User:Z3333429

From Embryology

Lab Attendance

Lab 1: --Z3333429 (talk) 12:52, 6 August 2014 (EST)

http://www.ncbi.nlm.nih.gov/pubmed

PubMed

Lab 2: --Z3333429 (talk) 11:03, 13 August 2014 (EST)

Lab 3: --Z3333429 (talk) 11:12, 20 August 2014 (EST)

Lab 4: --Z3333429 (talk) 11:09, 27 August 2014 (EST)

Lab 5: --Z3333429 (talk) 11:32, 3 September 2014 (EST)

Lab 6: --Z3333429 (talk) 11:26, 10 September 2014 (EST)


Online Lab Assessments

Lab 1 Assessment

Article 1

Effect of vitamin D status on clinical pregnancy rates following in vitro fertilization[1]

Summary

Research was carried out to investigate the possible effect of vitamin D on human reproduction. The goal was to detect whether vitamin D levels Recent studies suggest that vitamin D may play a role in human reproduction. Our goal was to investigate whether there is a correlation between vitamin D levels and implantation and clinical pregnancy rates in infertile women following IVF.

Method
  • Participants in this investigation were 173 women undergoing IVF at Mount Sinai Hospital, Toronto, Ontatrio.
  • Serum 25(OH)D samples were collected within a week of oocyte retrieval from the patients.
  • The vitamin D levels of the participants were measured according to serum 25-hydroxy-vitamin D (25[OH]D) levels
  • Patients were classified in two categories according to serum levels of 25(OH)D: sufficient (≥ 75 nmol/L) or insufficient (< 75 nmol/L). Of the 173 patients, 54.9% presented with insufficient 25(OH)D levels and 45.1% has sufficient levels.
  • A comparison was made between patient demographics and IVF cycle parameters between sufficient and insufficient groups.
  • Clinical pregnancy, as identified by ultrasound following 4-5 weeks after embryo transfer; was the primary outcome measurement.
Findings

The research found that women who presented with sufficient 25(OH)D levels had significantly higher rates of clinical pregnancy per IVF cycle (52.5%) as compared to women with insufficient levels (34.7%). A higher rate of implantation was detected in the sufficient 25(OH)D group, however the results were not statistically significant. The research calls for further investigation the findings showed that vitamin D levels might be a predictor of clinical pregnancy and vitamin D supplementation could provide a simple and economical method of improving clinical pregnancy rates, not only in women undergoing IVF, but also across the board.

Reference

<pubmed>25077107</pubmed> Alcohol consumption and quality of embryos obtained in programmes of in vitro fertilization

Article 2

Alcohol consumption and quality of embryos obtained in programmes of in vitro fertilization[2]

Summary

Alcohol consumption has been identified as one of the main stimulants that negatively affect the reproductive systems of both sexes. An investigation was carried out to analyse the effect of alcohol consumption of female participants on the quality of embryos obtained through IVF programmes.

Method
  • The study covered 54 women who received treatment due to infertility.
  • Of the 54 women who participated, 42.59% consumed alcohol. Records were examined of the class of embryos (A, B and C) that each woman presented in during treatment.
  • The database and statistical analyses were performed using computer software STATISTICA 7.1.
Findings

A statistically significant correlation was found between the occurrences of class B embryo in patients who consumed more than 25 grams of ethyl alcohol daily (72.72%). Women who consumed alcohol sporadically or those who abstained entirely from alcohol presented with 44.44% and 30% rates of class B embryos respectively. It was concluded that alcohol consumption (over 25 grams of ethyl alcohol) increases the likelihood of developing pooper quality embryos. More research should be carried out to investigate this further and it was suggested that active campaigns should be established to inform women of the negative affects of alcohol consumption on embryonic development.

Reference

<pubmed>24959808</pubmed> Effect of vitamin D status on clinical pregnancy rates following in vitro fertilization


References

  1. <pubmed>25077107</pubmed>
  2. <pubmed>24959808</pubmed>


--Mark Hill These are good articles and well written summaries (5/5).

Lab 2 Assessment

[[File:RatLungGADGABA.jpeg|framed|center|800x432px|Microscopic Field Image of GAD and GABA in Fetal Rat Lung Tissue. Location of glutamic acid decarboxylase (GAD) and γ-aminobutyric acid (GABA) in fetal lungs of rats: Detection of antigens was used to identify the location of GAD and GABA on fetal lung tissue sections.[1]

Reference

  1. <pubmed>21152393</pubmed>

--Mark Hill This image and associated information meet the assessment criteria. I have fixed a few formatting issues with the figure referencing information. See the file history for changes. (4/5)

