User:Z5020175

From CellBiology

My Student Page

Attenndance

Z5020175 (talk) 11:53, 10 March 2016 (AEDT)

Z5020175 (talk) 12:38, 17 March 2016 (AEDT)

Z5020175 (talk) 11:21, 24 March 2016 (AEDT)

Z5020175 (talk) 11:08, 7 April 2016 (AEST)

Z5020175 (talk) 11:12, 14 April 2016 (AEST)

Z5020175 (talk) 11:00, 21 April 2016 (AEST)

Z5020175 (talk) 11:03, 28 April 2016 (AEST)

Z5020175 (talk) 11:35, 5 May 2016 (AEST)

Z5020175 (talk) 12:55, 19 May 2016 (AEST)

Z5020175 (talk) 13:02, 26 May 2016 (AEST)

Z5020175 (talk) 11:05, 2 June 2016 (AEST)


  • Z8600021 Attended 11 practical classes.

Lab Assessment Information

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.

In Class Assessments

Lab 1 Assessment

Search PubMed

BioMed Central

Prokayrotic Cytoskeleton

Eukaryotic Cytoskeleton

PMID 26756351

Katherine Ann Hurley, Thiago M A Santos, Gabriella M Nepomuceno, Valerie Huynh, Jared T Shaw, Douglas B Weibel Targeting the bacterial division protein FtsZ. J. Med. Chem.: 2016; PubMed 26756351


How to make an in-text citation

Bacterial division protein FtsZ.[1]


Links

Carnegie stage table

Lecture 1

SMH Sydney Paper

Testz8600021


What I've learnt so far?

Today I learnt how to create and edit a wiki page, which surprisingly was not as difficult as I had expected. Although, there are many codes to remember, I found the process quite fun and helpful. I have always done my referencing manually and learning that there is a quick code to generate a reference was quite exciting. Furthermore, I have become more efficient at searching for articles on popular medical databases. Prior to this lab, I did not know that you could change the amount of articles you can view on one page or that can you narrow down the search to review articles. I can now add websites and articles easily to the wiki page and it was really useful to know that you can name them with a short title. Forming headings and subheadings on a wiki page was quite a simple process and it does make the page look very structured. Overall, my computer and webpage editing skills have vastly expanded and I am looking forward to becoming more adept with these skills through applying them in the group assessment.

Lab 2 Assessment

  • Z8600021 Image has reference, copyright and student template in summary box. (5/5)

Role of the domain interface in channel activation.png

Role of the domain interface in channel activation[2]

Individual Assessment

Lab 1: Student Image

Role of the domain interface in channel activation.png

Role of the domain interface in channel activation[2]


Lab 2: Summary of Article

SIM images and graphs demonstrating the need for WASp in the formation of actin nodules in both mouse and human platelets[3]

The actin cytoskeleton is a crucial component in the survival and function of platelets along with their precursor cells, the megakaryocytes. It is involved in the maintenance of platelet morphology and enables quick changes in shape upon platelet activation. This is essential for the ability of platelets to aggregate and form a clot at existing sites of vascular injury. Actin filaments can be assembled into a wide range of specialised structures and the two studied within this article, are the podosomes and actin nodules. Both of these F-actin structures are known to play an important role in normal platelet adhesion and aggregation. In mice that are Wiskott – Aldrich Syndrome protein (WASp) deficient, these structures are not formed and so they exhibit low platelet counts (thrombocytopenia) and excessive bleeding upon injury. Hence, this study was established to determine if WASp may have a regulatory role in the formation of podosomes and actin nodules.


To effectively study the relationship between WASp and podosome/nodule formation, several microscopy techniques were utilized within this study, one of which is structured illumination microscopy (SIM). This super resolution microscopy technique, was able to demonstrate that nodule formation is dependent upon the presence of functional WASp proteins. Both mouse and human platelet cells that lacked WASp (WASp KO) or contained a defective WASp protein (WASp Y293F) were unable to form a significant number of nodules in comparison to the wild type platelet cells. This can be seen in the image inserted in the thumbnail. Furthermore, the study was able to illustrate the mechanism by which WASp enables the formation of actin nodules. Through SIM imaging, it was apparent that platelet cells of patients with Wiskott - Aldrich Syndrome were unable to form large foci of ARP2/3 complexes whilst normal platelet cells showed otherwise. This therefore suggests that the presence of functional WASp is needed to recruit ARP2/3 complexes, in order to form actin nodules. [3]

