Difference between revisions of "User:Z3465531"

From CellBiology
Line 77: Line 77:
[[File:Super-resolution improves skin surface imaging.jpg|thumb|Image of the surface of intact skin<ref name="PMID26751684"><pubmed>26751684</pubmed></ref>]]
[[File:Super-resolution improves skin surface imaging.jpg|thumb|Image of the surface of intact skin<ref name="PMID26751684"><pubmed>26751684</pubmed></ref>]]
==Lab 3 Assessment==
==Lab 3 Assessment==

Revision as of 13:19, 7 April 2016

My Student Page


Z3465531 (talk) 11:53, 10 March 2016 (AEDT)

Z3465531 (talk) 11:06, 17 March 2016 (AEDT)

Z3465531 (talk) 14:39, 24 March 2016 (AEDT)

I forgot to submit the above attendance until I returned home from the lab.

Z3465531 (talk) 11:13, 7 April 2016 (AEST)

Weekly Assignment

Group Projects
This year's main topic is Blood Cell Biology. Each group should discuss with group members the specific sub-topic that will be covered by their project.

Here is a list of some of the cell types (Structure and Function)

Cell Type (PuMed citations)

Below are the groups to which students have been randomly assigned. You should now on the project discussion page add your own suggestion for a specific topic. Once your group has agreed on the topic, add this as a heading to the project page before Lab 3.

2016 Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7

Group 1: User:Z5017493 | User:Z3330991 | User:Z5020043 | User:Z5020175 | User:Z3489355

Group 2: User:Z5018320 | User:Z5015980 | User:Z3376375 | User:Z3461106

Group 3: User:Z5019595 | User:Z5019962 | User:Z5018925 | User:Z3461911

Group 4: User:Z5020356 | User:Z3463895 | User:Z3376502 | User:Z3423497 | User:Z5021149

Group 5: User:Z5015719 | User:Z3462124 | User:Z3463953 | User:Z5017292

Group 6: User:Z5018866 | User:Z3329177 | User:Z3465531 | User:Z5105710

Group 7: User:Z5021060 | User:Z5016365 | User:Z5016784 | User:Z3414546 | User:Z3417773

Group Assessment Criteria

Group Assessment Criteria

  1. The key points relating to the topic that your group allocated are clearly described.
  2. The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area.
  3. Content is correctly cited and referenced.
  4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations.
  5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities.
  6. Relates the topic and content of the Wiki entry to learning aims of cell biology.
  7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki.
  8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.
  9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning.
  10. Develops and edits the wiki entries in accordance with the above guidelines.
Individual Lab Assessments
Lab 8 Assessment
2016 Lab 8 - Lab 8 Assessment (to be completed before Lab 9)
  1. Add your peer assessment to your own student page to the site.
  2. Add your peer assessment to each project discussion page to the site.
Lab 6 Assessment
2016 Lab 6 -
  1. Identify an antibody against your group blood cell protein that is commercially available.
  2. Add a link to the original data sheet page and identify the type of group blood cell protein.
  3. Include the following information: type of antibody (polyclonal, monoclonal), species raised in, species reacts against, types of application uses, and if available any reference using that antibody.
Lab 2 Assessment
2016 Lab 2 - Super resolution microscopy
  1. Find a recent research article (not review) that uses super resolution microscopy technique.
  2. Write a brief summary of the paper (referenced) and what the super resolution microscopy technique showed.
    1. This should not simply be the abstract of the paper.
    2. This can be 2-3 paragraphs no longer.
  3. Include a super resolution microscopy image from the paper.
    1. Therefore the paper must be from a source that you can reuse.
    2. Image uploaded as in Lab 1 (summary box - description/reference/copyright/student image)
    3. Image should appear as a "thumbnail" (thumb) next to your paper summary (with citation legend) See Test page
Lab 1 Assessment
2016 Lab 1 - Lab 1 Assessment (to be completed before Lab 2) The test page I set up in the Lab
  1. Add your own student page to the site.
  2. Add your signature for Lab attendance.
  3. Add a sub-heading.
  4. Add an external Link.
  5. Add an internal Link.
  6. Add an image from PubMed, PloS or BioMed Central journal related to prokaryote cellular component. Make sure it includes both the reference and copyright information, with the file and where it appears on your page.

