Lab 4 Online Assessment
- The allantois, identified in the placental cord, is continuous with what anatomical structure?
- Identify the 3 vascular shunts, and their location, in the embryonic circulation.
- Identify the Group project sub-section that you will be researching. (Add to project page and your individual assessment page)
Laboratory Assessments and Attendance Records
Laboratory Assessment 1
--Z3289991 12:55, 28 July 2011 (EST)
Questions and Answers to Lab Assessment 1
1. Identify the origin of In Vitro Fertilization and the 2010 nobel prize winner associated with this technique.
1. In vitro fertilization originated from the American doctor John Rock’s extraction of an intact fertilized egg. Since IVF (In Vitro Fertilization) involves the artificial insemination of sperm and eggs outside of the body, John Rock’s method paved the way of IVF clinics coming into practice (Gladwell, 2000). The first pregnancy which began off as successful using IVF was reported in the Lancet medical journal by scientists from the Australian Monash University (IVF, 2011). Unfortunately, the pregnancy did not progress any further as the embryo failed to implant properly in the uterine wall. This occurred in 1973. Robert Edwards, who was the 2010 Nobel Prize winner (Committee, 2010), carried out the successful insemination of a sperm and egg outside of the body which led to the healthy birth of a newborn in 1978 (News, 2011). Embryos can now be successfully frozen and transferred from embryonic donors to acceptors.
2. Identify a recent paper on fertilisation and describe its key findings.
2. In 2010, a study was done into finding a therapy for allowing fertilization to occur even when there was sperm centrosomal dysfunction. Reproductive technologies will be invented in the coming years to analyse sperm centrosomal function and counter sperm centrosomal dysfunction. These reproductive technologies will be referred to as assisted reproductive technologies (ART). These technologies are necessary since the sperm centrosome was found to play an important role in the fertilization process after the intracytoplasmic sperm injections (ICSI). This all occurs within the cytoplasm of the oocyte. The answer was sourced from the single reference, (Yukihiro Terada, 2010), details of which can be found in the reference list.
3. Identify 2 congenital anomalies.
4. Two distinct congenital anomalies are amniotic band syndrome and atrial septal defect. Amniotic band syndrome is a limb anomaly which is caused by foetal parts such as limbs of the foetus being stuck in amniotic fibrous bands whilst the baby is in utero. Two main theories have been brought forward to explain how it is caused. The amniotic band theory suggests that there was partial rupture of the amniotic sac (Rapini, Bolognia, & Jorizzo, 2007). However, the chorion remains stable. Hence, fibrous bands of the ruptured ammonium float in fluid and entrap the limbs. The second theory suggests that there may have been vascular disruption to the foetus whilst in utero. Atrial septal defect is a congenital anomaly of the heart. It enables blood flow between the left and right atria via the inter arterial septum (Ira H Gessner, 2008). Thus, there is a mix of venous and arterial blood. This can be clinically significant, depending on how bad the defect is due to mixing oxygenated blood with deoxygenated blood.
Committee, N. P. (2010). The Nobel Prize in Physiology or Medicine 2010. Retrieved July 30, 2011, from Nobel Prize: http://nobelprize.org/nobel_prizes/medicine/laureates/2010/press.html
Gladwell, M. (2000, October 3rd ). John Rock's Error. The New Yorker . New York, New York, America.
Ira H Gessner, M. (2008). Ostium Secundum Atrial Septal Defects. Retrieved July 30, 2011, from Medscape Reference: http://emedicine.medscape.com/article/890991-overview
IVF, M. U. (2011). History of IVF. Retrieved July 30, 2011, from Monash IVF- Life Starts Here: http://www.monashivf.com/About_Monash_IVF/History_of_IVF.aspx
News, B. (2011). On This Day. Retrieved July 30, 2011, from BBC News: http://news.bbc.co.uk/onthisday/hi/dates/stories/july/25/newsid_2499000/2499411.stm
Rapini, R. P., Bolognia, J. L., & Jorizzo, J. L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby.
Yukihiro Terada, G. S. (2010). Essential Roles of the Sperm centrosome in human fertilization: Developing the therapy for fertilization failure due to sperm centrosomal dysfunction. Journal of Experimental Medicine , 247-258.
--Z3289991 09:02, 3 August 2011 (EST)
--Mark Hill 09:47, 3 August 2011 (EST) A very complete answer to all 3 questions, well done.