Lab 3: Summarising Reference Papers related to Megakaryocytes

  • Z8600021 Good paper summaries, these relate to the group project. Image has reference, copyright and student template in summary box. (5/5)


Paper 1: Ciovacco et al. [4] examined the complex interplay between megakaryocytes and bone development. They had done so through studying the effect of megakaryocyte (MK) maturation and numbers on osteoblast proliferation and osteoclast inhibition. Megakaryocytes from the wild type C57BL/6 mice were assorted into 3 sub - populations based on their increasing levels of maturity: megakaryoblasts, immature MK and mature MK. These cells were incubated with the same numbers of osteoblasts in separate cultures respectively. In conjunction, two other cultures were also made: osteoblasts alone and osteoblasts with BSA separated MKs. These were the negative and positive controls respectively. The same experiment was repeated with the use of osteoclasts instead. The numbers of bone cells within each experiment were recorded after 3 days of incubation and it was determined that megakaryoblasts do not exhibit a proliferative or inhibitory effect on osteoblasts and osteoclasts respectively. However, this was not the case for immature and mature MKs, as they were able to enhance the proliferation of osteoblasts and inhibit the formation of osteoclasts at virtually identical levels. This study was also able to demonstrate that as the numbers of megakaryocytes increase, so does the level of osteoblast proliferation. Overall, it was illustrated that the effect of megakaryocytes on bone growth is complex and determined by multiple factors such as their level of maturity and population numbers. This article is therefore relevant to the 'function and roles' subsection as one of the main functions of megakaryocytes is the regulation of skeletal homeostasis.


Paper 2: Uchiyama et al. [5] studies the role of growth differentiation factor 15 (GDF15) in the pathogenesis of primary myelofibrosis (PMF) which is a severe disorder that involves bone marrow fibrosis. The serum of patients with PMF were analysed within this study and nearly all patients demonstrated abnormally high levels of GDF15. This led the researchers to determine the source of this cytokine and it was found to be megakaryocytes within the bone marrow. Relative to other cell populations within the bone marrow of patients with PMF, megakaryocytes demonstrated greater haematoxylin and eosin staining and this means that the expression of GDF15 predominantly occurs in megakaryocytes. The numbers of these precursor cells are also known to be elevated in PMF and GDF15 was shown to be upregulated in megakaryocytes of patients with PMF when compared to expression levels in normally healthy individuals. The study had further found that GDF15 was responsible for the abnormal proliferation of fibroblasts and osteoblasts in the bone marrow of PMF patients. These two cells are known to cause the fibrosis of the bone marrow in PMF which leads to an inability to generate cells of the blood. Hence, megakaryocytes appear to play a regulatory role in the biogenesis of fibroblasts and osteoblasts in the bone marrow, through signalling molecules such as GDF15. This undoubtingly highlights the relevance of this article to both our 'disease' and 'function/roles' subsections as it explores the complex interaction between megakaryocytes and the cells that lead to fibrosis in PMF.


Paper 3: Within this study, Nishimura et al. [6] has identified an alternative pathway that involves megakaryocyte rupture and thereby enhanced platelet release in response to acute platelet needs mediated by Interlukin-1α (IL-1α). The main mode of platelet production is regulated by the molecule 'thrombopoietin' (TPO) which promotes a "microtubule - dependent extension of elongated pseudopodal structures" that eventually break off from the megakaryocyte as platelets. The process of generating these megakaryocyte projections is known as 'proplatelet formation' (PPF). The results of this study illustrate that PPF alone is not sufficient in producing the rapid platelet turnover required to meet acute platelet needs in inflammatory reactions. They demonstrate that there is an additional pathway of platelet production (thrombopoesis) mediated by IL-1α. Using a screening assay, it was determined that IL-1α is able to increase platelet production from megakaryocytes to a greater degree than TPO. By studying the effects of exogenous IL-1α on bone marrow megakaryocytes in vivo, it was found that IL-1α significantly enhanced megakaryocyte rupture but notably reduced PPF without altering the serum levels of TPO. The loss of PPF was due to the impairment of microtubule assembly and weakening of the plasma membrane by the IL-1α signalling pathway. The platelets from this cytokine mediated rupture were larger in size than those produced by PPF but demonstrated the same aggregation and thrombotic functions. This article evidently related to the 'function and roles' subsection as it illustrates the importance of megakaryocytes in platelet production under both physiologically normal and stress conditions.