Lab 3 Assessment

<pubmed>22151899</pubmed> <pubmed>22214468</pubmed> <pubmed>12547712</pubmed>

Congenital Diaphragmatic Hernia

Laryngo-tracheo-oesophageal clefts



--Mark Hill These are all good references, I would have also liked some explanation as to why they were relevant. (4/5)

Lab 4 Assessment

Cord Stem Cell Therapeutics

Human umbilical cord blood-derived mesenchymal stem cell transplantation for the treatment of spinal cord injury[1]

Summary

The aim of this study was to find investigate if the transplantation of Human Umbilical Cord Blood Mesenchymal Stem Cells (HUCB-MSC’s) can offer an effective therapeutic treatment of Spinal Cord Injuries (SCI) and provide evidence for clinical applications. Recent studies have shown that there are possible treatments for SCI. These studies have shown that changing the local environment following after SCI (through transplantation of umbilical cord blood stem cells and other various cells and tissues) can aid in regenerating injured nerve axons and lead to functional restoration of SCI. In this study, HUCB-MSC’s were transplanted into rat models for the treatment of SCI and the therapeutic effects were evaluated through the observed behaviour and histological changes shown in the rats.

Method
  1. HUCB was retrieved from consenting donors from the Departments of Gynaecology and Obstetrics at the First and Third Affiliated Hospitals of Zhengzhou University and Zhengzhou People’s Hospital (Zhengzhou, China). The HUCB samples were screened against the hepatitis B virus.
  2. 46 adult female Wistar rats were used from the Experimental Animal Center of Henan (Zhengzhou, China). The rats were kept in a pathogen-free room at 25°C and humidity of 45% humidity and were 250-280g in weight.
  3. The Allen’s method (laminectomy of the spinous process and vertebral plates of T8-T10, exposing the dorsum of the spinal cord) was used to create the SCI rat models. After the exposing of the spinal cord at T-8-T10 a weight was dropped to simulate SCI and then the rats were separated into three groups: the injury group (received no treatment following injury), the control group (treated with saline) and the transplantation group (treated with HUCB-MSC suspension).
  4. The HUCB cells were isolated and screen for viability then cultured.
  5. The cultured HUCB-MSC’s were collected and diluted then the suspension was injected at the SCI site of the rat models. The same procedure was carried out on the control group using physiological saline.
  6. Following transplantation, locomotor ratings were obtained from the control and transplant groups at two and four weeks. Histological changes were observed via samples collected at week one and four. These samples were then underwent statistical analysis.
Findings

Following treatment, the transplantation group displayed recovery of spinal nerve function and immunohistochemistry identified that there was production of novel nerve cells at wee four. These findings suggest that transplanting HUCB-MSCs help the functional recovery of the damaged of spinal cord nerves in rats with SCI.

Reference

  1. <pubmed>24940417</pubmed>

Vascular Shunts

Foramen Ovale: located in the interatrial septum of the heart, allows blood to travel from the right atrium to the left atrium. Becomes fossa ovalis postnatally.

Ductus Venosus: located within the liver, becomes ligamentum venosum postnatally and allows blood from the umbilical vein to bypasses the liver and enter directly into the IVC.

Ductus Arteriosus: located within the aortich arch, allows blood to pass from the pulmonary artery into the descending aorta allowing blood from the right ventricle to bypass the non-functional lungs of the fetus. Postnatally it becomes the ligamentum arteriosum.


Lab 5 Assessment

Newborn Respiratory Distress Syndrome (Hyaline Membrane Disease)

Newborn Respiratory Distress Syndrome (NRDS), also known as Hyaline Membrane Disease is characterised by the lack of or inability to synthesise surfactant in the premature lung of neonates.

The incidence of NRDS occurs in babies suffering form immature lung development, usually from premature birth with increased severity and incidence in correlation to decreased gestational age [1]. Preterm births do not allow for full lung maturation of the preterm infant due to process in which the respiratory system forms (from upper respiratory tree to lower). Type II Pneumocytes secrete surfactant into the alveoli, reducing surface tension and thus preventing the collapse of the alveolus – they are the last respiratory cells to differentiate. Preterm infants usually lack Type II Pneumocytes in their lung tissue causing the instability of their alveoli, oedema from immature alveolar capillaries and hyaline membrane formation[2].