To Do: Find a research article and write a brief summary. Upload an image of the super resolution as a thumbnail sitting next to the shortcut. The image has to be taken from an allowable article.

Lab 1 Assessment

Search PubMed

prokaryotic cytoskeleton


PMID 26756351


BioMed Central

How to make an in-text citation

Bacterial division protein FtsZ.[1]



Carnegie stage table


Lecture 1

SMH Sydney Paper

What I have learned so far

The most useful information I have learned so far is multiple specific computer programming language commands necessary for organizing information on wiki pages. In particular, I have learned the incredibly useful command for instantly creating a citation of a PubMed article. I have also learned how to rename links a wiki page so that full website address itself is not necessarily listed and is instead whichever name I select. The simple coding language use of equals signs will be extremely helpful for organizing my work into simple headings and subheadings. Additionally, I learned that all of the edits to the wiki will be completely preserved so that there is no risk of information and progress being lost. In general, I learned how to execute several wiki commands, and now I have a useful template available for the purposes of creating wiki pages throughout the rest of the course.

Student Image

Here is the uploaded image

Bacterial Phylogenic Tree Example.png

Bacterial phylogenetic tree reconstructed from a concatenated alignment of 50 nearly ubiquitous r-proteins[2]

You can also set it to any size you want, this is 200px wide.

Bacterial Phylogenic Tree Example.png]

Bacterial phylogenetic tree reconstructed from a concatenated alignment of 50 nearly ubiquitous r-proteins[2]

Lab 2 Assessment

In their article, Superresolution and Fluorescence Dynamics Evidence Reveal That Intact Liposomes Do Not Cross the Human Skin Barrier, Dreier et al investigate the mechanism by with liposomes act to deliver drugs in human skin. Very few drugs are easily delivered across the skin barrier, but lipid vesicle carriers are one of the methods by which the permeably of human skin is able to be enhanced. Specifically liposomes, also known as large unilamellar vesicles (LUVs), are of particular interest when considering options for drug delivery across the dermis. Despite the widespread use of LUVs commercially, much has historically been unknown about the mechanism of action due to the minute scale at which the liposomes are functioning.

Dreier et al used stimulated emission depletion (STED) microscopy to create superresolution images able to resolve the 100nm liposomes of interest in the skin. STED microscopy allowed for high enough resolution to determine that hardly any liposomes were intact deep to the skin surface. Therefore, Dreier et al were able to conclude that liposomes used for transdermal drug delivery mostly burst fusing to deliver their contents to the outmost layers of the skin rather than directly transporting intact liposomes through the skin barrier. [3]

Thumbnail version of image

You can also set it to a thumbnail image.

Image of the surface of intact skin[3]


  1. <pubmed>26756351</pubmed>
  2. 2.0 2.1 <pubmed>22615861</pubmed>
  3. 3.0 3.1 <pubmed>26751684</pubmed>

Lab 3 Assessment

The following assessment for Lab 3 I completed before Lab 4, but forgot to copy over to my individual page before Lab 4:


1. Summary: Cathepsin B controls the persistence of memory CD8+ T lymphocytes, Byrne, S. M., et al. [1]

This study investigates the mechanisms by which memory T lymphocytes persist, even in the absence of antigen.

The findings indicate that one of the major limiting factors to memory CD8(+) T cell populations is the stability of the cell lysosomes. The genes IL-15 and IL-7 contribute to the production of serine protease inhibitor (Spi) 2A, which inhibits cytosolic cathepsin and thus inhibits apoptosis. In animal models, Spi2A inhibition results in less CD8+ T lymphocyte maturation and less homeostatic proliferation as well. The experimental results indicated that Spi2A is required in order for the memory CD8(+) T lymphocytes to maintain population numbers after viral infection and that one specific mechanism of action is protection from lysosomal breakdown via cathepsin B inhibition. Furthermore, it was found that T cells deficient in Spi2A could have their homeostatis restored by concurrently blocking cathepsin B, which strongly suggested that the physiological target of Spi2A was indeed cathepsin B.