Overview of the biological phases involved in platelet generation from HSCs and subsequent platelet activation[7]

Paper 4: Zhao et al. [8] sets out to illustrate the dual role of megakaryocytes (MKs) in maintaining HSC quiescence during homeostasis and promoting the repletion of haematopoietic stem cells (HSCs) following chemotherapeutic stress. Many cell types in the bone marrow stroma have been identified as HSC-regulating niche cells. However, whether a HSC progeny is recruited as a HSC niche cell is not clearly known and is thought to be regulated by megakaryocyte secretions. The results of this study show that MKs have physical interactions with HSCs in mice bone marrow and that a deficiency of MKs will lead quiescent HSCs to become activated and thereby proliferate rapidly. In comparison to other stromal niche cells, MKs were revealed to express higher levels of biologically active transforming growth factor β1 (TGF-β1 ) through analysing RNA sequencing data. When MKs are removed from the bone marrow, the levels of functional TGF-β1 protein and nuclear-localized phosphorylated SMAD2/3 (pSMAD2/3) is significantly lowered in the resident HSCs. This insinuates that the HSCs are kept in the quiescent state through the TGF-β-SMAD signalling pathway triggered by megakaryocyte secretions. In order to prove this further, the researchers had injected TGF-β1 into mice with MK ablation and this had reverted the actively proliferating HSCs into a quiescent state. When this injection was depleted, the quiescent HSCs became activated and there was an increase in their proliferative activity. Thus, it is apparent that TGF-β1 which is primarily expressed by MKs, is the key signal in maintaining HSC quiescence. Moreover, there was a significant impairment in the expansion of HSCs when the test mice were under chemotherapy. During this stress phase, megakaryocytes were observed to release fibroblast growth factor 1 (FGF1) which had appeared to override the inhibitory signal induced by TGF-β1. This had temporarily enabled the quiescent HSCs to become activated and clonally expand. On the whole, the data produced in this article is relevant to the 'function and roles' subsection as it highlights the importance of megakaryocytes in maintaining HSC homeostasis through the secretion of signalling molecules.

Lab 5: Upload graph depicting analysis of cell morphologies

Comparison of the morphology of undifferentiated B35 cells over-expressing Tm4 and wild type B35 cells.jpg

Lab 6: Immunochemistry

  • Z8600021 All information is here. Why not use the PMID 15797992 for the published reference. (5/5)


1. Identify an antibody against your group blood cell protein that is commercially available: Anti-CD41 antibody [M148] (ab11024)

2. Add a link to the original data sheet page and identify the type of group blood cell protein:

- http://www.abcam.com/cd41-antibody-m148-ab11024.html

- Anti-CD41 Antibodies target the CD41 surface marker found specifically on the cell membrane of megakaryocytes and platelets.It is a transmembrane glycoprotein that interacts with CD61 (integrin β3) to generate complexes that whhich can associate with fibrinogen, fibronectin, von Willebrand factor, and thrombin. This is essential for the processes of platelet adhesion and aggregation.


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:

- Type of antibody: Monoclonal antibody

- Species raised in: Mouse

- Species reacts against: Humans

- Types of application uses: The antibody can be used to identify megakaryocytes and platelets in bone marrow and blood samples. It can also be used to bind to some medulloblastoma and neuroblastoma cells and rhabdomyosarcoma and certain other solid tumours.

- Reference using this antibody: Sato Y, Fujiwara H, Zeng BX, Higuchi T, Yoshioka S, Fujii S. Platelet-derived soluble factors induce human extravillous trophoblast migration and differentiation: platelets are a possible regulator of trophoblast infiltration into maternal spiral arteries. Blood. 2005 Jul 15;106(2):428-35.

