User:Z5020117

Student Information (expand to read)
Individual Assessments
Please leave this template on top of your student page as I will add your assessment items here. Beginning your online work - Working Online in this course Make your own page. Log-in to the embryology website using your student ID and Zpass. Click your student number (shown in red at the top right of the screen following log-in) Create page using the tab at the top of the page, and save. Add the following to the top of your page exactly as shown - {{ANAT2341Student2016}} How would you identify your Type in a group and add to your page. What was the most interesting thing you learnt in the fertilisation lecture? If you have done the above correctly your ZID should be blue and not red on this page link - ANAT2341 2016 Students. Here is the example page I made in Lab 1 Student Page. With a few more explanatory notes. Click here to email Dr Mark Hill Editing Links: Editing Basics | Images | Tables | Referencing | Journal Searches | Copyright | Font Colours | Virtual Slide Permalink | My Preferences | One Page Wiki Card | Printing | Movies | Language Translation | Student Movies | Using OpenOffice | Internet Browsers | Moodle | Navigation/Contribution | Term Link | Short URLs | 2018 Test Student
Lab 1 Assessment - Researching a Topic
In the lab I showed you how to find the PubMed reference database and search it using a topic word. Lab 1 assessment will be for you to use this to find a research reference on "fertilization" and write a brief summary of the main finding of the paper. Add a new Sub-heading "Lab 1 Assessment" (without the quotes). Search the database for a reference on "fertilisation" published in the last 5 years. It must be a research article not a Review. The full paper must be available online, not just the abstract. Add a link to this reference using its PMID using this code <pubmed>XXXXX</pubmed> replacing the Xs with just the PMID number (no text). Under the reference write a short summary of the papers main findings. Only 1-2 paragraphs. Must not be a copy of the paper abstract. Save and you are done.
Lab 2 Assessment - Uploading an Image
Upload a research image using the guide information below. The image uploaded for your individual assessment can relate to your project or from fertilisation to week 3 of development (upload only a single image). Add that image to your own individual page (see Images) including an image title and its reference link. No two students should upload the same image, check new images before you upload. No student can delete an image once uploaded, please contact me by email with the image address and I will delete (with no penalty, just glad to help out). 2016 Group Project Topic - Signaling in Development OK you are now in a group Go to the blank group page and add a topic that interests you along with your student signature. No two groups can do the same topic, but at this stage the final topic has not yet been decided (next week). Initially the topic can be as specific or as broad as you want. Chicken embryo E-cad and P-cad gastrulation References
Lab 4 Assessment - GIT Quiz
ANAT2341 Quiz Example | Category:Quiz | ANAT2341 Student 2015 Quiz Questions | Design 4 quiz questions based upon gastrointestinal tract. Add the quiz to your own page under Lab 4 assessment and provide a sub-sub-heading on the topic of the quiz. An example is shown below (open this page in view code or edit mode). Note that it is not just how you ask the question, but also how you explain the correct answer.
Lab 5 Assessment - Course Review
Complete the course review questionnaire and add the fact you have completed to your student page.
Lab 6 Assessment - Cleft Lip and Palate
Identify a known genetic mutation that is associated with cleft lip or palate. Identify a recent research article on this gene. How does this mutation affect developmental signalling in normal development.
Lab 7 Assessment - Muscular Dystrophy
What is/are the dystrophin mutation(s)? What is the function of dystrophin? What other tissues/organs are affected by this disorder? What therapies exist for DMD? What animal models are available for muscular dystrophy?
Lab 8 Assessment - Quiz
A brief quiz was held in the practical class on urogenital development.
Lab 9 Assessment - Peer Assessment
This will form part of your individual assessment for the course. Each student should now look at each of the other Group projects in the class. Next prepare a critical assessment (should include both positive and negative issues) of each project using the project group assessment criteria. This assessment should be pasted without signature on the top of the specific project's discussion page. (minimum length 3-5 paragraphs/project) This critical assessment should also be pasted on your own student page. Each student should therefore have 5 separate reports pasted on their own page for this assessment item. Length, quality and accuracy of your reports will be part of the overall mark for this assessment. there will be a greater loading on this than simple question assessments.
