the the anatomy and development of each gland so very well done for working on the difficult system! I like how you have divided the page into different glands; I can imagine having the four major headings (development, historic findings, current research and abnormalities) and then subdividing it into different organs would be more confusing. Just try to follow the same structure for each organ; I recommend doing a brief introduction, anatomy, function, timeline, development, historic findings, current research and abnormalities for each organ. It is important that your page has a coherent flow by following the same structure for each subheading. An overall introduction on endocrine system might also be very useful. You can then include in the introduction how you are planning to structure your page.&lt;br /&gt;
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The content and number of references show that extensive research has been conducted. It would be great if you could use in-text referencing and place all the references under one subheading at the end of the page. Arranging the information into tables is a great idea but you need to complete your tables for pineal gland, hypothalamus and placenta. You also need to include more images in your page (you can include at least one image for the abnormality associated with each organ). There are a few images included at the moment and they are well done and appropriately referenced. You can also try to draw your own diagrams. In my opinion, a timeline showing the development of all the systems would be a great way to compare the different stages in development of different endocrine glands. Maybe think about including this in a table after you finished all the sections; it is a good way to connect the information provided separately for each organ. Overall the content of this page is very good but it needs to be formatted so that it can have a coherent flow. Also there is no information for introduction, historic findings and development of placenta, make sure you include those.&lt;br /&gt;
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The breaking down of this system into organs is a real strong point of this page and there is plenty of information under each of these subheadings. The page could benefit from a ‘Current Findings’ section or perhaps by including relevant articles under each organ. &lt;br /&gt;
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The text in this page is great but it could really benefit from the inclusion of some more images to support the information. I can see that your group did plenty of research but in text citations need to be included with your text with a ‘References’ section at the bottom of the page to stop the reference lists scattered along the page from interrupting the flow of your page.&lt;br /&gt;
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Overall the page is definitely well resourced and has plenty of detailed text. Along with the inclusion of images and some minor improvements with the organisation of your text, this page will become a very good finished product. &lt;br /&gt;
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I noticed that there is no introduction, however the page does have introduction heading, I’m assuming you didn’t get the chance to upload information there or you haven’t had the time. This is something you need to work on so that the audience has some note of what this page is about, instead of just going straight into the pineal gland. It would make your page more appealing and professional if you followed through with an introduction.  &lt;br /&gt;
There is great amount of reference at the end of each section however there is no in- text referencing. Having in-text referencing will allow the audience to  know exactly where the information was read from and for the interest of the audience can read that specific paper in detail. &lt;br /&gt;
There is a great amount of information in almost every section with great detail however, consider subheadings to make the section easier to read and allows the audience to navigate the page effortlessly. Also consider some images in each section, to make it more inviting and not overwhelming with just content. &lt;br /&gt;
I do appreciate that each section is subdivided into “development, timeline”, maybe consider adding in the current research, historic research and abnormalities to ensure that you can get all the marks possible by addressing all the key concepts. &lt;br /&gt;
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Overall this page is coming along nicely, I can appreciate the difficulty of this system in trying to make the page more coherent. However if you work on the subheading within each section and add some images as well as some in text referencing I think that should make a significant difference by making this page more inviting, easier to navigate and also appear greatly organised. &lt;br /&gt;
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You have covered the main topics by listing the endocrine organs. However the sections are lacking some key information which I assume you will add later. The introduction is empty and it would be very helpful it outlined what the page was about and what the page was focusing in terms of endocrine development. Also historic findings and current research models and findings haven’t been addressed yet. It is present to a small extent in some endocrine organ descriptions. By identifying these topics the page could be greatly contributed too. The page has good use of timeline for all the organ descriptions. However the timelines need to be expanded on with more detail. &lt;br /&gt;
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Maybe a better use of headings is possible, where subheadings under each sections can be made. For example under hypothalamus the following subheadings can be added and used; historic findings, recent models and findings, hypothalamus development during fetal period, abnormalities occurring during fetal period. These topics are covered in some sections, but if subsection headings were made, it would be much more easy to read and navigate through. As there is a lot of organs to cover this may be useful.&lt;br /&gt;
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Diagrams and tables could really help fill the page up and help in giving a more comprehensive coverage of the topic. Some tables aren’t fully filled up, for example the table under ‘hypothalamus’ and ‘Associated Abnormalities’. The filled up tables which are in the pancreas and adrenal gland really help these sections and if added and fully filled up for other sections could really add to the page. There is a helpful use of dot points within the page which helps make the material readable and structured, particularly in thymus, pancreas and gonad development. &lt;br /&gt;
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Some sections don’t have adequate information on fetal development for example the Hypothalamus and Pituitary sections. There seems to be a teaching level of knowledge being displayed. Deeper research could be done to further enhance the project and fulfil project aims. Also more tools for helping peers understand the topic could be used, for example diagrams and hand drawn diagrams, video links etc. &lt;br /&gt;
References are done and there is a lot of in text citations. Some sections like the ‘Pineal Gland’ and ‘Hypothalamus’ section has no in text citations, which need to be added. The official references section is empty. If all the references from each of the sections could be added to the main reference section it would be great for the page. This can easily be done by referring to the how to reference page on the website; https://embryology.med.unsw.edu.au/embryology/index.php/Help:Reference_Tutorial. &lt;br /&gt;
Overall good job guys ! Good luck &lt;br /&gt;
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Diagrams that have been used are good and show what the text has been explaining. Tables have been used well to illustrate some of the information; tables could also possibly be used to show the developmental timeline more clearly.  References could all be collated at the end of the project to make the text flow better from one section to another. &lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
&lt;br /&gt;
The page is well formatted in terms with heading and choice of content such as diagrams, tables and graphs. Having the different organs as headings is good as it allows the readers to take in information in a logical manner.  It is good that timeline is included under each organ heading shows understanding of the whole endocrine system by breaking it down organ by organ however each sections is not consistent with the other one. Some has development overview while others write timeline I would suggest to keep it as same heading for all.  There is good description of each organ at the beginning of each section and in the timeline there is key events described showing understanding and helping to learn. &lt;br /&gt;
&lt;br /&gt;
All sections are incomplete in some form or another. The diagram used are good and relevant especially the pancreas cells diagram. It is well explained and shoes evidence of research. Pineal gland timeline looks incomplete or doesn’t show evidence of enough research however the recent finding is relevant and good in this section, other sections have not included recent finding showing some lack of research. Other sections also have incomplete tables and could put diagrams or drawings to so information can be better understood for readers. A video or two could also be added on the page and a section for historic finding should be added under each headings. &lt;br /&gt;
&lt;br /&gt;
Overall there is some good information that shows evidence of research in the development of the different endocrine organs however there is lack of models and research findings as well as historic findings, even abnormalities are not well explained in each headings. It is not easy to navigate as each headings are not consistent with each other however the diagrams used are relevant and properly explained and citied. There is also good use of table to enhance understanding of hormones involved and with few adjustments page will look organised and be logical to read. Reference is done correctly however it would make it more engaging and easier to follow if in text reference was done and having a list of the reference at the end. A short paragraph in the introduction would also help readers understand exactly what is involved in endocrine system. &lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
&lt;br /&gt;
== Group Project Topic - Endocrine ==&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:17, 20 August 2014 (EST) We have chosen our group project to be on the endocrine system.&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418702|Z3418702]] ([[User talk:Z3418702|talk]]) 13:07, 20 August 2014 (EST) We have decided to allocate 2 topics (endocrine organs) to each group member. We will go and research each and look for research articles and then figure out the best way to structure the content.&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:19, 26 August 2014 (EST) This is a draft allocation for research topics for our project. &lt;br /&gt;
Janaki - Pineal, Hypothalamus.&lt;br /&gt;
Ali (z3414648)- Pituitary, thyroid.&lt;br /&gt;
Samrah (z3418837) - parathyroid, thymus, pancreas.&lt;br /&gt;
Ruth - Adrenal, gonad, placenta.&lt;br /&gt;
Samrah and Ruth if there is heaps to do on those three parts that i've allocated just let Janaki and I know and we can also help out. If anyones topics are sparse on info also let us know and we can reshuffle the allocations&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418698|Z3418698]] ([[User talk:Z3418698|talk]]) 22:02, 26 August 2014 (EST) Hey guys, I was thinking we should maybe have a heading 'Recent findings' for maybe a few of the topics and have a short, brief summary of any new developments. I think it would be really interesting!&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418702|Z3418702]] ([[User talk:Z3418702|talk]]) 00:00, 27 August 2014 (EST) That's a good idea, should we put a separate section on recent findings, or just some information on recent findings under each section? Also we need historical findings&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418837|Z3418837]] ([[User talk:Z3418837|talk]]) 00:44, 27 August 2014 (EST)Hey guys, it's better to post student numbers to the parts allocated to each group member so it's easier for the tutor to mark. I would do this but i'm not sure about who is who :P Also I like the idea of recent findings. I think it's also better to post articles related to the recent findings and abnormalities as we go along as this will make it easier instead of leaving it to the end. For now, I think we should just post up as many articles related to each topic as possible and then figure out how to structure the content.&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 21:22, 2 September 2014 (EST) Hey guys, I've done some research on the prenatal development of the thyroid gland so I'll add that to my section. We can always change it up later.&lt;br /&gt;
&lt;br /&gt;
I also found this review article that goes into a lot of detail about the pituitary gland. It explains the cellular differentiation involved to create the cells responsible for manufacturing hormones like ACTH. There is a lot of complex gene involvement but I was thinking we could condense a lot of the information into a table. I suggest you guys do that for your organs too rather than having a lot of jargon on our page that only an advanced biochemist will understand. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;22872762&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 10:09, 9 September 2014 (EST) Hey i found a great article on normal and abnormal thyroid development and it's given me a lot of great information for the timeline part. &lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1016/j.beem.2013.08.005&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
 &lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418698|Z3418698]] ([[User talk:Z3418698|talk]]) 12:44, 10 September 2014 (EST)We are going to incorporate the Timeline and Abnormalities under each individual sub heading rather than at the end of the page. We are also going to find image links and post them in the discussion page before uploading them. We are also going to tabulate the hormones released by the glands under the subheadings. This will summarise the function of the glands in the embryo and how they contribute to fetal development.&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418702|Z3418702]] ([[User talk:Z3418702|talk]]) 00:46, 17 September 2014 (EST) Hi guys, I've added some info about adrenal development through gestation, at this stage some simple dot points which will probably be expanded upon later. There is a lot of content about the cell morphology at different weeks but I'm not sure as yet whether it's necessary to include that level of detail?&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:59, 17 September 2014 (EST) Hey guys, i found this link for an image that i'm thinking of using on the project. It's from PLOSone which is good because it's free to use those images. This is the link for it: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016752&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418698|Z3418698]] ([[User talk:Z3418698|talk]]) 13:06, 17 September 2014 (EST) Hey guys, I found this image I wanted to use for hypothalamus development in a rodent, it basically illustrates the different nuclei in the hypothalamus once it it fully developed but I will be focusing on those that are present during development and the role of hormones each of them releases. &lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2082685/figure/fig1/&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418702|Z3418702]] ([[User talk:Z3418702|talk]]) 23:50, 23 September 2014 (EST)--[[User:Z3418702|Z3418702]] ([[User talk:Z3418702|talk]]) 23:50, 23 September 2014 (EST) Hi guys, I think I might use this image (figure 3), it's from the PLoS too so totally fine to re-use and shows the fetal adrenal gland using 3 different techniques, like MRI, gross imaging and histological stain. I like it because it shows the gland from different perspectives. I'll upload it soon but here's the link:&lt;br /&gt;
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0075511&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418837|Z3418837]] ([[User talk:Z3418837|talk]]) 03:29, 24 September 2014 (EST) I might use this image for the pancreas section http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0007739 . It basicallys shows the development of the islet of langerhans and the ratio of alpha &amp;amp; beta cells at different phases of fetal development. Also Z3418698, I don't think that image can be used as it has copyright restrictions. Try looking in Plos One =]&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418698|Z3418698]] ([[User talk:Z3418698|talk]]) 11:59, 15 October 2014 (EST) Hi guys, for our stem cell research presentation task I've found an interesting article on adipose tissue-derived stromal cells and their potential for cardiovascular regeneration. Have a look and let me know what you think! :) http://www.sciencedirect.com/science/article/pii/S1873506114001068&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:15, 15 October 2014 (EST) Hey i found an article on stem cell biology that we can send in to be checked. This is the link if you want to have a look at it. We just need one more and then we're sweet. Sorry I didn’t respond, I can’t make it this Thursday evening since I’m tutoring and I’ve got tickets to an Oktoberfest party. From next week onwards my Thursday evenings will be free, obviously. I’d love to be updated with what happens tomorrow night if someone is going to take minutes of the meeting? http://download.springer.com/static/pdf/736/art%253A10.1007%252Fs11626-014-9818-2.pdf?auth66=1413334955_76faa5c3ff5dcfff697deaf907881825&amp;amp;ext=.pdf &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
&lt;br /&gt;
*Firstly, props on choosing the endocrine system. It seems like one of the harder ones to take on&lt;br /&gt;
*I don't understand why you chose to divide tasks based on endocrine organs as that has seemed to cause your research to become really disjointed. I guess now work harder to collaborate your separate findings particularly for things like having 1 united timeline overview&lt;br /&gt;
*Ensure uniformity throughout the page with little things like is it &amp;quot;fetal&amp;quot; or &amp;quot;foetal&amp;quot;? Choose one then go with it&lt;br /&gt;
*Maybe have labels for tables more distinguished as being separate to the main text&lt;br /&gt;
*Include the references throughout discussion, rather than a collection at the end of each section. Then have the entire reference list at the bottom like all the other pages have. You can look at the &amp;quot;edit&amp;quot; of other pages to copy and paste the codes&lt;br /&gt;
*Your timeline isn't really a timeline if there are no times mentioned in the &amp;quot;pineal gland&amp;quot; section. Try using a week-by-week format and separating information that way for all of your findings altogether. Then format that into a table&lt;br /&gt;
*Proofread for typos &amp;quot;Abnormalities&amp;quot; in &amp;quot;pineal gland&amp;quot; section&lt;br /&gt;
*Need more images for earlier sections&lt;br /&gt;
*Great formatting of images and tables for the adrenal gland, parathyroid and pancreas sections&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=150419</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=150419"/>
		<updated>2014-10-15T00:08:42Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Lab Attendance */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
&lt;br /&gt;
[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
&lt;br /&gt;
==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
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===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
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===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
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===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
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===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
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===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
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===Lab 10===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:08, 15 October 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 1 ==&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
&lt;br /&gt;
The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
&lt;br /&gt;
These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
&lt;br /&gt;
These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
&lt;br /&gt;
The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&lt;br /&gt;
===Thyroid===&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&lt;br /&gt;
&lt;br /&gt;
--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
&lt;br /&gt;
'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
&lt;br /&gt;
The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
&lt;br /&gt;
1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
&lt;br /&gt;
2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
&lt;br /&gt;
3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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&lt;br /&gt;
==Online Assignment 5==&lt;br /&gt;
&lt;br /&gt;
===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
&lt;br /&gt;
Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;br /&gt;
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Project 7: Neural &lt;br /&gt;
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This project has a great introduction and overview of the brain and spinal cord anatomy. The first image is eye catching however I find it hard to follow and it seems like there is too much information on it. Perhaps it would be better positioned further down in the report after more neural developmental stages have been explained. The timeline section is clear and to the point. There is an excellent use of images to support the information. The fluorescent stained images make the ventricular, subventricular and other cortical layers clear and easy to understand. The information under the brain development section is simple and effective. However there are some terms mentioned that are not explained in enough detail like the specific layering of the cortex. It is a complicated migration process that deserves some more research. It is good that the student has explained gyration and sulcation in this section. &lt;br /&gt;
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This project is clearly still in progress however the information in the first section of the wiki page indicates a very promising final product. The spinal cord and meninges development section still needs to be written up. If it follows along the course of the brain development section, it will be flawless. The current research models and finding section reveals an in-depth understanding of complex ideas. However for a student embryology wiki page, there is too much detail. If the student wants to illustrate a complicated research finding, images or tables of the results found from this research would help convey the message to the student. A table would help summarise the results in the first current research description, particularly for the results gathered from the different parts of the brain. &lt;br /&gt;
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The final part of this report on abnormalities is unfinished however the bulk of the information presented already is very good. The images supporting the abnormality are excellent and important for keeping the student reading this page engaged. However there are a few spelling and grammar errors in the neural tube defects section: “which affect the either the brain”, “the openings remain which leas”. There is still room for more research and information on other neural development abnormalities and the subheadings the student has incorporated indicates their intention of adding more information. This report has excellent reference formatting and citation throughout the page. The tables and images are referenced correctly and the long list at the end is very neat. &lt;br /&gt;
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Project 8: musculoskeletal &lt;br /&gt;
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This project is still in its early days but the layout and plan is very good. With additional information added to the subheadings, it will be a very interesting student wiki page. Reviewing what has already been completed on this page, it is too content heavy. There are a lot of large chunks of text indicating the student has gone to a lot of effort to find complex research papers. This is further supported by the huge amount of references at the end of the page. However as this is to be a student embryology wiki page, it would help if the passages of text were broken up into bullet points and tables. Furthermore there are no images or student drawn diagrams. These would also help convey the main messages of musculoskeletal development. The sections after tendon development are unfinished and very brief. Furthermore the only in text referencing present is in the first two sections. Citations should be carried through the entire page. &lt;br /&gt;
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The second trimester muscular development section is particularly clear and to the point. However the information present doesn’t stretch much further than what was covered in the lecture material. By adding diagrams of the pharyngeal arch origins and including further research into this section, its quality will be greatly improved.&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=150329</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=150329"/>
		<updated>2014-10-14T23:39:18Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Online Assessment - Peer Reviews */&lt;/p&gt;
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&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
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==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
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===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
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===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
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===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
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===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
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===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
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== Online Assignment 1 ==&lt;br /&gt;
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Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
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The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;br /&gt;
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Project 7: Neural &lt;br /&gt;
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This project has a great introduction and overview of the brain and spinal cord anatomy. The first image is eye catching however I find it hard to follow and it seems like there is too much information on it. Perhaps it would be better positioned further down in the report after more neural developmental stages have been explained. The timeline section is clear and to the point. There is an excellent use of images to support the information. The fluorescent stained images make the ventricular, subventricular and other cortical layers clear and easy to understand. The information under the brain development section is simple and effective. However there are some terms mentioned that are not explained in enough detail like the specific layering of the cortex. It is a complicated migration process that deserves some more research. It is good that the student has explained gyration and sulcation in this section. &lt;br /&gt;
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This project is clearly still in progress however the information in the first section of the wiki page indicates a very promising final product. The spinal cord and meninges development section still needs to be written up. If it follows along the course of the brain development section, it will be flawless. The current research models and finding section reveals an in-depth understanding of complex ideas. However for a student embryology wiki page, there is too much detail. If the student wants to illustrate a complicated research finding, images or tables of the results found from this research would help convey the message to the student. A table would help summarise the results in the first current research description, particularly for the results gathered from the different parts of the brain. &lt;br /&gt;
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The final part of this report on abnormalities is unfinished however the bulk of the information presented already is very good. The images supporting the abnormality are excellent and important for keeping the student reading this page engaged. However there are a few spelling and grammar errors in the neural tube defects section: “which affect the either the brain”, “the openings remain which leas”. There is still room for more research and information on other neural development abnormalities and the subheadings the student has incorporated indicates their intention of adding more information. This report has excellent reference formatting and citation throughout the page. The tables and images are referenced correctly and the long list at the end is very neat. &lt;br /&gt;
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Project 8: musculoskeletal &lt;br /&gt;
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This project is still in its early days but the layout and plan is very good. With additional information added to the subheadings, it will be a very interesting student wiki page. Reviewing what has already been completed on this page, it is too content heavy. There are a lot of large chunks of text indicating the student has gone to a lot of effort to find complex research papers. This is further supported by the huge amount of references at the end of the page. However as this is to be a student embryology wiki page, it would help if the passages of text were broken up into bullet points and tables. Furthermore there are no images or student drawn diagrams. These would also help convey the main messages of musculoskeletal development. The sections after tendon development are unfinished and very brief. Furthermore the only in text referencing present is in the first two sections. Citations should be carried through the entire page. &lt;br /&gt;
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The second trimester muscular development section is particularly clear and to the point. However the information present doesn’t stretch much further than what was covered in the lecture material. By adding diagrams of the pharyngeal arch origins and including further research into this section, its quality will be greatly improved.&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_8&amp;diff=150323</id>
		<title>Talk:2014 Group Project 8</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_8&amp;diff=150323"/>
		<updated>2014-10-14T23:36:42Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Peer Reviews */&lt;/p&gt;
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==Peer Reviews==&lt;br /&gt;
===1===&lt;br /&gt;
Let me start by saying that the “Muscle Gains” section is funny but obviously very irrelevant to the project. Looking at the contents of this page, there seem to be a lot of focus on the development and very little on the other sections. The development section is well-researched and great job on the in-text citations! Some parts look a bit bulky though so maybe try to break some of them down into bulletpoints if possible. A timeline of development is also very helpful in this project.&lt;br /&gt;
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On abnormalities, very concise and detailed. Try to  write about 3-4 abnormalities and find information on how they’re treated or managed presently. As for historic findings, there is a section on the Wikipage that has old books on embryology. It’s under the “Explore” tab and you’ll see “Historic embryo”. Those books have a lot of information regarding that section. Don’t forget to write about current findings as well. Another thing, try to use images since these really help with understanding the content of the page. Overall, a lot of work has to be done before the due date. I do understand why because there are only two people in this group. Goodluck and I wish you the best in finishing this project!&lt;br /&gt;
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===2===&lt;br /&gt;
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The key points of musculoskeletal development appear as headings however there is still much that needs to be clearly discussed beneath each of these points. The main headings are good and specific but some are way too specific and should be under much larger headings, for example, 1.2-1.9 could be subheadings that come under the heading ‘System Development’. ‘Background embryonic development’ is useful to understand but perhaps it is better to not have so much detail, or summarise it in a table. The ‘Abnormalities’ heading is done well, with one disease listed (Duchenne Muscular Dystrophy).  It might be better to have more than one abnormality listed and clearly described as well. I particularly like the use of statistics and genetic references. It seems most of the key points relating to system development have been clearly described, but some tidying up in terms of editing needs to be done. &lt;br /&gt;
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Also, more work needs to be done on historic findings, current research, models and findings.  Once all the research parts are completed, the timeline can be correctly constructed. Also like the idea of putting a timeline and the heading shows that this is intended. More subheadings could be used to make the page look more organised and pleasing to the eye. &lt;br /&gt;
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There are also no graphs or tables as well as pictures. A table could be used to make the timeline or highlight the differences between the second, third trimesters and neonatal periods of fetal muscular development. Maybe the initial heading of the page should be changed to ‘Muscular Fetal Development’ to indicate that muscular development is actually being covered instead of both muscular and skeletal. There also isn’t much information regarding limb fetal development, so maybe it would be good to go through that on a deeper level. &lt;br /&gt;
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It could also help to have images loaded onto the page or to draw flow diagrams to assist in the description of how the muscles develop in the fetal period. For example, upload an image showing the difference between slow twitch and fast twitch muscle fibres or draw a flow chart to show better understanding of the molecular and cellular regulation of fetal myogenesis. &lt;br /&gt;
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References need to be in one larger section at the end under the heading ‘References’, not two and scattered throughout as is seen. The major section of references appears to be referenced correctly and in-cite references are done very well. There are also many references which are good and show that this group has thoroughly researched their topic. &lt;br /&gt;
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Overall, this group has done very well and just needs to add more information for certain headings, as well as organise the page a bit better in neater headings and subheadings. Pictures should be added, as well as graphs, tables and own student-drawn images.&lt;br /&gt;
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===3===&lt;br /&gt;
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There is no introduction that allows the audience an insight to your project page. This is something that needs to be worked on and maybe add some images also. I’m not sure what I think about the “making gains” section, it’s funny however needs a bit of work. However I do see what you are trying to do here, trying to make it more inviting, interesting and alluring the audience and I appreciate that. &lt;br /&gt;
The Muscle development timeline needs some work and progress. I don’t see a timeline, or dot points, maybe work on format here even if it’s in a table format for this section.&lt;br /&gt;
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Most of the following sections have great amount of detail with a number of in text citations and this is great to see. However I do notice that there is no images what so ever, not sure if you are having trouble finding, or if you have left this until the last thing, try and draw images, or look at a youtube video that sums one section or maybe the entire system. This could help balance the amount of text you have, making the page more interesting, not overwhelming. Also work on making things more concise and simplifying paragraphs. &lt;br /&gt;
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Third trimester, neonatal and mechanisms are all sections that need more content in there whether it be images or information there is not much attention given to these areas. &lt;br /&gt;
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Overall this project page has room for improvement by giving certain sections of the page the attention they deserve. Images are imperative in allowing a balance between text and the image itself. It can sometimes be refreshing, and less overwhelming to see an image among paragraphs of content. Also try and look for a youtube video that can help summaries the content on your page. Try and work on time management, or set a group deadline that everyone has to meet so that all the information can be well up before the due date so your group can have time to edit and add images and play around with the page comfortably. &lt;br /&gt;
