User:Z3292373
The Completer Finisher is a perfectionist and will often go the extra mile to make sure everything is "just right," and the things he or she delivers can be trusted to have been double-checked and then checked again. The Completer Finisher has a strong inward sense of the need for accuracy, and sets his or her own high standards rather than working on the encouragement of others. They may frustrate their teammates by worrying excessively about minor details and by refusing to delegate tasks that they do not trust anyone else to perform.
I had no idea that Oocytes and spermatozoa were not matured at the time of release, for no reason at all i assumed that it was bucket science and the two just needed mixing and "let them do their thing". Which is ridicules now that i think about it.
Laboratory Work
Lab 1
A summery of two recent research articles on fertility or fertilization.
Article One:Degradation of Paternal Mitochondria by Fertilization-Triggered Autophagy in C.elegans Embryos [1]
Miyuki Sato,Ken Sato
Using C.elegans as a model organism this paper investigates the possible mechanisms in which paternal mitochondria might be removed from the Oocyte after fertilisation. Initially mitochondria from the spermatozoa were track through embriogenisis via marking with MitoTracker red (MT) and Heat Shock Green Fluorescence Protein (HS-GFP). This initial tracking showed paternal mitochondria entering the cell at fertilisation and being randomly inherited by blastomeres through to the 4 cell stage then clearing by the 16 cell stage.
To establish a link between this pattern and autophagy, autophagisomes with GFP marked homologue of a protein in their membrane (LGG-1) were fertilised. These autophagisomes were built up around the pronuclear paternal DNA (C.eleigans spermatazoa have their mitochondria distributed around the head of the gamete and posses no tail) and then dispersed around the cytoplasm as the blastocyst developed. Like the paternal mitochondria the autophagisomes then cleared by the 16 cell stage as well as appearing sparadicaly in places related with regular development.
Further fertilisation with mutant sperm line spe-9, that cannot produce the proteins for normal fertilisation, did not produce the initial induction of autophagy. Whilst insertion of sperm line spe-11, that cannot fertilise but permit embryogenesis but show the same patterning of auto phagisomes around the paternal pronuclei. This suggested that induction of autophagy is based on the entry of paternal proteins. By arresting the Oocyte in metaphase 1 by emb-27(RNAi) it was also shown that the induction happens independent of progress into anaphase 1.
Confirmation of the role of autophagy in the removal of paternal mitochondria was done by the use of mutants with compromised autophagy regulators. Gamete mutants lgg-1(tm3489) that could not produce the autophagicyte membrane could proceed through fertilisation at a reduced capacity however could not progress past the L1 larval stage. In these matings the paternal mitochondria persisted past the 16 cell stage. In contrast if mutant Oocytes were mated with wild type spermatozoa then paternal mitochondria would be present until the Lima Bean stage and then cleared. Spermatozoa that contained the same lgg-1 mutation however had no change to the regular clearing of paternal mitochondria when mated with wildtype oocytes. This suggested that the maternal autophagocytes were the main contributors to paternal mitochondrial clearing. However paternal lgg-1 expression could, at a reduced capacity, compensate for compromised maternal autophagy.
Atricle Two: Developmental potential of zona pellucida–free oocytes obtained following mild in vitro fertilization [2]
Satoshi Ueno et al.
In this research, from a Japanese fertility clinic normal oocyte and zona free (ZF) oocytes where taken from the same patient in the same collection cycle. The ZF oocytes did not have an intrinsic absence but breakages of the zona palucida through which the oocyct was protruding. The oocyte was retrieved from the extrusion. These were then fertilised via intracytoplasmic sperm injection, cultured and followed through cleavage and blastocyst formation.
A comparison of the blastocyst formation from successfully fertilised ZF and normal oocytes showed no statistical difference in viability. The same was found of thoughs ZF derived blasticysts that were carried to full term.
--Mark Hill (talk) 10:28, 4 September 2015 (AEST) These are accurate suppers of these 2 papers (5/5)
Lab 2
Introduction to addition of images to website.
Cells of the innate and adaptive immune system present in the uterus at the time of implantation [3]| frontiers in Immunology
--Mark Hill (talk) 10:30, 4 September 2015 (AEST) Image uploaded with correct reference, copyright and student template. Please in future use a briefer image title for example, File:Cells of the innate and adaptive immune system present in the uterus at the time of implantation.jpg, could have been simply File:Cells of the innate and adaptive immune system at implantation.jpg. (5/5)
Lab 3
Brief description of 3 research articles on your subject.
Article 1:
PMID 25629662 Mitocondrial donation--how many women could benefit?[4]
This is a statistical analysis of the prevalence of women of child bearing age that have pathogenic mutation to their mitochondria that could benefit from mitochondrial donation in the UK. And the affects of the mitochondrial mutation on fertility as compared to background natural birth rate. They found no difference in fertility rates and 4% of women at risk of passing on symptomatic mitochondrial disease.
Article 2:
PMID 20393463 Pronuclear tranfer in human embryos to prevent transmition of mitochondrial DNA disease[5]
As the name suggest this paper looks at pronuclear transfer as way to remove donor mitochondria measured by mt-DNA. And it effectiveness in doing so. And the processes that occur in the oocyte when this method is used.
Article 3:
PMID 18674747 Pathogenic mitochondrial DNA mutations are common in the general population.[6] Another on the prevalence of mitochondrial mutations in the populous. This time via mtDNA sequencing from umbilical samples from live births, looking for ten specific mt-DNA mutations. It found a frequency rate of 0.54% for these mutations. Although they had limited data on the prevalence of these mutations maternally.