Lab 10 Assessment - Stem Cells
As part of the assessment for this course, you will give a 15 minutes journal club presentation in Lab 10. For this you will in your current student group discuss a recent (published after 2011) original research article (not a review!) on stem cell biology or technology. Lab 10 - Stem Cell Presentations 2016 Group Mark Assessor General Comments Group 1: 15/20 Group 2: 19/20 Group 3: 20/20 Group 4: 19/20 Group 5: 16/20 Group 6: 16/20 The students put great effort in their presentation and we heard a nice variety of studies in stem cell biology and regenerative medicine today. The interaction after the presentation was great. As general feedback I would like to advise students to: Never discuss M&M as a separate section in journal clubs. I gave this advice prior to the lab, but still most groups did talk through the M&M section. Do not use your slides as cheat sheets, avoid text on slides, know what messages you need to get across, use images to illustrate these Engage with your slides. Talk through them. Point at panels. Gauge your audience’s understanding by making eye contact with them Avoid using abbreviations. Most people do not readily understand these and will lose track
Lab 11 Assessment - Heart Development
Read the following recent review article on heart repair and from the reference list identify a cited research article and write a brief summary of the paper's main findings. Then describe how the original research result was used in the review article. <pubmed>26932668</pubmed>Development
ANAT2341Lectures - Textbook chapters   Lecture (Timetable) Textbook - The Developing Human Textbook - Larsen's Human Embryology Embryology Introduction Introduction to the Developing Human Fertilization First Week of Human Development Gametogenesis, Fertilization, and First Week Week 1 and 2 Second Week of Human Development Second Week: Becoming Bilaminar and Fully Implanting Week 3 Third Week of Human Development Third Week: Becoming Trilaminar and Establishing Body Axes Mesoderm Fourth to Eighth Weeks of Human Development Fourth Week: Forming the Embryo Ectoderm Nervous System Development of the Central Nervous System Early Vascular Cardiovascular System Development of the Vasculature Placenta Placenta and Fetal Membranes Development of the Vasculature Endoderm - GIT Alimentary System Development of the Gastrointestinal Tract Respiratory Respiratory System Development of the Respiratory System and Body Cavities Head Pharyngeal Apparatus, Face, and Neck Development of the Pharyngeal Apparatus and Face Neural Crest Nervous System Development of the Peripheral Nervous System Musculoskeletal Muscular System Development of the Musculoskeletal System Limb Development of Limbs Development of the Limbs Renal Urogenital System Development of the Urinary System Genital Urogenital System Development of the Urinary System Stem Cells Integumentary Integumentary System Development of the Skin and Its Derivatives Endocrine Covered through various chapters (see also alternate text), read head and neck, neural crest and renal chapters. Endocrinology Textbook - Chapter Titles   Nussey S. and Whitehead S. Endocrinology: An Integrated Approach (2001) Oxford: BIOS Scientific Publishers; ISBN-10: 1-85996-252-1. Chapter 1. Principles of endocrinology Chapter 2. The endocrine pancreas Chapter 3. The thyroid gland Chapter 4. The adrenal gland Chapter 5. The parathyroid glands and vitamin D Chapter 6. The gonad Chapter 7. The pituitary gland Chapter 8. Cardiovascular and renal endocrinology Full Table of Contents Heart Cardiovascular System Development of the Heart Sensory Development of Eyes and Ears Development of the Eyes Fetal Fetal Period Fetal Development and the Fetus as Patient Birth and Revision Additional Textbook Content - The following concepts also form part of the theory material covered throughout the course. Principles and Mechanisms of Morphogenesis and Dysmorphogenesis Common Signaling Pathways Used During Development Human Birth Defect ANAT2341 Course Timetable   Week (Mon) Lecture 1 (Mon 1-2pm) Lecture 2 (Tue 3-4pm) Practical (Fri 1-3pm) Week 2 (1 Aug) Introduction Fertilization Lab 1 Week 3 (8 Aug) Week 1 and 2 Week 3 Lab 2 Week 4 (15 Aug) Mesoderm Ectoderm Lab 3 Week 5 (22 Aug) Early Vascular Placenta Lab 4 Week 6 (29 Aug) Gastrointestinal Respiratory Lab 5 Week 7 (5 Sep) Head Neural Crest Lab 6 Week 8 (12 Sep) Musculoskeletal Limb Development Lab 7 Week 9 (19 Sep) Renal Genital Lab 8 Mid-semester break Week 10 (3 Oct) Public Holiday Stem Cells Lab 9 Week 11 (10 Oct) Integumentary Endocrine Lab 10 Week 12 (17 Oct) Heart Sensory Lab 11 Week 13 (24 Oct) Fetal Birth and Revision Lab 12 ANAT2341 2016: Moodle page | ECHO360 | Textbooks | Students 2016 | Projects 2016