--z3289991 11:23, 4 August 2011 (EST)
Laboratory Assessment 2
Lab Assessment 2 Questions and Answers
1. Identify the ZP protein that spermatozoa binds and how is this changed (altered) after fertilisation.
1. ZP-3 (Zona pellucida sperm binding protein-3) is a protein which is coded for by the ZP3 gene. It is the receptor in the zona pellucida which binds with sperm at the beginning of fertilization. The protein encoded by this gene is a major structural component of the zona pellcida and functions in the primary binding and stimulation of the sperm acrosome reaction. Typically, the acrosome reaction will not occur until the sperm comes into contact with the jelly layer of the oocyte. After the jelly layer has been penetrated, the acrosomal enzymes will dissolve and the actin filaments will contact the zona pellucida. A signalling cascade will happen as the calcium influx occurred. ZP3 will not bind sperm to the membrane after this and it will now act to block polyspermy.
2. Identify a review and a research article related to your group topic. (Paste on both group discussion page with signature and on your own page)
2. See main group assessment page, group 3, as well as below:
Below is a review article:
It is entitled: Termination Rates After Prenatal Diagnosis of Down Syndrome, Spina Bifida, Anencephaly, and Turner and Klinefelter Syndromes: A Systematic Literature Review
The Research Article:
It is entitled: Prenatal and Postnatal Prevalence of Klinefelter Syndrome: A National Registry Study
Both articles explore more the epidemiology of klinefelter's syndrome as I felt that it would be interesting to look at its prevalence, and frequency of distribution within a population. The first review article that I hasve linked to explores the frequency of Klinefelter's syndrome in a population along with various other genetic anomalies.
--z3289991 06:22, 9 August 2011 (EST)
Laboratory Assessment 3
Date Stamp: --z3289991 11:07, 11 August 2011 (EST)
Questions and Answers for Lab Assessment 3
1. What is the maternal dietary requirement for late neural development?
1. Iodine is very important in preventing late stage neural tube defects. Many defects have arisen from neural tube defects in the past, such as Iniencephaly, which is where the head is bent quite severely towards the spine. Usually, the infant lacks a neck and doesn't survive for more than a few hours. Another neural tube defect that can arise is Hydranencephaly, whereby the cerebral hemispheres are missing and are full with sacs of cerebrospinal fluid (CSF). It prevents cretinism if taken properly.
2. Upload a picture relating to you group project. Add to both the Group discussion and your online assessment page. Image must be renamed appropriately, citation on "Summary" window with link to original paper and copyright information. As outlined in the Practical class tutorial.
Laboratory Assessment 4
Date Stamp:--Robert Klein 11:08, 18 August 2011 (EST)
Questions and Answers for Lab Assessment 4
1.The allantois, identified in the placental cord, is continuous with what anatomical structure?
1. 1. The allantois is continuous with the endoderm andr hindgut of the embryo.
2. Identify the 3 vascular shunts, and their location, in the embryonic circulation.
2. Three vascular shunts and their respective locations in the embryonic circulation are as follows: • Ductus venosus - Found between the umbilical view and the inferior vena cava of the heart • Ductus arteriosus - Found between the pulmonary artery and the descending aorta of the heart • Ductus arteriosus - Found between the pulmonary artery and the descending aorta of the heart
3. Identify the Group project sub-section that you will be researching. (Add to project page and your individual assessment page)
3. I will be researching Epidemiology, Similar defects and the Glossary of terms for Klinefelter's Syndrome.
Laboratory Assessment 5
Date and Time Stamp:--Robert Klein 11:17, 25 August 2011 (EST)
Questions and Answers for Lab Assessment 5
1. Which side (L/R) is most common for diaphragmatic hernia and why?
1. Around 90% of hernias of the diaphragm do occur on the left side, so it is the most common place for them to occur. This can be caused by uneven diaphragm closure during embryonic development, and the left side is supposed to close after the right side, therefore there is higher risk of herniation on the left side.
Dr Hill, I have completed my Project sections for the time being as you requested.Cheers --Robert Klein 06:06, 1 September 2011 (EST)
Laboratory Assessment 6
Lab Attendence:--Robert Klein 11:05, 1 September 2011 (EST)
Questions and Answers for Lab Assessment 6
1.What week of development do the palatal shelves fuse?
1. Week 9 is when the palatal shelves usually fuse. The fusion of the palatal shelves is also referred to as the fusion of the secondary palate.
