User:Z3422484: Difference between revisions
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lab 7 --[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]]) 11:04, 17 September 2014 (EST) | lab 7 --[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]]) 11:04, 17 September 2014 (EST) | ||
lab 8 (Apologises, forgot to sign to this lab but still attended) --[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]]) 11:01, 8 October 2014 (EST) | |||
Lab 9 --[[User:Z3422484|Z3422484]] ([[User talk:Z3422484|talk]]) 11:01, 8 October 2014 (EST) | |||
http://www.ncbi.nlm.nih.gov/pubmed | http://www.ncbi.nlm.nih.gov/pubmed | ||
Revision as of 10:01, 8 October 2014
Welcome to the 2014 Embryology Course!
- Links: Timetable | How to work online | One page Wiki Reference Card | Moodle
- Each week the individual assessment questions will be displayed in the practical class pages and also added here.
- Copy the assessment items to your own page and provide your answer.
- Note - Some guest assessments may require completion of a worksheet that will be handed in in class with your student name and ID.
Individual Lab Assessment |
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Lab 12 - Stem Cell Presentation Assessment | More Info | |
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Group | Comment | Mark (10) |
1/8 |
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7 |
2 |
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7.5 |
3 |
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7.5 |
4 |
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8.5 |
5 |
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8.5 |
6 |
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8.5 |
7 |
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7.5 |
LAB ATTENDANCE
lab 1 --Z3422484 (talk) 12:51, 6 August 2014 (EST)
lab 2--Z3422484 (talk) 12:42, 13 August 2014
lab 3 --Z3422484 (talk) 11:11, 20 August 2014 (EST)
lab 4 --Z3422484 (talk) 11:18, 27 August 2014 (EST)
lab 5 --Z3422484 (talk) 11:21, 3 September 2014 (EST)
lab 6 --Z3422484 (talk) 10:57, 10 September 2014 (EST)
lab 7 --Z3422484 (talk) 11:04, 17 September 2014 (EST)
lab 8 (Apologises, forgot to sign to this lab but still attended) --Z3422484 (talk) 11:01, 8 October 2014 (EST)
Lab 9 --Z3422484 (talk) 11:01, 8 October 2014 (EST) http://www.ncbi.nlm.nih.gov/pubmed
<pubmed>25084016</pubmed>
Lab 1 Assessment
<pubmed>25100708</pubmed>
The article above investigates in detail, the acrosome reaction occurring within spermatozoa and whether other roles are involved with [Ca2+]i. This was facilitated by using FM4-64, Fluo-4 AM (fluorescent dye) and Sytox green (represent whether cell death has occurred) as well as progesterone, Ham's F-10 media, FITC-PSA and ionomycin. The three major steps undertaken in the experiment (method) involve the preparation of the human sperm samples, viewing of spermatozoa samples and the use of the scanning electron microscope. The preparation of the sperm samples involved culturing sperm in a Ham’s F-10 medium in an incubator at room temperature and then placed into medium allowing capacitation to occur. Spermatozoa were then suspended in various reagents including the FM4-64 DYE, incubated then viewed under an inverted microscope. The spermatozoa (given progesterone) were then viewed under a scanning electron microscope.
The study found that applying ionomycin with the FM4-64 dye led to a more accurate image forming on the acrosomal region of spermatozoa due to an increase in fluorescence. With this in mind, distribution changes occurred when AR inducers (ionomycin and progesterone) were applied. The acrosomal reaction is heavily dependent on extracellular Ca2+. The staining revealed the formation of tube-like structures on the spermatozoa head. These structures were unique in that developed while capacitation was underway. Also, it was found that progesterone did not affect spontaneous Ca2+ oscillation and therefore no correlation was found.
<pubmed>25031361</pubmed>
The aim of the experiment was to identify and discuss how nuerotensin affects the functioning of sperm. The above article utilised an epididymis removed from mice and placed in a human tubal fluid medium containing various reagents. Cumulus oocyte complexes were then isolated from antral follicles and then applied with IVM. NTR1 and NTR2 were then analysed using immunofluorescence in spermatozoa. The oviduct and uterus dissected from four to five mice was then immersed in Bouin’s fixing solution and then viewed under a fluorescence microscope. RT-PCR was then used to analyse cumulus tissues and female reproductive tissue as well as the monitoring of neurotensin levels in samples.