Goodluck!&lt;br /&gt;
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===4===&lt;br /&gt;
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Overall the Group project page seems to be set out quite well with its headings and sub headings.  Just needs a bit more info for some of the sub headings particularly from ‘second trimester muscular development’ onwards and a few formatting adjustments. The use of timelines, tables and dot points might help in those sections. The content provided is written well and in a detailed manner, which is still understood.  There is a significant amount of research presented and this is seen through the in text citations and then further identified in the reference list. A good use of referencing is seen supporting the content info provided.  The content uses examples of past and current research to help develop and establish ideas that are presented well. The abnormalities section on ‘Duchenne muscular dystrophy’ is described really well, maybe other abnormalities could also be added later. &lt;br /&gt;
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To improve the page some suggestions include the use of diagrams and images, would help to add a bit more vibrancy to the page. Images and drawings are a great way to help in understanding the content.  They are also a great way to make the content clearer especially if there are a number of processes involved in the development.  Some of the longer paragraphs of content may also be formatted into dot points just to avoid lengthy paragraphs of info. It might also be useful to include some of the headings mentioned on the assessment page (identify current research models and findings, historic findings etc.). &lt;br /&gt;
Finally, the page so far is done well however it will need a little bit more work to be completely finished. Try to just gather as much info as you can to ensure you have enough content and then add images and any other visual aids later. Keep up the good work and good luck :).&lt;br /&gt;
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===5===&lt;br /&gt;
Firstly, I thought the “Making Gains” bit was great- and I can guess who came up with that. I know you’ll take it our prior to submission though haha. The structure of your project is quite good, and the subheadings would make it much easier to read- the only thing is you need to add more content! I think because your system encompasses quite a lot, it would be a better idea for you to put as much information as you can into tables and include diagrams- I saw that musculoskeletal development has quite a few visual resources so it you should use them!&lt;br /&gt;
There are some areas where the content is really sparse, yet others where it is extremely heavy. In these areas, you may benefit from putting your information into bullet points so as to alleviate any confusion that may arise and overall enhance the clarity of your work. The references you have done are quite good, but there appears to be some missing.&lt;br /&gt;
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Overall, I think your project would greatly benefit from the incorporation of images and diagrams. Because you are describing so much, a visual aid will help you immensely and also assist in retaining the attention of the reader throughout the entirety of the piece.  Also, I see that you have deviated from the recommended headings. This may be a good idea to individualise your project- but make sure all topics are covered.  I think it’s a good start considering you only have two team members, and I’m sure you will be able to pull it all together by the time it is due.&lt;br /&gt;
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===6===&lt;br /&gt;
Musculoskeletal&lt;br /&gt;
There is no introduction that has been added - you should really add one because its great to introduce the readers to what will be in the wiki page. I hope the person incharge of the first two sections of your group will / does have some work to add soon. Hardly any information has been added to the majority of the assignment, and to be honest, this wiki project has had the least amount of work done on it. You need pictures, diagrams, graphs and a LOT more information. You guys are doing a “musculoskeletal” topic, and I can’t find anything on “skeletal” on your page yet. Mark has posted that your page will only be focusing on fetal muscle development - why not change the name of the page from musculoskeletal to muscular only? That will prepare the reader in regards to the topic being addressed. &lt;br /&gt;
As for abnormalities, all the other pages have on average 5 abnormalities being introduced, whereas this page only has 1. Although it is really well worded and introduced, I think you should try to find at least another 2 abnormalities to put into your group project. &lt;br /&gt;
Sections for historic findings, current research, models and findings will need to be added. &lt;br /&gt;
Your page seems to focus only on how the actual muscle fibres develop, but perhaps, you could write about skeletal muscle development contributing to limb development or something to widen your topics? &lt;br /&gt;
Overall, your page needs a lot more work! Hope you can get a lot of work done until the project is due, make sure to add pictures!&lt;br /&gt;
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===7===&lt;br /&gt;
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In this project the development section is well-researched however introduction, historical findings, current models and abnormalities still need some work. The development section is very informative with appropriate use of in-text referencing. However, to prevent having bulks of text, you can create diagrams and flow charts or use bullet points. It would also be great if you could provide a timeline under “muscle development general timeline” section. Background embryonic development section is very helpful but we do not need this much information on embryonic period for this project. You can summarise this information in introduction, so that it provides a starting point and fetal development can be further expanded through the project. The rest of the information regarding system development seems to cover the important points; however it still needs work (for e.g. “second trimester muscular development” section is clearly missing some bits).&lt;br /&gt;
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The abnormality section only includes one abnormality (Duchenne Muscular Dystrophy). This abnormality is well described but it needs to be referenced. An image of the clinical manifestation of the disease can clearly help with understanding. There are lots of other abnormalities that you can include in this section (We learnt from the musculoskeletal development lecture that musculoskeletal conditions form 20% of all abnormalities at birth). You can also refer to “limb development lecture” to find information on musculoskeletal abnormalities.&lt;br /&gt;
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Finding information on historic findings might be a little challenging. A suggestion I can make is to search for old articles in PubMed (by adjusting the year). These articles can include key historical events. Review articles that summarise historic findings related to musculoskeletal development may also be helpful. You also need to find information on current research.&lt;br /&gt;
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Finally, you should add an introduction to your project. It seems like you are more focused on muscular development rather than “musculoskeletal” so you can mention that in your introduction. You can also show creativity by drawing your own diagrams, adding images, and tabulating timeline data. You should also fix the references by putting all the references under one subheading in the bottom of the page.&lt;br /&gt;
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===8===&lt;br /&gt;
I think this page needs a lot of work in improving the overall layout. First, I think the page would benefit from a more formal introduction that introduces the content of the page in a way that is helpful to your audience. The age could also be improved by breaking it up into ‘Development’, ‘Historic Findings’, ‘Current Research Models and Findings’ as well as the Abnormalities section already included to make it flow better.&lt;br /&gt;
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The text in under the ‘Molecular and Cellular Reputation of Fetal Myogenesis’ is really good but it is appears as a large slab of information that would be better presented with dot points to break it up and images to make it more interesting. The Abnormalities section is well written but is very brief. This section could be improved by including more abnormalities and the appropriate images. &lt;br /&gt;
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Overall there is a lot of work to be carried out for this page but I understand that this is a smaller group. Perhaps breaking the work up into those smaller headings mentioned will help you split the work evenly. When all the text is uploaded, make sure that there is an effort to include in text citations to support all your information and images to make the page interesting. Try to avoid writing big slabs of information – tabulate or use dot points to break up large portions of text.&lt;br /&gt;
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===9===&lt;br /&gt;
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I think the group has found some useful and relevant sources of information however there still needs to be work done in writing up content under some headings. The structure of the wiki page has been laid out and I think the idea of splitting up the developmental process into three trimesters is a good idea to avoid lengthy paragraphs or an overly lengthy timeline that may be difficult to absorb. I would suggest using a table to write up the timeline with a brief description of what exactly the process occurring involves. There are some references that are missing in the tendon development section. &lt;br /&gt;
I think the ‘Molecular and Cellular regulation of fetal myogenesis’ section was the most well written section with a thorough description of the process involved. Try to find relevant pictures and diagrams to accompany this text, they will make the explanation much more beneficial and easier to understand. Overall a good  structure has been laid out for the wiki page but more content still needs to be added.&lt;br /&gt;
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===10===&lt;br /&gt;
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I understand that you only have two people in your group so you have made a good start considering this. It does seem a bit unorganized at the moment though. Be aware that mark has set out guidelines that include that include making sure you have an introduction, historic findings and models. These can be found when you click on the student projects at the top of the page. &lt;br /&gt;
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The information you do have is good but your page isn’t visually entertaining as there are no images. Adding images makes it more interesting and I particularly recommend student images to make it more student-like and in my opinion these will attract attention from the viewer. Obviously the making gains part, while blatantly funny it is quite irrelevant. &lt;br /&gt;
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Referencing appears to be a bit of an issue at the moment as some parts have been done well with in text citations but you need to make sure all of the text has in text citations. Also it would be a good idea to put all your references down the bottom of the page to make it look more tidy and aesthetically pleasing. &lt;br /&gt;
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I like how you have split your page into different parts, it would be a good idea if you were to finish off the general timeline at the start as well. Think about tabulating it as this has been done by other projects and it looks really good. I think the fact that you have only two people you have got just about all the information you need there as it is difficult to do as much as the other groups when there is only two of you. So even the abnormalities part it’s good that you have even one to the effort to have it there. &lt;br /&gt;
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Overall, a very good start from both of you. I think it’s important to make sure that everything mark has mentioned is put into your page at the start even if there isn’t as much information in each as other pages have. Also make sure you include some sort of images because it’s a bit monotonous at the moment. The referencing needs  a bit of tweaking as well. Best of luck with the rest of the assignment.&lt;br /&gt;
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===11===&lt;br /&gt;
The Making Gains section is quite funny but as you said, this is not Broscience and I’m sure it will be removed for the final submission. Once that is removed, begin the project with an introduction and the developmental general timeline. The main idea of the timeline is present, however when constructing one, use specific weeks within the foetal period and what developmental changes occur in those weeks. The information found under Background Embryonic development may be used to form the introduction, but if you are going to do that do not make the introduction as detailed as this section is, particularly in terms of the transcription factors and signalling molecules, they can be moved and added into the other sections that look at the various musculoskeletal developments individually.&lt;br /&gt;
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It is evident that there is great understanding of this topic and that it is only a case of further research and addition of those information to complete the sections. Certain sections lack information all together, such as the Third Trimester Muscular development and Recent findings, whereas other sections only contain the research articles and no summaries of them such as Abnormalities. However I understand this is a draft and that all those areas will be addressed adequately, contributing to the final copy. &lt;br /&gt;
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Only the Background Embryonic development and Molecular and Cellular regulation of foetal myogenesis have in text citations, whereas the other sections that do contain information are not cited. It might become difficult to later find the correct article from which you obtained the information so it is advised to cite the text while adding it. In terms of the citations present, there is no need for a comma between the superscripts and you have also allocated two sections to references, one subsequent to Abnormalities and another at the bottom of the page, it is best to collate all the references in one list at the end of the page. This is also the case for Abnormalities as there are two subheadings for it, merge them into one. &lt;br /&gt;
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No images, tables, or timelines are added. The information you have now is well written and divided into small paragraphs, which is a good way of presenting the information, however other forms such as images and tables should be used. A timeline should be added under the Muscle development General Timeline subheading, this may be done as a table or a drawing and uploaded as it simplifies the information and breaks the page from continuous writing. &lt;br /&gt;
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Overall this group project page is great, containing all the headings and articles present. It is only a matter of summarising those articles and adding the information. All the information present thus far is appropriate and emphasises great research skills.&lt;br /&gt;
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===12===&lt;br /&gt;
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The project is split up into different sections well but you need to include an introduction to your project. Really good information and references but use bullet points and diagrams to break up the text so that it is easier to read. There is good information on DMD but you could possibly write about another abnormality linked to muscle development.&lt;br /&gt;
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===13===&lt;br /&gt;
Introduction is missing. Some information about the functions of the systems and topics going to be covered should be included here. The section ‘making gains’ is funny. However, more work has to be done to make it more interesting.&lt;br /&gt;
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For the timeline, more information is needed. It would be great to include a table here and describe the changes during different stages (microfibers formation…). Table is also useful to explain the second trimester muscular development&lt;br /&gt;
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The information under background embryonic development can be summarised and put under introduction as this project should be focused on fetal development.&lt;br /&gt;
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It is great to have molecular and cellular regulation. However, more diagrams are needed here. It would be better if they are stated in several points rather than a big paragraph. Also, more images are needed for other sections, it would be good to draw the picture as well.&lt;br /&gt;
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For abnormalities, in-text references are needed. Also, some more abnormalities should be included with the use of images to illustrate them.&lt;br /&gt;
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Overall, there is a pretty good structure of the website. It could be improved by including some current and historic researches on this topic. Also, more images are needed (as there is none now) to make the webpage more interesting and informative. More contents should be included as well.&lt;br /&gt;
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The page is disorganised in certain aspects. The first heading is not appropriate and is not teaching at peer level. Timeline is incomplete could have phases (first trimester, second trimester etc.) and key events put into a table and shown. &lt;br /&gt;
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There’s good information about the muscle development from myofiber to tubules etc. however there is no period of time given to when the event occurs so it can get confusing maybe include the week in the information. Molecular and cellular regulation is well described but some information such as how IFG1 has found to enhance protein synthesis could be put into a different heading specific on research findings.   Tendon development is much clearer and easier to understand as it to the point and tells it as a series of event. Could include when the process ends only has shown that it started in 20th Carnegie stage&lt;br /&gt;
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Second and Third trimester information is incomplete although the summary in second Trimester heading is easy to understand it can be expanded upon.  Does anything happen to limb buds in fetal stage maybe could include information of muscles in that. The one Abnormality given is relevant and well summarised. It has been defined and shows how common it is which is good to include. There should be more abnormalities added into this section and possibly picture or diagram helping to visualise how it may look. &lt;br /&gt;
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Referencing is done in the correct format and it’s good everything is shown as a list on the bottom of the page. Overall the page needs improvement there is some evident of research done however there needs to be more headings added such as Historic findings. The recent finding heading could be placed more up on the page, before abnormality heading. Can have the different trimesters as subheading instead of separate headings. Can include a timeline in table format and also some diagrams or pictures of muscle development in head region and tendon development as well as possibly a video. Good background of embryonic development but since embryonic development is not related the project can summarise it a bit more and add more into fetal development of muscles.&lt;br /&gt;
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This project is still in its early days but the layout and plan is very good. With additional information added to the subheadings, it will be a very interesting student wiki page. Reviewing what has already been completed on this page, it is too content heavy. There are a lot of large chunks of text indicating the student has gone to a lot of effort to find complex research papers. This is further supported by the huge amount of references at the end of the page. However as this is to be a student embryology wiki page, it would help if the passages of text were broken up into bullet points and tables. Furthermore there are no images or student drawn diagrams. These would also help convey the main messages of musculoskeletal development. The sections after tendon development are unfinished and very brief. Furthermore the only in text referencing present is in the first two sections. Citations should be carried through the entire page. &lt;br /&gt;
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The second trimester muscular development section is particularly clear and to the point. However the information present doesn’t stretch much further than what was covered in the lecture material. By adding diagrams of the pharyngeal arch origins and including further research into this section, its quality will be greatly improved.&lt;br /&gt;
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==4==&lt;br /&gt;
This page needs a lot of work; there are sections with little to no information, while others have just slabs of text, some of which have no references. Of those that have info presented, the topic is well covered with the large amount of content. You should use some dot points for some areas where you have a lot of info. You also need to use some images!! They will help to alleviate the slabs of content you have and add some colour to the page. Make sure you caption and reference them correctly, and add the correct copyright info. &lt;br /&gt;
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Overall, there isn’t much I can say except add content, reference is correctly both in text and at the bottom of the page, and images and use some dot points and/or tables; don’t write everything in large slabs of text. Also, maybe get rid of that 'Muscle Gains' section, unless you actually plan to write something relevant in there haha. Otherwise, Good luck!&lt;br /&gt;
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==5==&lt;br /&gt;
Let me start by saying, for only having two people in the group, well done. The page should have an introduction though, and this is missing. Just by simply summarizing all the information that will be covered in the page and adding it to the introduction, will improve the overall presentation significantly, you may wish to leave this to last, or edit as you go along. &lt;br /&gt;
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The section “Making gains” is amusing, but inappropriate and should be omitted from the final submission. The timeline for the page I believe should be put into a table to save time and add to the presentation of the page, it can be easily done if you follow the steps outlined in the ‘editing basics’ page &lt;br /&gt;
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The background information is comprehensive, however, the page is in desperate need of some images as there are just slabs of text. Images will really help break up the contents of the page and make it visually appealing. &lt;br /&gt;
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The abnormalities section also seems to be coming along quite well. Keep up the good work. &lt;br /&gt;
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==6==&lt;br /&gt;
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This is great work so far from a group consisting of only 2 people. Keep up the good work and continue to work hard in finishing this page. Very admirable.&lt;br /&gt;
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Overall, I would suggest reformatting and adding pictures to enhance the presentation of this page. Consider the use of lists and tables, throughout this wiki.&lt;br /&gt;
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Instead of the rather hilarious (but rather inappropriate) ‘Making gains’ subheading, I believe an introduction should be added. Remember to clearly indicate the outcomes that the page hopes to achieve.&lt;br /&gt;
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I also believe that the development/timeline section of this page is informative, with a very good use of headings and sub-headings. There is excellent evidence of significant scientific research and is correctly referenced and cited. However, this section could be further summarised or improved through the use of a table I believe- just a suggestion however. Adding pictures would also add to the overall understanding of this section.&lt;br /&gt;
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This page has no information for the “recent findings” or “historic findings” section. Remember to include relevant information/pictures and references to these sections.&lt;br /&gt;
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The abnormalities section is also looking very promising. Include more varying abnormalities. The abnormality included, DMD, is well written and informative. It needs to be correctly referenced however. &lt;br /&gt;
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==7==&lt;br /&gt;
In this review I hope to highlight the merits of your project and suggest some areas for improvement in line with the marking criteria. &lt;br /&gt;
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I see that you have conducted a great amount of research on the fetal development of the musculoskeletal system. The content clearly goes beyond the material covered in the lectures. It was interesting to read about the different transcriptions factors involved in induction and regulation of myoblast differentiation. I think it will be good to see a summary of all this information in a timeline format. I suggest simply highlighting the main developments at each stage. &lt;br /&gt;
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You have made a good start on abnormalities. I suggest that you begin by selecting one abnormality include Description; Epidemiology; Cause and Treatment. You can add more later.&lt;br /&gt;
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The page needs a little more structure. Make sure you include appropriate sub-heading and organise the information before you submit the project. Remember we were asked specifically to address the topics of current research and historic findings. &lt;br /&gt;
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Finally it would be good see some images to support the text. Perhaps diagrams on tendon development would help summarise the process. &lt;br /&gt;
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Great work so far!! Hope this feed back helps. &lt;br /&gt;
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==8==&lt;br /&gt;
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Overall, the project has some very detailed sections and some sections where content is scarce. It would be helpful to start off with an introduction of the musculoskeletal system so the reader is aware of its components and what the page intends to cover. The timeline of muscle development has good potential, I understand it is still being planned at this stage and with further research, it could definitely be effective. A table format would be useful to present this information. The following sections on background embryonic development and fetal myogenesis are well-researched and have a lot of content, however I would consider breaking it down into dot points to improve readability. The sections are cited correctly in-text though, which is good to see.&lt;br /&gt;
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There is much more improvement in the tendon and second trimester development sections, as the chunks of text have been reduced to provide a succinct summary, however these need to have citations also. The use of some images here, either hand-drawn or from online would be beneficial, to have a balance between text and pictures and make the page more visually appealing. Other than the abnormalities section which provides a good, concise summary of Duchenne Muscular Dystrophy, the following sections seem to be only references at this stage. As long as these are used to compose some relevant paragraphs/dot points, this is fine considering there is still time to improve the page. &lt;br /&gt;
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Overall, this page has good potential as the groundwork has been completed; it is now more a matter of writing up more information, adding images and possibly a relevant video. The part on ‘making gains’ would need to be removed for the final, but otherwise, it is definitely a decent amount of work so far, especially considering the few group members involved.&lt;br /&gt;
&lt;br /&gt;
==9==&lt;br /&gt;
&lt;br /&gt;
“Making Gains” is pretty funny but offcourse irrelevant to this project.&lt;br /&gt;
Your timeline needs a lot of work done as it is missing copious amounts of information.&lt;br /&gt;
Background embryonic development section is well detailed though it lacks images to aid the information. Also molecular and cellular regulation of fetal myogenesis section is the same; it is well informed but lacks images.&lt;br /&gt;
Much more is needed on tendon development, second and third trimester muscular development, neonatal, mechanisms/structure of muscle fibres and abnormalities.&lt;br /&gt;
Over all very good in text citations for the development (top) section. References from the background section should be at the bottom of the page with other references. The page mostly looks like a bulk of writing so include images where possible. A LOT more work is needed but I understand your situation as your group only has 2 members now so do as much as you can and GOOD LUCK!&lt;br /&gt;
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==10==&lt;br /&gt;
&lt;br /&gt;
The project doesn’t have an introduction yet; however information such as what the Musculoskeletal system is about, the features of the system as well as the difference between the embryonic and fetal stages of development should be mentioned. Not to mention a brief summary of each key subheading such as abnormalities under introduction e.g. any deformations in the fetal stages of musculoskeletal development can result in to such and such abnormalities which will be addressed. This will help the viewer’s understand what the project will be going through. I like the ‘making gains’ subheading as it adds humour to the page and engages the viewers. The general timeline needs information including what events take place at certain phases of fetal development. This could be present in a table to make the information more clear. It’s good that the project has information on the embryonic development so that the viewers can understand how the fetus arises to that point in development (fetal period). &lt;br /&gt;
&lt;br /&gt;
All of the content seems to relate to the key topic and is appropriately paragraphed. However much of the content is still missing such as in ‘recent findings’ and ‘introduction’. More information could be added under the associated ‘trimesters’ and ‘abnormalities’. There are no historic findings which is great to have on your page for viewer’s fascination into the group project. Members could search on pubmed about the musculoskeletal system and view dates on the side that may contain key findings for historical events. Also a glossary list should be added to help viewers understand the content more instead of just being confused at some sections.&lt;br /&gt;
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There are no images on this page and definitely needs to be added with the appropriate information such as the description, referencing, copyright issues and ‘student template’. If images are not readily available, it is best to draw them. Also captions should be added on the page to state what the images are showing. As for referencing, there are  some sections which shows incite referencing such as in the content under ‘Molecular and Cellular regulation of fetal myogenesis’ and some that don’t have any like in ‘tendon development’. There needs to be references in all sections. There is a huge list of references under ‘abnormalities’ which need to be placed all under one ‘references subheading’; similarly to any other reference list on the page. Number 15 of the reference list has an error in it and needs to be fixed right away. Overall, this is a working progress and if the group makes edits based on the peer-reviews received, this could enhance their project.&lt;br /&gt;
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Week 5 &lt;br /&gt;
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--[[User:Z3418989|Z3418989]] ([[User talk:Z3418989|talk]]) 22:34, 26 August 2014 (EST)&lt;br /&gt;
Hi guys &lt;br /&gt;
After discussing in lab last week we tried to divide the categories and work as following; &lt;br /&gt;
* skeletal and cartilaginous development - Joel&lt;br /&gt;
* muscular development - Gowtem&lt;br /&gt;
* overall skeletal and muscular arrangement macroscopically - Danny &lt;br /&gt;
What do you guys think about addressing these topics as well &lt;br /&gt;
* Historical findings&lt;br /&gt;
* Abnormalities &lt;br /&gt;
* New findings&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418779|Z3418779]] ([[User talk:Z3418779|talk]]) 12:44, 27 August 2014 (EST)&lt;br /&gt;
Great idea m8 Danny can probably also do abnormalities, remember to post any articles of particular relevance to New/historical findings. To complete after main content assembled&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418779|Z3418779]] ([[User talk:Z3418779|talk]]) 01:02, 28 August 2014 (EST)&lt;br /&gt;
I would suggest that we narrow down the topic to focusing on the appendicular musculoskeletal system, so that;&lt;br /&gt;
*To make work load more managable&lt;br /&gt;
*To avoid the multiple highly specialised and irregular muscles/bones of the head&lt;br /&gt;
*The muscles I would suggest to include in are all muscles which have attachments to the appendicular skeleton including axioappendicular muscles (petoralis major, pectoralis minor, subclavious, serratus anterior, Latissimus Dorsi, Traps, levator scap, rhomboid major and minor.&lt;br /&gt;
*Joints and tendons are included in the musculoskeletal system, we should about wether we want to have a section for them.&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418779|Z3418779]] ([[User talk:Z3418779|talk]]) 09:05, 31 August 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
Hi guys just posted the topics of abnormalities of muscle and skeletal system im gonna talk bout and references of relevant articles to the topics. Sorry for being late btw&lt;br /&gt;
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--[[User:Z3418779|Z3418779]] ([[User talk:Z3418779|talk]]) 14:57, 9 September 2014 (EST)&lt;br /&gt;
Disregard the rest of the stuff I said in earlier discussions, I believe that to make it significantly easier we just do muscular system. I will Reformat everything to make it make sense.&lt;br /&gt;
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--[[User:Z3418989|Z3418989]] ([[User talk:Z3418989|talk]]) 01:51, 10 September 2014 (EST) &lt;br /&gt;
Yeah completely agree, I think focusing on the muscular system would be much easier than doing both. Appendicular muscles sounds good - so muscles of limbs. Could divide it into upper and lower limbs. May have to talk about bone/cartilage a bit to describe how the muscle forms around it. Maybe how developing of muscles in embryonic development is important and eventually affects origin and insertions and actions of muscles when fully developed.&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418779|Z3418779]] ([[User talk:Z3418779|talk]]) 12:56, 17 September 2014 (EST) This link shows a very good description of myogenesis; http://books.google.com.au/books?id=1ZRCMRXbbwoC&amp;amp;pg=PA38&amp;amp;lpg=PA38&amp;amp;dq=primary+secondary+myofibers&amp;amp;source=bl&amp;amp;ots=RSRcVVe5xr&amp;amp;sig=eDJBF_3qkYzA8WSin1tnbzT2xYY&amp;amp;hl=en&amp;amp;sa=X&amp;amp;ei=OegYVL_UHpOB8gWMxoDYAw&amp;amp;ved=0CCoQ6AEwAw#v=onepage&amp;amp;q&amp;amp;f=false&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418989|Z3418989]] ([[User talk:Z3418989|talk]]) 12:27, 20 September 2014 (EST)&lt;br /&gt;
Ill add a bit more on embryonic muscle development guys&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418779|Z3418779]] ([[User talk:Z3418779|talk]]) 22:30, 6 October 2014 (EST)&lt;br /&gt;
Here are some article which would probably be helpful&lt;br /&gt;
Nrk2b-mediated NAD+ production regulates cell adhesion and is required for muscle morphogenesis in vivo: Nrk2b and NAD+ in muscle morphogenesis&lt;br /&gt;
Coexpression of two distinct muscle acetylcholine receptor a-subunits during development&lt;br /&gt;
&lt;br /&gt;
At the moment I have a general structure for tendon development and abnormalities will add to wiki tommorrow.&lt;br /&gt;
&lt;br /&gt;
the good indepth morphogenesis studies focus on gluteus maxximus, extrenal urethra spincter, tensor veli palatini very little are done of the other muscles, so will try to apply the conclusions from these studies to related skeltal muscles&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_7&amp;diff=150293</id>