NRDS mostly occurs in preterm neonates but can occur in post-term and term babies for a variety of reasons including:[3]

  • Intrauterine Asphyxia – commonly caused by wrapping umbilical cord around the neck of the neonate, impairing development[1]
  • Maternal diabetes – high levels of insulin can delay surfactant synthesis[4]
  • Multiple pregnancy (twins, triplets etc) – associated with high rates of preterm births and resulting lung immaturity [4]
  • Rapid labour, fetal distress, placenta previa, preeclampsia, placental abruption – that impair lung maturation in final stages of pregnancy [4]
  • Preterm Caesarean delivery – not allowing for lung maturation[5]
  • Genetic abnormalities that impair surfactant synthesis (ABCA3)[6]
  • Meconium Aspiration Syndrome (MAS) - damage to lower respiratory epithelium after aspiration of Meconium in amniotic fluid [7]

References

  1. 1.0 1.1 <pubmed>20468585</pubmed>
  2. <pubmed>6071188</pubmed>
  3. <pubmed>10829971</pubmed>
  4. 4.0 4.1 4.2 <pubmed>20848797</pubmed> Cite error: Invalid <ref> tag; name 'PMID20848797' defined multiple times with different content Cite error: Invalid <ref> tag; name 'PMID20848797' defined multiple times with different content
  5. <pubmed>14629318</pubmed>
  6. <pubmed>15044640</pubmed>
  7. <pubmed>10612363</pubmed>


Lab 7 Assessment

Endocrine Development

The signalling of Gonadotropin-releasing hormone (GnRH) is responsible for regulating the actions of the gonads. The experiments in this study show that luteinising hormone expressing gonadotropes express the GnRHR and that increases in the secretion of luteinising hormone encourages gonadotropes expressed through follicle-stimulating hormone to develop. A functional role of GnHRH was suggested because removal of GnRHR cells increased the number of GnRH neurons in the hypothalamus meaning that it played a role in defining the amount of GnRH neurons present.[1]


This study was carried out on mice models where GnRHR cells were ablated to reveal the functional role in the embryonic development of the reproductive axis. The study suggests that luteinising gonadotropes acts as target cells for GnRH neurons in the forebrain and that maturation of follicle-stimulating hormone gonadotropes is dependent on the increased secretion of luteinising hormone. The method in which gonadotropes in the anterior pituitary gland mature was revealed as GnRH neurons migrate to the forebrain in the first step, secreting GnRH at this point. This is followed by the expression of GnHRH by the luteinising hormone gonadotropes. [1]


Tooth Development

The following embryonic layers and tissues contribute to the development of the teeth: The ectoderm of the first pharyngeal arch and neural crest, and ectomesenchymal cells.


  1. Odontoblasts - mesenchymal cells derived from the neural crest responsible for the secretion of predentin which calcifies to form the dentin if the teeth.
  2. Ameloblasts - cells derived from the differentiation of pre-ameloblasts from inner enamel epithelium. Responsible for he production if enamel.

References

  1. 1.0 1.1 <pubmed>20805495</pubmed>

Lab 8 Assessment

Embryonic Development of Testes

The gonads are derived from three sources during embryonic development:

  • Mesothelium
  • Underlying mesenchyme
  • Primordial germ cells: undifferentiated germ cells

Week 3: During week 3, the primordial germ cells migrate towards the primitive streak.

Week 5: Proliferation of the mesothelium and underlying mesenchyme occurs during week 5 of development and the gonadal ridge begins to form as a bulge on the medial region of the mesonephros. At this stage of development the gonadal cords begin to grow into the underlying mesenchyme. The gonadal structure at this stage of development is sexually indifferent.

  • Testes will form in the development of an XY embryo.

Week 6: Further migration of the primordial germ cells to the junction of the hindgut and yolk sac and then onto the gonadal ridge occurs at week 6. The differentiation of the primordial germ cells then begins at gametogenesis. Supporting cells are differentiated into Sertoli cells via the presence of sex-determining region Y gene – a protein-coding gene of the Y chromosome. Sertoli cells:

  • Involved in the differentiation of the male gonad
  • Secrete anti-Mullerian hormones – involved in the differentiation of the internal genital organs, ducts and gonads.
  • Differentiate sex-hormone-secreting cells into Leydig cells - release testosterone.
Transverse section of pig testicle revealing seminiferous tubules (derived from testis cords) and rete testis (derived from mesonephric tubules)

The gonadal cords begin differentiate into seminiferous cords or testis cords and this is controlled by the Y chromosome via testis-determining factor (TDF).

Week 7: At week 7 the testes begin to develop. Mullerian duct inhibitory factor is responsible for the obliteration of the paramesonephric duct and the mesonephric duct (Wolffian duct) begins to differentiate when acted upon by testosterone produced by the Leydig cells.

In these final stages of embryonic development, the male gonads have differentiated into two main parts:

  • Mesonephric duct: differentiates into the epididymis with the portion of the mesonephric duct lying outside of the gonad becoming the ductus deferens. The rete teste are formed from the mesonephric tubules growing towards the medullary sex cords.
  • Testis cords: containing the Sertoli cells and germ cells. In fetal development this will further differentiate into the seminiferous tubules – the area responsible for the production of spermatozoa during puberty in males.