The relevance of this topic to T lymphocytes, specifically memory T lymphocytes, is manifold. The primary function of memory T lymphocytes is to persist within the organism until such time as they are necessary to promote a fast, powerful targeted response to a second infection. If the population of the memory T lymphocytes is allowed to deplete, then immunological memory will not remain. If, on the other hand, memory T lymphocytes proliferated over abundantly, then this would be a likely mechanism for the development of possible leukemia.

2. Summary: The majority of HIV type 1 DNA in circulating CD4+ T lymphocytes is present in non-gut-homing resting memory CD4+ T cells, McBride, K., et al. [2]

This study investigates the locational distributions of integrated HIV-1 DNA copiers within memory CD4+ T lymphocytes for the purposes of better understanding the efficacy of disease treatments.

A proposed site of prominent HIV-1 replication with Memory CD4+ T lymphocytes is the gut-associated lymphoid tissue, where such cells tend to recirculate. The researchers of this study hypothesized that regulatory T cells and activated CD4+ T lymphocytes tend to recirculate and disproportionately make up a source of the HIV-1 reservoir, serving as a difficulty needing to be solved in any possible eradication of the disease.

Real time polymerase chain reaction was used to localise HIV-1 DNA within the human immune cells. More than 80% of total HIV-1 DNA was found in non-gut-homing CD45RO+ memory T lymphocytes, while less than 10% was found in regulatory T cells and CD38+ activated memory cells. The researchers found that most of the HIV-1 DNA was present in non-gut homing resting CD(+) T cells. The findings of the experiment are significant because they work toward better understanding the locational pathogenesis of HIV-1 in memory CD4+ T lymphocytes, which is necessary for developing a cure.

3. Summary: Interleukin-22 is produced by invariant natural killer T lymphocytes during influenza A virus infection: potential role in protection against lung epithelial damages, Paget, C., et al. [3]

During viral infections, invariant natural killer T (iNKT) cells are a type of non-conventional T lymphocyte that plays a key role through quickly producing cytokines. While the mechanism of their action is not entirely well known, it has been proposed that they play a useful role during influenza A virus (IAV) infection.

The findings of the article support that iNKT cells produce IFN-γ and IL-22, cytokines critical to muscosal immunity. The specific mechanisms of the production and mediation of these cytokines are investigated, especially with respect to the morality of those infected by the virus. It was demonstrated in vitro and vivo, at least during early IAV infection, that IL-22 helps to prevent epithelial cell death in a IAV-infection of the airway. In total, iNKT cells were revealed to provide a quick source of IL-22 that possibly is critical to protecting the lung epithelium. These findings are significant to better understanding how T-lymphocytes, and specifically natural killer T lymphocytes, play a role in proactively protecting from early infections in critical exposed areas, such as the lungs.

4. Summary: Microbial exposure during early life has persistent effects on natural killer T cell function, Olszak, T., et al. [4]

This study investigated the importance of microbial exposure at a young age to the function of natural killer T cells, which are supposed to play a critical role in diseases relating to the immune system such inflammatory bowel disease (IBD) and asthma.

The findings of the article are that germ-free (GF) mice tended to accumulate invariant natural killer T (iNKT) cells in the lungs and in the lamina propria of colon, increasing morbidity as compared with specific pathogen-free mice. Also, the GF mice had increased intestinal and pulmonary expression of CXCL16, a chemokine ligand associated with increased iNKT cells of the mucosa.

On the other hand, when neonatal GF mice were colonized with conventional microbiota, the mice tended to be protected from iNKT accumulation within the mucosa and associated pathogenicity. The results of the experiments as a whole suggested that contact with commensal microbes by a critical early age are crucial to developing a healthy levels of mucosal iNKT. These findings are significant to better understanding iNKT cells because they address both the natural function of iNKT cells in providing resistance to environmental exposures, but the experimenters also investigate the double edged nature to this immunity. If a the host fails to interact with any conventional microbiota during the early stages of life, then the natural killer T-cells themselves seem to be a source of pathogenicity. The results of the experiment provide crucial insight for better understanding T lymphocytes as a whole.

Migratory challenges faced by T cells [5]


  1. <pubmed>22745374</pubmed>
  2. <pubmed>23971972</pubmed>
  3. <pubmed>22294696</pubmed>
  4. <pubmed>22442383</pubmed>
  5. <pubmed>26635800</pubmed>