		<title>Talk:2014 Group Project 7</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_7&amp;diff=150293"/>
		<updated>2014-10-14T23:22:45Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Peer Reviews */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014discussionheader}}&lt;br /&gt;
==Peer Reviews==&lt;br /&gt;
===1===&lt;br /&gt;
Good introduction but I would move what happens in the embryonic development to the “development” section. Also, don’t forget any references and in-text citations for this section. Maybe add more on what the page is about and what the readers should be expecting. Nonetheless, it gives a good background of the key organs in this system. The diagram for the timeline of development is quite complex. Try to explain what is happening in this diagram within the “development” section. For example, maybe try to have the same headings (cell multiplication, cell migration, etc.) as the diagram for the “development” subheadings.  Or, if you’re willing, make a timeline of your own. At least, you can make a simpler diagram where only relevant information is included. Good job on the “Visible Anatomical Details” table. &lt;br /&gt;
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On current findings, good choice on research articles. They’re very relevant to the topic and to the project as well. Maybe try to add some images if possible. Also, try to add some dates or anything to show how recent these studies are. There is a bit of imbalance in terms of the amount of content for each study but nonetheless, this section was written well. Good job! As for “abnormalities”, this section was done well. Each disease was written with lots of detail but very concisely. I do suggest adding more images that show the clinical manifestation of each disease. Also, don’t just focus on the manifestations of each defects. Try to look for current treatments or techniques on managing the abnormality. Also, maybe look for more references. &lt;br /&gt;
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On historic findings, where is it? There is a section on the Wikipage that has old books on embryology. It’s under the “Explore” tab and you’ll see “Historic embryo”.&lt;br /&gt;
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I’ve check all the images and there are no issues with them in terms of copyright. I can see that you tried to add captions to each photo, which is good but you can format the image in a way so that the caption is framed with the photo. Check out the [[https://embryology.med.unsw.edu.au/embryology/index.php/Help:Image_Tutorial#Image_Formatting| Image Formatting]] guide to do this. Overall, this page is very detailed and written very well. Just try to edit the page and make it look cleaner. &lt;br /&gt;
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===2===&lt;br /&gt;
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This project page is very nicely organised with the group clearly specifying what aspect of neural development they are covering, being the CNS. The use of headings and subheadings is done very neatly, however sections 1.1-1.5 could be subheadings for the larger title ‘system development’. The key points have been clearly described but there is no referencing throughout the ‘Introduction’, ‘Brain development’ and ‘Abnormalities’ sections. Most key points have at least some information on them which is good for this stage of the project; however some of the headings without could use some more work. &lt;br /&gt;
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The choice of content is highly appropriate and the use of diagrams and pictures help show the groups understanding of the project thus far. I particularly like the use of subheadings in this project as they make the page look neater and organised. The image showing the timeline of fetal neural development is good however perhaps it would be better to draw or make a timeline on the computer in order to show better understanding of the time course of fetal development. Most images that have been uploaded are also well referenced and when clicking onto them, it takes the reader to a page that has more information related to the image. The table to describe anatomical details is also done well and is important that such a key point is mentioned seeing as this is an anatomy course. &lt;br /&gt;
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I also really like how the ‘Current research, models and findings’ section is split into ‘Current research’ and ‘Future Research’, however it seems future research needs to be further looked into. The ‘Abnormalities’ section is done very well, with multiple abnormalities listed with images used to show each one. The bolding of several key words is seen and is helpful in showing understanding of some of the key points.  There are also no historic findings so try and find some information on that.&lt;br /&gt;
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Referencing is correctly done with most references being in one main section at the end, and ordered correctly. In-cite referencing is also done correctly. All images are correctly referenced with copyright information present and the student image template. I also like the way the current research findings sources have been referenced with the use of dot points assisting learning by not just presenting to the reader as a blob of information.&lt;br /&gt;
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Overall, well done group 7! Keep up the great work!&lt;br /&gt;
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===3===&lt;br /&gt;
The content looks well organized. The introduction could use a bit of work; it does a good job of introducing the CNS, but it should also mention all the other sections this page will cover regarding the topic. You might want to get rid of the using bold for brain and spinal cord, it just makes it look a little weird. Otherwise, a good embryonic developmental background is provided, it’s a good way to set the stage for when fetal development will commence from.&lt;br /&gt;
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The information is organized well, no chunky slabs of texts. But the use of dot points is a bit extensive; almost every section of the page has dot points or makes up the complete majority of the info presented. You might want to present some of it in paragraph form e.g. the abnormalities part, as that section can still be kept quite short and not be packed with text. As long as you mention what it is, how you get it/how it forms, some statistics and use a picture, the section can be still visually appealing.&lt;br /&gt;
The images are captioned ok, but there is a better way of doing it. In the command to input the image, continue the command with: |thumb|’whatever you want to write’], and the section in the apostrophes will be the caption under the picture (go into edit mode on another project page for a better idea, I might not have explained well). &lt;br /&gt;
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The use of the table is well done, makes all that info easily presentable, though I see the meninges development still needs to be done. The current research models and findings looks kind of messy with just the referenced PubMed article there. It might look better if you had the article name written in bold and a couple sentences underneath each to describe what the article was trying to achieve, like what has been done under current research. A couple pictures may be included to make it all more visually appealing and colourful.&lt;br /&gt;
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Overall, this was done well. You have a good amount of information, just try not to present it all in dot points. Make sure all your info is referenced in text, will all references displayed at the bottom of the page. Another note, try to organise your pictures in different areas of the page as well, as they are all currently on the left hand side. &lt;br /&gt;
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===4===&lt;br /&gt;
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This group page shows a good amount of work completed however there are quite a few sections that clearly still need some more info. A good introduction to the neural development and a accurate description of what will be covered. Although it seems to be missing the in text citations. The section on ‘development during fetal period’ is presented clearly and structured really well. The info is not too overwhelming and the use of dot points for this section is great as neural development is quite complex.  There’s a good identification of images and the use of in text citations.  The brain development section is written really well with enough detail and it’s nice to see a table for the timeline of changes during each week. It does however seem to be a bit short, maybe that’s because it’s all in dot point form. It would be useful if the ‘brain, spinal cord and meninges development’ were combined under one heading, this might be a better way to structure it. Otherwise just keep each section separate but format the info into paragraph form. In the ‘current research’ section a thorough amount of info was provided. It seems as though it hasn’t been finished and more info will be added later that will be great. The abnormalities content is sufficient and well organised. Just consider using more in text citations in this section, add some more images and complete all the sub headings.&lt;br /&gt;
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Finally a good effort in this project page, it is structured well and the info provided is easy to understand. However it needs some more research and content to fill all the sub headings in order for it to be finished. Some suggestions that may be considered include; having all the references under one main heading at the end of the page. The use of more in text citations in some of the paragraphs throughout the whole page would be effective. There is an adequately amount of images already shown, so maybe the use of videos or drawings would also be good especially in the abnormalities section and current research.  The key is to focus on filing the info and then just making a few adjustments in terms of formatting. Otherwise the page is set out well , just needs a little more work. The page will look really great once completed. Good luck ☺&lt;br /&gt;
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===5===&lt;br /&gt;
This page is organized well, all the headings and subheadings are thought through. Although, I’m unsure while the sections brain and spinal cord are in bold? The development during fetal period image lacks the necessary “student template” at the bottom of the description summary and I was unable to open the link http://www.nichd.nih.gov/publications/pubs/acute/images/p44.gif.&lt;br /&gt;
Otherwise, all the other images uploaded on the page look really good and are referenced correctly.  &lt;br /&gt;
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The table under the section brain development is very brief, and expansions on the content will allow for a better understanding of the content. Adding images to appear after the table will also add to the appearance of the page and give it a cleaner look. &lt;br /&gt;
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The spinal cord and menegies development have been left untouched and the current research models have no content, just pubmed references. I understand the current research models are probably the hardest part of the assignment, but the content appears to be quite good, the formatting of the section could be improved by following the structure Mark uses. You could look at the other group projects as examples. &lt;br /&gt;
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In regards to referencing, there are no in-text citations for the first two subheadings. I would also like to recommend just adding a final list of references at the bottom of the page, as it looks much neater. &lt;br /&gt;
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The abnormalities section is done well. But try to minimise the use of dot points as this section lacks any structured paragraphs. It use of images are great, although there is an image that appear to have been removed and as a result, there is a broken link. &lt;br /&gt;
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Overall, great job so far!&lt;br /&gt;
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===6===&lt;br /&gt;
This is a really good project so far. The introduction is really well done and I especially like that you have included a diagrams in it. The brain development is good, however I’m not completely sure about the dot points. It would look better if they were not there.&lt;br /&gt;
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Well done with the images that you have got there they all appear to be well described and referenced when you click on them. Only problem with the images is that there is a lack of them. It appears that there is an imbalance between written information and images tipping in favor of the information. I think it would be a good idea to add some more images to elicit more excitement in the page. Student images are a good idea as they highlight that it is a student project and make it more interesting for the viewer. &lt;br /&gt;
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The current research models and findings shouldn’t be left like it is at the moment. You will need to go into more detail and reference properly. While on referencing it is important that you put all your references at the bottom of the page. You only have 20 at the bottom at the moment and it is clear that you have used many more than twenty. Also you need to add in text citations so that we know exactly where you have got your information from. &lt;br /&gt;
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The current research part is good with plenty of information, but again look at adding more images to make it a bit more interesting. There are obviously some parts that you need to finish off which I’m sure your aware of. &lt;br /&gt;
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Overall it is a really good project with the potential to be excellent because of the amount of effort you have put into the research. Just make sure you change your references so that they are all down the bottom and have in text citations, add more images and maybe student images as well to make your page more presentable. Very well done so far and good luck with finishing the project off. &lt;br /&gt;
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===7===&lt;br /&gt;
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In this review I intend to highlight the merits of your project and suggest some areas for improvement in light of the marking criterial provided. &lt;br /&gt;
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The introduction provides the perfect preface for your project, it serves to summarise the topic and highlight the areas that you will be addressing.&lt;br /&gt;
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In the first section you have discussed fetal development of the neural system in great detail. I feel that a lot of research has gone into the collection and presentation of this date. The diagrams have been appropriately selected. Each image really ties in with the content and helps explain that stage development; I particularly like the diagram summarising the cell migration. In addition the images are well referenced. In the link you provide a brief description of the image and effectively explain the meaning of all the abbreviations. &lt;br /&gt;
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The topics addressed under the heading of current seem quite interesting. The project really succeeds in providing insight into this new MIR technology, a technology that will certainly allow us to build on current knowledge of fetal neural development. I see that the heading of future research has not been completed. However I feel that this is a very interesting sub heading and shows a clear aspiration to go beyond the scope of the course. &lt;br /&gt;
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A number of abnormalities have been addressed. I only suggest that you ensure that each of these subheading is addressed for each abnormality. Description; Epidemiology; Cause and possible Treatments, an image would be good too. &lt;br /&gt;
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All the content on this page is well written. I feel that all the subheadings are relevant, though some sections are not complete. The only major drawback of your project is that, at this point the area of historic findings has not been addressed at all. Make sure you address this area.&lt;br /&gt;
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===8===&lt;br /&gt;
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I believe the introduction of this page is excellent. A good choice of appropriate headings and subheadings. The addition of images would just add to the presentation of the introduction.&lt;br /&gt;
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The development section of this page is excellent! There is very informative, easy to follow and well-presented. There is clear evidence of significant scientific research and correct referencing. The choice and use of graphs and diagrams is excellent and does indeed add to the overall understanding of this section. I do believe, however, that this section could be included with the use of more tables? (Eg. The first four bolded subheadings)- but this is only a suggestion. Excellent nevertheless. Really enjoyed the ‘Visible anatomical details’ table.&lt;br /&gt;
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The current research section is a bit lacking in detail and appropriate choice of pictures. There is a good choice of subheadings and references though. The first included study is excellent though and should serve as a benchmark for the other remaining studies.&lt;br /&gt;
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The historic findings section is not presented on the page yet? I cant seem to find this section on your page. &lt;br /&gt;
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The abnormalities section is excellent, well presented and well researched. There is a very good use of subheadings and an excellent varying amount of abnormalities/defects included. The use of dot-points is effective, as well as, the accompanying pictures- really aids in understanding. This section, however, needs to be correctly referenced and cited. The other remaining abnormalities should be finalised (although I believe not all of the abnormalities should be discussed in great detail!). Great work, overall.&lt;br /&gt;
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===9===&lt;br /&gt;
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Overall, the project contains a decent amount of content as it is, split up into appropriate subheadings, considering the large scope of the nervous system. The introduction provides a succinct description of the CNS, however including an outline of what topics the page intends to cover would be good to orient a reader that approaches the page for the first time. The descriptions of the brain and spinal cord are well-written, however require in-text citations and some words need not be capitalised e.g midbrain, hypothalamus. These can be easily fixed with proof-reading and further editing.&lt;br /&gt;
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The use of an image to illustrate fetal development was a very good idea; although the diagram is itself seems complicated, it can be explained well with the accompanying text beneath. The segmentation of the timeline into 4 different parts made it easier to follow, although I would consider placing the images on the right hand side of the page to reduce the vertical length of the page and the scrolling required to navigate through it. The section on ‘brain development’ contained some relevant information, formatted in dot points which improves readability, however in-text citations are needed to allow the reader to source the information if required. The use of the table in this part was effective also; it was concise and straight to the point. &lt;br /&gt;
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Although the brain development section was very well detailed, there was no information in the spinal cord and meninges sections; with further research, these need to be evened out, along with the current findings section which is just references at this stage, but still a good start to finding sources of information. The section on current research is well-detailed and contains a lot of information too, which is good to see. Fiinally, I thought the section on abnormalities was very well done, using subheadings to segment the content. The use of dot points allowed the information to be easily read off the page, and use of images to accompany them helped the reader to visualise the conditions. There is one image however that has been incorrectly uploaded; consulting Dr Hill’s Wiki help page can remedy this. Also, the placement of all references under one list at the end of the page was effective in neatening it up, that was very well done too. &lt;br /&gt;
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Overall, the project’s content has been well-researched and there is evidence of good teamwork and communication. Perhaps the use of some student-drawn images and inclusion of a relevant video may be areas of improvement. &lt;br /&gt;
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===10===&lt;br /&gt;
This project is coming along quite nicely! The introduction is very thorough and provides a really sound basis for the topics which you covered. I enjoyed the use of diagrams in your introduction- although I admit your flow diagram was very scary! I think you should be a bit more clear in your timeline of the human neural development – it took me a moment to figure out what was happening, so it may be a better idea to put all this information into a table. &lt;br /&gt;
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The images that you have used are great as they are relevant and provide interest to your project page. The referencing on them appears consistent and there doesn’t appear to be any copyright issues- so I think you should include a few more diagrams, just to make your message even clearer. &lt;br /&gt;
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The current research models could do with some reformatting. I don’t think it is a good idea to put the references at the start, and secondly it seems like your work is not so well structured. I think if you included some bullet points in your work, it would greatly aid the clarity. The abnormalities is off to a good start, I see that it is well researched but you want to consider adding some more pictures or diagrams just to make it a bit more visually appealing. Overall this project is off to a good start, I think it may be a good idea to leave all your references until the end just to make your work more cohesive.  &lt;br /&gt;
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===11===&lt;br /&gt;
Very good introduction! Very informative and gives a great jist as to what the project will be about. The developmental timeline is very well done and easy to comprehend and understand.  You should add a lot more pictures in general to the whole page, there’s a lot of information and is organised nicely. &lt;br /&gt;
I feel the usage of dot points is a bit excessive, maybe try to organise some of the information into paragraphs to make it match the wiki page style.  The references aren’t organised at the bottom of the page yet; maybe something for the group to start when the page is unlocked for editing? Some parts of the page still do need a lot of information still to be added.  &lt;br /&gt;
I think you could go more into detail with the brain development; maybe you could make sub sections for development of the cerebrum, cerebellum, brain stem etc to add more information.&lt;br /&gt;
I’ve noticed that there is an image that hasn’t been uploaded correctly; have a look at the page on how to upload pictures, I’ve found that using Mark’s tutorial has been really helpful when I was doing my page. Hope this helped!&lt;br /&gt;
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===12===&lt;br /&gt;
Introduction is a bit too focussed on anatomical division of brain and spinal cord, doesn’t address current/historical research or abnormalities. Change the word “website” to page or project. The embryonic development is explained well and should have its own subheading. Referencing is required for the whole of the introduction, Brain development and abnormalities sections. The Sections 1.1 through to 1.5 could be subheadings under the “system development” main heading.&lt;br /&gt;
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Image showing fetal development timeline is quite overly complex and captioning/referencing is required. Additional explanation of the timeline image narrowing the viewer’s focus onto key fetal development processes will provide greater clarity allowing them to relate the image to surrounding content. The 3 images included in the project also are absent of referencing/captions present on the project page, though info after clicking on the image is great. Brain development information is in-depth and well presented(great use of table), the Spinal Cord and Meninges section have content yet to be added. There is an unusual caption [11] at the end of brain development which should be removed. Like the focus on anatomical structures. &lt;br /&gt;
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There is an absence of historical research which could be found searching on Pub Med for studies completed before a certain date(1970 for example). Current Research content is sufficient. Removal of the different types of dot-points, with addition of images would make the section more attractive.Abnormalities content is great for sections covered, removal of surplus abnormalities and “500px” at the bottom of the section is need unless they are still to be added to.&lt;br /&gt;
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===13===&lt;br /&gt;
The page had plenty of detail in some of the sections especially in the ‘Abnormalities’ section. This section in particular could benefit from the use of in text citation to support the text and some images to give a visual representation of the information. It is clear that it is not yet finished so it when the rest of the abnormalities are completed I think that this could be a strong point of your page.&lt;br /&gt;
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The ‘Current Research Models and Findings’ section has a good selection of articles but some subheadings need to be explained (e.g. ‘Future Research’). If possible, it might be beneficial to include some images break up this section but the summaries of most subheadings were very good. I think this page needs a ‘Historic Findings’ heading with the relevant information. A good place to start is to look under the ‘Historic Embryo’ tab for information. &lt;br /&gt;
&lt;br /&gt;
Overall this page contained some good information but still needs some work. Focus on including a ‘Historic Findings’ subheading and in text citations to support your text. &lt;br /&gt;
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===14===&lt;br /&gt;
Introduction is well informed and written. Maybe write a bit more about what the page is about rather than just a background on the central nervous system. I suggest maybe putting up an image to aid the text. In text citations are missing.&lt;br /&gt;
Development during fetal period has great images to aid the information written so well done. Although I suggest not using bullet points a lot.&lt;br /&gt;
Brain development section has a very good table and an image.&lt;br /&gt;
Spinal cord development section needs more information.&lt;br /&gt;
Meninges development section is empty so research needs to be done as soon as possible.&lt;br /&gt;
Current models and findings section just has references so do start to write on what those research articles say.&lt;br /&gt;
Current research is well informed but images will help aid the information. Future research is blank which needs to be filled up with information.&lt;br /&gt;
Abnormalities section is quite good as the image and information relate to each other and the images help aid the information. A bit incomplete towards the end which you should write up on.&lt;br /&gt;
Overall, some of the images are a bit too complex so maybe try hand drawing some images in a simplified manner. All the references would look more professional and neat if it was at the end of the page in a bulk. Also historic findings section is missing so suggest you add that if possible. Good so far just missing bits and pieces of information which I am sure you can write up on within a week. Good luck!&lt;br /&gt;
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===15===&lt;br /&gt;
&lt;br /&gt;
The introduction is great as it mentions the features of the neural system, their anatomical positions and highlights the key events in the embryonic and fetal stages of development. The last paragraph of the introduction clearly addresses how the page will be divided and what the viewers are to expect which is good. The content under all subheadings are relating to the key topic and are formatted appropriately. I really like the image used under the subheading ‘Development during fetal period’ as it presents a diagrammatic representation of the content mentioned. The use of a table to briefly describe the events that occur at certain periods of fetal development is really helpful in grasping the main details. Some information is missing such as in ‘spinal cord development’, ‘Meninges development’, ‘future research’ and some ‘abnormalities’. This should be added right away. There are no historic findings which is great to have on your page for viewer’s fascination into the group project. Members could search on pubmed about the neural system and view dates on the side that may contain key findings. Also a glossary list should be added to help viewers understand the content more instead of just being confused at some sections.&lt;br /&gt;
&lt;br /&gt;
In terms of images, there are still many potential spaces for images such as under ‘introduction’, ‘current research’ and some ‘abnormalities’.  The images used under ‘Development during fetal period’ are great and relate to the content. All images have correct description, referencing, copyright issues and ‘student template’, which shows that members of the group have followed correct ‘uploading image’ procedures. The images however need a caption to describe what the image is showing.&lt;br /&gt;
&lt;br /&gt;
There needs to be more use of incite referencing such as in the ‘introduction’, ‘brain development’ and ‘abnormalities’. There is a huge list of references under ‘current research models and findings’ which need to be placed all under one ‘references subheading’; similarly to any other reference list on the page. References 7 and 8 are the same reference under the ‘references’ subheading and need to be combined into one number. Overall, this is a good project and if the group makes edits based on the peer-reviews received, this could enhance their project.&lt;br /&gt;
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===16===&lt;br /&gt;
&lt;br /&gt;
Group 7 has definitely put in a lot of effort into the project however there are some points for improvement I’d like to suggest. The introduction is quite succinct and short which is good however I felt some more could be detailed about what the project was about and what aspects of development were being focused on. I would also suggest having a timeline either in dot-point form or as a table to summarise the changes that occur during fetal development of each of the organs. Though this was done with the visible anatomical details table, it would be a good idea to include some more information on function or implications of the stages of development. I think overall a good variety of images and diagrams have been used to support the text however the structure and format of the text needs to be edited and made more consistent between the headings. With the current research findings heading, the layout is a bit confusing and hard to follow and the references listed here seem out of place. I would suggest finding at least 2-3 recent research papers and under each one, summarise the purpose of the study, the out come and then the implications. This will give a lot more meaning and purpose to the text and be an interesting read. I am not really sure if the future research subheading is necessary, but if you have found good sources of proposed research plans then it would be a good idea to include it. The abnormalities section still needs to be completed, but from whatever work has been done, I think the information was informative and well written. There is an issue with the ‘facial expressions associated with fetal alcohol syndrome’ picture which can be sorted out by reformatting. Overall, the referencing was done well and most were listed under an exclusive references heading which is great. Bit of work still needs to be done but other than that, great job!&lt;br /&gt;
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===17===&lt;br /&gt;
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The introduction is helpful in introducing the CNS. However the introduction is a good opportunity to outline what the page will be focusing on about the CNS, for example that it is focusing on fetal development. More could be added to the introduction for it mention briefly other things like recent findings, historic findings and fetal development introduction. In the content box ‘Brain’ and  ‘Spinal Cord are in bold, it would be good to make it normal. Most of the key topics were addressed on your page. However you guys should add historic findings if you get time. It is part of the criteria and it would be good for your page. &lt;br /&gt;
The table under Brain development is really good and it is simple and easy to follow. If it were possible, if appropriate images were put into the table it would make the table really good. You guys have a lot of different articles for research models and findings, but as you are probably already going to do, would be good to explain each of them. Some sections are empty like the ‘Meninges Development’ which I’m sure you guys will get too before the dead line. &lt;br /&gt;
&lt;br /&gt;
There was a good use of diagrams. The first diagram is particularly useful. It is a good pictorial representation of the CNS development. It is a good medium to try explaining it effectively to peers. In the ‘Brain Development section (-)  was used to demarcate points. And in the ‘Development during fetal period’ dot points where used instead. It might be a good idea to use the dot points throughout the page for consistency. &lt;br /&gt;
It is evident that you guys have done a considerable amount of information. Some more research wouldn’t hurt so that you guys can go beyond normal teaching level descriptions. Different teaching tools for peers might be a good idea, or some sort of way to make the page more interactive or captivating. For example hand drawn diagrams or video links. &lt;br /&gt;
The references are done well but there are some references throughout the page which can be added to the main reference section. Overall it was good project guys all the best. &lt;br /&gt;
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===18===&lt;br /&gt;
Good use of bullet points and images to clearly show the stages that occur during development. Table is effective at showing the visible anatomical details at different weeks. More work needs to be done on the spinal cord development and meninges development sections. The references in the current research models and findings need to be expanded or put into the references section at the end.&lt;br /&gt;
&lt;br /&gt;
===19===&lt;br /&gt;
This project has a great introduction and overview of the brain and spinal cord anatomy. The first image is eye catching however I find it hard to follow and it seems like there is too much information on it. Perhaps it would be better positioned further down in the report after more neural developmental stages have been explained. The timeline section is clear and to the point. There is an excellent use of images to support the information. The fluorescent stained images make the ventricular, subventricular and other cortical layers clear and easy to understand. The information under the brain development section is simple and effective. However there are some terms mentioned that are not explained in enough detail like the specific layering of the cortex. It is a complicated migration process that deserves some more research. It is good that the student has explained gyration and sulcation in this section. &lt;br /&gt;
&lt;br /&gt;
This project is clearly still in progress however the information in the first section of the wiki page indicates a very promising final product. The spinal cord and meninges development section still needs to be written up. If it follows along the course of the brain development section, it will be flawless. The current research models and finding section reveals an in-depth understanding of complex ideas. However for a student embryology wiki page, there is too much detail. If the student wants to illustrate a complicated research finding, images or tables of the results found from this research would help convey the message to the student. A table would help summarise the results in the first current research description, particularly for the results gathered from the different parts of the brain. &lt;br /&gt;
&lt;br /&gt;
The final part of this report on abnormalities is unfinished however the bulk of the information presented already is very good. The images supporting the abnormality are excellent and important for keeping the student reading this page engaged. However there are a few spelling and grammar errors in the neural tube defects section: “which affect the either the brain”, “the openings remain which leas”. There is still room for more research and information on other neural development abnormalities and the subheadings the student has incorporated indicates their intention of adding more information. This report has excellent reference formatting and citation throughout the page. The tables and images are referenced correctly and the long list at the end is very neat. &lt;br /&gt;