It was found that tyrosine phosphorylation was not enhanced when neurotensin was present. However, NT did speed up the rate at which the acrosome reaction occurred. Furthermore, when expression levels were monitored in female reproductive tissues and cumulus cells, the ampulla displaced a significantly higher expression level compared to the isthmus or uterus. Lastly, when cumulus oocyte complexes in the presence of FSH or EGF, neurotensin released from cumulus was affected greatly (significant increase).
--Mark Hill These are good summaries of the 2 research articles. (5/5)
Where are your submissions for Lab 2 and 3 assessments?
Lab 4 Assessment
Part 1
<pubmed>19156219</pubmed>
The article above looks at whether regulatory T lymphocytes cultured with human cord blood stem cells prevents the occurrence of type 1 diabetes in non-obese mice. Diabetes mellitus type 1 is caused by the immune system attacking and destroying beta cells distributed within the islets of Langerhans. Beta cells are imperative for survival as they responsible for producing the peptide hormone insulin, responsible for lowering blood glucose levels. Therefore, the destruction of these insulin producing beta cells by auto-reactive effector T cells is a major issue. It has been noted that Tregs (Regulatory T cells) display an essential role by having an inhibitory effect on auto-reactive effector T cells. Defects or abnormalities in Tregs accelerates the occurrence of type 1 diabetes.
The findings show that by applying purified autologous CD4(+)CD62L(+)co-cultured with human blood stem cells boots the regeneration of beta cells and an increase in beta-cell mass and hence an increase in insulin production and restoring the framework of pancreatic islets. Furthermore a decrease in islet inflammation, re-establishment of blood cytokine balance (Th1/Th2) and inhibiting leukocyte triggered apoptosis in pancreatic islets. The implications of these findings provide as possible strategy in treating type 1 Diabetes in regenerative medicine.
Part 2
Ductus Arteriosus - shunts pulmonary artery to aorta above heart
Ductus venosus - shunts left umbilical vein to inferior vena cava near the liver
Foramen ovale - located in atrial septum, allowing blood from right atrium to enter left atrium
Lab 5 Assessment
Alveolar Capillary Dysplasia
Alveolar capillary dysplasia is a developmental condition occurring in newborns involving improper positioning of pulmonary veins and unsuccessful formation alveolar capillaries where there is no contact to the alveolar mucosa as well as increased thickness of the alveolar wall as well as reduced distribution of these capillaries. Associated with this is also pulmonary hypertension leading to respiratory distress and can eventually be fatal for newborns as well as lead to other congenital abnormalities.
It has been strongly noted that a genetic abnormality is major contributing factor to the cause of alveolar capillary dysplasia. This involves mutations such as micro- deletions in a specific gene referred to as the FOX1 gene. The FOX1 gene is important in lung development and its vasculature as well as gastrointestinal tract development. The FOX1 gene produces a transcription factor responsible in regulation activity of other genes by binding to specific regions of DNA. A mutation in the FOX1 gene leads to an inactivated protein leading to lung blood vessel abnormalities. Furthermore deletion in genes along the region of 16q24.1 of chromosome 16 can further lead to the progression of this disease.
--Mark Hill (talk) 11:27, 26 August 2014 (EST) This image should also be on your student page.
File:Trophoblast_and_villous_epithelium_of_the_placenta.png
Lab 6 Assessment
Part 1
<pubmed>23274887</pubmed>
The article looks at whether the occurrence of beta-cell dysfunction is in relation to the peroxisome proliferator-activated receptor-y coactivator-1a or PGC-1a. PGC-1a, co-regulates the activity of glucocorticoids binding onto the GC receptor. It was found that PGC-1a overexpression affected glucose tolerance and glucose stimulated insulin secretion (GSIS). Furthermore, impairment in B-cell gene expression reduced B-cell mass and insulin composition in the pancreas as well as Langerhans cell islets and islet mitotic growth (hypertrophy). A unique finding demonstrated in the article is that PGC-1a overexpression in the adult stage does not affect glucose tolerance and GSIS but only in the fetal stage. Furthermore, neurod1; which has a regulatory effect on insulin gene expression is reduced by PGC-1a overexpression. This transcription factor when leads to the above exhibited effects on GSIS and pancreatic islet number and growth.