Lab 7: Peer Review

  • Z8600021 You have provided valuable peer feedback in some detail. I would suggest including an overview or summary at the beginning of each as the information you have provided is very specific and I do not get a feel for what you thought of the project quality or how they rank against each other. (17/20)

Group 2

Introduction:

  • Different points flow well
  • Summarises the different topics discussed under RBCs
  • Referencing is done correctly
  • Unfinished sentence at the end

History:

  • Layout is great & everything is referenced
  • The written findings is worded well and easy to understand

Structure:

  • Good use of subheadings
  • You might want to show the electron/light microscopy images of erythropoiesis
  • There are a few punctuation and spelling errors for eg. Remove 's' from "protective mechanisms" and add an "a" in between lack and celll nucleus
  • Membrane composition is not really mentioned but the function of the membrane has lots of information
  • What sort of filamentous systems make up the erythrocyte cytoskeleton.
  • The function of the cytoskeleton was explained very well
  • What is the structure of Hb? - Include an image

Function:

  • "To bind O2 in the pulmonary capillaries in an area of high O2tension and release O2 in the periphery where there is low O2 tension" - This did not make sense
  • What is the name of the process where O2 binding enhances the binding affinity of other subunits
  • Helping this process… - be careful of diction
  • Diagrams are needed in this section to complement the information.
  • The buffering ability should be explored further
  • Another role of RBCs is to transport immune complexes in the bloodstream to the spleen and liver for breakdown

Synthesis and regualtion:

  • Great diagram used
  • Great use of subheadings
  • Writing is suitable level for student learning but minor spelling errors can be found here and there
  • Erythropoietin should be labelled EPO so that we know on the diagram
  • Great referencing

Diseases:

  • The use of a table for the symptoms is a very smart idea
  • "insufficient iron available for Hb synthesis in rbcs"
  • IDA was explained very well
  • Diseases set out nicely and explained thoroughly
  • Outlines the pathogenesis of disease (genetic basis) well and then talks about clinical manifestations
  • Talks a bit of epidemiology
  • Talks about treatment for thalassemia
  • Links cause and effect well such as how increased RBC in polycthemia can lead to reduced blood flow & making patients susceptible to thromboembolism --> death
  • Demonstrates diversity in diseases associated with RBCs - nutritional, genetic and microbial
  • Doesn't explain how the infestation leads to illness - what are the clinical manifestations

Current Research:

  • This section could be imrpoved by adding in other examples as well
  • The connection between erythrocyte death and Parkinson's Disease (PD) is really interesting
  • Connected how the signalling molecules in PD also affect RBCs and highlights the relevance of studying RBC --> engaging to the reader

Overall:

  • Great written expression and has lots of clarity
  • Spelling and punctuation errors here and there
  • Engaging to read as diseases are diverse - nutritional…
  • Links in cause & progression of disease to the effects
  • Function requires more images
  • Structure component is focused on function of structural components rather than the structure itself
  • Current research was engaging but only shows one example of the importance of studying RBCs
  • Referencing is good but missing in a few places
  • Lacking student made diagrams
  • Table idea, subheadings and layout were great


Group 3

Introduction:

  • Clear & written very well - suitable for student learning
  • States general info about B cells - where they form? What they do?
  • No referencing
  • Antibody secreting effector cell is called what? - Plasma cells

History:

  • This section could be improved by adding more information and references
  • Does not mention any significant individuals.

Development:

  • Subheadings for the different B cell stages should be included
  • Logically outlines the different stages of B cell development but hasn't formatted it well
  • Genetic recombination & specificity has not been explored very well
  • How are autoreactive B cells deleted or become anergic?

Location and activation:

  • Location clearly stated
  • Easy to read
  • T cell dependent activation is missing information - Types of receptor binding, cytokines released & what class switching occurs?
  • T cells and not t cells!
  • Writing has great clarity but detail is not enough for student learning

Types of B cells:

  • This is an appropriate subheading
  • Layout was executed very well
  • States what the specific cell type does and where it's located. For example, Memory B Cells are dormant until re-exposure to antigen where they differentiate into plasma cells to secrete antibodies for antigen clearing. Found in germinal centre
  • Lacking diagrams

Structure:

  • Lacks referencing
  • Appropriate subheadings
  • This section was Well written
  • Shows complexity in surface marker expression
  • Split the dotpoints under surface marker section
  • Plasma cell structure explained well and has a good accompanying diagram
  • No copyright caption included in diagram
  • Summary table of surface molecules is helpful
  • Diagram for structure of antibodies

Functions:

  • Summarised well
  • Clarity in expression
  • Needs more referencing
  • What do the cytokines do to maintain immune system? Provide examples!
  • Why is class switching such as to IgE or IgA important and where does it occur?