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--[[User:Z3418981|Z3418981]] ([[User talk:Z3418981|talk]]) 14:21, 16 August 2014 (EST) Hey everyone,&lt;br /&gt;
&lt;br /&gt;
What's everyone's ideas about doing the neural system for our project? there are lots of interesting Neurologic deficits that we could talk about!!!&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3419587|Z3419587]] ([[User talk:Z3419587|talk]]) 23:25, 16 August 2014 (EST) That's a good idea. Neural system is a complex structure and it should be fun to work on it! Any other ideas?&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3374116|Z3374116]] ([[User talk:Z3374116|talk]]) 23:51, 19 August 2014 (EST)&lt;br /&gt;
I talked to Yas before, sorry couldnt respond faster haha. Agree that Neural system would be interesting to research :p&lt;br /&gt;
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Do you guys have facebook as well? It might be an additional way to communicate&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]])&lt;br /&gt;
I also agree on this topic being quite interesting as well&lt;br /&gt;
--[[User:Z3418981|Z3418981]]&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3418981|Z3418981]] ([[User talk:Z3418981|talk]]) 10:54, 25 August 2014 (EST) hey guys it's yas! so we each need to choose one of the following:&lt;br /&gt;
Review the neural system development during the fetal period.&lt;br /&gt;
Identify current research models and finding.&lt;br /&gt;
Identify historic findings.&lt;br /&gt;
Identify abnormalities that can occur in this system during fetal period.&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3419587|Z3419587]] ([[User talk:Z3419587|talk]]) 21:07, 25 August 2014 (EST) Thanks! This is vivian. Can I do &amp;quot;the review of the neural system development during the fetal period&amp;quot;? Or if anyone wants to do this section?&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3374116|Z3374116]] ([[User talk:Z3374116|talk]]) 12:07, 26 August 2014 (EST)&lt;br /&gt;
Hey guys, Can i do historic findings for fetal neutral system development :) - Sean&lt;br /&gt;
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&lt;br /&gt;
--[[User:Z3419587|Z3419587]] ([[User talk:Z3419587|talk]]) 17:47, 26 August 2014 (EST)I have put some subtitles to give a brief structure to our webpage, feel free to change them if you want!&lt;br /&gt;
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--[[User:Z3418981|Z3418981]] ([[User talk:Z3418981|talk]]) 17:51, 26 August 2014 (EST) sure and I'll do the abnormalities - Yas&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3419587|Z3419587]] ([[User talk:Z3419587|talk]]) 18:25, 26 August 2014 (EST) hey Yas, see if this helps. &amp;lt;pubmed&amp;gt;25007063&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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--[[User:Z3418981|Z3418981]] ([[User talk:Z3418981|talk]]) 21:14, 26 August 2014 (EST) Thanks Vivian!! the article is very helpful! and the page looks really good too :)&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3374116|Z3374116]] ([[User talk:Z3374116|talk]]) 20:18, 26 August 2014 (EST)&lt;br /&gt;
Hey guys, I think the last entry from my section will help alot in the ''Development'' section for our project :) - Sean&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;17848161&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3419587|Z3419587]] ([[User talk:Z3419587|talk]]) 23:14, 26 August 2014 (EST) That's true! thanks Sean :) - vivian&lt;br /&gt;
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--[[User:Z3422484|Z3422484]]--[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]]) 12:50, 27 August 2014 (EST)&lt;br /&gt;
Hey guys, this is a useful article for the abnormalities area &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24664314&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3374116|Z3374116]] ([[User talk:Z3374116|talk]]) 23:55, 1 September 2014 (EST) nice one :D&lt;br /&gt;
How are you guys going with your sections?&lt;br /&gt;
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--[[User:Z3374116|Z3374116]] ([[User talk:Z3374116|talk]]) 12:58, 17 September 2014 (EST) &amp;lt;pubmed&amp;gt;10226791&amp;lt;/pubmed&amp;gt; maybe for development&lt;br /&gt;
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--[[User:Z3374116|Z3374116]] ([[User talk:Z3374116|talk]]) 21:12, 20 September 2014 (EST) http://www.ehd.org/cache/pdf/fd7e47f291dded855c38ffb3418fbdc8/timeline.pdf&lt;br /&gt;
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something which might help us figure out a timeline structure&lt;br /&gt;
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--[[User:Z3374116|Z3374116]] ([[User talk:Z3374116|talk]]) 11:56, 24 September 2014 (EST) http://discovery.lifemapsc.com/library/review-of-medical-embryology&lt;br /&gt;
A textbook which has great information on the development of the CNS during the fetal period&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]]) 11:35, 8 October 2014 (EST)&lt;br /&gt;
Hey guys i will be adding a few extra research articles to the current research tab&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]]) 11:35, 8 October 2014 (EST)&lt;br /&gt;
Also is there anything else anyone needs help on as well?&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]]) 12:09, 8 October 2014 (EST)&lt;br /&gt;
Forgot to mention that I'll also be adding spinal cord abnormalities&lt;br /&gt;
&lt;br /&gt;
For Historial Research and Findings&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19339620&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;8005032&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;9311417&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17848161&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;12768653&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;17060425&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21042938&amp;lt;/pubmed&amp;gt; for brain de&lt;br /&gt;
&lt;br /&gt;
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abnormalities&lt;br /&gt;
&amp;lt;pubmed&amp;gt;12454899&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;25007063&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;16530991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;7504639&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;19651588&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;25135350&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;25128525&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24397701&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
----&lt;br /&gt;
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*Good start on the introduction. Maybe have it used to explicitly state what your entire page will be covering rather than just a background on what the CNS is. &lt;br /&gt;
*You're missing references for the huge chunks of information in the introduction section&lt;br /&gt;
*The image of the timeline of development seems overly complex and I can't tell if you've explained it. If it's not relevant, maybe just come up with your own concise table of what happens during the course of development&lt;br /&gt;
*Maybe think of re-creating some simpler images by hand and uploading them. That way you can choose to focus on what you actually need from the image to show what you're explaining&lt;br /&gt;
*Include the years of when your current findings were discovered&lt;br /&gt;
*For the &amp;quot;abnormalities&amp;quot; section, as there are many, maybe the amount of detail you've included for the first couple of ones isn't needed, but of course, use your own discretion to how much is relevant. Otherwise, the bullet points are a good way to simplify information &lt;br /&gt;
*Collate all your references in the bottom from all the separate sections&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=149750</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=149750"/>
		<updated>2014-10-14T12:35:00Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Online Assessment - Peer Reviews */&lt;/p&gt;
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&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
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==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
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===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
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== Online Assignment 1 ==&lt;br /&gt;
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Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
&lt;br /&gt;
The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
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		<updated>2014-10-14T12:33:30Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
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==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
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===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
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===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
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===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
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===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
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===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
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== Online Assignment 1 ==&lt;br /&gt;
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Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
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The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;br /&gt;
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==Online Assessment - Peer Reviews==&lt;br /&gt;
Project 1: Respiratory system&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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Project 2: Renal system&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end.  &lt;br /&gt;
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Project 3: gastro-intestinal system&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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Project 4: genital system&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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 Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources. &lt;br /&gt;
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Project 5: Integumentary system&lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
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The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
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The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_5&amp;diff=149738</id>
		<title>Talk:2014 Group Project 5</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_5&amp;diff=149738"/>
		<updated>2014-10-14T12:30:33Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Peer Reviews */&lt;/p&gt;
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&lt;div&gt;{{ANAT2341Project2014discussionheader}}&lt;br /&gt;
==Peer Reviews==&lt;br /&gt;
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Group Project 5 – Integumentary Development&lt;br /&gt;
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This page looks very neat and well organised, with an introduction that explains exactly what is going to appear and be discussed on the page. The Development Overview section is very well done, with the appropriate use of subheadings and content. The use of dot points is very effective, making the page look neater. Perhaps it would be good to draw a histological diagram of the skin layers, and uploading it to the skin development section. Specialised cells or important names throughout the page could be highlighted in bold or underlined as well, to highlight important terms and make it easier to learn and remember from. The title ‘Some Recent Findings’ accurately portrays what we as students can only do, which is identify SOME of the recent findings. This section could have more than 2 recent findings however and could be further subdivided by subheadings into the different components of the integumentary system – perhaps have 2-3 research articles for each component of the system. Historic findings are well researched but some more information would be good. The ‘Abnormalities’ section is so far the best looking section as it seems it is almost completed. Perhaps a few more abnormalities would be even better.&lt;br /&gt;
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The table of the timeline in the ‘Development Overview’ section is superbly done and the use of histological images is fantastic as it provides the anatomical information visually. When I clicked on an image however, there was no proper referencing of the image and the copyright information and student image information was not present. The images are described very well. &lt;br /&gt;
One image has a problem and is present in red writing, so might need to remove this as something is wrong with the file and it could not be uploaded. There are no student-drawn images and I think if this group did this, it would really benefit their project and emphasise their understanding. &lt;br /&gt;
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The ‘Some Recent Findings’ section has a purple background, which makes the page look more aesthetically pleasing and less monochrome. I like the ‘More recent papers’ box that can be expanded to reveal any more research papers related to the integumentary fetal development, in case anyone wants to have a further read- very clever. &lt;br /&gt;
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Journal articles are correctly referenced but website references need to be improved upon- to find how to do this go to the ‘How to reference’ page. References are all over the place and need to be compiled under each heading or one main heading titled ‘References’ at the bottom of the page.&lt;br /&gt;
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Overall, this page is looking fantastic at this point in time so keep up the great work!&lt;br /&gt;
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Introduction is short though luckily few words can go a long way, with all sections of the wiki page being properly addressed. Development overview content is good; the use of table integrated with pictures allows viewers to visually grasp the progression in skin and teeth development. The changing between dot-points and paragraph format should be standardized or use paragraphs with dot-point only for list based information. References need to be properly integrated into the page, instead of at the bottom of each section. &lt;br /&gt;
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In the recent findings section 2 out of the 4 studies presented have any content. To improve cutting some of excess information for the 2 studies already addressed and creating summaries for the other 2 will create better scope of recent findings. The formatting of recent findings is unusual, proper placement of the “Hematoxylin/eosin” image”, removal of dot-point and removal of purple highlighting, will make the section easier for viewers to understand. Historical findings okay, more detail could be added to “skin”, “glands”, “nails”. Use of capital letters like “DEVELOPMENT” show be replaced with subheadings, the image “File:Screen Shot 2014-10-08 at 10.38.04 am.png” has not appeared properly, should be easy to fix.&lt;br /&gt;
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Straight up the abnormalities section is amazing, no improvement needed. All 4 diseases have in-depth relevant information, sufficient referencing and images to allow viewers to visualise clinical manifestation. To improve use of dot-points or paragraphs should be standard throughout the project, referencing in beginning sections needs to compiled at ending of each Main heading or bottom of page, recent findings need 1-2 more studies, and recent findings need significant reformatting.&lt;br /&gt;
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This page seems to be done extremely well. It looks very visually appealing as multiple images are used, information is presented in tables, bullet points and very few slabs of text. The introduction is short and to the point. You could possibly add to this area a tiny bit of info concerning the embryonic development of this system, where it first started, then mention how you will expand on the fetal development. Otherwise it just seems way too short.&lt;br /&gt;
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Explanation of the organs in this system is well done and concise. In the glands section, I would suggest not using dot points for the function of the vernix caseosa as it looks as though the dot points continue from those of the glands, therefore can be confusing when first looked at. Other than that, I would suggest that you make sure your referencing is correct and is used within the text.&lt;br /&gt;
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The recent findings area is nicely done, but I still can’t help but feel the amount of text is just too much, even though the section is made better looking by making it purple (keep the colour, it looks awesome). The slab of text is just too much, so you should try and simplify it a bit. Historic findings are few but there is at least one for every organ which is good (more would be better). The abnormalities covered are done well, going into detail and providing a good image to describe what it looks like. I would suggest having at least 5 abnormalities, one for each organ discussed.&lt;br /&gt;
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Overall, this page is very well done, with lots of images and colour used. The main thing I would suggest would be to make sure correct referencing is used. There were some paragraphs were no references were used at all. Also, all references should be at the bottom of the page, not within individual sections.&lt;br /&gt;
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This page has great overall structure and presentation. The introduction gives good insight of the overall contents of the page, however it is very brief and should be expanded upon. &lt;br /&gt;
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The table included in the developmental overview serving, as a timeline is excellent, really well done. It’s easy to follow and looks very neat. I like how there is an image for each of the weeks mentioned, just don’t forget to add in-text citations for its contents. The glands sub-section is very brief and would benefit if there were more contents added. Great job on the images though. The nail section is the same, more contents needs to be added and image would look really good. &lt;br /&gt;
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The developmental overview and historic findings sections also seems to lack in-text citations. There is also has an image with a broken link. The subsection hair seems to be well researched, however I would also suggest either bolding or underlining the words you want to emphasize such as “structure” for a neater look. &lt;br /&gt;
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The recent findings section looks superb I love the purple background colour. Its very well researched and the link to more research papers are very helpful for readers. I would suggest you put the image at the bottom of the mentioned content though, just to avoid the big gap on the page, or even if you can manage to wrap the text around the image, it would look much better in terms of presentation. &lt;br /&gt;
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Although disturbing, the abnormalities section I could not fault. Very well done. It is evident that it has been research well and the images allow for great visualization of the diseases mentioned. &lt;br /&gt;
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Overall, excellent page just needs a very formatting edits and some expanded contents mentioned above. Good luck! &lt;br /&gt;
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This is a really well done project. You have made sure that that you have ticked all the boxes as well that Mark has asked for. The abnormalities section is really good. You have done well with most of your images as when you click on them there is a good description and they are well referenced. The development overview table is exceptional and makes the project easy to understand. For the week 22 maybe include the study in which you got your information from.  &lt;br /&gt;
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Apart from the abnormalities section it appears as though the referencing is a bit all over the place. Need to follow the abnormalities section and put  references into the specific parts of the information you are using it for. Because otherwise it becomes difficult to know exactly where you got your information from. The historic findings are really good and well done however there is probably a space for more information to be included as I feel as though some of the findings are a bit hard to follow at times. It may have just been my computer I couldn’t see the picture of ‘fetal hair development’. &lt;br /&gt;
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I think it would give a nice touch to the project if you were to add some student images because it would give the page a more ‘student’ and also make it easier to understand. Don’t mind the purple background on the ‘some recent findings’ part but it just looks a bit out of the blue. It’s certainly unique and attracts the eye but it puts a lot of emphasis on this section which I’m not entirely sure you want. &lt;br /&gt;
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Overall though a really good project with excellent information. There needs to be a bit more focus on referencing technique, some minor edits which I have mentioned and maybe introduce some student pictures to make the project more student-like. Great work though and good luck in finishing it off. &lt;br /&gt;
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The introduction of this page was good as it provided a great overview and insight into what the project would later go on to discuss. Perhaps a little information on defining the integumentary system itself would be valuable though, to let the reader know the constituents.&lt;br /&gt;
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The sub-sectioning of the page’s content into ‘introduction, ‘development overview’, ‘recent findings’, ‘historic findings’ and ‘abnormalities’ was clever, as the development section then went on to describe each component such as skin, nails etc. This effectively segmented the information into smaller chunks that could easily be navigated to. I especially liked the use of the table in the ‘skin’ section, showing the week of development, description and image corresponding alongside it, as it provided a holistic approach to that section. However, there were no in-text citations in the ‘skin’, ‘hair’, ‘nail’ or ‘teeth’ sections, hence the source of the information is unclear. To do this correctly, Dr Hill’s Wiki help page should be consulted.&lt;br /&gt;
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The use of various images with labelled captions was a strength of this project, as the pictures were effective in balancing the text components to make the page more visually appealing. Most of the sections under ‘development overview’ have a decent amount of content, however the ‘nails’ part is a bit lacking and also needs to be correctly cited. The use of the table of images alongside the description of developmental stage in the ‘teeth’ section was very good to include, however the image is captioned ‘The stages of embryonic teeth development’. This may be irrelevant as the project’s focus is on fetal development. Further research into this area may uncover more relevant information. &lt;br /&gt;
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Although the section on ‘recent findings’ contains a lot of information, the use of chunky paragraphs detracts from the readability of the page and the purple boxes could be summarised into dot points to help the reader understand the content more quickly. The section on historic findings seems concise and relevant, however the image included says it has been removed/deleted, so this requires editing. Lastly, the ‘abnormalities’ section was very well-structured and written, as each example had a captioned image accompanying it to help the reader visualise. This section was also well-done in terms of in-text citations, with an extensive reference list provided at the end. Perhaps consider adding some student-drawn images and possibly a relevant video, but otherwise it is very good as it is. Overall, the project has a good layout and a decent amount of content; with some editing and formatting it can be improved further. &lt;br /&gt;
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Overall this is an impressive and well researched wiki page incorporating lots of pictures and tables to keep the reader engaged and interested. However there are a few areas that have the potential to be tweaked. Firstly there are references scattered throughout the page. A more attractive way of presenting the references is as a long list at the end of the page. The introduction is clear, concise and short. All the organ development section is well presented and has the right amount of information. It is well structured in the sense that the student introduces the organ, it’s embryonic origin, the fetal growth stage and then goes into slightly more depth in a bullet point form. Along with complementary pictures, this is a very effective way of presenting their topic. This page could be improved by adding student-drawn schematic diagrams to summarise the layers of the skin in particular since histological images can be confusing and unclear to a non-expert embryology student. &lt;br /&gt;
&lt;br /&gt;
The skin development section appears to dwell on the content that was covered in lectures. Considering there appears to be only three references associated with the entire integumentary organ development section, the depth of the information is limited. By doing some more research you might be able to find interesting additional information that can be added. The recent findings section is interesting and the images are great. However the dense block of information and slightly odd formatting make it hard to follow. Perhaps using diagrams to explain the differing gene expression and breaking down the information into bullet points would make it more readable. &lt;br /&gt;
&lt;br /&gt;
The historic findings and abnormalities section is particularly well done. The images complement the minimal yet important points made. I was left wanting to read more into it so that suggests there’s room for further development and a deeper explanation of skin abnormalities.&lt;br /&gt;
&lt;br /&gt;
==Week 5==&lt;br /&gt;
Hey guys!! I found some research material that we can use to construct our time line! &lt;br /&gt;
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Historic information is hard to find! I might go look at some text books  in the library &lt;br /&gt;
--[[User:Z3418340|Z3418340]] ([[User talk:Z3418340|talk]]) 12:50, 27 August 2014 (EST)&lt;br /&gt;
How is everyone else going?&lt;br /&gt;
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--[[User:Z3417843|Z3417843]] ([[User talk:Z3417843|talk]]) 12:52, 27 August 2014 (EST) Hey!! That's great! I also found some material for abnormalities. There seem to be a lot about septal defects. I'm gonna try to look up for more defects.&lt;br /&gt;
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--[[User:Z3417843|Z3417843]] ([[User talk:Z3417843|talk]]) 22:53, 30 August 2014 (EST)Woo!! Nice to see more links in the page! Rehmina and I also thought that it would be easier for marking if one of the two people in current research do timeline instead because that would make marking easier and less confusing. But that's not final, it's only a suggestion. Also, Dr. Hill gave us some tips on what to focus/include in our research such as:&lt;br /&gt;
*Remodelling during the fetal period&lt;br /&gt;
*Changes during ossification - haematopoietic elocution from liver to bone marrow&lt;br /&gt;
*Early development of WBCs — hot topic right now!!&lt;br /&gt;
&lt;br /&gt;
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Hey everyone, yeah that sounds good with me..  :) so rather each person focuses on 1 of the 4 topics right? --[[User:Z3417796|Z3417796]] ([[User talk:Z3417796|talk]]) 12:35, 31 August 2014 (EST)&lt;br /&gt;
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--[[User:Z3417843|Z3417843]] ([[User talk:Z3417843|talk]]) 18:36, 1 September 2014 (EST)Yep, exactly! I'm really glad that's alright with you but we can still talk about more in the lab. &lt;br /&gt;
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--[[User:Z3417843|Z3417843]] ([[User talk:Z3417843|talk]]) 12:14, 2 September 2014 (EST)Hey everyone! I just asked Dr. Hill about using review articles. He said it's alright to use review articles as long as you say that the information came from a review article when citing. We can also use images from review articles and there is no need to say that it came from a review article.&lt;br /&gt;
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==Week 6==&lt;br /&gt;
--[[User:Z3418488|Z3418488]] ([[User talk:Z3418488|talk]]) 20:19, 3 September 2014 (EST)Hey guys, I had a good talk with Mark today after the lab. Since we're doing the Cardiovascular system, it incorporates the (i) development of the heart, (ii) development of the blood vessels and (iii) the formation of red blood cells/white blood cells. But Mark said that as a group, we would be able to create and produce this web-site in a manner that we thought was appropriate. We could focus on one of the specific areas or more broadly on each area, if we chose to. But, MOST IMPORTANTLY, our project should be cohesive. What we talk about should be introduced well at the start and should be cohesive through out all of the subsections that we're working on. He really stressed the importance of us having a single, unified vision of our end product and that it should be succinct throughout it all. Im proposing that we actually decide what to focus on very soon. &lt;br /&gt;
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: --[[User:Z3418488|Z3418488]] ([[User talk:Z3418488|talk]]) 20:19, 3 September 2014 (EST) I'd particularly like to just focus on the development of the heart? Maybe incorporate the formation of blood cells if the research in the other areas is interesting and notable?&lt;br /&gt;
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--[[User:Z3418488|Z3418488]] ([[User talk:Z3418488|talk]]) 20:24, 3 September 2014 (EST)In regards to the use of the textbook, we are allowed to use the information from it if we cite it properly, but he really want us to be using articles (and even Review articles) to   discuss our information.&lt;br /&gt;
&lt;br /&gt;
I agree, the heart should remain our focus, but of course other aspects such as blood vessel formation/ blood cells would naturally fall into it as well- maybe just a brief mention wherever appropriate? --[[User:Z3417796|Z3417796]] ([[User talk:Z3417796|talk]]) 21:22, 3 September 2014 (EST)&lt;br /&gt;
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==Week 7==&lt;br /&gt;
--[[User:Z3417843|Z3417843]] ([[User talk:Z3417843|talk]]) 21:05, 8 September 2014 (EST) Hmm. I agree. Let's try and focus on the heart for now and see how we go? And if time permits, maybe we will be able to include the development of blood vessels and blood cells. Sorry I didn't reply so soon, kinda busy week for me haha!&lt;br /&gt;
: --[[User:Z3418488|Z3418488]] ([[User talk:Z3418488|talk]]) 00:24, 10 September 2014 (EST)Ok that sounds really good and reasonable! I'd be happy to follow that plan. And yeah, same! Very busy week for me as well! But yeah, I think lets just focus and refine our research to just the development of the heart at the moment&lt;br /&gt;
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--[[User:Z3418488|Z3418488]] ([[User talk:Z3418488|talk]]) 00:40, 10 September 2014 (EST)Hey guys, Im having difficulty knowing whether the use of an article is fine or not?! If it says &amp;quot;Full-free-text&amp;quot; does that mean we're allowed to incoporate it? Because a lot of the copyright information, is very brief.  Thanks heaps, if you guys know an answer haha&lt;br /&gt;
: --[[User:Z3418488|Z3418488]] ([[User talk:Z3418488|talk]]) 00:55, 10 September 2014 (EST)Ok, never mind.. I find out the answer haha. If it says &amp;quot;Open-Access&amp;quot; or &amp;quot;Full-free-text&amp;quot; it is only free to read online and may/may not be allowed for re-use. You'; have to read carefully or apply for permission lol. I guess i'll just be sticking to mainly the Public Library of Science (PLoS), Biomed central (BMC) and Springer Open... which we are pretty much able to use, with the right referencing and acknowledgement. I read this on the 'Copy rights' page on this wiki. http://php.med.unsw.edu.au/embryology/index.php?title=Help:Copyright_Tutorial. Can someone verify or correct me if i'm wrong haha?&lt;br /&gt;
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--[[User:Z3417843|Z3417843]] ([[User talk:Z3417843|talk]]) 11:56, 10 September 2014 (EST) I thought copyright only applied on images and not on content. It would be really difficult to write a report when the most papers have copyright. We can ask Dr. Hill in the lab just to confirm.&lt;br /&gt;
&lt;br /&gt;
==Week 8==&lt;br /&gt;
--[[User:Z3417796|Z3417796]] ([[User talk:Z3417796|talk]]) 12:56, 17 September 2014 (EST) Hey guys, so Carl and I had a talk with Dr. Hill and he has agreed to allow us to change topics from Cardio to Integumentary. To finalise the change all members have to personally email him saying we all agree to the topic change. Carl and I have started thinking about our approach to the topic and we think we should have a main focus on skin and smaller sub-topics on hair, nails, glands and teeth. Each members role just remains the same and any problems we will all still help eachother :)&lt;br /&gt;
&lt;br /&gt;
==Week 9==&lt;br /&gt;
--[[User:Z3417796|Z3417796]] ([[User talk:Z3417796|talk]]) 12:46, 22 September 2014 (EST)Hey guys, I've added some headings for our new page just to get a start, we've got alot to catch up on, I guess we still have to talk about it as a group for the overall layout, we should all start adding some content soon.&lt;br /&gt;
&lt;br /&gt;
--[[User:Z3417843|Z3417843]] ([[User talk:Z3417843|talk]]) 12:41, 23 September 2014 (EST) Thank you for fixing it! Yeah, we have a lot to do but that's okay. Midsem break is next week and hopefully we can get most of the bulk done before week 10.&lt;br /&gt;
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==Midsem Break==&lt;br /&gt;
--[[User:Z3417843|Z3417843]] ([[User talk:Z3417843|talk]]) 23:24, 29 September 2014 (EST) Just wanted to let you guys know that Dr. Hill gave us some tips on what to look at a few weeks back. He mentioned &amp;quot;vernix caseosa and fetal hair.&amp;quot; Here's a wikipedia link to vernix caseosa (http://en.wikipedia.org/wiki/Vernix_caseosa) just to give you guys an idea on what it is. I'm aiming to finish before the end of the week so that I could help anyone with their parts. Anyway, I hope everyone's having a good break!&lt;br /&gt;
&lt;br /&gt;
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&lt;br /&gt;
*Great overview given in the introduction. Maybe look to replacing the words &amp;quot;this page&amp;quot; to something else to avoid repetition&lt;br /&gt;
*I'm really liking how everything has been simplified into dot points and tables where relevant. Don't forget to include relevant references all throughout though, to justify all that you've included in each section&lt;br /&gt;
*I can't express how much I love your first table. Great work! &lt;br /&gt;
*Proofread so that you don't repeat the same things in your table though. You mention &amp;quot;in a study&amp;quot; numerous times but there's no indication to which studies they are&lt;br /&gt;
*I'm sure Mark would be thinking this same thing, but look to getting different references outside of this Embryology website, maybe from textbooks or otherwise for preliminary information on development&lt;br /&gt;
*The &amp;quot;recent findings&amp;quot; section looks nicely formatted but just a bit wordy. Maybe think of dividing the text up with bullet points or images&lt;br /&gt;
*Really liking your &amp;quot;historic findings&amp;quot; section! Great research&lt;br /&gt;
*Maybe think of re-creating some of the simpler pictures by drawing them yourselves. That way you're not using too many pictures from this Embryology website, Mark warned our group about this point&lt;br /&gt;
*Great choices for the &amp;quot;abnormalities&amp;quot; section. Traumatising at first, but very well-researched and presented&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_4&amp;diff=149678</id>
		<title>Talk:2014 Group Project 4</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_4&amp;diff=149678"/>
		<updated>2014-10-14T11:24:31Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Peer Reviews */&lt;/p&gt;
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&lt;div&gt;{{ANAT2341Project2014discussionheader}}&lt;br /&gt;
==Peer Reviews==&lt;br /&gt;
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The Introduction, Current Models and Current Research section all in dot-point form, which obviously allowed you to more easily, put information on the page. These need to be converted into paragraph form to give the content greater readability and flow.&lt;br /&gt;