Lab Attendance

Z5020117 (talk) 14:34, 5 August 2016 (AEST) Z5020117 (talk) 14:41, 12 August 2016 (AEST) Z5020117 (talk) 14:07, 19 August 2016 (AEST) Z5020117 (talk) 14:11, 26 August 2016 (AEST) Z5020117 (talk) 13:21, 9 September 2016 (AEST) Z5020117 (talk) 15:01, 16 September 2016 (AEST) Z5020117 (talk) 13:27, 23 September 2016 (AEST)

Lab 1 Assessment

'Preimplantation genetic screening for all 24 chromosomes by microarray comparative genomic hybridization significantly increases implantation rates and clinical pregnancy rates in patients undergoing in vitro fertilization with poor prognosis' Summary

<pubmed>27382234</pubmed>

The use of Preimplantation Genetic Screening (PGS) in association with IVF has not been prevalent due to its expensive and highly invasive nature, almost doubling the cost of IVF. Currently, morphology evaluation is predominantly used due to its non-invasive nature despite its variable efficacy. Majumdar et al. designed an experiment to evaluate an improved PGS system that analyses all 24 chromosomes. They believe the incorporation of chromosomal analysis will increase pregnancy and implantation rates in patients with poor prognosis. The twenty subjects of this study were classified into one of three groups, advanced maternal age (AMA), repeated miscarriage (RI) and recurrent implantation failure (RIF).

This study found that the transfer of only a few embryos, particularly euploid embryos, resulted in higher implantation rates in those receiving PGS in comparison to the control non-PGS group. Overall, it was found that in comparison to the traditional morphology evaluation previously used, the incorporation of PGS allows for improved outcomes following IVF even when no euploid embryos were transferred. With recent research establishing the correlation between high prevalence of aneuploidy embryos in patients with AMA and unsuccessful implantations, PGS can be used to successfully identify and eliminate the possibility of aneuploidy embryo transfer, thus allowing for increased implantation and pregnancy rates. In saying this, Majumdar et al. emphasise how successful implantation cannot be guaranteed with PGS as some pregnancy failures occur as a result of factors other than chromosomal abnormalities. Though further research is needed to consolidate the benefits of PGS, this study identified the possibility of achieving successful implantation and pregnancy in a shorter time period with fewer miscarriages when utilising PGS rather than morphology evaluation in association with IVF.

Mark Hill 18 August 2016 - You have added the citation correctly and written a reasonable summary of the papers findings. Why would you thing PGD would improve implantation rates and clinical pregnancy rates? Note that this is not a high impact Journal, try those first for your article selections.

Assessment 5/5

Lab 2 Assessment

Primitive streak development in chick embryo

Primitive streak development in chick embryo

Mark Hill 29 August 2016 - All information Reference, Copyright and Student Image template correctly included with the file and referenced on your page here. The citation on the page here could also have appeared in the image legend as shown below. I have also added a reference sub-heading to fix the formatting issue.

Assessment 5/5

Primitive streak development in chick embryo

Lab 3 Assessment

Mark Hill 31 August 2016 - Lab 3 Assessment Quiz - Mesoderm and Ectoderm development. Question 1 - somites Question 3 - brain vesicles Question 5 - maternal diet

Assessment 2.5/5

Lab 4 Assessment

GIT Abnormalities Quiz

1

What are some of the symptoms experienced by infants suffering from intestinal malrotation? (select one or more options)

	Bloody stools
	Common bile duct obstruction
	Abdominal distention
	Bilious vomiting
	Recurrent abdominal pain
	Asymptomatic

2 Gastroschisis is a congenital defect.

	true
	false

3 What percentage of all congenital malformations is accounted for by defects of the digestive system in 1981 - 1992?

	5.7%
	7.3%
	11.3%t
	19.8%

4 What is the cause of Meckel’s Diverticulum?

	Incomplete recanalization resulting in parallel lumens
	Lack of the enteric nervous system in the intestinal tract
	Herniation of the bowel, liver and other organs into the intact umbilical cord
	Improper closure and absorption of the vitelline duct during early development

Lab 6 Assessment

Completed course questionnaire

Cleft Palate

Genetic mutation of the transcription factor TBX22, which encodes for the DNA binding-domain, T-Box, causes cleft palate. . It has been shown that during palatogenesis TBX22 is found within the tongue and palatal shelves, thus indicating its role in the development of both the tongue and palate. Various mutations of TBX22 can occur, including frameshift mutations resulting in the production of truncated proteins, as well as missense mutations causing a change of a single nucleotide. These mutations result in an inefficient or reduced capability of DNA to bind to the T-Box. In the case of missense mutations, it could also lead to the inability to activate transcription factors. As a result, the lack of formation of functional proteins leads to a dysfunctional palatogenesis process and thus, significantly affecting signalling in normal development to cause formation of cleft palate.