Role in disease:

  • Lacks referencing and could be improved by more information
  • You should provide a prominent example of an autoimmune disease that involves autoreactive B cells
  • The process of forming autoreactive B cells is somewhat explained but lacking key information - Genetic susceptibility, epigenetic factors, environmental factors, loss of immune tolerance
  • What about multiple myeloma?
  • How does one gene mutation lead to the alteration in B cell signalling? - give an example
  • Immunodeficiency? Agammaglobulemia

Applications:

  • What are other applications?

Overall:

  • The written expression is very clear and suited to student level
  • However, there is a lack of detail and information - lots of knowledge gaps
  • Lack of referencing and images are not from copyrighted source
  • The choices of headings and subheadings was good
  • No student diagrams & barely any tables
  • Introduction flows well and so is development but the latter needs to have subheadings
  • History is lacking
  • B cell structure and types of B cells is missing diagrams
  • Maybe you can have a collage of the different B cell types or a timeline image showing immature B cell to mature one
  • The importance of certain functions such as class switching and maintenance of IS was missing
  • Role in disease and applications is lacking sufficient information


Group 4

Introduction: The introduction summarises the main features of Natural Killer Cells quite well but there is a lack of flow with the last 2 paragraphs. The history table is formatted well but there appears to be limited information on the history of NK cells.

Structure:

  • Easy to read
  • Its good that you recognised the need to add a drawing
  • "which are then differentiated into the bone marrow allowing circulation around the body as peripheral blood after the homeostasis" - This doesn't make sense although I understand what you mean
  • Spelling and grammatical errors need to be corrected
  • You have to establish that NK cells are classified as large granular lymphocytes (LGL). However, a LGL is not always an NK cell; it can also be a CD8+ T cell.
  • The three different divisions of NK cells can be put under subheadings
  • You're missing information on the activating and inhibitory receptors but at least you've pointed it out

Function:

  • Can you please explain how a surface marker (CD56) is a cell function?
  • You didn't really explain how NK cells distinguish self and non-self clearly and you could add in a simple diagram here
  • This section is written well and not dense with jargon
  • Great use of a study to add onto the function in cancer
  • Is it cytokinesis or cytokine production? Cytokinesis is a process that occurs in cell division and is not the same as cytokine production

Abnormalities In disease:

  • The addition of a table was a good idea
  • Lack of referencing in Rheumatoid Arthritis
  • An extensive list of different diseases was explored which is good

Current Research:

  • Use subheadings
  • Written well and contains ample information.

Overall Points:

  • Missing Development and Maturation of NK cells
  • The writing is at a suitable level for students
  • Certain parts such as history and function is lacking information
  • Uncompleted bits and need some more diagrams


Group 5

Introduction:

  • Very well written introduction on mast cells
  • Clearly introduces the main points about mast cells such as their origin, location, roles in our body and a bit about their structure (contains granules)
  • Information is clearly referenced
  • The Introduction may need to be split into 2 paragraphs particularly at the words "Mast cells are highly granulated…" since this is a completely different point about mast cells.

History:

  • The formatting of the table is really pleasant aesthetically
  • The Findings weren't too dense with information which is good and suitable for student learning
  • All information was referenced

Physiology:

  • Morphology was really well written and provided sufficient detail. The language was not to dense with jargon and was suitable for student learning. It could be broken up into a few paragraphs for easier reading and for the different points to stand out.
  • Function: The diverse roles of mast cells was established within this paragraph. There is a missing word in the very last sentence of the second paragraph. The information on mast cells and their involvement in tumour growth should be placed in a separate paragraph. Maybe 1 or 2 diagrams could be added to enhance the information. Overall, this was a really solid section as you have clearly illustrated a connection between the molecules secreted by mast cells and their diverse roles: inflammation, tumour inhibition and pathogen clearance.
  • Origin and migration: This section was engaging to read as it briefly mentioned the historical context in which mast cell precursors were discovered. It is very clear that Group 5 has been actively reading through research papers on mast cells and their origins. The addition of 'integrins' in this section really ties in well with what we have learnt in cell biology. Diagrams were well chosen and demonstrate mast cell development comprehensively.
  • Differentiation: The table summarises the intrinsic and extrinsic factors that lead to mast cell differentiation really well. This is easy to read and would be very helpful for students.
  • Activation: The hand - made drawing is really easy to follow and this section was not too information dense. However, the main intermediate steps in the signalling pathways may need to be elucidated.
  • Mediators: The two main classes of mediators produced by mast cells is thoroughly covered and images have been added to enhance this section.
  • Degranulation: The addition of a video and EM images was a really smart idea. The use of a table in this section made learning about mast cell degranulation easier to understand. It also clearly shows the differences between piecemeal and anaphylactic degranulation such as how they are stimulated by TLR and FCeR1 cross - linking respectively.

Pathology:

  • The diagram really summarises the involvement of mast cells in the various forms of immunity very well
  • The information presented on mast cells is correct
  • Mast Cell Activation Disease is really interesting to read
  • The addition of pathogenesis and clinical manifestations really provides a more holistic picture of the mast cell related diseases.
  • The signs and symptoms table was really set out since it shows how the different organs are affected
  • Using a table for treatment was a really wise choice
  • You’ve extensively covered the allergic disorders and how mast cells are involved in their pathogenesis. However, the addition of treatment can improve this section for e.g. loratadine is used to treat allergic rhinitis and ventolin is used to treat asthma. Sodium cromoglycate stabilises mast cells and prevents their degranulation.

Overall:

  • You have clearly shown that they have done extensive research on mast cells.
  • The overall formatting was really well executed
  • The written expression was spectacular and would be easy for a student to follow.
  • The information was really engaging to read especially since it was briefly contextualised. For example, the origin of mast cells was discovered through a patient with leukaemia.
  • The use of tables for certain sections was really effective in teaching the reader about mast cell differentiation or degranulation.
  • Certain sections need to be divided into paragraphs
  • Has good use of diagrams and contains a student diagram
  • Covers many diseases associated with mast cells


Group 6

Introduction:

  • This section is really well written
  • Clearly introduces distinguishing features of T cells
  • It is good that you have briefly mentioned their function in the immune system
  • I don't think it is conventional to cite articles by saying "as shown in (7)(8)". You usually just add the citation numbers at the end of the information.
  • It might be a bit too much information to discuss the classes of T cells in the introduction.

Function:

  • This section could be improved by correcting the wording, grammar and sentence structure.
  • Information is cited and comes from a wide variety of sources.
  • A table would be useful to highlight the differences between Tregs and other effector T cells.
  • The cytoskeleton information should be placed under structure and not function.
  • The diagram doesn't really correspond with the functions of T cells.
  • The mechanisms in which T cells eliminate tumours, virally infected cells or regulates the immune response should be explored.
  • This section is not solely focused on the functions of T cells and this should be corrected.

Structure:

  • The first paragraph bears no relevance to the structure of T cells
  • T cell Morphology: It is better if you do not mention B cells and just focus on the morphology of the T cells. All the necessary information such as cell size, shape and nucleus appearance is stated but the B cell information should be removed.
  • Location shouldn't be placed under the structure subheading
  • T Cell Receptor and Co-receptors: A good diagram was used . The genetic background of the TCR is extensively covered but there is too much detail and this can be difficult for a student who is trying to learn about TCRs for the first time. Not every student will have knowledge about VDJ genes and their rearrangement.

Development:

  • The written expression in this section was clear but is very heavy in information and this may be difficult to facilitate student learning.
  • Information is clearly cited but you don't need to put in "reviewed in". Simply add the numbers to the end of the information you intend to cite.
  • A diagram could really be shown in this section particularly if you are trying to teach a difficult concept such as VDJ rearrangement to students.
  • There are many images for positive and negative selection which simplify the process so that it can be understood well. Adding in one of these images may assist the reader in understanding the process.