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Presuming the system development is supposed to be the introduction, there should be inclusion of current research, historical research and abnormalities. Without these the reader will not know all the sections of the page after reading the introductory section, which is the intros purpose. The use of bold and capital letters is unneeded. The existence of a table is good though has a bunch of formatting and text problems (capitals, bold, captions, lack of lines). “(around week 4-6) that sexual differentiation occurs in the fetus ” this statement is incorrect since it is an embryo during the week4-6, it becomes a later around week 10. “450px” has not been inserted properly, the sexual differentiation image requires caption and references.&lt;br /&gt;
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Current Research and Models has in-depth content for undifferentiated and male, though limited information on current female genital research. The headings are repetitive also many without any content, similar content needs to be merged under single headings. In Historic findings the content and wording is good but same trend continues significantly more text on Male development compared to female. &lt;br /&gt;
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Abnormalities section is great with even attention given to female, male and both. Information is appropriately in-depth and referenced, addressing causes, process and treatment. Addition of 1-2 images in the “both” section is advised, to allow readers to identify clinical features of the diseases. Like the use of drawings especially “Abnormalities of the Uterus and Vagina” and “Anat of Testes”, you should change the caption of the testes drawing from “alt text”.&lt;br /&gt;
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For improvement; covert of dot-points into paragraphs, expand on female sections of “current research” and “historical research”, fix a few image problems and remove unnecessary bold/capitals/captions.&lt;br /&gt;
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A great start on tabulating the information about the development of this system. There are references but I don’t see any in-text citations. The image used in this section is really good and relevant. It clearly shows the major processes in the development of the genital system. However, it is a bit pixelated so maybe try resizing the image to a smaller size. Maybe try uploading the image again with a different filename, change it to something more appropriate rather than “Image.jpg”. And also, if possible, try to include it in the table. Good job on embedding a video! I think this is the only group so far that has included a video. It’s a good video about the development, I just wish it had a voice-over explaining what is happening but that’s not really the group’s fault. Nonetheless, great job on the development section. &lt;br /&gt;
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With the current research section, great use of dot points but a bit excessive. Maybe try to make paragraphs where it is appropriate. It is well-researched, very detailed and very informative. It’s good to see student drawings. Great job on that. I see that an image was not properly uploaded into the page, so just fix that. Good job on referencing. All research articles seem to be relevant to this section but try to incorporate some of the in-text citations of the remaining articles, not just the first three. Overall, really great job on the content of this section. It is evident that the person responsible for this section put a lot of effort in research.&lt;br /&gt;
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As for historic findings, great job! I know this is probably the hardest of all the four sections in terms of finding information and this section is well-researched, very detailed, and very informative much like the current research section. Maybe try to use some dot points to lessen the bulk of this section. Great drawing included in this section. Try to add more, especially for the males since that is the bulk of this section. &lt;br /&gt;
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Lastly, for abnormalities, great job on finding lots of abnormalities! Lots of references and each area of this section seems to be well-cited. The content of this section is very concise. All the important information about the disease is included, from the cause to the treatment. Good work! Try to find more images for the other abnormalities. It may be tedious but it will help in visualising the clinical manifestations of each disease. Overall, this group has done their research and did it well. Great job on the table for development and images. Their page is very clean and very organised, particularly the references. Don’t forget to write an introduction for your project’s page.&lt;br /&gt;
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Just looking at the contents, if feels a little intimidating both in that it is so long as well as the use of caps. You should try and limit both; the use of all caps can be quite annoying in text and the extensive contents list can make people dread reading through your page if it looks like it’s quite long.&lt;br /&gt;
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An introduction is recommended as it is usually a good starting point to provide the reader as sense of everything the page will cover. The system development is a little messy, but I will heed your note and pay attention to only the table. The table itself is a great idea to lay out all the events happening in the corresponding weeks, making it look neat and concise. However, the use of all caps, bold text, and two different fonts still makes this section look messy. Having both male and female events on the same table makes it look as if there is a chunk of info missing for the female side as well. I would suggest having them in separate tables next to each other, which would eliminate the empty rows in both areas. Both the image and the video (congrats on finding a video! Really good addition to the page) should be captioned.&lt;br /&gt;
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The current research, models and findings seems well researched as there are a lot of points made. However, it is all presented in bullet points which can be visually unappealing. Some sections look incomplete as well, so an effort needs to be made to finish these areas as well as present them in an appealing manner e.g. in paragraph form with a picture next to it to both describe the text visually and offset the amount of text. The drawing of the testes should be captioned appropriately instead of the ‘alt text’ provided. It should also be enlarged, as its current size isn’t large enough to view any of the labels properly.&lt;br /&gt;
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Historic findings looks well researched on first glance, but then I saw that only 4 sources were used to reference the section. It looks really bad when only one source is used to reference a large slab of text, which you have done twice. I suggest finding articles that state similar information and using them as references as well, to back up your current information found. Other than that, I suggest possibly formatting your section in a more appealing way; either summarize some areas in dot points, and add a picture. &lt;br /&gt;
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The abnormalities section is nice and concise, without going into too much detail which is good. Just make sure you explain what it is, how it is formed/how you get it, some statistics and possibly an image to show what it looks like, and that’s all I believe you really need for this section.&lt;br /&gt;
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Overall, your page is well researched with lots of info. Just make sure it looks visually appealing, is consistent in terms of font and presentation, images are used and captioned correctly, and all references are placed at the bottom of the page.&lt;br /&gt;
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Firstly, great job on all the contents you guys managed to present, it’s quite detailed. There seems to be no introduction though, and the page jumps straight into explaining genital development. I think if an introduction were added, it would give the whole page better structure and formatting so the reader knows what to expect when they decide if they want to read on. The dot points used for the developmental section allows for easy readability of the contents, however, the use of caps lock and arrows takes away from the overall presentation of the page. I would suggest any text you want to emphasize to make bold or underline the word. I also noticed that there was a note stating the attempt to put all the developmental information into a table, but had issues. I suggest you look at the editing basic page you can search for in the top right hand corner as it outlines a step-by-step guide into making tables etc. &lt;br /&gt;
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In regards to referencing, there are no in-text citations for the first two subheadings. The sections were they do have citations also have a list of references at the bottom of each section. I would recommend just adding a final list of references at the bottom of the page, as it looks much neater. &lt;br /&gt;
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I’m impressed with the level of hand-drawn diagrams uploaded. I would also recommend adding captions to the image. For example:&lt;br /&gt;
[[File: Flow Diagram of Fetal Development of External Genitalia.pptx|1000px|thumb|right|alt text]]. The “alt text” should be edited to describe the caption of the drawing. This particular image seems to have a broken link though; the “alt text” also appeared in the labeled diagram of the testes. Otherwise, good job on the other images. &lt;br /&gt;
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The current findings section seems to be untouched, with the exception of some pubmed journal article links, I’m assuming you are still in the process of adding content. The historic findings, however, is extensive and well researched. Good job. &lt;br /&gt;
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The abnormalities section is done well. There is more than enough abnormalities listed, and they are researched well, I would just suggest adding a few more images for better visualization. Overall, great page, just needs better formatting for the mentioned sections.&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. &lt;br /&gt;
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It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources.&lt;br /&gt;
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==Group Topic==&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 14:08, 18 August 2014 (EST)&lt;br /&gt;
Hi everyone :),&lt;br /&gt;
We all need to decide on a system for our group asap, does anyone have any suggestions ? I was thinking we could do the Genital or Musculoskeletal ?&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 17:45, 19 August 2014 (EST)&lt;br /&gt;
Hello, I was thinking of covering the genital system development as well.&lt;br /&gt;
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--[[User:Z3417753|Z3417753]] ([[User talk:Z3417753|talk]]) 20:39, 19 August 2014 (EST)&lt;br /&gt;
Genital it is :)&lt;br /&gt;
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--[[User:Z3416697|Z3416697]] ([[User talk:Z3416697|talk]]) 11:07, 20 August 2014 (EST)&lt;br /&gt;
Great can't wait! there seems to be a lot of info about genital embryogenesis&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 21:07, 26 August 2014 (EST) Hey everyone, just wanted to make a note of what each of us was going to research. So as we all discussed last week, I am happy to do part 5. Abnormalities :)&lt;br /&gt;
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--[[User:Z3417753|Z3417753]] ([[User talk:Z3417753|talk]]) 23:18, 26 August 2014 (EST) Hey ! Yes im doing current research models and findings :)&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 01:05, 27 August 2014 (EST) Thank you all for referencing your articles. I am having some difficulty with referencing 1 of my 3 articles mainly because they are not from Pubmed. I will consult with Mark tomorrow and have my part completely uploaded during the lab. Thanks for your understanding.&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 14:57, 1 September 2014 (EST) Hey All, just wanted to let you know that there are some really good pictures showing the differentiation between the male and female genital development in the textbooks. So maybe this week we could decide which ones we like and then I can try to draw them.  :)&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 17:27, 2 September 2014 (EST) That sounds really good. If we are not given some time tomorrow during the lab to meet with our group and if you all don't mind we can stay back for 10 minutes or so to have a look at the images you found and if anyone has found any interesting material. See you all tomorrow in the lab.&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 18:06, 9 September 2014 (EST) Hi, I know we can only use one image from wikipedia so maybe we could use this one ? Or has anyone found any others ?  Heres the link -- &amp;gt; http://en.wikipedia.org/wiki/Sexual_differentiation#mediaviewer/File:2915_Sexual_Differentation-02.jpg&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 18:14, 16 September 2014 (EST) Hi everyone, I am going to post 2 images on here tonight, please let me know which you prefer :)&lt;br /&gt;
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1. [[File:Image.jpg|350px]]&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 21:04, 16 September 2014 (EST) Or this one -&amp;gt;&lt;br /&gt;
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2.  [[File:Sexual Differentiation.jpg|350px]]&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 14:42, 21 September 2014 (EST) Since my part is historical findings, I have found a few old articles around 50-100+ years old. Below I'm going to past a paragraph about the female genital system development I have composed from information of two articles, one is from the 1950s and the other is 1890s. My only concern is what I have written doubles up with the system development part of this assignment so I have not uploaded onto the page but if you guys think it's fine for historical finding then I will, if not we can add that into system development and the timeline. I am still searching for historical teachings and images that can be used in this assignment. &lt;br /&gt;
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The mullerian (paramesonephric) ducts, found laterally to the wolffian ducts, are the original structures of the female reproductive system. Female sexual organs (the fallopian tubes, uterus and vagina) originate from the mullerian ducts, which differentiates within the foetal developmental phase. Initially the foetus contains two mullerian ducts, however by the ninth week fusion of the lower portion of the ducts is complete, creating the fundamental structure of the uterus and the vagina, however the these two organs are not continuous with vagina being solid. The non-fused upper part of the ducts emerge into the fallopian tubes. It is not until the fourth and fifth month of development that the uterus becomes continuous with the vagina, with both organs developing a hollow lumen. The muscular layers of the uterus is also present by this stage. The cervix begins to form within the fifth month, between the continuous vagina and uterus. Also within the same month, the formation of the hymen occurs. The hymen is described as a pouting vertical slit and represents the remains of the mullerian eminence&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 21:05, 22 September 2014 (EST) I think it can be added under your heading of historical findings :)&lt;br /&gt;
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--[[User:Z3417753|Z3417753]] ([[User talk:Z3417753|talk]]) 12:26, 1 October 2014 (EST) hey guys hope you are all enjoying your break :) Hope your assignments are all going well :) &lt;br /&gt;
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Also, I found this article that might be useful if you havent already found it - it goes under historic findings - it is from 1942!!&lt;br /&gt;
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Schonfeld  WABeebe  GW Normal growth and variation in the male genitalia from birth to maturity. J Urol 1942;8759- 777&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 21:59, 2 October 2014 (EST) Hey, hope your enjoying your break too. Thats great :). If you any of you guys come across an image that we could use for the first page, post in on here so we can decide if we want to use it. :)&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 16:16, 5 October 2014 (EST) Thank you, I'm doing the historical findings and I will have a look into that article. Thanks again. I have just redrawn an image from one of my articles about the Mullerian ducts and forming the female genital system. I will try and upload it following the steps Mark gave to us in the first lab so once it is up please let me know if you guys like it or not. Thanks&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 16:57, 5 October 2014 (EST) Also another thing, please let me know if I am being too specific in my part (Historical findings). I still have more to add on other areas of genital development, so if what I am doing is fine then I will continue this way, if not please let me know so I can change what I have. Thanks again.&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 16:15, 6 October 2014 (EST) Hey Everyone, I've found a video we could use on our page, the background music is a bit annoying but the drawings are really good, detailed and clear heres a link. Let me know if any of you have found some too. :)&lt;br /&gt;
https://www.youtube.com/watch?v=MureNA-RSZM&lt;br /&gt;
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*Great progress on the table. Maybe once you've managed to format everything you need into it, don't forget to reference bits you need to&lt;br /&gt;
*I liked the diagram you used to show the different pathways of genital development for the different genders. It's just a bit blurry so maybe think of re-uploading a clearer image or of making the image on your page a little smaller&lt;br /&gt;
*Good use of dot points under the &amp;quot;current research&amp;quot; section but maybe think of connecting the separate points a bit more as it seems a bit disjointed and difficult to follow. Maybe think of having your write-up as normal and using points in particular parts that show a sequence of events, or separate components of something&lt;br /&gt;
*Look to getting more references for the current research and models section because you're just using 1 at the moment&lt;br /&gt;
*Proofread. I know maybe you guys are still at the collation of information stage, but I find it's easier to get it right as you go along rather than coming back to it later &lt;br /&gt;
*Re-phrase some bits like: female and male fetuses’ external genitalia --&amp;gt; The external genitalia of the female and male fetus&lt;br /&gt;
*Great drawn images! They're all so clear, well thought out and identify all relevant components of what you're trying to show all throughout your page&lt;br /&gt;
*I liked the detail of your &amp;quot;historical findings&amp;quot; section&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_4&amp;diff=149675</id>
		<title>Talk:2014 Group Project 4</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_4&amp;diff=149675"/>
		<updated>2014-10-14T11:23:41Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Peer Reviews */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{ANAT2341Project2014discussionheader}}&lt;br /&gt;
==Peer Reviews==&lt;br /&gt;
&lt;br /&gt;
The Introduction, Current Models and Current Research section all in dot-point form, which obviously allowed you to more easily, put information on the page. These need to be converted into paragraph form to give the content greater readability and flow.&lt;br /&gt;
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Presuming the system development is supposed to be the introduction, there should be inclusion of current research, historical research and abnormalities. Without these the reader will not know all the sections of the page after reading the introductory section, which is the intros purpose. The use of bold and capital letters is unneeded. The existence of a table is good though has a bunch of formatting and text problems (capitals, bold, captions, lack of lines). “(around week 4-6) that sexual differentiation occurs in the fetus ” this statement is incorrect since it is an embryo during the week4-6, it becomes a later around week 10. “450px” has not been inserted properly, the sexual differentiation image requires caption and references.&lt;br /&gt;
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Current Research and Models has in-depth content for undifferentiated and male, though limited information on current female genital research. The headings are repetitive also many without any content, similar content needs to be merged under single headings. In Historic findings the content and wording is good but same trend continues significantly more text on Male development compared to female. &lt;br /&gt;
&lt;br /&gt;
Abnormalities section is great with even attention given to female, male and both. Information is appropriately in-depth and referenced, addressing causes, process and treatment. Addition of 1-2 images in the “both” section is advised, to allow readers to identify clinical features of the diseases. Like the use of drawings especially “Abnormalities of the Uterus and Vagina” and “Anat of Testes”, you should change the caption of the testes drawing from “alt text”.&lt;br /&gt;
&lt;br /&gt;
For improvement; covert of dot-points into paragraphs, expand on female sections of “current research” and “historical research”, fix a few image problems and remove unnecessary bold/capitals/captions.&lt;br /&gt;
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A great start on tabulating the information about the development of this system. There are references but I don’t see any in-text citations. The image used in this section is really good and relevant. It clearly shows the major processes in the development of the genital system. However, it is a bit pixelated so maybe try resizing the image to a smaller size. Maybe try uploading the image again with a different filename, change it to something more appropriate rather than “Image.jpg”. And also, if possible, try to include it in the table. Good job on embedding a video! I think this is the only group so far that has included a video. It’s a good video about the development, I just wish it had a voice-over explaining what is happening but that’s not really the group’s fault. Nonetheless, great job on the development section. &lt;br /&gt;
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With the current research section, great use of dot points but a bit excessive. Maybe try to make paragraphs where it is appropriate. It is well-researched, very detailed and very informative. It’s good to see student drawings. Great job on that. I see that an image was not properly uploaded into the page, so just fix that. Good job on referencing. All research articles seem to be relevant to this section but try to incorporate some of the in-text citations of the remaining articles, not just the first three. Overall, really great job on the content of this section. It is evident that the person responsible for this section put a lot of effort in research.&lt;br /&gt;
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As for historic findings, great job! I know this is probably the hardest of all the four sections in terms of finding information and this section is well-researched, very detailed, and very informative much like the current research section. Maybe try to use some dot points to lessen the bulk of this section. Great drawing included in this section. Try to add more, especially for the males since that is the bulk of this section. &lt;br /&gt;
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Lastly, for abnormalities, great job on finding lots of abnormalities! Lots of references and each area of this section seems to be well-cited. The content of this section is very concise. All the important information about the disease is included, from the cause to the treatment. Good work! Try to find more images for the other abnormalities. It may be tedious but it will help in visualising the clinical manifestations of each disease. Overall, this group has done their research and did it well. Great job on the table for development and images. Their page is very clean and very organised, particularly the references. Don’t forget to write an introduction for your project’s page.&lt;br /&gt;
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Just looking at the contents, if feels a little intimidating both in that it is so long as well as the use of caps. You should try and limit both; the use of all caps can be quite annoying in text and the extensive contents list can make people dread reading through your page if it looks like it’s quite long.&lt;br /&gt;
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An introduction is recommended as it is usually a good starting point to provide the reader as sense of everything the page will cover. The system development is a little messy, but I will heed your note and pay attention to only the table. The table itself is a great idea to lay out all the events happening in the corresponding weeks, making it look neat and concise. However, the use of all caps, bold text, and two different fonts still makes this section look messy. Having both male and female events on the same table makes it look as if there is a chunk of info missing for the female side as well. I would suggest having them in separate tables next to each other, which would eliminate the empty rows in both areas. Both the image and the video (congrats on finding a video! Really good addition to the page) should be captioned.&lt;br /&gt;
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The current research, models and findings seems well researched as there are a lot of points made. However, it is all presented in bullet points which can be visually unappealing. Some sections look incomplete as well, so an effort needs to be made to finish these areas as well as present them in an appealing manner e.g. in paragraph form with a picture next to it to both describe the text visually and offset the amount of text. The drawing of the testes should be captioned appropriately instead of the ‘alt text’ provided. It should also be enlarged, as its current size isn’t large enough to view any of the labels properly.&lt;br /&gt;
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Historic findings looks well researched on first glance, but then I saw that only 4 sources were used to reference the section. It looks really bad when only one source is used to reference a large slab of text, which you have done twice. I suggest finding articles that state similar information and using them as references as well, to back up your current information found. Other than that, I suggest possibly formatting your section in a more appealing way; either summarize some areas in dot points, and add a picture. &lt;br /&gt;
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The abnormalities section is nice and concise, without going into too much detail which is good. Just make sure you explain what it is, how it is formed/how you get it, some statistics and possibly an image to show what it looks like, and that’s all I believe you really need for this section.&lt;br /&gt;
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Overall, your page is well researched with lots of info. Just make sure it looks visually appealing, is consistent in terms of font and presentation, images are used and captioned correctly, and all references are placed at the bottom of the page.&lt;br /&gt;
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Firstly, great job on all the contents you guys managed to present, it’s quite detailed. There seems to be no introduction though, and the page jumps straight into explaining genital development. I think if an introduction were added, it would give the whole page better structure and formatting so the reader knows what to expect when they decide if they want to read on. The dot points used for the developmental section allows for easy readability of the contents, however, the use of caps lock and arrows takes away from the overall presentation of the page. I would suggest any text you want to emphasize to make bold or underline the word. I also noticed that there was a note stating the attempt to put all the developmental information into a table, but had issues. I suggest you look at the editing basic page you can search for in the top right hand corner as it outlines a step-by-step guide into making tables etc. &lt;br /&gt;
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In regards to referencing, there are no in-text citations for the first two subheadings. The sections were they do have citations also have a list of references at the bottom of each section. I would recommend just adding a final list of references at the bottom of the page, as it looks much neater. &lt;br /&gt;
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I’m impressed with the level of hand-drawn diagrams uploaded. I would also recommend adding captions to the image. For example:&lt;br /&gt;
[[File: Flow Diagram of Fetal Development of External Genitalia.pptx|1000px|thumb|right|alt text]]. The “alt text” should be edited to describe the caption of the drawing. This particular image seems to have a broken link though; the “alt text” also appeared in the labeled diagram of the testes. Otherwise, good job on the other images. &lt;br /&gt;
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The current findings section seems to be untouched, with the exception of some pubmed journal article links, I’m assuming you are still in the process of adding content. The historic findings, however, is extensive and well researched. Good job. &lt;br /&gt;
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The abnormalities section is done well. There is more than enough abnormalities listed, and they are researched well, I would just suggest adding a few more images for better visualization. Overall, great page, just needs better formatting for the mentioned sections.&lt;br /&gt;
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This project would benefit from having an introduction to prepare the reader for what is to come and summarise everything briefly. The system development part is interesting and clearly there has been a lot of research put into finding the information. I suggest adding pictures or student-drawn diagrams, particularly of the chromosome and the SRY gene location to make it more comprehendible. If you’re not a geneticist, it can be difficult to picture that much detail at an embryonic level. &lt;br /&gt;
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It is clear you have considered inserting images so it would be important to follow through with that before the final stages of marking. I’m not really sure why you’ve inserted a table here as well since a lot of the information was already covered previously. Maybe use less information in the table. The references at the end of this section should appear at the very end of the wiki page. A lot of other groups have already done that so if you need to copy the formatting, it’s definitely possible. The use of a video on your page is commendable and sets this project above others in that sense. It’s a great idea to have a youtube clip. However, it is 9 minutes long which is a bit long for a student page that is designed to inform students on the genital system on a wholistic scale rather than tackling complicated ideas. Maybe try editing the youtube video so you only use a 30 second or 1minute clip. &lt;br /&gt;
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The male and female genital development section is clearly presented and the use of bullet points make it easy to follow. However reading the information, it appears that a lot of it I recognised from the lectures. This doesn’t suggest the student explored external embryology sources. On another note, perhaps the lecture on the genital system was very indepth and this student did do research but found all the relevant information had already been covered. None the less, I think it would be advantageous to add a subheading in the section that looks at recent findings. This would broaden the understanding an embryology student can achieve by reading this wiki-page. Also there has been an error uploading an image so that should be fixed.&lt;br /&gt;
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 Although the information is presented well, the bulk of references should be included at the very end of the page. This project is very good but there is still some further research needed, particularly under the current findings subheading. The information presented under the historical findings subheading is quite dense and would benefit from being broken up into a table or simple bullet points. The abnormalities part is excellent and there has clearly been broad research into different embryological resources.&lt;br /&gt;
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==Group Topic==&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 14:08, 18 August 2014 (EST)&lt;br /&gt;
Hi everyone :),&lt;br /&gt;
We all need to decide on a system for our group asap, does anyone have any suggestions ? I was thinking we could do the Genital or Musculoskeletal ?&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 17:45, 19 August 2014 (EST)&lt;br /&gt;
Hello, I was thinking of covering the genital system development as well.&lt;br /&gt;
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--[[User:Z3417753|Z3417753]] ([[User talk:Z3417753|talk]]) 20:39, 19 August 2014 (EST)&lt;br /&gt;
Genital it is :)&lt;br /&gt;
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--[[User:Z3416697|Z3416697]] ([[User talk:Z3416697|talk]]) 11:07, 20 August 2014 (EST)&lt;br /&gt;
Great can't wait! there seems to be a lot of info about genital embryogenesis&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 21:07, 26 August 2014 (EST) Hey everyone, just wanted to make a note of what each of us was going to research. So as we all discussed last week, I am happy to do part 5. Abnormalities :)&lt;br /&gt;
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--[[User:Z3417753|Z3417753]] ([[User talk:Z3417753|talk]]) 23:18, 26 August 2014 (EST) Hey ! Yes im doing current research models and findings :)&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 01:05, 27 August 2014 (EST) Thank you all for referencing your articles. I am having some difficulty with referencing 1 of my 3 articles mainly because they are not from Pubmed. I will consult with Mark tomorrow and have my part completely uploaded during the lab. Thanks for your understanding.&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 14:57, 1 September 2014 (EST) Hey All, just wanted to let you know that there are some really good pictures showing the differentiation between the male and female genital development in the textbooks. So maybe this week we could decide which ones we like and then I can try to draw them.  :)&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 17:27, 2 September 2014 (EST) That sounds really good. If we are not given some time tomorrow during the lab to meet with our group and if you all don't mind we can stay back for 10 minutes or so to have a look at the images you found and if anyone has found any interesting material. See you all tomorrow in the lab.&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 18:06, 9 September 2014 (EST) Hi, I know we can only use one image from wikipedia so maybe we could use this one ? Or has anyone found any others ?  Heres the link -- &amp;gt; http://en.wikipedia.org/wiki/Sexual_differentiation#mediaviewer/File:2915_Sexual_Differentation-02.jpg&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 18:14, 16 September 2014 (EST) Hi everyone, I am going to post 2 images on here tonight, please let me know which you prefer :)&lt;br /&gt;
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1. [[File:Image.jpg|350px]]&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 21:04, 16 September 2014 (EST) Or this one -&amp;gt;&lt;br /&gt;
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2.  [[File:Sexual Differentiation.jpg|350px]]&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 14:42, 21 September 2014 (EST) Since my part is historical findings, I have found a few old articles around 50-100+ years old. Below I'm going to past a paragraph about the female genital system development I have composed from information of two articles, one is from the 1950s and the other is 1890s. My only concern is what I have written doubles up with the system development part of this assignment so I have not uploaded onto the page but if you guys think it's fine for historical finding then I will, if not we can add that into system development and the timeline. I am still searching for historical teachings and images that can be used in this assignment. &lt;br /&gt;
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The mullerian (paramesonephric) ducts, found laterally to the wolffian ducts, are the original structures of the female reproductive system. Female sexual organs (the fallopian tubes, uterus and vagina) originate from the mullerian ducts, which differentiates within the foetal developmental phase. Initially the foetus contains two mullerian ducts, however by the ninth week fusion of the lower portion of the ducts is complete, creating the fundamental structure of the uterus and the vagina, however the these two organs are not continuous with vagina being solid. The non-fused upper part of the ducts emerge into the fallopian tubes. It is not until the fourth and fifth month of development that the uterus becomes continuous with the vagina, with both organs developing a hollow lumen. The muscular layers of the uterus is also present by this stage. The cervix begins to form within the fifth month, between the continuous vagina and uterus. Also within the same month, the formation of the hymen occurs. The hymen is described as a pouting vertical slit and represents the remains of the mullerian eminence&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 21:05, 22 September 2014 (EST) I think it can be added under your heading of historical findings :)&lt;br /&gt;
