User:Z3292373

From Embryology
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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.jpg


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

1 Which of these is NOT a part of Tertiary Chorionic Villi formation?

Mesenchyme differentiating into blood vessels and cells.
Fusing with placental vessels.
Extra-embryonic mesoderm grows into the villi.
All of the above

2 Which of these structures make up part of the maternal surface of the placenta?

Amniotic membrane.
Cotyledons
Chorionic plate.
Syncytiotrophoblasts

3 What is the name given to the abnormal development of the placenta described by the attachment of the placenta deep into the uterine wall and also penetrating into the uterine muscle but not into the uterine serosa ?

Placenta Increta.
Placenta Accreta
Placenta Percreta
Placenta Previa


--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 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)

Notes

Test student 2015


Uploading Images in 5 Easy Steps  
First Read the help page Images and Copyright Tutorial.
Hint - This exercise is best done by using separate tabs on your browser so that you can keep all the relevant pages easily available. You can also use your own discussion page to copy and paste links, text. PMIDs etc that you will need in this process.
  1. Find an image .
    1. Search PubMed using an appropriate search term. Note that there is a special library of complete (full online) article and review texts called PubMed Central (PMC). Be very careful, while some of these PMC papers allow reuse, not all do and to add the reference link to your image you will still need to use the PMID.
    2. You can also make your own search term. In this link example PMC is searched for images related to "embryo+implantation" http://www.ncbi.nlm.nih.gov/pmc/?term=embryo+implantation&report=imagesdocsum. simply replace "embryo+implantation" with your own search term, but remember not everything in PMC can be reused, you will still need to find the "copyright notice" on the full paper, no notice, no reuse.
    3. Where else can I look? BioMed Central is a separate online database of journals that allow reuse of article content. Also look at the local page Journals that provides additional resources.
    4. You have found an image, go to step 2.
  2. Check the Copyright. I cannot emphasise enough the importance of this second step.
    1. The rule is unless there is an obvious copyright statement that clearly allows reuse (there are several different kinds of copyright, some do not) located in the article or on the article page, move on and find another resource. Not complying with this is a serious academic infringement equivalent to plagiarism."Plagiarism at UNSW is defined as using the words or ideas of others and passing them off as your own." (extract from UNSW statement on Academic Honesty and Plagiarism)
    2. You have found the statement and it allows reuse, go to step 3.
  3. Downloading your image.
    1. Download the image to your own computer. Either use the download image on the page or right click the image.
    2. To find the downloaded image you may have to look in your computer downloads folder, or the default location for downloaded files.
    3. The image file will have its own original name, that you will not be using on the wiki. You can rename it now (see renaming below), but you should also make a note of the original name.
    4. Make sure you have everything ready then for the
    5. You have the image file on your computer, go to step 4.
  4. Uploading your image.
    1. First make sure you have all the information you want to use with the file readily available. There is also a detailed description below.
    2. Towards the bottom of the lefthand menuunder “Toolbox” click Upload file. This will open a new window.
    3. In the top window "Source file", click "Choose file" and then navigate to find the file on the computer. and select the image.
    4. If you have done this correctly the upload window will now have your image file shown in choose file and also in the lower window "File description" in "Destination filename:" DO NOT CLICK UPLOAD FILE YET.
    5. Rename your file in "Destination filename:" this should be a brief filename that describes the image. Not any of the following - the original file name, image, file, my image, your ZID, etc. Many of the common embryology names may have already been used, but you can add a number (01, 02, 03, etc) or the PMID number to the filename to make it unique.
    6. If the filename or image has already been used or exists it will be shown on the upload page. If another student has already uploaded that image you will have to find another file. Duplicated images will not receive a mark, so check before you upload as you cannot delete images.
    7. In the "Summary" window for now just paste the PMID. You will come back and edit this information.
    8. Now click "Upload image" at the bottom of the window, go to step 4.
  5. Edit and Add to your page.
    1. Edit - Open the image with the "Edit" tab at the top of its page. You should see the PMID you had pasted earlier in the new edit window. Add the following information to the summary box.
      1. Image Title as a sub-heading. Under this title add the original figure legend or your own description of the image.
      2. Image Reference sub-sub-heading. Use the PMID link method shown in Lab 1 and you can also have a direct link to the original Journal article.
      3. Image Copyright sub-sub-heading. Add the copyright information under this sub-sub-heading exactly as shown in the original paper.
      4. Student Image template, as shown here {{Template:Student Image}} to show that it is a student uploaded image.
    2. Add - Now add your image to your own page under a subheading for Lab 2 Assessment including a description and a reference link. If still stuck with this last step, look at the example on the Test Student page.
    3. Done!

Students cannot delete images once uploaded. You will need to email me with the full image name and request deletion, that I am happy to do with no penalty if done before I assess.

Non-Table version of this page

Stress Relief....

<html5media height="480" width="640">http://www.youtube.com/watch?v=i9Hwn2DOgKo</html5media>

[1]

Please do not use your real name on this website, use only your student number.

2015 Course: Week 2 Lecture 1 Lecture 2 Lab 1 | Week 3 Lecture 3 Lecture 4 Lab 2 | Week 4 Lecture 5 Lecture 6 Lab 3 | Week 5 Lecture 7 Lecture 8 Lab 4 | Week 6 Lecture 9 Lecture 10 Lab 5 | Week 7 Lecture 11 Lecture 12 Lab 6 | Week 8 Lecture 13 Lecture 14 Lab 7 | Week 9 Lecture 15 Lecture 16 Lab 8 | Week 10 Lecture 17 Lecture 18 Lab 9 | Week 11 Lecture 19 Lecture 20 Lab 10 | Week 12 Lecture 21 Lecture 22 Lab 11 | Week 13 Lecture 23 Lecture 24 Lab 12 | 2015 Projects: Three Person Embryos | Ovarian Hyper-stimulation Syndrome | Polycystic Ovarian Syndrome | Male Infertility | Oncofertility | Preimplantation Genetic Diagnosis | Students | Student Designed Quiz Questions | Moodle page

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References

  1. <pubmed>21998252</pubmed>
  2. <pubmed>25256934</pubmed>
  3. <pubmed>26136750</pubmed>
  4. <pubmed> 25629662 </pubmed>
  5. <pubmed> 20393463 </pubmed>
  6. <pubmed> 18674747 </pubmed>
  7. <pubmed>17514199</pubmed>
  8. <pubmed>6691093</pubmed>
  9. <pubmed>9722005</pubmed>
  10. <pubmed>8565847</pubmed>
  11. <pubmed>9753687</pubmed>
  12. <pubmed>12399307</pubmed>
  13. <pubmed>16624853</pubmed>
  14. <pubmed>16339294</pubmed>
  15. <pubmed>12702665</pubmed>