2.What early animal model helped elucidate the neural crest origin and migration of neural crest cells?
2. The early animal model used was quail chick chimeras, which are essentially quail chicks made of genetically distinct groups of cells. These were used in the 1980s to investigate neural crest migration. These organisms are appropriate for the purpose, since there are differences in the nucleoli of chicks and quail, so it was easy to see the migration of the neural crest cells in the organisms.
3.What abnormality results from neural crest not migrating into the cardiac outflow tract?
3.This is known as a 'Tetralogy of Fallot', and this can result in truncation or the complete absence of the outflow tract.
Laboratory Assessment 7
Questions and Answers for Lab Assessment 7
1. Are satellite cells (a) necessary for muscle hypertrophy and (b) generally involved in hypertrophy?
1(a) satellite cells are really not all that necessary for muscle hypertrophy. Studies and our Embryo theory have shown that satellite cell-depleted muscles can still undergo hypertrophy. After a period of around 2 weeks, it showed the same increases in the muscle mass, in satellite cell positive muscle and satellite cell depleted muscle. 1(b) Satellite cells are very important for new fiber formation and regeneration. In normal muscle, satellite cells definitely contribute to the process of hypertrophy. .
2. Why does chronic low frequency stimulation cause a fast to slow fibre type shift?
2. This form of muscle shift has been linked with increases in the myoneuclear content and satellite cell activation in the muscle. Chronic low frequency stimulation causes changes in the oxygen and metabolite demands of the muscle fibres. The fast fibres tend to be glycolytic and thus do not have the appropriate capacity for oxygen metabolism. The outcome of this demand is changes in structure and type (example, from fast to slow) where the formed slow fibres are able to withstand this chronic activation. The fast to slow fibre type shift is carried out by the "neighbour rule" , for example, move from Type IIB (fast) to IIA to IIX to I (slow).
Trisomy 21 Page Judgement
Some areas were quite lacking in content, such as ‘Trisomy 21 Karotypes’. More detail needs to be included so that the audience is more informed. Most images have no copyright clearance statement this leaving UNSW Embryology open to legal issues. Something to consider. We are not told how Karyotype works and what it is clearly at all. Screening by country needs to have more than one country listed. Spain is only one country, not many. All the images on the page were not explained very clearly. An example of this is the Trisomy 21 graphs, which are poorly explained. It appears as if the project was rushed. All areas of the project need to be expanded upon. Otherwise, the students cannot grasp what they need to know about Down Syndrome. The section on Prevalence needs to have more than the two countries of Ireland and the USA listed. It needs to have at least 6 or 7 for a somewhat valid comparison. The section entitled meiosis 1 and 2 with aneuploidy did not link in with the rest of the project. Where was its relevance? The introduction needs more information. It is too fluffy and wordy. Wordiness is not equivalent to extra information. The research conducted needs to be explained more clearly and be linking in with the rest of the page. There is still a long way to go yet before the page is suitable for the site. As well, the glossary needs more terms. There are not enough of them at the moment.
Laboratory Assessment 8
LAB ATTENDENCE: --Robert Klein 11:06, 22 September 2011 (EST)
Questions and Answers for Lab 8
Group 1 Critique
- • The introduction is quite interesting. Clinical features of the disease, even if given as an example, should not be mentioned in the introduction
- • The graph comparing common malformations of Turner Syndrome in the epidemiology is quite good, however it should be explained a little more clearly. Also, where is the copyright information for the graph?
- • The aetiology has terms in it which are not properly explained e.g. random assortment. Give clearer explanations
- • Clinical manifestations are explained ok. Maybe put it in sentence form instead of listing it in bullet points
- • Diagnostic Procedures is labelled and explained ok. Maybe expand upon the techniques a little more instead of just summarizing them in a table
- • Treatment is ok. Could have a little more explanation though
- • Research and future research is good
- • Glossary is incomplete- random assortment, sister chromatids
Group 2 Critique
- • The introduction needs to be re-written in proper English. Some of the sentences don’t make proper sense. Also, the introduction should focus primarily on DiGeorge’s Syndrome and not explain what a congenital abnormality is
- • Historical background was good
- • Epidemiology should not explain clinical features, such as the baby making a noise which is nasally in tone
- • Aetiology is ok
- • Pathogenesis is quite detailed, however genes should be explained a little more clearly
- • Diagnostic tests section was impressive
- • Clinical manifestations was good
- • Treatment was good
- • Future research was good
- • Glossary was good
Images were appropriately used.