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--[[User:Z3417753|Z3417753]] ([[User talk:Z3417753|talk]]) 12:26, 1 October 2014 (EST) hey guys hope you are all enjoying your break :) Hope your assignments are all going well :) &lt;br /&gt;
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Also, I found this article that might be useful if you havent already found it - it goes under historic findings - it is from 1942!!&lt;br /&gt;
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Schonfeld  WABeebe  GW Normal growth and variation in the male genitalia from birth to maturity. J Urol 1942;8759- 777&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 21:59, 2 October 2014 (EST) Hey, hope your enjoying your break too. Thats great :). If you any of you guys come across an image that we could use for the first page, post in on here so we can decide if we want to use it. :)&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 16:16, 5 October 2014 (EST) Thank you, I'm doing the historical findings and I will have a look into that article. Thanks again. I have just redrawn an image from one of my articles about the Mullerian ducts and forming the female genital system. I will try and upload it following the steps Mark gave to us in the first lab so once it is up please let me know if you guys like it or not. Thanks&lt;br /&gt;
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--[[User:Z3415716|Z3415716]] ([[User talk:Z3415716|talk]]) 16:57, 5 October 2014 (EST) Also another thing, please let me know if I am being too specific in my part (Historical findings). I still have more to add on other areas of genital development, so if what I am doing is fine then I will continue this way, if not please let me know so I can change what I have. Thanks again.&lt;br /&gt;
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--[[User:Z3417458|Z3417458]] ([[User talk:Z3417458|talk]]) 16:15, 6 October 2014 (EST) Hey Everyone, I've found a video we could use on our page, the background music is a bit annoying but the drawings are really good, detailed and clear heres a link. Let me know if any of you have found some too. :)&lt;br /&gt;
https://www.youtube.com/watch?v=MureNA-RSZM&lt;br /&gt;
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*Great progress on the table. Maybe once you've managed to format everything you need into it, don't forget to reference bits you need to&lt;br /&gt;
*I liked the diagram you used to show the different pathways of genital development for the different genders. It's just a bit blurry so maybe think of re-uploading a clearer image or of making the image on your page a little smaller&lt;br /&gt;
*Good use of dot points under the &amp;quot;current research&amp;quot; section but maybe think of connecting the separate points a bit more as it seems a bit disjointed and difficult to follow. Maybe think of having your write-up as normal and using points in particular parts that show a sequence of events, or separate components of something&lt;br /&gt;
*Look to getting more references for the current research and models section because you're just using 1 at the moment&lt;br /&gt;
*Proofread. I know maybe you guys are still at the collation of information stage, but I find it's easier to get it right as you go along rather than coming back to it later &lt;br /&gt;
*Re-phrase some bits like: female and male fetuses’ external genitalia --&amp;gt; The external genitalia of the female and male fetus&lt;br /&gt;
*Great drawn images! They're all so clear, well thought out and identify all relevant components of what you're trying to show all throughout your page&lt;br /&gt;
*I liked the detail of your &amp;quot;historical findings&amp;quot; section&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_3&amp;diff=149570</id>
		<title>Talk:2014 Group Project 3</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_3&amp;diff=149570"/>
		<updated>2014-10-14T10:29:31Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Peer Reviews */&lt;/p&gt;
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==Peer Reviews==&lt;br /&gt;
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Good introduction, initial description of fore/mid/hindgut with listing of respective structures gives the reader an anatomical starting point. Fetal development is presented in appropriate depth. There is no acknowledgement of embryonic origin, research or abnormalities. These sections should feature in the introduction to present all parts of the report in the intro. The three separate timelines defeat the purpose of a timeline. These should either be merged into a single large timeline and remain at their present location or moved to introduce the foregut/midget/hindgut sections later on. Recent findings has a single study which is covered in good detail though 2-3 more studies would allow the reader to further understand current GIT Research.&lt;br /&gt;
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In foregut section the dot-points used should match your subheadings. For example duodenum development is covered in the stomach section but is not mentioned in the subheading resulting in its development being hard to find without trawling through the text or “Ctrl-f”. Additionally you seemed to have missed out on pancreas development entirely. Foregut could also use some more images 2-3 would be suffice. Midgut development has great information, strong table, 8/8 drawings(captions required though). Inclusion of histological features gives viewer a microscopic perspective on development. Hindgut cloaca partitioning content is well worded though references are lacking. &lt;br /&gt;
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Anorectal deformities sections should be moved under the Deformities section. The type of dot-point style used should be standardized. Too few abnormalities in the deformities section, though after the hindgut deformities are mover there should be sufficient. There are no references supporting the possible causes of Gastroschisis. The referencing it very good unlike other pages there are no random reference subheadings. In overview format wise quite attractive, information is adequately in-depth in all sections, introduction fails to address whole page,  referencing is great for a draft (exceptions being “introduction” “Liver, Gallbladder and Bile Duct”), some captions aren't present, abnormalities in development section should be moved into deformities/abnormalities section.&lt;br /&gt;
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The introduction is good as it accurately describes what the GIT system is about and the anatomical positions of the features in this system. It also briefly highlights the development stages at embryonic and fetal stages, however ‘embryonic development’ should be mentioned in a little more detail to understand how far in development the fetal stage begins. I also think the introduction should include a sentence or two describing how abnormalities in such organs can lead to these diseases. Basically a bit from each major subheading should be incorporated including current research as an introduction is a summary of the whole page. As for the ‘timeline’, it would’ve been more appropriate to place the timelines under each section, e.g foregut timeline under the ‘foregut’ subheading. This is because viewers would be confused on why there is so much difference in development in one section of the page. A glossary list should be incorporated in a separate subheading to define some of these words such as hematopoiesis so that viewers can fully grasp the information. &lt;br /&gt;
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The information under recent findings is quite interesting and relatable to the content which is GIT fetal development. However, I believe more findings could be incorporated under this subheading. The information under each organ of the three ‘guts’ are quite detailed in fetal development which is good and shouldn’t be too difficult for the viewers to understand. However, I believe the group could include information on the function of these organs as well. The structure of the information under ‘guts’ does not flow in the sense that the midgut includes features and structure whereas the other ‘guts’ do not. The innvervation and bloody supply of the hindgut should be incorporated in a paragraph instead of being listed like that. All the deformities should be places under one subheading to make it easier for viewers to navigate. The abnormalities were also concise and related to the topic. Overall, the content is relating to the topic of the project and addresses key points. It also shows good amount of research, however there seems to be too much information in some parts which could be reduced a bit. The project needs a  coherent flow of the structure.&lt;br /&gt;
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As for images, there needs to be an image under introduction which includes all features of the GIT tract. There are a lot of potential images missing under each subheading except for the ‘midgut’ section. This shows that there has been one person working on this section or one section being focused on in comparison the others. The information used to reference the images is missing in some images such as the ‘Human- fetal week 10 sagittal plane D.jpg’ (although this is uploaded from a different user so this is understandable. However images such a ‘GIT 2.jpg’ need more information including ‘student template’ as well as the reference where the image idea may have come from. Also, if this is a hand-drawn image then please state this as one member did in ‘Week 11 midgut herniation.png’. Overall, I enjoy the use of self-drawn images as it makes it easier to show what the content is saying without going through the stress of looking for an image online that doesn’t relate to the content. However more images definitely need to be added. The use of footnotes is also good and indicates what the images are showing.&lt;br /&gt;
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There are sections where incite referencing are used, however some sections are void of them such as the ‘introduction’ and ‘Liver, Gallbladder and Bile Duct’ (the [6],[7] should be placed next to the text not above the text. The use of a ‘references’ subheading is good the same references have been combined into one number showing that the group knows how to make the references set out. The use of a table in formatting the ‘Percentage of Foetuses Herniated’ is great and shows more that the group has done research.  Overall, this is a good project and if the group makes edits based on the peer-reviews received, this could enhance their project.&lt;br /&gt;
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A good introduction to the page but only outlines the developmental part of the project. Don’t forget to include other sections as well like current findings, abnormalities, etc. Also, no need for the hyphen for foregut, midgut, and hindgut. The development timeline is really good. Its very concise and well-referenced. It could be improved by tabulating the whole thing and maybe try to fuse the three sections together. Also, add an image or drawing of the development of the system. It will definitely help in terms of understanding what is happening at each stage. On recent findings, it’s not as good as the other groups but it’s definitely a start. Most groups write about 2-4 research articles for their current findings sections. As for the development section, each section is very detailed and informative. Maybe add a few images for the foregut section because images are really helpful. As for midgut, great to see images and student drawings. Good job on that. The same can be said for the hindgut section. It’s written well but maybe put the deformities in this section with the “Deformities” section. Deformities (abnormalities) section is good. It is detailed and the image used clearly shows what the disease is like. Maybe writing about 1-2 more abnormalities would make this section better. &lt;br /&gt;
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It terms of citation and referencing, midgut section did the best job. I recommend the other sections to look for a lot more related material. I understand that this topic was divided depending on the region of the GIT, particularly the development section, but make sure to reorganise each section to make the page coherent. As for the images, most of them are well referenced. It wouldn’t hurt to add a few more. It’s great to see a lot of student drawings. Overall, a good project page very detailed in most areas but very little in referencing. In summary, focus on adding more references, making the whole page coherent, and a few more on the abnormalities.&lt;br /&gt;
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The introduction provides a good basic outline of the overview of the GIT. Although, there are no in-text citations in the introduction and all sub-headings are not included into the overview. Be wary of spelling errors such as “GIT (Gastrointestinal Track) consist of the Fore-gut, Mid-gut and Hind-gut” that should read Gastrointestinal Tract consists of the foregut, midgut and hindgut. This section would be better it was expanded upon and images were added. The timeline provides good detail, though would benefit by better formatting and organisation of the information, maybe putting it all into a table, by week will tidy it up. &lt;br /&gt;
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Adding images for the sections will definitely be beneficial. The images hand-drawn are great, although the colours used make it hard to read. If you plan to add anymore drawings, try and use dark colours that allow for easy readability. The images already uploaded are missing copyright, referencing and “student template” information for images such as “fetal week 10 sagittal plane”. I would suggest you look up the tutorial for uploading images on the pages as Mark has extensive information for the proper steps required for uploading images.&lt;br /&gt;
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The deformities section should be re-titled abnormalities as per the assessment criteria and would ensure the group is following similar structure from the other projects. Again, adding an image per disease would be great. Try and do about 1-2 more abnormalities. Great job on putting all the references at the bottom of the page, it makes it very neat and accessible. Overall, a good project just needs a few edits. &lt;br /&gt;
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A good overview of the GIT, very descriptive. This section would need some referencing as most of this info isn’t exactly common knowledge. Some of the sentences seem too short for me e.g. I would reconfigure the third sentence and combine the fourth and fifth sentences into one: ‘The GIT (gastrointestinal tract) consists of three regions: the foregut, midgut and the hindgut. The majority of the organs are located in the foregut, including…..’. You also need to make sure not to use capital letters in the middle of sentences.&lt;br /&gt;
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The timeline is sort of well organized; it’s good that you have it separated for each region so they’re not all muddled up together, but is the info in dot points under the week, or is it just written next to the week? It needs to be kept consistent.  I feel like this section is a bit too spread out as well, a large portion of the left hand side has text, while the entire right side of the screen is empty. You could possible put in a picture showing these 3 regions of the gut to fill in the space? Or maybe format the info into a table, it would make it look more formal and structured. The proper referencing technique should also be used here, not added hyperlinks.&lt;br /&gt;
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The recent findings area is a little sparse, so you should try to find a few more. The title does say findings (plural), so maybe add at least one more. The foregut section is very extensive on the information provided which is good, a lot of research has been made. Visually however, it looks a little bad as all that can be seen is a mass of text. This can be alleviated if the same thing is done as has been with the midgut and hindgut region: the use of bullet points, a small table and the use of images to offset the slabs of text. It makes it more visually appealing. Unlike the midgut portion of the page, if the images are hand drawn, make sure they are clear, legible, and with colours used that will not strain the eye. For the images drawn in that section are messy and the labels hard to read both due to the colour of the pen used and the handwriting. In both the foregut and hindgut, referencing needs to be done. There are slabs of text in both sections where no references are made.&lt;br /&gt;
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The deformities section is good, kept simple with no extensive explanations. Are there only 2 possible deformaties? If so, might be good to write a sentence mentioning that. If not, would be good to have at least 2 more deformities listed. The image drawn in this section is very neat, I like it a lot. The only problem with it is that it’s too small, making it hard to read some of the labels.&lt;br /&gt;
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Overall, I think this page is very well done in terms of content. You have a lot of text, but I think it could do with some more pictures especially to offset some of the large slabs of texts in some areas. Make sure the pictures you have a clear and neat, and make sure you are referencing and doing it correctly.&lt;br /&gt;
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The introduction part of this project provided a good overview of the gastrointestinal tract and its components, also mentioning briefly the changes that occur in the fetal period. However, care must be taken to not capitalise words that are not needed e.g. Foregut, Midgut, Appendix etc. Although the information in the ‘timeline’ section is relevant, its formatting needs a bit of review as there are inconsistencies between the foregut, midgut and hindgut parts. It also seems that the in-text citations have just been arbitrarily placed in chronological order, with each line having a new reference. Also, this information may be better presented in table format to improve readability. Some simple editing may be needed to fix this.&lt;br /&gt;
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The section on ‘Recent findings’ has some good information, however the reference needs to be properly cited and maybe a couple more articles would help give this part some substance. I thought it was effective to have the GIT split into the foregut, midgut and hindgut and then detail the fetal development under those titles. This gave the page a good structure. However, adding some images, both from online and student-drawn to the foregut and hindgut sections would help improve the aesthetics of the page. The hand-drawn images on the midgut section are effective learning tools to a student, but maybe could be drawn a little neater with darker colours as the blue labelling is difficult to read. They should also be captioned. The use of a table to show midgut herniation of fetuses was a good tool as it makes the information easier to read also.&lt;br /&gt;
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Lastly, the section on abnormalities was well-detailed and I liked that the deformities were split into a definition and cause. An image of gastrochisis may be helpful for a reader to visualise the condition though. The in-text citations in this part were properly done and a long list of references being at the end of the page made the project look neat overall. Areas of improvement may be some simple formatting changes and evening out the information across sections, however a solid project so far.&lt;br /&gt;
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This project overall is very good with a lot relevant information. There is some use of images and hand-drawn images that are excellent. It would be good to see more images, perhaps to complement the timeline section. It is clear the group have worked well together to create a wiki page that flows well and covers all the organs of the gastrointestinal system. All the citations formatted correctly and it is good that all the references appear in one long list at the end of the page. There is still room to add tables, maybe to summarise the timeline. Other groups who presented their timelines in a table achieved an element of wiki-sophistication. There are a few spelling errors in some of the sections (specified below) which need to be corrected so as to not interrupt the flow of information when the reader is reading it. Again, there are only minimal errors or problems with this page, overall it is excellent!&lt;br /&gt;
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The section on the midgut is well presented and thoroughly researched, well done! It is easy to follow and the way it is described makes it easy to imagine visually. However just double check for typos, for example “to that of” is spelt “tot hat of”. Simple error that is easily fixed. These hand drawn images are excellent. The colour coding and minimal use of words is very effective in supporting the written material. &lt;br /&gt;
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The hindgut section is also well written and there is a lot of extensive information. Also double check for spelling, mesenchyme is spelt “esenchyme” in one of the sentences. This area of the project is lacking images detracting from its readability and level of interest. &lt;br /&gt;
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--[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 20:38, 13 August 2014 (EST)&lt;br /&gt;
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Alright so lets choose a topic quickly before it gets taken. I would like all of you to post 3 topics that you would like to do (here) in order of importance and the topic that gets chosen the most will win. This is the only way I could think of in order to decide, so sorry. By the way Cardiovascular is taken so we cannot do that any more. My three choices are: Gastrointestinal System, Immune System and Placenta. What are yours?&lt;br /&gt;
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i choose renal, head and neck, GIT --[[User:Z3415242|Z3415242]] ([[User talk:Z3415242|talk]]) 22:22, 14 August 2014 (EST)&lt;br /&gt;
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Im thinking GIT. Everyone so far has said GIT so I reckon that might be the best option as i think it will be relatively easy to understand and follow with the whole mid gut, hind gut formation ect.&lt;br /&gt;
--[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 12:58, 15 August 2014 (EST)&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] ([[User talk:Z8600021|talk]]) 10:16, 16 August 2014 (EST) I have just reformatted your project page heading as the major heading (single =) and capitalised the words). All page sub-heading (two ==).&lt;br /&gt;
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z3415141: I am going to be looking up research of the midgut.--[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 13:08, 20 August 2014 (EST)&lt;br /&gt;
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I choose to research on abnormalities of the GIT system--[[User:Z3415242|Z3415242]] ([[User talk:Z3415242|talk]]) 13:14, 20 August 2014 (EST)&lt;br /&gt;
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z3375627: I'm going to be doing Hind gut development research --[[User:Z3375627|Z3375627]] ([[User talk:Z3375627|talk]]) 13:10, 20 August 2014 (EST)&lt;br /&gt;
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z3414515: I will be researching foregut. --[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 13:12, 20 August 2014 (EST)&lt;br /&gt;
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Alright people lets get some work done on this project. I hope everyone could at least write up few paragraphs on their chosen section by Tuesday. Thanks :) --[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 22:18, 30 August 2014 (EST)&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] ([[User talk:Z8600021|talk]]) 22:47, 30 August 2014 (EST) I agree, times a wasting. While you have met the required addition of references, tarts all that is currently on your project page.&lt;br /&gt;
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--[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 12:23, 2 September 2014 (EST)The reference below might help you guys. &lt;br /&gt;
&amp;lt;pubmed&amp;gt;12943221&amp;lt;/pubmed&amp;gt; &lt;br /&gt;
--[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 12:23, 2 September 2014 (EST)&lt;br /&gt;
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Is it only me or is everyone finding it hard to differentiate between embryo and fetal development?--[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 12:23, 2 September 2014 (EST)&lt;br /&gt;
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Yeh I agree there are so many times where they talk about it as one in the same thing. Just have to read really carefully as we don't want to cross over. --[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 14:46, 2 September 2014 (EST)&lt;br /&gt;
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Also with what you have written so far about the oesophagus, it looks good but what are you doing about referencing. Are you just keeping a list that you will put down later or are you getting the information from the resources that you found last week?? --[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 14:53, 2 September 2014 (EST)&lt;br /&gt;
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I have my references saved on my laptop so when the time comes I can relate the information to specific reference. How are you coming along with your research so far?--[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 00:08, 3 September 2014 (EST)&lt;br /&gt;
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Just been reading heaps to make sure I get the information right. I'm trying to get a really good understanding of the midgut rotation as I believe it is a critical part in the development of the ftus. --[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 09:31, 3 September 2014 (EST)&lt;br /&gt;
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I am still waiting for some information from z3375627 and z3415242. Common people get moving!!! Also I meant that in the nicest way possible :) --[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 10:52, 3 September 2014 (EST)&lt;br /&gt;
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I have found a picture to go with the adnormality that i am doing however i will not upload it until everyone is ok with it. I will work to add on the first abnormality i have started and done and continue to research on a second one. If i come across any useful articles for you guys i will post it on this. --[[User:Z3415242|Z3415242]] ([[User talk:Z3415242|talk]]) 19:02, 9 September 2014 (EST)&lt;br /&gt;
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Show the group in class your image so we can discuss on it. Also I know everyone must be busy with mid semester exams or assessments so I appreciate the effort you guys are putting in so far. BUT do remember as soon as the mid semester exams are over we need to pick up the pace or pull up our socks for this embryology project. --[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 09:27, 10 September 2014 (EST)&lt;br /&gt;
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Common people lets get a move on. I have put up some information on my section though it is on the embryo period, the fetal period is in progress and in detail. The embryo period is only there as a guideline to understand how the stomach actually attains its shape. --[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 12:47, 16 September 2014 (EST)&lt;br /&gt;
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i have come across some research articles on omphalocele (abnormality occurs in week 10-12 YAY ) just reading through them as they are pretty long and abit difficult understanding so i'm trying to put some stuff into a paragraph or two will try and upload the stuff for it by this week sometime. cheers --[[User:Z3415242|Z3415242]] ([[User talk:Z3415242|talk]]) 21:50, 16 September 2014 (EST)&lt;br /&gt;
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Alright this is the week to really get a good chunk of it done now that most of our mid sems are over. Not sure if anyone else has any good youtube videos, but because we only get one I'm gonna put this one out there relating to midgut rotation: https://www.youtube.com/watch?v=AscKR_cQExY --[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 08:09, 17 September 2014 (EST)&lt;br /&gt;
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Also we need to start our list of references so I reckon we just put them down under this heading. Leave the references at the bottom of the page ie. write above the heading references.--[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 08:18, 17 September 2014 (EST)&lt;br /&gt;
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i found a simple sketch drawing of omphalocele just so we have some picture on our page but i don't want to put it on the page yet incase you guys don't like i and since we cant delete it once its up so after your approval i will put it up also i am trying to find good video on organ development since im sure alot are formed by week 10 as i have read in articlese. --[[User:Z3415242|Z3415242]] ([[User talk:Z3415242|talk]]) 00:42, 24 September 2014 (EST)&lt;br /&gt;
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Apologies with my lack of input on this. I’ve added a bit of the Cloacal partitioning and deformities that I’ll expand upon. I’ve also found some great pictures on some of the other GIT deformities. If I’m unable to source permission for them, I’m happy to recreate them --[[User:Z3375627|Z3375627]] ([[User talk:Z3375627|talk]]) 07:55, 24 September 2014 (EST)&lt;br /&gt;
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Definitely put that picture up about Omphalocele. That will work well because I'm talking about midgut herniation so if I talk about it in my stuff then I can just link it so that when you click on it goes down to the bottom of the page to where you talk about it in abnormalities. Not exactly sure how we do that but I'm sure we will work it out.--[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 13:02, 6 October 2014 (EST)&lt;br /&gt;
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Hey all just wanted to note that when your referencing from now look at the editing page to see what mark does so that the references are footnotes down the bottom of the page. Obviously you will need to change the reference in the brackets but you get the point. This means that when you do this all the references will come up down the bottom of the page. --[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 23:34, 6 October 2014 (EST)&lt;br /&gt;
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Not sure if we are supposed to get rid of the references that we used for our group assignment but I just did because they were taking up uneccesary space on our page. Just thought i would say this here just in case we were not meant to.--[[User:Z3415141|Z3415141]] ([[User talk:Z3415141|talk]]) 09:17, 8 October 2014 (EST)&lt;br /&gt;
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Everyone please take off your student signature from the group page as it looks unprofessional. Thanks guys and girls :) --[[User:Z3414515|Z3414515]] ([[User talk:Z3414515|talk]]) 10:07, 8 October 2014 (EST) &lt;br /&gt;
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'''References'''&lt;br /&gt;
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Won Kyu Kim, Hyun Kim, Dae Ho Ahn, Myoung Hee Kim, Hyoung Woo Park Timetable for intestinal rotation in staged human embryos and fetuses. Birth Defects Res. Part A Clin. Mol. Teratol.: 2003, 67(11);941-5 PMID:14745932. I used this in describing midgut rotation.&lt;br /&gt;
&amp;lt;gallery&amp;gt;&lt;br /&gt;
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&amp;lt;/gallery&amp;gt;&lt;br /&gt;
&lt;br /&gt;
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*References are missing from the overview section. Although it serves as an introduction, you can still include references to support what you're saying. Also, maybe the language of this section should be edited to be a bit more formal, like the 2nd sentence in particular&lt;br /&gt;
*GIT = Gastrointestinal tract, not track&lt;br /&gt;
*The hyphens between &amp;quot;foregut&amp;quot; etc are not needed&lt;br /&gt;
*The timeline is a good idea! Everything was simplified. Maybe look to see if you can add some images to this section&lt;br /&gt;
*Week 6 of timeline: I don't think a liver can &amp;quot;obtain&amp;quot; a colour. Look to change the wording&lt;br /&gt;
*Maybe to simplify the timeline section better, tabulate the findings according to time (weeks), rather than dividing it by the midgut, foregut and hind gut section. It makes it hard to follow&lt;br /&gt;
*Need some more work on the recent findings section. Just some tips, when researching on pubmed, there's an option to look at recent articles by customising dates to say 2012-onwards&lt;br /&gt;
*Many potentials for adding images to the &amp;quot;foregut&amp;quot; section. If you find that copyright is too difficult to get around, then you can sketch or trace images from textbooks and upload them&lt;br /&gt;
*Great effort with the drawn images in the &amp;quot;midgut&amp;quot; section! Be wary of colour choice though, as the green highlighter and blue pen can be a bit difficult to see. Otherwise think of adjusting contrast on the images to make the diagram stand out more&lt;br /&gt;
*Maybe think of adding a video from YouTube to show some features of GIT fetal development, like the rotations. If you do that, be sure to include the 11-digit cache code as your reference point&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_2&amp;diff=149240</id>
		<title>Talk:2014 Group Project 2</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_2&amp;diff=149240"/>
		<updated>2014-10-14T00:47:28Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Peer Reviews */&lt;/p&gt;
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&lt;div&gt;{{Template:ANAT2341Project2014discussionheader}}&lt;br /&gt;
==Peer Reviews==&lt;br /&gt;
Really good introduction! It clearly outlines what is in the page. Most key points were done really well except for historic findings. There is a section on the Wikipage that has old books on embryology. It’s under the “Explore” tab and you’ll see “Historic embryo”. The developmental timeline would’ve been better if it was in a table, has an image showing the major steps in development, and is within the development section of the page. Regarding the development section, very detailed and informative. It clearly outlines the development of the renal system in the fetal stage. Dividing this section into the different organs is a very smart decision. It makes it a lot less confusing to the reader. Maybe try to breakdown some of the information and use dot points. There are lots of images to give the readers a visual of the developmental process. Also, the images have captions, which is great. &lt;br /&gt;
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Great job on the current research section. The articles chosen for current research is highly relevant to the topic and to the project. This section is written concisely and very detailed. The image really helps to understand the findings of the research. The same can be said to the abnormalities section. Each disease was written concisely and is very informative. The images really help in terms of understanding the clinical manifestation/s of each disease. Try to find information on current treatments and/or management techniques for each disease. &lt;br /&gt;
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Looking at the images included, all of them seems to be properly uploaded except for the “Kidney ascent.jpg”. It is missing its copyright information. From what I know, images from textbooks normally can’t be used because of copyright. Other than that, all the images are relevant and function as an aid to understanding what each section is about. In regards of citation and references, everything looks good. Each section was well-researched and properly cited. Great job on organising most of your references at the bottom of the page. The page looks very clean. In summary, focus on getting the historic findings section done and just minor fixes on images. Well done!&lt;br /&gt;
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In this review I will attempt to highlight the strengths of your project and identify some areas for improvement, in light of the criteria provided. &lt;br /&gt;
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I believe the developmental timeline is a great way to summarise the major events at each stage in fetal development and serves as a simple introduction to the project. However I think it would be best if you presented this information in a tabulated format, and include a little more detail. For instance “Week 8 – Mature kidney is formed” could  also mention some structures features seen at this stage, hallmarks that allows us to recognise a mature kidney.&lt;br /&gt;
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I think the current research section delves into a number in interesting areas, mentioning studies  on the treatment of congenital renal abnormalities. However, I think that there needs to be additional discussion on the molecular signalling that drives the underlying process of renal development in the fetus. &lt;br /&gt;