History:

  • All historical findings have been cited
  • A few more historical findings can be added especially since T cell research is such a big field

Types of T cells:

  • The line separation here was a bit confusing and should be removed
  • Each type of T cell was thoroughly examined but the amount of information added doesn't follow Mark's 'keep it simple' rule and would make it difficult for students to remember key features of the different T cell types
  • A table illustrating differences between the T cell subtypes can be a useful tool in 'simply' presenting the information.
  • Good use of diagrams
  • It is commendable that you explored the structure, function, development and diseases associated with each T cell type.


Current Research and Future Directions:

  • It is good that you have raised several different applications of T cells.
  • The T cells and Cancer section had too much contextual information and not much on how T cells can be used to fight cancer. What molecular mechanisms are being studied?
  • The Crispr/Cas9 and T cells section does not really illustrate the relationship between these proteins and T cells.
  • The CAR race was interesting to read and clearly illustrated the use of T cells in CAR therapy. However, some of the contextual information can be removed and the information should be condensed to the essence of the wiki page - to 'simply' explain how T cells are used in CAR therapy and for what purpose.

Final thoughts:

  • This section is not needed on a wiki page

Overall:

  • This page was rich in information but there needs to be 'concision' and should be easy to read and remember for students.
  • The introduction was very well written
  • The functions section requires editing and should solely focus on the different functions of T cells such as anti - viral activity, anti - tumour activity, immune regulation, tolerance induction etc.
  • Diagrams are needed for functions and development
  • Good referencing but you don't need to say "as reviewed in [42]"
  • Comparison of T cells can be done in a table format
  • The current research section had too much contextual information and could be improved by focusing on how T cells can be exploited for future treatment of cancers etc.
  • This page has a very extensive amount of information and it is very commendable that you have actively read through many research articles.


Group 7

Overall:

  • An introduction should be added to the page. It's essential to introduce the cell type and its importance in eliminating extracellular parasites. Talk a bit about how it’s a granulocyte and where it is found i.e. the bloodstream
  • The written expression was suitable for student learning
  • Maybe a section on current research or future applications should be explored
  • There needs to be more information on the page

History:

  • Well Referenced
  • History is quite dense with information and can be shortened
  • There is no mention of any historical findings following 1879 for Eosinophil

Birth, Life and Death in the Body:

  • The information in the first bit of this section should be placed inside of the introduction
  • Good use of references
  • Clearly states the different locations of eosinophils through their life cycle
  • Written expression is a suitable level for student learning
  • Main cytokine in eosinophil development - IL-5 was discussed quite well
  • Clearly outlines the need for regulating eosinophil activation and cell death.
  • A flow diagram of the eosinophil's development would be a good addition to this section

Structure:

  • Very good diagram illustrating the effects of different bioactive molecules released from eosinophils and it also has copyright approval
  • Change "which containing" to "which contain"
  • What is the importance of catalysing "2-lysophosphatidylcholine +…"
  • The subheadings underneath granules make it more engaging for students to read
  • A brief explanation of what MBP-1 and MBP-2 should be mentioned in the 'What are they' paragraph
  • The sentence structure in the 'What are they' paragraph needs to be corrected. You cannot begin a sentence with 'suggesting'.
  • The idea of using dotpoints for the granular contents is good in that it makes it easier for the person to read. However, this could also be formatted in a table which includes brief functions of each of these molecules.
  • Mechanisms for content release shouldn't be placed under the structure sub-heading. It should be made a subheading on its own and diagrams illustrating eosinophil exocytosis and cytolysis should be used for a better understanding of the release mechanisms.
  • The role of each mediator was concisely displayed
  • Good choice of granule pictures

Role in Allergy and Disease:

  • The time lapse video didn't work on the wiki itself
  • It should be "There is some evidence" and not "They is some…"
  • The wording of the Helminth paragraph can be improved upon
  • Maybe go into a bit more depth about how the Eosinophil granular proteins are able to degrade ssRNA viruses specifically.
  • How exactly does the EDN and MBP kill the fungal organisms?You have only mentioned that they do but have not gone into a bit more detail about their action on fungal organisms. Do they cleave molecules in the cell wall or is it another mechanism?
  • The 'bacterial' paragraph requires a bit more information and maybe an image of the 'bacterial traps' to show their appearance. Also, you may consider adding in information about how these traps kill the bacteria.
  • There is no information that describes how eosinophils contribute to the pathogenesis of Atopic Dermatitis even though the subheading was 'Role in Allergy'. This should be explored further in order to improve the page and overtly demonstrate the ways in which eosinophils trigger or participate in the allergic response.
  • The paragraph on asthma could be improved by adding more detail about the pathogenesis. You should talk about how eosinophils are recruited and release inflammatory mediators which increase…. As a result, the epithelial lining of the airway becomes damaged and there is a thickening of the wall as well as the excess production of mucus. All of these effects of eosinophil degranulation can lead to obstruction of the airways which in asthma patients manifests as wheezing and shortness of breath.
  • Explore the clinical manifestations of asthma!
  • Good use of diagrams
  • You have not explained what constitutes 'severe eosinophilia' and its effects. Explain how the mechanism of action prevents the generation of disease. For example, by inhibiting receptor tyrosine kinase activity, how does Imantinib treat eosinophil related disease?

References

  1. Katherine Ann Hurley, Thiago M A Santos, Gabriella M Nepomuceno, Valerie Huynh, Jared T Shaw, Douglas B Weibel Targeting the bacterial division protein FtsZ. J. Med. Chem.: 2016; PubMed 26756351
  2. 2.0 2.1 Carlo Bertozzi, Iwan Zimmermann, Sibylle Engeler, Ricarda J C Hilf, Raimund Dutzler Signal Transduction at the Domain Interface of Prokaryotic Pentameric Ligand-Gated Ion Channels. PLoS Biol.: 2016, 14(3);e1002393 PubMed 26943937
  3. 3.0 3.1 Natalie S Poulter, Alice Y Pollitt, Amy Davies, Dessislava Malinova, Gerard B Nash, Mike J Hannon, Zoe Pikramenou, Joshua Z Rappoport, John H Hartwig, Dylan M Owen, Adrian J Thrasher, Stephen P Watson, Steven G Thomas Platelet actin nodules are podosome-like structures dependent on Wiskott-Aldrich syndrome protein and ARP2/3 complex. Nat Commun: 2015, 6;7254 PubMed 26028144
  4. Wendy A Ciovacco, Ying-Hua Cheng, Mark C Horowitz, Melissa A Kacena Immature and mature megakaryocytes enhance osteoblast proliferation and inhibit osteoclast formation. J. Cell. Biochem.: 2010, 109(4);774-81 PubMed 20052670
  5. Tatsuki Uchiyama, Hiroshi Kawabata, Yasuo Miura, Satoshi Yoshioka, Masaki Iwasa, Hisayuki Yao, Soichiro Sakamoto, Masakazu Fujimoto, Hironori Haga, Norimitsu Kadowaki, Taira Maekawa, Akifumi Takaori-Kondo The role of growth differentiation factor 15 in the pathogenesis of primary myelofibrosis. Cancer Med: 2015, 4(10);1558-72 PubMed 26276681
  6. Satoshi Nishimura, Mika Nagasaki, Shinji Kunishima, Akira Sawaguchi, Asuka Sakata, Hiroyasu Sakaguchi, Tsukasa Ohmori, Ichiro Manabe, Joseph E Italiano, Tomiko Ryu, Naoya Takayama, Issei Komuro, Takashi Kadowaki, Koji Eto, Ryozo Nagai IL-1α induces thrombopoiesis through megakaryocyte rupture in response to acute platelet needs. J. Cell Biol.: 2015, 209(3);453-66 PubMed 25963822
  7. S Chen, Y Su, J Wang ROS-mediated platelet generation: a microenvironment-dependent manner for megakaryocyte proliferation, differentiation, and maturation. Cell Death Dis: 2013, 4;e722 PubMed 23846224
  8. Meng Zhao, John M Perry, Heather Marshall, Aparna Venkatraman, Pengxu Qian, Xi C He, Jasimuddin Ahamed, Linheng Li Megakaryocytes maintain homeostatic quiescence and promote post-injury regeneration of hematopoietic stem cells. Nat. Med.: 2014, 20(11);1321-6 PubMed 25326798