Difference between revisions of "User:Z3288729"
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--[[User:Z3288729|Sarah Jenkins]] 11:31, 15 September 2011 (EST)
--[[User:Z3288729|Sarah Jenkins]] 11:31, 15 September 2011 (EST)
Revision as of 12:45, 22 September 2011
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)
--Z3288729 12:16, 28 July 2011 (EST)
--z3288729 11:12, 4 August 2011 (EST)
--Sarah Jenkins 11:10, 18 August 2011 (EST)
--Sarah Jenkins 11:11, 25 August 2011 (EST)
--Sarah Jenkins 12:28, 1 September 2011 (EST)
--Sarah Jenkins 11:31, 15 September 2011 (EST)
--Sarah Jenkins 11:45, 22 September 2011 (EST)
Identify the origin of In Vitro Fertilization and the 2010 nobel prize winner associated with this technique.
In vitro fertilisation began in 1978 when Edwards RG successfully carried out the process. He won the nobel prize for his work in 2010.
Identify a recent paper on fertilisation and describe its key findings.
Actin, more than just a housekeeping protein at the scene of fertilization.
This research project looked into the role of actin in fertilisation. It was found that it is an important molecule, significant in modulation of fertilisation. The rearrangement of the actin cytoskeleton of a fertilised egg plays a role in allowing only one sperm to enter the cell. 
Identify 2 congenital anomalies.
Ectrodactyly- a lack of one or more digits of the hand or foot
Spina Bifida- incomplete closing of the embryonic neural tube
Identify the ZP protein that spermatozoa binds and how is this changed (altered) after fertilization.
zona pellucida glycoprotein 3 (ZP3) acts as a sperm receptor. . ZP3 surrounds the oocyte, and the sperm binds to it as a way to enter the cell. Once a sperm has entered the oocyte, mechanisms to prevent polyspermy are put in place. The IP3 pathway is activated and in increase in intraceellular calcium results in alteration of ZP3 to prevent any more sperm entering the oocyte.
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)
What is the maternal dietary requirement for late neural development?
Upload a picture relating to you group project.
--Mark Hill 12:20, 16 August 2011 (EST) Good image and the information included is correct. I don't really like the image name as it does not indicate what the image is about. Looking at the original figure legend is also not as helpful, perhaps modified from the paper title "T-cell receptor diversity with thymus transplantation for DiGeorge anomaly" or along those lines.
The allantois, identified in the placental cord, is continuous with what anatomical structure?
The allantois is a membranous sac that is continuous with the splanchnic mesoderm and the embryonic gastrointestinal tract.
Identify the 3 vascular shunts, and their location, in the embryonic circulation
- Ductus arteriosus- It attaches the pumonary artery to the aortic arch so that blood bypasses the lungs.
- Ductus venosus - shunts half of the arterial blood flow from the umbilical cord so that it is able to bypass the liver
- Foramen ovale- shunts oxygenated blood from the right atrium to left atrium so bypass the ventricles.
Identify the group project subsection you will be researching
- Historical background
Which side (L/R) is most common for diaphragmatic hernia and why?
Diaphragmatic heriation occurs most commonly on the left side . Herniation occurs when there is abnormal closure of the pleuroperitoneal folds. These folds close to separate the lungs from the gut. The right side often closes first, and as such leaves it more likely for gastrointestinal structures to move up before the membrane is fused closed.
What week of development do the palatal shelves fuse?
What animal model helped elucidate the neural crest origin and migration of cells?
What abnormality results from neural crest not migrating into the cardiac outflow tract?
Tetralogy of Fallot
Are satellite cells (a) necessary for muscle hypertrophy and (b) generally involved in hypertrophy?
b) they contribute but are not 'necessary'
Why does chronic low frequency stimulation cause a fast to slow fibre type shift?
After chronic low-frequency stimulation, cellular destruction and regeneration are noticed. There is also evidence of satellite cell recruitment and differentiation from fast to slow fibre types. Long term stimulation creates cells of a lower calibre with an increase aerobic capacity so that they are more resistant to fatigue. they demonstrate a decrease in relaxation time. These changes are associated with changes in the calcium regulation proteins that control the process of excitation, contraction and relaxation. The fibre shift is a form of conditioning and protective so that the fibres are not damaged. They adapt to suit the conditions that they are exposed to.
Trisomy 21 assessment
- Although it is nice that the 'nondisjunction' definition is linked to a medical dictionary, it was confusing having to scroll down to find it. It would have been easier if the link was to a page that only had the nondisjunction definition on it.
- The introduction is very vague and does not indicate much as to what the project is about. It gives one historical reference, a definition that seems out of place and a few extra links to other genetic conditions. It would have been better to have a little more information on the actual condition rather than a definition, a few statistics and a date. Also, while the image does represent the cause of the problem, I believe it would be much more effective to have an image of a child with Trisomy 21 so that the reader is able to gauge the severity of the condition. Genetic details will (hopefully) be discussed later and this image will fit in later.
- "recent finsings" would be better placed at the end of the project. It is difficult to understand their significance without understanding the topic
- No historical findings are noted (other than the one date in the introduction). This should be elaborated on.
- In the kayrotypes section, there should be an image of the normal set of chromosomes so that the reader can see the difference between that and the trisomy karyotype
- It would also be interesting to note HOW trisomy 21 develops.
- The list of congenital abnormalities could be expanded on to say why they are associated with trisomy 21.
- The image in the congenital abnormalities section is not at all useful. Also, the list does not explain what the actual problems are and their significance.
- Human idiogram-chromosome 21.jpg is not referenced
- Heart defects need to be explained- what are they?
- Limb abnormalities = interesting with a useful image
- prevalence should be earlier in the project and Australia should be included in these statistics
- The Image of Down is out of place, it has no significance here and is halfway between two sections
- terms should be put in a glossary at the end (which is non existent)
- the Aneuploidy section could be removed, and these terms put into a glossary instead
- Meiosis I and Meiosis II is not a suitable heading as it does not actually explain how meiosis occurs. This information needs to be included and would be better at the top of the project
- Overall, most of the information is present, it just needs to be rearranged into the right order.
- Angelo DiGeorge. In the mid 1960's, Angelo DiGeorge noticed a similar combination of clinical features in some children. He named the syndrom after himself. The symptoms that he recognised were hypoparathyroidism, underdeveloped thymus, conotruncal heart defects and a cleft lip/palate. 
- Robert Shprintzen described patients with similar symptoms (cleft lip, heart defects, absent or underdeveloped thymus, hypocalcemia) and named the group of symptoms as velo-cardio-facial syndrome. 
- Lischner and Huff determined that there was a deficiency in T cells was present in 10-20% of the normal thymic tissue of DiGeorge syndrome patients (1975). 
- ‘’’Cleveland’’’ determined that a thymus transplant in patients of DiGeorge was able to restore immunlogical function (1975). 
- Finley and others identified that the cardiac failure of infants suffering from DiGeorge could be related to abnormal development of structures derived from the pouches of the 3rd and 4th pouches in the pharangeal arches. 
- 1980s technology develops to identify that these patients have part of a chromosome missing. 
- '’’De La Chapelle’’’ suspects that a chromosome deletion in 22q11 is responsible for diGeorge syndrome (1981) 
- ’’'Ammann'’’ suspects that DiGeorge symdrome may be caused by alcoholism in the mother during pregnancy. There appears to be abnormalities between the two conditions such as facial features, cardiovascular, immune and neural symptoms (1982). 
- http://www.ncbi.nlm.nih.gov/pubmed/21786196 Actin, more than just a housekeeping protein at the scene of fertilization