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The abnormalities associated with renal development in the feral period have been well researched and the information provided is well structured. However this section seems incomplete. I see a number of additional links to interesting scholarly articles. I think you should discuss some more abnormalities at the stages of early and late fetal development. I also suggest including images to supper the text. &lt;br /&gt;
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There is has been little information added on the historic findings. I suggest looking at text books in the library or searching the UNSW database to find information for this vital section.&lt;br /&gt;
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I really like how you have selected labeled diagrams to compliment and break up the text. Each image is relevant to the topic being discussed and the small description attached really help the reader orient them selves. Overall this project is coming along nicely. Just ensure that you are making progress on all the sections. Also only include relevant references. Finally proof read and review your work before the final submission.&lt;br /&gt;
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This is an excellent introduction and gives a great expectation for the information to come later in the project. The current research models section needs to be checked for spelling and grammar. The information here is good but is also very dense and hard to follow. It would be great if you could break it up a bit with bullet points or more images or tables. This style of writing is very professional and would be perfect for a report or essay, however as a wiki page it is too hard to follow. Breaking up the information into bullet point and tables would allow you to guide the reader through a journey of renal system development.&lt;br /&gt;
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There has clearly been a lot of research and work put into this project and that is very commendable. However on a whole, there is too much information. It’s difficult to read and grasp a wholesome understanding of the renal system when it delves too deep too quickly. One suggestion is giving a more brief explanation of the timeline of nephrogenesis, urethra, ureter and bladder development and then go into more detail in a subheading called “current research findings”.  The references under the abnormalities heading should be incorporated at the very end. &lt;br /&gt;
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[[RENAL SYSTEM]]&lt;br /&gt;
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Introduction&lt;br /&gt;
Background&lt;br /&gt;
Timeline of development - everyone will research first to get general idea of when,what and how long it will develop. Divide this area up from there.&lt;br /&gt;
Development of Actual system - all organs and parts that contribute to it (will be divided up later)&lt;br /&gt;
Abnormalities&lt;br /&gt;
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ACTUAL RESEARCH FIRST, THEN DIVIDE. SEE HOW MUCH INFO AND PARTS THERE IS FIRST&lt;br /&gt;
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==ANNOUNCEMENTS==&lt;br /&gt;
http://www.ehd.org/science_main.php?level=a&amp;amp;submit3.x=73&amp;amp;submit3.y=21&amp;amp;s18=on&amp;amp;ops=&amp;amp;re=on&amp;amp;L1=1&amp;amp;L2=0 have a look at this web site, good time line --[[User:Z3463310|Z3463310]] ([[User talk:Z3463310|talk]]) 10:50, 26 August 2014 (EST)&lt;br /&gt;
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Looks good. There wont be much we can say for all the individual events that occur since all of it is up to the 8th week, but it'll give us a good starting point. We can say 'such and such has been formed during the embryo period' and we can move on from there. I also found the following site which gives a nice intro into the components of the renal system and some general info on each part. Thought we might be able to incorporate a bit of it, talk about what the system/organ does, then follow on how it develops. Use it as a bit of a guide to how we could do our own. http://www.myvmc.com/anatomy/urinary-system-renal-system/ --[[User:Z3465654|Z3465654]] ([[User talk:Z3465654|talk]]) 13:48, 24 August 2014 (EST)&lt;br /&gt;
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https://docs.google.com/viewer?url=http%3A%2F%2Fpediatrics.med.unc.edu%2Feducation%2Fcurrent-residents%2Frotation-information%2Fnephrology%2Ffiles-1%2FNephrogenesis.ppt this web site goes into quite a lot of detail regarding how the renal system develops. &lt;br /&gt;
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I think in terms of dividing the work: &lt;br /&gt;
*1- urine formation (week 11~12) &amp;amp; amniotic sac&lt;br /&gt;
*2- kidneys descending from where they developed to adult anatomical positions (week 9)&lt;br /&gt;
*3- development of trigone of the bladder and allantois&lt;br /&gt;
*4- structures that arise from the Metanephric mesoderm&lt;br /&gt;
*5- structures that arise from the Ureteric bud&lt;br /&gt;
*6- abnormalities (developmental and genetic)&lt;br /&gt;
*7- introduction&lt;br /&gt;
*8- timeline of events in development&lt;br /&gt;
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I've thought of 8 topics we can divide the work into, so lets choose 2 each?&lt;br /&gt;
I preferably want to do abnormalities and urine formation (number 1 and 6), is that ok? we need this sorted out for our lab homework thing for this week. please reply asap. --[[User:Z3463310|Z3463310]] ([[User talk:Z3463310|talk]]) 10:50, 26 August 2014 (EST)&lt;br /&gt;
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On the actual project page when you expand the bit at the top there are 5 bullet point but the first one is just to come up with our title, shall we divide our project into those 4 different headings?:&lt;br /&gt;
Review that system development during the fetal period.&lt;br /&gt;
Identify current research models and finding.&lt;br /&gt;
Identify historic findings.&lt;br /&gt;
Identify abnormalities that can occur in this system during the fetal period&lt;br /&gt;
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Hey guys, i have now gone and updated the page and added sub-headings as suggested by above, please feel free to add or delete anything you seem unfit for the page. As for the online assessment due tomorrow, i agree that 2 each is appropriate although the timeline will be very long and would be unfair if one person to do the whole thing... We should probably divide the timetable based on weeks and then assign who wants to do what. Although i thought we agreed that i would do the abnormalities as discussed in the last lab...? i have already started to do some research on the topic....&lt;br /&gt;
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Here is a basic summary of some of the development structures in the renal system, as well as their abnormalities &lt;br /&gt;
https://web.duke.edu/anatomy/embryology/urogenital/urogenital.html&lt;br /&gt;
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--[[User:Z3465141|Z3465141]] ([[User talk:Z3465141|talk]]) 16:52, 26 August 2014 (EST)&lt;br /&gt;
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Ill look at 4 and 5 if that is alright with everyone (structures that arise from the Metanephric mesoderm&lt;br /&gt;
and the Ureteric bud), I think we need to also write a bit about Historic findings and current research models&lt;br /&gt;
--[[User:Z5030311|Z5030311]] ([[User talk:Z5030311|talk]]) 17:24, 26 August 2014 (EST)&lt;br /&gt;
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I can do the descending of the kidneys and the development of the bladder (2 and 3) if everyone is fine with that --[[User:Z3465654|Z3465654]] ([[User talk:Z3465654|talk]]) 18:39, 26 August 2014 (EST)&lt;br /&gt;
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Uh I guess that leaves 1 &amp;amp; 8 then, since no one wants to do the timeline xD&lt;br /&gt;
It doesnt look too hard so i dont mind doing timeline :)&lt;br /&gt;
so whoever only took 1 topic, can you please do the intro as well please? &lt;br /&gt;
Also im not 100% on the topics, but it'll have to do for now. add as we go i guess. &lt;br /&gt;
--[[User:Z3463310|Z3463310]] ([[User talk:Z3463310|talk]]) 20:26, 26 August 2014 (EST)&lt;br /&gt;
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yeah no worries, there will most likely be changes to the topics, or at least the headings. It's only set out the way it is now just so we can have a general layout, have some idea what to research. I also dont think we'll end up sticking to the subheading we chose, as there is a lot of stuff that will cross over to other topics.&lt;br /&gt;
I think we said that the timeline would be one of the last things we would do yeah? cause after we research all the organs and stuff as it develops, it would be easier to determine when it all develops as well, so we could just stick all that info together at the end. --[[User:Z3465654|Z3465654]] ([[User talk:Z3465654|talk]]) 21:04, 26 August 2014 (EST)&lt;br /&gt;
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--[[User:Z3463310|Z3463310]] ([[User talk:Z3463310|talk]]) 12:53, 27 August 2014 (EST)&lt;br /&gt;
*kidney(nephrogenesis0 - Sam&lt;br /&gt;
*ureter - Bahar&lt;br /&gt;
*urethra &amp;amp; fetal urination - Emily&lt;br /&gt;
*bladder - Rachel&lt;br /&gt;
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*intro - Emily&lt;br /&gt;
*historic findings - Emily&lt;br /&gt;
*abnormalities - Bahar &lt;br /&gt;
*current models - Rachel&lt;br /&gt;
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*developmental timeline (everyone)&lt;br /&gt;
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HOW IS EVERYONE GOING WITH THEIR PART????&lt;br /&gt;
www.lab.anhb.uwa.edu.au/hsd212/.../KidneyDevelopmentPrint.ppt&lt;br /&gt;
--&amp;gt; this powerpoint gives a good general intro to renal development btw if anyone wants to see?&lt;br /&gt;
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GIRLS&lt;br /&gt;
are we going to keep the whole assignment as apa referencing or as harvard? --[[User:Z3463310|Z3463310]] ([[User talk:Z3463310|talk]]) 01:36, 22 September 2014 (EST)&lt;br /&gt;
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umm i guess APA since thats the actual formal type of referencing. or you can just try and structure it the way its auto generated when you type in pubmed links haha. im gonna try and put some more content up about the kidneys in a couple days and a drawing or two. ill get some historic findings done as well.--[[User:Z3465654|Z3465654]] ([[User talk:Z3465654|talk]]) 21:16, 23 September 2014 (EST)&lt;br /&gt;
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hey guys, sorry i havent been putting anything up recently. i moved in to my new place over the weekend but the internet isnt up yet so i havent been able to upload anything. i dont know how much longer until its up, so ill be coming to uni just to use the internet (its where i am now lol). so when did the majority of our content have to be up by? was it friday or sunday? i cant remember. --[[User:Z3465654|Z3465654]] ([[User talk:Z3465654|talk]]) 12:48, 1 October 2014 (EST)&lt;br /&gt;
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i found this really good article. it mainly focuses on the kidneys but there are a couple of lines here and there where it mentions some facts about the rest of the renal system. thought u guys might wanna take a look. i dont know whether full access to the article is normal or whether i only managed it because im using the uni library internet, but if u cant access it just let me know and ill send u the article (i downloaded it haha). --[[User:Z3465654|Z3465654]] ([[User talk:Z3465654|talk]]) 14:15, 1 October 2014 (EST)&lt;br /&gt;
oh i also just found this book, it has A LOT of info about the embryology of the renal system, though half the chapters seem to be focused towards abnormalities and defects of the organs http://books.google.com.au/books?id=IKexq6xCRmIC&amp;amp;pg=PA542&amp;amp;lpg=PA542&amp;amp;dq=rotation+of+fetal+kidney&amp;amp;source=bl&amp;amp;ots=0O-4VfybHS&amp;amp;sig=3VeDlTrB9HnJsdYQLP66IKNGPDU&amp;amp;hl=en&amp;amp;sa=X&amp;amp;ei=1ocrVPuiIoKUoQSyroEQ&amp;amp;ved=0CCoQ6AEwBA#v=onepage&amp;amp;q=rotation%20of%20fetal%20kidney&amp;amp;f=false --[[User:Z3465654|Z3465654]] ([[User talk:Z3465654|talk]]) 15:10, 1 October 2014 (EST)&lt;br /&gt;
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Hey Girls hows the &amp;quot;break&amp;quot; going? :) i was wondering how many abnormalities we should have? 3/4? Also, is it just me or can we not access some of the journals that are free on Pubmed for e.g.&lt;br /&gt;
http://www.ncbi.nlm.nih.gov/pubmed/11458035 ?? --[[User:Z3465141|Z3465141]] ([[User talk:Z3465141|talk]]) 19:20, 1 October 2014 (EST)&lt;br /&gt;
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Sorry this is way too late but I think 3/4 abnormalities sound good and for references I have just been doing the automated way of the references --[[User:Z5030311|Z5030311]] ([[User talk:Z5030311|talk]]) 23:07, 7 October 2014 (EST)&lt;br /&gt;
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Also at the moment I have done 2 research models, do you think that is enough or shall I do another one? --[[User:Z5030311|Z5030311]] ([[User talk:Z5030311|talk]]) 00:01, 8 October 2014 (EST)&lt;br /&gt;
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*Great introduction! Your entire page's contents was introduced well and simple. I'm just wondering if you'd have to include more references to further justify some of the aspects you've mentioned in your explanation of the renal system development&lt;br /&gt;
*I noticed the historic findings have been left untouched. This section is in my opinion the trickiest because of the difficulty in finding information out there. My suggestions are to go onto pubmed and use key words like &amp;quot;Renal system development: a historical perspective&amp;quot; and then work from there. You can also adjust years to look at earlier papers from the 1920s and onwards. Also use Mark's historical textbooks on this website as a starting point, it's helpful too to see how ideas in fetal development have changed over the years&lt;br /&gt;
*I like how the timeline overview has been simplified. Maybe think of tabulating the findings? You can get the template for doing that off any other group project that has tables by copy and pasting, then just editing in what you need&lt;br /&gt;
*I wouldn't add that first like under &amp;quot;Current research models&amp;quot; but if you wanted to do that, maybe think of rewording it. An example could be: &amp;quot;Animal models are ideal to work with when researching renal system development due to their short gestation periods, making the identification of mutations much quicker.&amp;quot; Although what you've said about ethics is technically true, the ethics of working with animal models are still lengthy considerations and the fact that our pages are accessed to the public, maybe something like ethics don't need to be mentioned&lt;br /&gt;
*Include the years of when the current research findings were discovered. Otherwise, good work on this section. Just proofread over it to fix minor errors&lt;br /&gt;
*Great images used throughout&lt;br /&gt;
*Maybe think of having some sections more concise rather than wordy by including dot points&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
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	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_1&amp;diff=149201</id>
		<title>Talk:2014 Group Project 1</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=Talk:2014_Group_Project_1&amp;diff=149201"/>
		<updated>2014-10-14T00:07:31Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Peer Reviews */&lt;/p&gt;
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&lt;div&gt;{{ANAT2341Project2014discussionheader}}&lt;br /&gt;
==Peer Reviews==&lt;br /&gt;
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The introduction was written quite well as it explains what the respiratory system is about and the origin of its development. It also briefly highlights the difference between the embryonic and fetal stage which is important in enabling the viewers to have an understanding on what the project will be focusing on. I also like how the group distinguished between the two zones of the respiratory tract and adequately described the features and function of each. The content in the lung development stages clearly relates to the topic and underlines fetal development. The group briefly mentioned the key features in each stage instead of pasting a whole lot of information; this makes it easier for viewers to understand. Overall the content relates to the learning objectives of embryology and the level of research is good as exemplified under ‘Current Research and Findings’ and ‘abnormalities’ (many forms of diseases described).&lt;br /&gt;
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The images under introduction and the image used for Meconium aspiration syndrome have not been referenced properly as there is missing information such as ((Template: Student Image)), description, copyright information and proper references for some. The image used under the ‘current research and findings’ subheading is a good example for the group to copy the referencing style. It is also vital that the group adds a brief description of what the image illustrates as a footnote to help viewers understand the relation of the content and image (this is seen in the image under ‘surfactant’). More images could be added such as in the ‘lung development stage’ and under abnormalities. If images for lung development stages aren’t easily accessible, it is perhaps a good idea to draw them. The table format used for ‘lung development stages’ makes it easy for the viewers to navigate which is a good feature used in the project.&lt;br /&gt;
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In terms of referencing, there are many in-cite references missing such as in the ‘introduction’ and in ‘lung development stages’. It is important to have these references formatted correctly under the one ‘references’ subheading. There seems to be many ‘references’ subheadings making it harder for viewers to navigate. Some references are shown as ‘&amp;lt;/span&amp;gt; &amp;lt;/li&amp;gt; which needs to be fixed right away. Overall, the content seems well written, formatted and concise making it easy to understand. However the problems related to referencing needs to be corrected as this is inconsistent throughout the project.&lt;br /&gt;
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This project was done really well. All key points, i.e. development, historic findings, etc., were clearly described. In terms of content, this group did a great job. It is very informative and all information they have included are relevant to the topic. There are a few mentions of embryonic stage but I do understand why, particularly for the development of the respiratory system. The developmental timeline is good but an image about the development would make it better. Remember to add in-text citations for this part. Historic findings section is very detailed and exceptional. Abnormalities is done well. A couple or more images would make this section really great. There are images that help with understanding the content. Try to find information on current treatments and/or management techniques for each disease. &lt;br /&gt;
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However, some images have no captions and so some seem vague as to what they’re about. There are a few images missing copyright, specifically the 2nd photo on the project page and the historical image of lung development. From what I know, images from textbooks normally can’t be used because of copyright. The content is cited and referenced correctly. A bit messy with the references right now but I understand why. Just don’t forget to organise it before submission. Also, don’t forget to mention the other sections in the introduction. Overall, this project is done really well. It is very informative and easy to understand. In summary, just a few more images and correction of typos and this project would be remarkable. Well done! &lt;br /&gt;
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Firstly, great job on the layout and formatting of the project, everything is easy to find and overall, it reads well. The introduction provides great insight of what to expect on the page. However, it lacks in-text citations for the first three subheadings of the page, as well as the table of lung developmental stages. The first two images also don’t have a description when I click on it, I don’t know what I’m looking at. The “student template” is also missing for the images. I would suggest you look up the tutorial for uploading images on the pages as Mark has extensive information for the proper steps required for uploading images. Otherwise, the lung developmental stages table is informative and easy to read. I would also recommend adding an image for better visualization of the developmental process. &lt;br /&gt;
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The historical findings and current research models have very detailed content, and look as though they have been referenced correctly using in-text citations, I’m impressed. Although, I would suggest you leave all the references to the end by simply putting &amp;lt;/references&amp;gt; at the bottom of the page, as it looks neater to have them all in one place, rather than at the bottom of each sub-heading. The abnormalities section is done well and there are a wide number of abnormalities covered. The detail of the first two is more in depth than the rest, I’m unsure whether they was more information on those particular abnormalities or their still needs to be information added, but I suggest to have the same amount of information on each disease, if possible. &lt;br /&gt;
Overall, the project is very informative and presented well. It just need a few minor edits. &lt;br /&gt;
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The introduction provided good background information about the lungs and its general development, however seemed to lack any further explanation as to what else would be covered on the page (current research, abnormalities). I found most of the sentences to be short and abrupt, and more in the form of statements rather than an explanation. This is the same for the following paragraphs regarding the two zones. I would combine several of the sentences together, and restructure them so that they do not start in the same manner e.g. of the first four sentence in your introduction, three of them begin with the words ‘The respiratory system’, and over half the sentences in the entire paragraph begin with ‘The’.  There are a few grammatical errors within the text that should be corrected e.g. ‘till’ of ‘until’, ‘id’ instead of ‘is’. The images used fit well, but there is no caption to explain what they are images of and what they are trying to show. This is also not indicated on the summary of the image, one of which also doesn’t include any copyright information.&lt;br /&gt;
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The lung development stages were done very well, simplified and tabulated making it very clear. My only concern for this part is that it should be the main part of the project, the area where the development of the lungs is fully explained, yet it is the smallest section of the page. Try to expand on it maybe? Or add a picture or two to enlarge the section?&lt;br /&gt;
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The current research and findings section seems very thorough, lots of content, good explanations. Very minor problems however; a slight tendency to over use commas in some areas, while not in others. The current models area has not been added to; make sure to fill it in, or will it be scrapped? I have also noticed a picture has been deleted so make sure to get that issue fixed if you still want to use the same image. Is the second picture under this heading part of the section? As it is after the references so I'm not sure where it lies exactly. The image should be captioned as well.&lt;br /&gt;
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I really like the historical findings section, the information seems more concise when it is presented in bullet points. The second picture within this section is well done and very neatly labeled (I thought it was an image from the internet). The first picture though, needs a caption added as well as copyright information. The abnormalities section is very extensive which can be bother good and bad. For some of the abnormalities there is a lot of detail presented, while for others there is very little. I think maybe that as long as you mention what it is, how you get it/how it forms, some statistics and maybe an image, that should be more than enough. Also, I would remove all the sub-headings under abnormalities and have them just written in bold. Otherwise, when looking at the contents at the top of the page, it looks as though half your page is solely focused on abnormalities. &lt;br /&gt;
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Overall, I think this page is well done and only a focus on sentence structure, a bit on grammar, and captioning pictures with correct copyright info is needed. Other than these main focus areas, one other point to make would be all the references should be at the bottom of the page.&lt;br /&gt;
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In this review I intend to highlight the merits of your project as well as provide some constructive criticism in light of the marking criteria of this task. &lt;br /&gt;
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The page is well structured and provides perfect balance between written text and images. However some of the included images do not compliment the text. I suggest adding labels or descriptive annotations to these images using paint. You could also include a simple written description of what each image showing. Alternatively you could refer to these images in your text e.g “ as seen in Figure 4a” and use them to make the content more engaging. I found the table on the stages of lung development really effective way of organising the content and I was able to understand much of it in a quick glimpse! I like how the text is summarised and highlights the main developmental changes that are occurring at each stage. Just to make it more engaging, perhaps you could include matching images in a another column. &lt;br /&gt;
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Under the section of current findings, I believe that most of the information included is relevant and incredibly appropriate articles have been selected. I think its good that this section is delving into the area of molecular signalling underlying the morphological changes that we see. I believe your project would greatly benefit if there was more material discussing the biochemical signalling and recent findings in relation to this. However, I am not sure if the details on cell type should be in this section, this section might need some re-organising. &lt;br /&gt;
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I understand that the history is a difficult topic to research. The information on our understanding of surfactant is appropriate, detailed and very informative. However I think you need to include more information on our understanding of stages in fetal lung development. Explore the transition in research focus investigating morphology to molecular changes. Perhaps use the library database to find relevant historic journal articles in the database. It was good to see the use of relevant historic images. &lt;br /&gt;
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A number of abnormalities have been identified and described, I think its great that each section includes a description of the abnormality, and goes on to discuss the cause and implications of each disease. I would only recommend including matching images to make this section more engaging to readers. Great Work!&lt;br /&gt;
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Overall the project is coming along really well ! Just ensure that you proof read and review before the final submission. Also include in-text references and compile all your references to one section at the end of the page. Good Luck!!&lt;br /&gt;
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Well explained introduction and the histological images provided are great.&lt;br /&gt;
In the first section the addition of in text citations would be useful. The content is explained really well and a good use of detail in the paragraphs is not too overwhelming.  Good use of formatting with the inclusion of the table, helps to keep the content clear and concise. The current research, findings and models is present really well, good use of referencing and in text citations. Current findings, models and research is presented really well, good use of referencing and in text citations. Information is clear and with sufficient detail. There are a variety of formatting techniques used which is great to see. Good use of images, however seems to be missing info, suggest filling it out and maybe fixing some of the formatting errors shown but otherwise really well done.  This section shows a good amount of research conducted. The historic findings are also well presented, the use of dot points to format the info is very useful and provides clarity. A timeline for the key historic dates might be helpful and another use of visuals. Great to see a variety of abnormalities, shows an extensive research really well presented. Would be great to see more images for this section and maybe drawings too. &lt;br /&gt;
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This group overall has done really well, there are only a couple of suggestions for the page to be complete these include filling in the missing info under the sub heading ‘current models’. The in text citations and referencing in the first section should be added in to avoid losing marks. Also try adding captions to some of the images,  a brief description of what the image is showing. Evidently the research conducted has been quite extensive and the group has worked well to ensure all parts are completed equally. Overall the page is structured really well and organized in an understandable manner. The use of a variety of images and formatting techniques is really great. Just a few minor adjustments and this page will be really great. Great work everyone !&lt;br /&gt;
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The intro is very good and the images are a good size but there needs to be some description to make it relevant to the project. Need to edit ‘Conducting Zone’ info since there are some grammatical and spelling errors. Also should have in-text referencing in this section of the project with a long list of all the references at the end. You can go onto other people’s reports to find the coding for this reference style. &lt;br /&gt;
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The information on the lung development timeline is fantastic but it is a bit dense. Splitting it into bullet points might be a better way of organising it so peers get a more effective learning experience when they read it. In the conducting system under current findings it looks like there has been an attempt to upload an image called “400px” however the link leads nowhere. It has great information, very interesting and concise. However the references at the end of this section should be incorporated at the very end of the wiki page. This would make it flow better. &lt;br /&gt;
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Excellent images of the diseased lung compared to normal lung, however it might make more sense for these to be under the lung abnormalities subheading. There is excellent information on the historical findings. It has been written in an easy to understand manner and all the information is relevant. There is also excellent referencing and good use of diagrams. However I still think that the references should all be together at the very end of the project page. &lt;br /&gt;
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The abnormalities section is very in depth however there is a bit too much information. It would be easier to follow and more interesting if there were images associated with the information, or maybe if the information was tabulated that would make it easier to follow. Well done on this project! It is clear that a lot of research has been done outside. &lt;br /&gt;
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--[[User:Z3333429|Z3333429]] ([[User talk:Z3333429|talk]]) 16:13, 17 August 2014 (EST)&lt;br /&gt;
Hey guys, it's Emanuel&lt;br /&gt;
I've had a look into the systems and respiratory caught my interest. I wanted to do cardio but another group has already chosen it so I think we should choose a system ASAP.&lt;br /&gt;
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Respiratory looks like it has plenty of resources and there are some interesting abnormalities gat I found on this page:&lt;br /&gt;
[http://embryology.med.unsw.edu.au/embryology/index.php?title=Respiratory_System_-_Abnormalities Respiratory Abnormalities]&lt;br /&gt;
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Do you guys have any other systems you would like to do or do you like respiratory?&lt;br /&gt;
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--[[User:Z3372817|Z3372817]] ([[User talk:Z3372817|talk]]) 20:07, 17 August 2014 (EST)&lt;br /&gt;
Hey Emanuel, its Ish here.&lt;br /&gt;
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As we said on the day, we're fine with anything. So if it's still free, let's lock it in before another group claims it?&lt;br /&gt;
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--[[User:Z3333429|Z3333429]] ([[User talk:Z3333429|talk]]) 20:59, 17 August 2014 (EST) Alright awesome, well I guess we're the Respiratory group. How do we let Dr Hill know?&lt;br /&gt;
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--[[User:Z3330991|Z3330991]] ([[User talk:Z3330991|talk]]) 22:30, 17 August 2014 (EST) Hi guys, it's Nadine. I'm happy to do the respiratory system :) I'm sure we have to email him, I'll do that now, since we all seem to be on the same page and in agreement with the respiratory system.&lt;br /&gt;
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--[[User:Z3330991|Z3330991]] ([[User talk:Z3330991|talk]]) 22:56, 17 August 2014 (EST)  Just emailed Dr Mark and put a heading &amp;quot;respiratory&amp;quot; on our group page :)&lt;br /&gt;
Also we each need to pick one of the following; &lt;br /&gt;
# Review that system development during the fetal period.&lt;br /&gt;
# Identify current research models and finding.&lt;br /&gt;
# Identify historic findings.&lt;br /&gt;
# Identify abnormalities that can occur in this system during fetal period.&lt;br /&gt;
I'm happy to do number 1. Unless someone else wants to?&lt;br /&gt;
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--[[User:Z3333429|Z3333429]] ([[User talk:Z3333429|talk]]) 06:09, 18 August 2014 (EST)Thanks Nadine, I'll do number 4 if that's all good with you guys?&lt;br /&gt;
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--[[User:Z3372817|Z3372817]] ([[User talk:Z3372817|talk]]) 19:54, 18 August 2014 (EST) Great work with allocating Nadine. I'd love to do the historic findings (number 3) that sounds interesting! Only if that's okay with you all though?&lt;br /&gt;
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--[[User:Z3332339|Z3332339]] ([[User talk:Z3332339|talk]]) 15:17, 19 August 2014 (EST) Hey Guys! It's marina here :), I'm happy with number 2. If anyone comes across information for other parts of the project, let's let each other know :)&lt;br /&gt;
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--[[User:Z3330991|Z3330991]] ([[User talk:Z3330991|talk]]) 21:07, 26 August 2014 (EST)Hi guys its Nadine, just wanted to let you guys know that i added in subheadings to our page :) So feel free to add to your sections  -pictures  -articles  -tables&lt;br /&gt;
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--[[User:Z3332339|Z3332339]] ([[User talk:Z3332339|talk]]) 23:58, 26 August 2014 (EST)Marina: Thanks Nadine :) I'm just going to add our names next to each section that we are looking at so its easier to communicate with with one another and who's doing what :)&lt;br /&gt;
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# Review that system development during the fetal period-Nadine&lt;br /&gt;
# Identify current research models and finding-Marina&lt;br /&gt;
# Identify historic findings-Ish&lt;br /&gt;
# Identify abnormalities that can occur in this system during fetal period-Emanuel&lt;br /&gt;
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--[[User:Z3333429|Z3333429]] ([[User talk:Z3333429|talk]]) 12:58, 27 August 2014 (EST) &lt;br /&gt;
'''Topics to cover'''&lt;br /&gt;
#Major stages of development - all fetal (only primordial embryonic development)&lt;br /&gt;
#Histological findings&lt;br /&gt;
#Separate into Functional elements (alveoli) and Tract (conducting system: upper and lower)&lt;br /&gt;
#Include diaphragm (musculoskeletal)&lt;br /&gt;
#Changes after birth&lt;br /&gt;
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--[[User:Z3333429|Z3333429]] ([[User talk:Z3333429|talk]]) 12:20, 2 September 2014 (EST) Emanuel: Hey guys just letting you know that I spoke to Dr Hill before the lecture with Carl from the cardio group about using review articles. He said we are allowed to use them as long as we refer to them appropriately (e.g as reviewed in..., according to review by..., etc).&lt;br /&gt;
He also said that any direct findings need to be referenced from the original article and not a review article. &lt;br /&gt;
We can reference to them as mentioned above and we can also add a subheading under references titled &amp;quot;review articles&amp;quot; if we want. When we start to formulate the page we can look at what previous projects have done when organising their review article references for ideas.&lt;br /&gt;
In regards to using images from review articles - there is no need to cite them as coming from review article.&lt;br /&gt;