Group 4 Critique
- • Introduction was quite good
- • History was good. I liked the timeline
- • Tables in the epidemiology were good
- • The genetics was clearly explained
- • Pathogenesis was really good. I quite liked it
- • Clinical manifestations is good
- • Diagnostic tests could be more detailed
- • Overall, quite a well written project. Well done. Maybe add a little more about the medications.
Group 5 Critique
- • Introduction should not contain clinical manifestations. It should introduce the topic as a whole. This section needs to be re-written
- • The history section is ok. The timeline could be explained a little better to give a clearer view of what the history of the disease is to the reader
- • Epidemiology should not contain the advantages and disadvantages of population testing. This should be another section in itself
- • Aetiology was fine
- • Development of the disease was ok
- • Signs and Symptoms was good
- • Diagnosis needs to be more detailed than what it is
- • Treatment and recent research is impressive
- • Glossary needs more terms added to it. It is too short, however that will be fixed when you add more explanations to the other sections and define the terms here.
Group 6 Critique
- • Introduction is ok, however it needs to be structured a lot better than what it is
- • History is interesting
- • Epidemiology needs a lot more detail. A few lines is not good enough
- • Signs and Symptoms is ok
- • Genetics needs to be explained a lot more clearly than what it is
- • Abnormalities is ok
- • Diagnostic tests table is impressive
- • Treatment/management section is very good
- • Prognosis and future directions section is great
- • Glossary is incomplete. Check the first term and fix this
Group 7 Critique
- • Introduction is good
- • History is really good. I like how you explain your table and introduce it
- • Epidemiology is too short. More statistics need to be included
- • Aetiology is ok
- • Pathogenesis is complicated. Maybe explain what the genes are and their function
- • Pathophysiology has the same problems as pathogenesis
- • The remaining sections are done pretty well. I wouldn’t really change anything
- • Great use of images throughout the project
Group 8 Critique
- • Epidemiologic figures should not be included in the introduction. Also, neither should pathogenesis. Maybe just explain very simply what the condition is and explain the genes in the pathogenesis. The introduction should be organised a little better.
- • The history is rather short. You need to explain in a little more detail how the disease was discovered, and don’t mention pathogenesis or gene function.
- • The epidemiology is ok
- • Aetiology is fine. Good use of images to support your points
- • Pathogenesis should include the sentences on genes found in the introduction
- • Neuropathology is good, but you need to explain the image of the cross section of the spinal cord
- • Clinical presentation is quite good
- • Diagnosis is very good. Your tables in this section are excellent. Good use of images
- • Treatment and Current Research is very good.
- • Glossary is fine
Group 9 Critique
- • Introduction is ok. Maybe add a picture or two to make the introduction look a little bit more interesting
- • History is pretty good. Nice work on the timeline!
- • The table in the section on genetic factors is appropriate. Good job!
- • Diagnosis is good
- • Epidemiology should be after introduction, not diagnosis, but otherwise ok
- • The overall project is quite good, however diagnosis should be at the end and not one of the first sections
- • Also, is it necessary to put in information about support groups? Something to think about
- • Glossary is unfinished
- • The current research and developments section should have more information in it. Two lines of information is not enough detail
Group 10 Critique
- • The introduction was very good. Good use of images to give it a little decoration!
- • History is good
- • Epidemiology is good, however if possible try and make it longer/ include more information
- • The Genetics section is a bit too short. Add more information. Good hand drawn image!
- • Pathogenesis is a little short. Needs more information
- • Signs and Symptoms is good
- • Clinical manifestations is ok
- • Diagnosis, treatment and glossary are all well written. These sections should not require any change
Group 11 Critique
- • Introduction is far too short and more work needs to be done
- • History is also very short and more information needs to be added
- • The timeline is quite good
- • Diagnosis is alright
- • Syndromes and anomalies associated with cleft is detailed. Good job!
- • Development is good. Maybe use more images
- • The other sections are good, up until current research. More work needs to be done here as there is not enough information
- • Glossary is too short
- • Is the gallery really needed if you have images illustrating your text?