It was also found that TBX22 serves as a transcriptional repressor and modification of this repressor activity occurs through SUMO-1, a small ubiquitin-like modifier that binds upstream from the T-Box domain. Therefore, mutations of SUMO-1 can also impair the function of TBX22 and can present as the craniofacial defect of X-linked cleft palate as found in many cases. Research shows that loss of function of SUMO-1 occurs as a result of exposure to an array of environmental and other factors during early pregnancy including, smoking, lack of nutritional supplements and maternal age and it is exposure to these factors that can have an effect on normal signalling in development encouraging the formation of cleft palate.

Lab 7 Assessment

1. What is/are the dystrophin mutation(s)?

Majority of the dystrophin mutations, approximately 60%, are due to deletions or insertions of nucleotides resulting in a downstream frameshift of the dystrophin gene. The remainder of dystrophin mutations are either point mutations, where there is a substitution of a single nucleotide or minor frameshift errors. These mutations can result in the complete absence or in milder forms, the alteration or reduction of the dystrophin protein.

2. What is the function of dystrophin?

The dystrophin protein found in both skeletal and cardiac muscle plays a structural role by linking the internal cytoskeleton of the muscle with the extracellular matrix. It is also responsible for protecting muscles during contraction and relaxation from injury by strengthening muscle fibres. Dystrophin also plays an additional role in cell signaling through interaction with other proteins involved in sending and receiving chemical signals. Research has shown that dystrophin may be present in minor amounts within the neurons of the brain. Thus, they may be involved in the formation of synapses
.

3. What other tissues/organs are affected by this disorder?

DMD can affect the respiratory muscles thus negatively impacting lung function. As the dystrophin protein is also found within cardiac muscle, the heart is also affected in DMD. Due to this dysrhythmia or arrhythmia, irregular heart rhythm and cardiomyopathy, abnormal pumping action can result. The presence of dystrophin in brain tissue can also result in learning and behavioural difficulties
.

4. What therapies exist for DMD?

Though there is no known cure for DMD, extensive research is being currently performed to treat DMD. The following are a few examples of research being conducted in the field of DMD.

Some of the therapies available include gene replacement therapy whereby plasmids or viruses are utilised to deliver dystrophin sequences but this is currently a work in progress. Myoblast transplantation where myoblasts are artificially delivered into the affected site can also be offered. This is because it has been shown that myoblasts can fuse to form new muscle fibres but upon exhaustion of the proliferative ability of the myoblasts, the skeletal muscle is converted into connective tissue. Unfortunately, studies have shown unsatisfactory results for such treatment. In saying this, stem-cell therapy has shown to be a good alternative to myoblast transplantation due to the extended proliferative life-span of stem cells.

Administration of aminoglycoside antibiotics is a potential therapy that targets DMD caused by premature stop codons. Results of such treatment have not been promising but have indicated that it may be more useful in only a select few DMD mutations. On the other hand, chimaeraplasts have been utilised as a vehicle to deliver the correct nucleotide to the site of dystrophin mutation. Unfortunately, the viability of such treatment is short-lived and requires further research.

Antisense oligonucleotides have been utilised to help redirect dystrophin splicing to exclude the inclusion of the premature stop codon, the most common cause of DMD. This will allow partial restoration of the reading frame and thus allow formation of the dystrophin, albeit shorter protein. Research has also shown that proteasome inhibitors can be used to improve the integrity of muscle. Lastly, upregulation therapy focuses on replacement of defective genes by increasing expression of alternative genes e.g. utrophin. These are promising areas of research in DMD therapy.

Currently, the only form of therapy available is management of DMD and this can be done through prescription of steroid medication to help maintain muscle integrity. Surgery can also be performed to release tightness of joints as well as treat scoliosis, the lateral curvature of the spine which can come as a result of DMD. Supportive equipment can also be provided including night splints, walking frames, wheelchairs, and other mobility aids. It is also important to regulate the patient’s diet and exercise routine. Muscle relaxants and anti-inflammatory medication can also be provided to help with any pain or discomfort
.

5. What animal models are available for muscular dystrophy?

Currently there are two animal models that have been utilised to further understand Duchenne Muscular Dystrophy, the mdx mouse model and the golden retriever muscular dystrophy (GRMD) dog. These models are significant as both these species lack the dystrophin protein.