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--[[User:Z3333429|Z3333429]] ([[User talk:Z3333429|talk]]) 15:41, 2 September 2014 (EST) Emanuel:  Hey guys just looking through the lecture and I noticed the part about the development of the pharynx. It develops with the foregut (oesophagus) of the GIT. What do you think if Nadine mentions that groups page in an appendix for her section to link the two pages? There is also a relationship between the development of the liver in wk7 that stops the descent of the heart and lungs so it could make our project more interesting in that it links out page with others offering a wider scope of information along with our specific topic.&lt;br /&gt;
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--[[User:Z3332339|Z3332339]] ([[User talk:Z3332339|talk]]) 11:37, 3 September 2014 (EST)Marina: Yeh I agree! I noticed that too Emanuel. The development of the oesophagus from the foregut and how it bifurcated from the common pharynx into the trachea is very much related to our topic. We can definitely include those relationships, and any others we come across&lt;br /&gt;
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--[[User:Z3333429|Z3333429]] ([[User talk:Z3333429|talk]]) 22:47, 9 September 2014 (EST) Emanuel: Hey Ish, just came across these articles regarding historical findings for pulmonary surfactant:&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed/18446178 Surfactants: past, preset and future.]&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed/14509914 The era of pulmonary surfactant from Laplace to nowadays]&lt;br /&gt;
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Mary Ellen Avery and Jere Mead seem to be the godparents of surfactant discovery.&lt;br /&gt;
I also noticed that there is a little tool on the right hand side of the pubmed page when you search for articles called &amp;quot;Results by year&amp;quot;. It's a little bar graph showing which years had the most articles and you can click on each year to bring up it's articles. This might be helpful if your looking for articles that sparked an increase in research by clicking on the years just before the spikes in articles.&lt;br /&gt;
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--[[User:Z3372817|Z3372817]] ([[User talk:Z3372817|talk]]) 15:49, 16 September 2014 (EST) That is just amazing Emanuel, thanks! Just another thing I wanted to ask, I noticed you took notes when Mark came by to talk to our group at the last lab. When he was saying to focus on things like..&lt;br /&gt;
Yeah, do you mind just typing up what you had written. That would be so helpful!&lt;br /&gt;
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--[[User:Z3332339|Z3332339]] ([[User talk:Z3332339|talk]]) 23:33, 16 September 2014 (EST)Marina: Hey guys, just uploaded an image onto our page. It's under current research because its something scientists are looking at the moment with tracking abnormalities. The picture compares the normal structure of a lung to a couple of diseased ones. I know this also links to other parts of our project so we can shift it around later if need be. Mark wanted a picture uploaded before tomorrow, so at least we have something up there for now :)&lt;br /&gt;
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--[[User:Z3330991|Z3330991]] ([[User talk:Z3330991|talk]]) 12:13, 17 September 2014 (EST) Nadine here, just wanted to inform you that we have a new group assessment that will be marked individually we need to pick 2-3 research papers on stem biology and we need to summarize the paper and present it in week 12 as a group. You will get an email in regards to this set assignment, just thought I'd give you a head up.&lt;br /&gt;
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--[[User:Z3333429|Z3333429]] ([[User talk:Z3333429|talk]]) 12:44, 17 September 2014 (EST) Emanuel: This is for Ish, I found a link on the respiratory pages that should help you out. Just go to one of the pages (e.g Respiratory System - Abnormalities) and there is a 'Historic Embryology' link just after the introduction. It's small and in a blue box so click on it to expand. It has some really good links that will hopefully help you. Something else that was interesting was the disclaimer at the bottom of the links stressing that the content and scientific understanding are specific to the time of publication. You may want to ask Dr Hill if you need to include that at the bottom of the page to make sure that our audience does not get confused.&lt;br /&gt;
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--[[User:Z3372817|Z3372817]] ([[User talk:Z3372817|talk]]) 13:27, 17 September 2014 (EST) Ish: Yup, I've seen that Emanuel. I sort of wrote a paragraph along those lines as an introduction to my section which serves as a type of disclaimer too, but I'll reconfirm with Mark whether it's necessary to have anything in addition to that. Nadine, thanks for the heads up.&lt;br /&gt;
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--[[User:Z3330991|Z3330991]] ([[User talk:Z3330991|talk]]) 16:21, 1 October 2014 (EST) Nadine: Hey guys, just wanted to remind you that by the end of this week all information should up for your section. Make sure that references are included, pictures if needed.&lt;br /&gt;
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--[[User:Z3372817|Z3372817]] ([[User talk:Z3372817|talk]]) 20:34, 1 October 2014 (EST) Ish: Hey guys, anyone else having issues with the website lately? I'm trying to upload an image - can't. I completed my latest lab assessment a couple days ago and saved it - lost it. So just to be safe, once you've written everything you need down in your sections, copy and paste EVERYTHING into a separate word doc. Don't want you guys to lose hours of work like I did.&lt;br /&gt;
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--[[User:Z3332339|Z3332339]] ([[User talk:Z3332339|talk]]) 19:02, 3 October 2014 (EST) Marina: Hey Ish yeh im also having trouble with it as well. Even the &amp;quot;uploading image&amp;quot; button is inactive for me, apparently others are having as few problems with this as well. Can you guys check if you yours is visible at the moment? I know this must be recent as you guys have uploaded images and i was able to before. Maybe it has to do with the website change Dr Mark was talking about.&lt;br /&gt;
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--[[User:Z3330991|Z3330991]] ([[User talk:Z3330991|talk]]) 21:10, 4 October 2014 (EST) Nadine: Thanks Ish! i had the same problem happened twice to me! But it worked out for me in the end. So i have been looking around -projects from years before us and i really like this layout. Have a look if you get the chance [https://embryology.med.unsw.edu.au/embryology/index.php/2012_Group_Project_3]&lt;br /&gt;
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--[[User:Z3332339|Z3332339]] ([[User talk:Z3332339|talk]]) 22:50, 4 October 2014 (EST) Marina: Hey Nardine, i really like that layout, hopefully we can get something similar to that going for us as well :) I'm sorry I havent been able to upload any images as the tab for me is unavailable, i emailed Dr mark about it though so hopefully that gets fixed soon.&lt;br /&gt;
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--[[User:Z3332339|Z3332339]] ([[User talk:Z3332339|talk]]) 22:51, 4 October 2014 (EST) Marina: I was thinking of adding a heading titled &amp;quot;Glossary&amp;quot; at the very end of our project for us to add any words we want to define.... what do you guys think of this?&lt;br /&gt;
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--[[User:Z3330991|Z3330991]] ([[User talk:Z3330991|talk]]) 20:33, 7 October 2014 (EST) Nadine: Hey Marina, i like that idea heaps and i was also thinking of drawing for my section i found a great paper with fantastic pictures but i cant find the copyright information its off Nature, or I'll just figure something out&lt;br /&gt;
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--[[User:Z3330991|Z3330991]] ([[User talk:Z3330991|talk]]) 20:36, 7 October 2014 (EST) Nadine: Hey I was thinking we need to get on top of the week 12 project maybe we can talk about this further tomorrow? I just dont want all of the good papers to go fast and we get left with really hard ones.&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=147830</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=147830"/>
		<updated>2014-10-08T00:22:59Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Lab Attendance */&lt;/p&gt;
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&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
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[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
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==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
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===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
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===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
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===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
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===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
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===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
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===Lab 9===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:22, 8 October 2014 (EST)&lt;br /&gt;
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== Online Assignment 1 ==&lt;br /&gt;
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Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
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The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
&lt;br /&gt;
The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{{Historic Disclaimer}}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
&lt;br /&gt;
:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=147725</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=147725"/>
		<updated>2014-10-07T23:36:05Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Online Assignment 3 */&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
&lt;br /&gt;
[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
&lt;br /&gt;
==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
&lt;br /&gt;
===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
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===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 1 ==&lt;br /&gt;
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&lt;br /&gt;
Article 1&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
&lt;br /&gt;
The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
&lt;br /&gt;
These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Article 2&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
&lt;br /&gt;
These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
&lt;br /&gt;
The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 2 ==&lt;br /&gt;
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&lt;br /&gt;
[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Thyroid===&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0080801&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1530/JOE-14-0025&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0016752&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Online Assignment 4==&lt;br /&gt;
&lt;br /&gt;
'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
&lt;br /&gt;
The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
&lt;br /&gt;
1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
&lt;br /&gt;
2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
&lt;br /&gt;
3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Online Assignment 5==&lt;br /&gt;
&lt;br /&gt;
===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
&lt;br /&gt;
Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Online Assignment 6==&lt;br /&gt;
&lt;br /&gt;
I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
&lt;br /&gt;
Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
 &lt;br /&gt;
&lt;br /&gt;
The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
&lt;br /&gt;
Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
&lt;br /&gt;
[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
&lt;br /&gt;
The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
&lt;br /&gt;
The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{{Historic Disclaimer}}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
&lt;br /&gt;
:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=147719</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=147719"/>
		<updated>2014-10-07T23:32:56Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
&lt;br /&gt;
[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
&lt;br /&gt;
==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
&lt;br /&gt;
===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
&lt;br /&gt;
===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 1 ==&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Article 1&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
&lt;br /&gt;
The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
&lt;br /&gt;
These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Article 2&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
&lt;br /&gt;
These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
&lt;br /&gt;
The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 2 ==&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1016/j.acthis.2014.04.003&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004815&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;ref name=&amp;quot;PMID10.1371/journal.pone.0004513&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
===Thyroid===&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
 &amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Online Assignment 4==&lt;br /&gt;
&lt;br /&gt;
'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
&lt;br /&gt;
The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
&lt;br /&gt;
1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
&lt;br /&gt;
2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
&lt;br /&gt;
3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
==Online Assignment 5==&lt;br /&gt;
&lt;br /&gt;
===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
&lt;br /&gt;
Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Online Assignment 6==&lt;br /&gt;
&lt;br /&gt;
I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
&lt;br /&gt;
* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
&lt;br /&gt;
Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
 &lt;br /&gt;
&lt;br /&gt;
The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
&lt;br /&gt;
Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
&lt;br /&gt;
[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
&lt;br /&gt;
The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&amp;lt;references/&amp;gt;&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
&lt;br /&gt;
The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
{{Historic Disclaimer}}&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
&lt;br /&gt;
:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;/div&gt;</summary>
		<author><name>Z3414648</name></author>
	</entry>
	<entry>
		<id>https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=147713</id>
		<title>User:Z3414648</title>
		<link rel="alternate" type="text/html" href="https://embryology.med.unsw.edu.au/embryology/index.php?title=User:Z3414648&amp;diff=147713"/>
		<updated>2014-10-07T23:30:07Z</updated>

		<summary type="html">&lt;p&gt;Z3414648: /* Online Assignment 3 */&lt;/p&gt;
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&lt;div&gt;{{StudentPage2014}}&lt;br /&gt;
&lt;br /&gt;
[http://www.ncbi.nlm.nih.gov/pubmed PubMed]&lt;br /&gt;
&lt;br /&gt;
==Lab Attendance==&lt;br /&gt;
===Lab 2===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:11, 20 August 2014 (EST)&lt;br /&gt;
Lab 2&lt;br /&gt;
I did not put my signature in my lab attendance last week however I did attend. The week 2 lab involved two guest researches discussing meiosis in mammalian oocytes and age-related vulnerability and the reproductive technology revolution.&lt;br /&gt;
&lt;br /&gt;
===Lab 3===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:12, 20 August 2014 (EST)&lt;br /&gt;
Lab 3&lt;br /&gt;
&lt;br /&gt;
===Lab 4===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:48, 27 August 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 5===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:10, 3 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 6===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:39, 10 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 7===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 12:07, 17 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
===Lab 8===&lt;br /&gt;
--[[User:Z3414648|Z3414648]] ([[User talk:Z3414648|talk]]) 11:04, 24 September 2014 (EST)&lt;br /&gt;
&lt;br /&gt;
== Online Assignment 1 ==&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;
Article 1&lt;br /&gt;
&lt;br /&gt;
&amp;lt;pubmed&amp;gt;24934154&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
&lt;br /&gt;
This article from PubMed explores the role of the ZP2 receptor and protein in female mice fertility and species-specific nature of the fusion of spermatozoa and oocyte during successful fertilisation. ZP2 is a glycoprotein found in a region of the extracellular oocyte-surrounding zona pellucida . Polyspermy is an abnormal and detrimental process where membrane fusion occurs between one oocyte and more than one spermatozoa. It is inefficient for more than one spermatozoa to bind to the oocyte because only one male and female gamete are required for successful fertilisation. The authors of this article used gamete samples from both mice and human origin to illustrate their findings.&lt;br /&gt;
&lt;br /&gt;
The authors used various materials and scientific methods in order to achieve their results. There were extensive, complex and repetitive biochemical and transgenic variations made in order to manipulate the gene expression and protein synthesis occurring in the test subjects, in this case mice. In order to control which cells could be genetically modified to express human or mice ZP2 protein, they scientists needed to first produce transgenic mouse lines from embryonic stem cells that had not yet differentiated into any of the ZP1, ZP2, ZP3 or ZP4. They created Bacterial Artifical Chromosomes carrying either the mouse or human form of the ZP2 gene and these were transformed into bacterial cells containing the gamma prophage. The recombinants could be identified by growing the transformed cells on minimal media with galactose. Once the transgenic mice line was established, they were genotyped using TP2 specific primers in extensive PCR reactions. The eggs and embryos were examined under the microscope and the scientists carried out immunohistochemistry. They examined the fertility of the females with and without the ZP2 binding ability through mice and human sperm assays. They also experimented with in vitro fertilisation of the female mice oocyte with mice sperm and then human sperm.&lt;br /&gt;
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These scientists accumulated results which revealed with following things. The transgenic female mice that did not express ZP2 in their zona pellucida where sterile. Female mice that were genetically modified to express the four human ZP proteins (ZP1, ZP2, ZP3 and ZP4) were recognised by human sperm to carry our successful fertilisation. However the female mice that did not express the human ZP2 protein did not attract the human sperm for fertilisation. This illustrated the species-specific gamete fusion that occurs in human fertilisation. &lt;br /&gt;
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Article 2&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;23909991&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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This journal article from PubMed compares the nature of embryo hatching between two different types of artificial fertilisation of a female gamete: in vitro fertilisation (IVF) and intracytoplasmic sperm insemination (ICSI). 'Hatching' is a term given to the process that occurs at around day 6 of embryo development, post zygote production, and it is where the blastocyst containing the maternal and paternal pronulei escapes the zona pellucida. In vitro fertilisation is where female follicles are isolated from the ovary and are exposed to spermatozoa. The spermatozoa acrosomal head naturally fuses to the zona pellucida of the female follicle and from there, there is no more external manipulation. The genetic material from the sperm mixes with the genetic material of the occyte resulting in fertilisation and a zygote. In intracytoplasmic sperm insemination, a fine needle is used to inject the sperm through the zona pellucida directly into the oocyte.&lt;br /&gt;
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These scientists performed a study in a fertility clinic and carried out in vitro fertilisation, embryo culture and embryo grading in order to obtain the results they wanted. Oocytes were inseminated either via IVF or ICSI and then the embryos were cultured and tested for successful fertilisation using an embryoscope. The grade the embryos were given was based on the size of the blastocele cavity and the cohesiveness of the inner cell mass. The embryos with the best morphology were used for further testing. The embryoscope took images every 20 minutes and this enabled the researchers to compare the nature of embryo hatching from the two different types of artificial fertilisation techniques.&lt;br /&gt;
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The results from these experiments showed there were two main types of spontaneous hatching which were specific for the two types of artificial fertilisation. One type of hatching was initial finger like projections reaching out of the zona pellucida before eventually the blastocyst emerged. The other type was spontaneous complete hatching out of the zona pellucida where the embryo completely ruptured through without the initial projections. The first type was mainly seen with the ICSI technique and the sudden rupture hatching was seen with the IVF technique.&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] These are good summaries of these 2 research articles (5/5)&lt;br /&gt;
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== Online Assignment 2 ==&lt;br /&gt;
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[[File:Cleavage stage embryo.png|200px|thumb|left|Cleavage stage embryo]]&lt;br /&gt;
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==Online Assignment 3==&lt;br /&gt;
===Pituitary gland===&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1016/j.acthis.2014.04.003&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004815&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0004513&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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===Thyroid===&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1371/journal.pone.0080801&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1530/JOE-14-0025&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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 &amp;lt;pubmed&amp;gt;10.1371/journal.pone.0016752&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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--[[User:Z8600021|Mark Hill]] You have included the references but not formatted the links correctly. (4/5) See [[Help:Reference Tutorial]]&lt;br /&gt;
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==Online Assignment 4==&lt;br /&gt;
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'''Therapeutic Cord Stem Cell Use''' &lt;br /&gt;
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The article written by S. Gopinath et al. looks into the therapeutic use of human umbilical cord blood (hUCB)-derived stem cells in reversing pathological hypertrophy of heart tissue in rats. It is an extensive research paper that uses the pre-existing knowledge that cord stem cells are pluripotent and have the potential to differentiate into any tissue of the body. Using this they investigated the ability for hUCB-derived stem cells to reverse the pathological hypertrophy that occurs when rats are induced with doxorubicin (DOX). Doxorubicin is a cancer-treating drug but is also known to induce cardiac hypertrophy. Cardiac hypertrophy involves the increase of size of cardiomyocytes, increased protein synthesis, increased interstitial fibrosis and higher organisation of a sarcomere. However there is also increased frequency of apoptosis that is dangerous considering myocytes have a limited self-renewal capacity. Hence if hUCB-derived stem cells have a cardiomyogenic potential, they could be used to reverse heart failure conditions. &lt;br /&gt;
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One key result that came about during this investigation was that after 24 hours of co-culture of normal rat cardiomyocytes and hUCB-derived stem cells, the structure of the red stained hUCB-cells began to look like myocytes. Immunocytochemistry staining showed that these new myocytes stained positive for molecules found in normal myocytes including connexion 43 and N-cadherin. There was also a clear image of striated cardiac α-actinin. Upon physical examination, the researchers found that these new myocytes beat in a strong, synchronised manner and also exhibited tight electrical coupling with the normal rat myocytes. Another finding was that hUCB-derived stem cells were able to decreases the apoptotic activity of DOX induced cardiac cells. This was indicated by the decrease expression of apoptotic proteins like caspase-9 and caspase-3 from the initially highly active apoptosis in the DOX-induced cells. &lt;br /&gt;
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Finally, the researchers were able to prove a significant finding involving the ability for hUCB-derived stem cells to reverse the pathological hypertrophy induced by the DOX. Part of the reason for this result was that the hUCB-derived stem cells were replacing the dead myocytes and there was increased paracrine secretion of IGF-1. This is significant because IGF-1 (insulin-like growth factor 1) is known to increase cell proliferation and inhibit apoptosis.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;20382121&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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'''There are a number of developmental vascular &amp;quot;shunts&amp;quot; present in the embryo that are closed postnatally. Identify these shunts and their anatomical location.'''&lt;br /&gt;
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1. Foramen ovale: a shunt in the aortic arch is present in the embryo meaning the blood flow bypasses the pulmonary circulation. The blood can flow from the right atrium to the left atrium without going via the pulmonary circuit. &lt;br /&gt;
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2. Ductus venosus: a shunt that exists between the left umbilical vein and the inferior vena cava. It mean the oxygenated blood from the placenta bypasses the liver on the way to the embryo&lt;br /&gt;
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3.Ductus arteriosus: a shunt that exists between the proximal descending aorta and the pulmonary artery. This is important in allowing the blood to run from the right ventricle to the aorta without entering the prenatal fluid-filled lungs.&lt;br /&gt;
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&amp;lt;pubmed&amp;gt;21513818&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assignment 5==&lt;br /&gt;
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===Congenital Pulmonary Airway Malformation===&lt;br /&gt;
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Congenital Pulmonary Airway Malformation (CPAM) is an abnormality that comes as a result of abnormal respiratory system development from week 4 to 10 of gestation. There are varying classes of CPAM depending on the level of differentiation of alveoli, the functional unit of the respiratory system, and the location of the abnormality. Although not completely understood, it is believed that this abnormality arises from unusual lung budding of the foregut endoderm during week 4 to 5 of development.&amp;lt;ref name=&amp;quot;PMID10.3109/15513815.2010.547556&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.3109/15513815.2010.547556&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Depending on the malformation observed, the embryological timing can help explain the deformity. Type I CAMP is where there is a localised cystic lesion in a lobe of the lung with pseudostratified ciliated columnar epithelium and relatively well differentiated alveolar cells. &amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; This suggests the malformation occurred during week 7 to 10 which is when bronchial cartilage and smooth muscle form in the fetus. &lt;br /&gt;
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Congenital Pulmonary Airway Malformations usually involve cystic changes in terminal bronchioles of the lung and are usually accompanied by recurrent pulmonary infections, lung abscesses and intra and extra lobar sequestration. They are usually recognised in the neonate within the first 2 years of life however they can also lie unobserved until later in life. CPAM in an adult can cause massive hemoptysis (coughing up blood) and respiratory distress but rarely causes symptoms like fever, headache, weight loss or chest pain that are typical of other respiratory disorders like pneumonia. If the malformation is isolated to a small part of a lobe, it can be removed surgically but type III CPAM has poor prognosis as it usually involves large lesions that are dispersed throughout the majority of a lobe of the lung.&amp;lt;ref name=&amp;quot;PMID24672262&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;24672262&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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Another theory on the cause of Congenital Pulmonary Airway Malforamtion is arrested development of the bronchial tree during week 6 to 7 of lung development. Furthermore it has been found that the thyroid transcription factor 1 (TTF1) plays a role in lung epithelium differentiation and lung development. It is found only in the lung, thyroid and in some parts of the brain so mutation or deletion to the gene coding for TTF1 could contribute to malformation of lung epithelium resulting in CPAM. &amp;lt;ref name=&amp;quot;PMID10.4187/respcare.00727&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.4187/respcare.00727&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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==Online Assignment 6==&lt;br /&gt;
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I have found a paper written in 2009 by a group of researchers from the University of California who have investigated the role of DNA methyltransferase 1 (Dnmt1) in pancreas development. Their paper Loss of Dnmt1 catalytic activity reveals multiple roles for DNA methylation during pancreas development and regeneration looks at the role of Dnmt1 in the development of the endodermal originating endocrine, duct and acinar cells of the pancreas. It uses a deductive method involving acquired Dnmt1 mutant zebra fish and looking at which pancreatic cells have inhibited, improved or unchanged growth and development. &lt;br /&gt;
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This paper is useful in consolidating our understanding of the control of various endodermal cells involved in pancreas growth and function. Dnmt1 is an enzyme that controls gene regulation and helps maintain chromosomal integrity. This paper found that in the early stages of pancreas development, Dnmt1 is a critical part of acinar cell development but not for beta cells or pancreatic duct cells. Their investigation using Zebrafish as a model showed that without this enzyme, the pancreas formed and then degenerated 84h post fertilization (hpf). With further investigation, they found that by 100hpf, almost all the acinar cells had undergone apoptosis but the endocrine and pancreatic duct cells still maintained integrity and remained functional.&lt;br /&gt;
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Although this paper uses zebrafish rather than humans to investigate pancreas development, it still reveals a relative timescale of the organ development. It also highlights the complex nature of endocrine organ development and how many enzymes are involved in assuring correct growth takes place. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2009.07.017&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2009.07.017&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt;&lt;br /&gt;
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&amp;lt;sup&amp;gt;'''Embryonic layers and tissues contributing to developing teeth:'''&amp;lt;/sup&amp;gt;&lt;br /&gt;
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* Ectoderm contributes to tooth enamel epithelium&lt;br /&gt;
* Neural crest derived mesenchyme contributes to dentin and pulp of the teeth&lt;br /&gt;
* The teeth develop around the stomodeum which is the origin of the oral cavity&lt;br /&gt;
* Some argument around vertebrates that have pharyngeal teeth, suggesting there is a pharumgeal endodermal origin involved as well, however it isn’t as thoroughly understood. &lt;br /&gt;
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&amp;lt;pubmed&amp;gt;10.1038/nature07304&amp;lt;/pubmed&amp;gt;&lt;br /&gt;
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==Online Assessment 7==&lt;br /&gt;
'''Embryonic Development of the Human Ovary'''&lt;br /&gt;
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Human gonad development begins around week 5 of embryological growth and the sex of the fetus depends on the X or Y chromosomal contribution from the male and female gametes at fertilization. Until around week 10, the human gonads are considered to be bipotential meaning they have the ability to differentiate into male testes or female ovaries. &amp;lt;ref name=&amp;quot;PMID10.1038/nrendo.2014.163&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1038/nrendo.2014.163&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; Gonad development is often referred to as urogenital development since it is closely related to the urinary system growth. Around week 4 the primordial germ cells are established at the site of umbilical vesicle near the origin of the allantois. In week 5 there is a thickening of the mesothelium on the medial side of the mesonephros which is the primitive kidney. &lt;br /&gt;
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During embryonic folding, the dorsal part of the umbilicus is incorporated into the embryo and by week 5, there is migration of the germ cells to the genital ridge. By week 6, there is proliferation of the epithelium and mesenchyme at the genital ridge that results in finger-like projections of epithelium forming genital cords producing an external cortex and internal medulla. The primordial germ cells migrate into the mesenchyme of the genital cords and this is controlled by various genes like stella and fragilis. In addition to the genital folds, by week 6 there are two types of genital ducts: mesonephric and paramesonephric. The mesonephric contributes to male gonad development whereas the paramesonephric contributes to female gonad development.&lt;br /&gt;
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The paramesonephric duct is also known as the Mullarian duct and in men there is an anti-mullarian gene that when switched on is responsible for the degradation of this duct. The Mullarian duct is a result of the invagination of the coelomic epithelium through the mesonephros. &amp;lt;ref name=&amp;quot;PMID10.1016/j.ydbio.2007.03.027&amp;quot;&amp;gt;&amp;lt;pubmed&amp;gt;10.1016/j.ydbio.2007.03.027&amp;lt;/pubmed&amp;gt;&amp;lt;/ref&amp;gt; The cranial end of the duct opens to the peritoneal cavity whereas the caudal end runs parallel and lateral to the Wolfian tube until it crosses over ventrally and fuse to form a y shaped uterovaginal primordium, the eventual uterus and vagina.  An XX genotype results in a female embryo and this is because testosterone is not produced, resulting in lack of maintencance of the mesonephric duct, no expression of anti-mullarian hormone hence maintenance of the paramesonephric duct. From week 10 onwards there is further gonad and external genital growth forming the ovaries, uterus and vagina.&lt;br /&gt;
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'''Historic Image of Human Urogenital Development''' &lt;br /&gt;
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Fig. 1109. Urogenital Sinus of Female Human Embryo of 8.5 to 9  weeks old&lt;br /&gt;
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[[File:Gray1109.jpg]]&lt;br /&gt;
(From model by Keibel)&lt;br /&gt;
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The Müllerian Ducts (Paramesonephric Ducts)&lt;br /&gt;
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|-&lt;br /&gt;
| [[File:The Developing Human, 8th edn.jpg|80px]]&lt;br /&gt;
| Moore, K.L. &amp;amp;amp; Persuad, T.V.N. (2008). &amp;lt;i&amp;gt;The Developing Human: clinically oriented embryology&amp;lt;/i&amp;gt; (8&amp;lt;sup&amp;gt;th&amp;lt;/sup&amp;gt; ed.). Philadelphia: Saunders.&lt;br /&gt;
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The following chapter links only work with a UNSW connection and can also be accessed through this  [http://searchfirst.library.unsw.edu.au/primo_library/libweb/action/search.do?vid=UNSW&amp;amp;amp;fn=search&amp;amp;amp;vl(freeText0)=UNSW_SFX14190000000048007 UNSW Library connection].&lt;br /&gt;
* [http://www.mdconsult.com/books/linkTo?type=bookPage&amp;amp;amp;isbn=978-1-4160-3706-4&amp;amp;amp;eid=4-u1.0-B978-1-4160-3706-4..50015-3 Chapter 12 - The Urogenital System]&lt;br /&gt;
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{{Historic Disclaimer}}&lt;br /&gt;
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The image is from the book Grays Anatomy from 1918 which can be accessed by the following link:&lt;br /&gt;
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:'''Links:''' [[Uterus Development]] | [[Anatomy_of_the_Human_Body_by_Henry_Gray#1108_Urogenital|Gray's Urogenital Images]]&lt;/div&gt;</summary>
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