Laboratory Assessment 9
LAB ATTENDENCE: ROSH HASHANAH (Jewish New Year, so I wasn't at the lab. Dr. Hill already knows this
Questions and Answers for Lab Assessment 9
1. NO QUESTIONS POSTED
Laboratory Assessment 10
LAB ATTENDENCE:--Robert Klein 10:43, 6 October 2011 (EST)
Questions and Answers for lab Assessment 10
1. Besides fetal alcohol syndrome, identify another environmental teratogen that can lead to hearing loss.
1. Amphetamines have been thought to cause deafness in the foetus as the baby is drugged along with the mother when she takes these drugs. Hence, when the drug passes from the mother’s bloodstream to the baby’s, foetal development is interfered with.
2. Identify 3 factors that contribute to poor neonatal drainage of the middle ear.
2. Three factors which may cause poor neonatal drainage of the middle ear occur when:
- The auditory tube in the neonate lies on an angle which is 10 degrees more horizontal, and the auditory tube in the adult lies on a 45 degree angle so that the middle ear can be drained.
- The adult middle ear has two muscles known as the tensor palati and the levator palati which helps drain the middle ear. The neonate has only one muscle, the tensor palati and so drainage is not as efficient as in the adult.
- Auditory tube size does change considerably since the adult auditory tube is longer and wide, and the neonatal auditory tube is narrow and short.
3. Identify 1 genetic abnormality that affects hearing development and link to the OMIM record. (Your individual abnormality should be different from all other students)
3. Treacher Collins Syndrome is a genetic disorder that affects growth and development of the head. It prevents the skull, cheek and jawbones from closing and developing and thus hearing defects are caused. Below is a link:
Laboratory Assessment 11
LAB ATTENDENCE:Robert Klein z3289991 11:03am Thursday 13th October 2011
QUESTIONS AND ANSWERS FOR LAB ASSESSMENT 11
1. Name the components that give rise to the interatrial septum and the passages that connect the right and left atria.
1. The first stage of development is the formation of the septum primum, which is the initial dividing crescent shaped piece of tissue between the left and right atria. The septum primum doesn’t fully block the space between the left and right atria due to its crescent shape; and thus the opening that remains is called the ostium primum. As the septum primum develops, the ostium primum progressively narrows. Before the ostium primum is fully closed, a second opening known as the ostium secundum begins to form within the septum primum. On the right of the septum primum, the septum secundum begins to develop. This thick, muscular structure initially takes on the same crescent shape as the septum primum, however it originates anteriorly, as opposed to the septum primum which originates posteriorly. As the septum secundum grows, it forms a small opening called the foramen ovale. The foramen ovale is continuous with the ostium secundum. The ostium secundum slowly enlarges and the size of the septum primum gets much smaller. Eventually, the septum primum is a small flap that covers the foramen ovale on its left side. This flap of tissue is known as the valve of the foramen ovale. It opens and closes due to pressure gradients between the left and right atria.
2. Identify the cardiac defects that arise through abnormal development of the outflow tract.
2. The cardiac defects that arise from abnormal development of the outflow tract are Ventricular Septal Defect (Result from growth failure of the membranous IV septum or endocardial cushions leading to a lack of closure of the IV foramen), Atrial Septal Defect (derived from multiple sources making various places susceptible to defects), Aortic Stenosis (Stenosis is caused either by a muscular obstruction below the aortic valve), Double Outlet Right Ventricle (This defect is considered to be present if the aorta obtains 50% of its blood from the right ventricle) and Tricuspid Atresia (Complete lack of formation of the tricuspid valve which results in an hypoplastic right ventricle).
Laboratory Assessment 12
LAB ATTENDENCE:--Robert Klein 10:54, 20 October 2011 (EST)
Questions and Answers for lab Assessment 12
1. Give examples of 3 systems that continue to develop postnatally.
1. Three systems that continue to develop postnatally are the myelin sheaths of the neural portion of the auditory system, which continues to develop until around 18 months after birth, the human nervous system which continues to develop after birth and also the pulmonary arteries of the heart (cardiorespiratory system) continue to develop after birth.
2. Identify the abnormalities detected by the Guthrie Test and link to one abnormality listed in OMIM.
2. The Guthrie test was designed mainly to detect abnormalities such as inborn or genetic errors of amino acid metabolism such as Phenylketonuria. The tests can detect other abnormalities as well, such as cystic fibrosis and sickle cell disease in the UK version of the test, and congenital adrenal hyperplasia and Galactosaemia in the New Zealand version of the test. Please click on PHENYLKETONURIAfor more information (OMIM database).