--Mark Hill (talk) 10:32, 4 September 2015 (AEST) These are relevant references to your group project. (5/5)
Lab 4
Three question quiz on Placenta Development
Take the Quiz
--Mark Hill (talk) 10:33, 4 September 2015 (AEST) Only 2 questions. I will come back later. ANAT2341 Student 2015 Quiz Questions
Quizzes
Medicine Practicals: Foundations Embryology - BGDA Fertilization to Implantation | Embryo | Fetal | Placenta - BGDB Gastrointestinal | Face and Ear | Sexual Differentiation
General Embryology: Ectoderm Quiz | Mesoderm Quiz | Early Heart Quiz | Placenta Quiz | Respiratory Quiz | Renal Quiz | Genital Quiz
Lab 5
Brief Overview of Hirschsprung's disease
Hirschsprung's disease (HSCR) also know as congenital aganglionic megacolon or intestinal aganglionosis is a disorder of the gastrointestinal tract characterised by a lack of neurons in the intestinal tract (IT). Most commonly affecting regions of the colon and more distal sections of the hindgut although can be prevalent from the stomach to the rectum. This causes the inability of the enteric nervous system (ENS) to control secretions and blood-flow in the affected area as well as maintain peristalsis leading to sustained contraction of the smooth muscle and hence obstruction and distension of the bowel [7]. Clinically this is displayed by the absence of a meconium stool in the first 48 hours after birth and confirmed by radiological examination with a barium enema [8]. Treatment requires removal of the defective region via surgery and has many possible complications [9].t
The ENS is derived from the Neural Crest. Vagal neural crest cells (NCC) contributing to the fore-,mid- and hind-gut[10], Sacral NCC's contributing to the distal hindgut[11]. Malformations of it's development such as HSCR are termed neurocristopathies. In the case of HSCR, most commonly it a restriction in the migration and proliferation of the neural crest cells in early development (weeks 4-7) impeding their colonisation of the gut. The cause of this impediment is varied. Around half of cases can be linked to the GDNF/RET (glial cell line derived neurotrophic factor/receptor tyrosine kinase)gene families that regulate to progression of the NCC cells through the mesoderm [12]. Mutations in any number of these genes can lead to delay or inability of the NCCs in their progress rostro-cordauly.
Another cuase comes from disruption of Endothelin pathways that although also control migration, maintain the enteric NCC progenitors cells in their proliferative state [13]. Mutations in this pathway have shown to stop differentiation of the NCC cells at the distal bowel [14], meaning although fully colonised the ENS cells have reduced excitatory fibres and abnormal neurotransmitter release.
Outside of genetic mutations retinal (vitamin A) deficiency has been link to HSCR [15]. Although vitamin A deficiency has been linked to numerous congenital defects of which HSCR is a small part. The complexity of systems that contribute the enteric nervous system mean that HSCR, although fairly understood as a disease, has many possible causes not yet linked.
Lab 6
Complete work on group project.
Lab 7
A brief description of the findings of a recent research paper on Odontogenisis.
Enamel hypomineralisation due to endocrine disruptors.
jedeon K et al.[16].
Endocrine disruptors and their possible health effects have been gaining a lot of traction in the media in the past decade. Most touted of these being the estrogen-like Bisphenol A (BPA) found in many plastic products. This study compared the affects of BPA and two other endocrine disruptors (EDs) genistein (G) and vinclozolin (V) on tooth development by use of mouse models and cell culture.
Their results showed that phenotypicaly rats exposed to BPA devolop the greatest degree of hypomineralisation, 75% of rats treated. Compared to lowest reading of 35% for though exposed to GV excluding the control group. Further more in HAT-7 rat ameloblast-like cell culture and analysis with RT-qPCR it was shown that BPA was up-regulating enamelin mRNA levels and down-regulating klk4 mRNA. The reson that mixtures of EDs were not as disruptive as BPA alone was discovered to be link to V which had a down-regulation effect on enamelin mRNA promoters only. It was suggested that there was most likely other target genes that the EDs affect that gave rise to there results.
Lab Attendance
--Z3292373 (talk) 13:45, 7 August 2015 (AEST)
--Z3292373 (talk) 13:31, 14 August 2015 (AEST)
--Z3292373 (talk) 13:43, 21 August 2015 (AEST)
--Z3292373 (talk) 13:36, 28 August 2015 (AEST)
--Z3292373 (talk) 13:20, 4 September 2015 (AEST)
--Z3292373 (talk) 12:08, 18 September 2015 (AEST)
--Z3292373 (talk) 14:00, 25 September 2015 (AEST)
--Z3292373 (talk) 12:55, 9 October 2015 (AEDT)
Notes
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References
- ↑ <pubmed>21998252</pubmed>
- ↑ <pubmed>25256934</pubmed>
- ↑ <pubmed>26136750</pubmed>
- ↑ <pubmed> 25629662 </pubmed>
- ↑ <pubmed> 20393463 </pubmed>
- ↑ <pubmed> 18674747 </pubmed>
- ↑ <pubmed>17514199</pubmed>
- ↑ <pubmed>6691093</pubmed>
- ↑ <pubmed>9722005</pubmed>
- ↑ <pubmed>8565847</pubmed>
- ↑ <pubmed>9753687</pubmed>
- ↑ <pubmed>12399307</pubmed>
- ↑ <pubmed>16624853</pubmed>
- ↑ <pubmed>16339294</pubmed>
- ↑ <pubmed>12702665</pubmed>
- ↑ <pubmed>25158179</pubmed>