Talk:Inflammatory bowel disease: Difference between revisions
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[[User:LiZhang1312|LiZhang1312]] ([[User talk:LiZhang1312|talk]]) 14:30, 14 October 2013 (UTC) |
[[User:LiZhang1312|LiZhang1312]] ([[User talk:LiZhang1312|talk]]) 14:30, 14 October 2013 (UTC) |
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{{ course assignment | course = Education Program:Case Western Reserve University/ANTH 302 Darwinian Medicine (Fall 2013) | term = 2013 Q3 }} |
Revision as of 21:57, 19 October 2013
![]() | Ideal sources for Wikipedia's health content are defined in the guideline Wikipedia:Identifying reliable sources (medicine) and are typically review articles. Here are links to possibly useful sources of information about Inflammatory bowel disease.
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![]() | Medicine: Gastroenterology C‑class Mid‑importance | ||||||||||||
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Helminthic therapy
I have significantly shortened the section on helminthic therapy. This is still in its experimental stages, and Wikipedia does not need to tell the public how a German company is trying to market this. When it hits the shelves, we'll see.
I have also replaced the news links with an actual scientific report in a peer-reviewed journal. The BBC link quoted the New Scientist, and the latter got its information from the article. This is much more direct. JFW | T@lk 23:17, 27 Nov 2004 (UTC)
Please note the link is broken for the scientific report (reference #19). This should be fixed. — Preceding unsigned comment added by 71.7.239.165 (talk) 13:27, 2 January 2012 (UTC)
Life events
Life events may herald onset of Crohn's but not IBD as a whole - doi:10.1111/j.1572-0241.2006.00931.x. JFW | T@lk 16:59, 11 March 2007 (UTC)
Clustering with immune conditions
doi:10.1111/j.1572-0241.2007.01215.x JFW | T@lk 06:23, 29 April 2007 (UTC)
Review on diagnostics
doi:10.1053/j.gastro.2007.09.001 JFW | T@lk 01:52, 23 November 2007 (UTC)
Rollback feature
I have been reverting a vandal, but I made a mistake the first time and I think I corrected it the second time. Just started using this so please if I still made any mistakes please bring it to my attentions and I will fix it or always feel free to fix anything I should do. Thank you, --CrohnieGalTalk 11:39, 25 April 2008 (UTC)
External links
I've pruned the external links section. I removed:
- a dead link (no content),
- a blog,
- a link to an organization that provides face-to-face meetings in two cities, and
- an online support group.
The first three are pretty obvious to most people: for example, Wikipedia is a worldwide encyclopedia, and something that happens half a world a way does you no good. The last one sometimes surprises people, so let me explain. Wikipedia's external links policy and the specific guidelines for medicine-related articles do not generally permit the inclusion of external links to non-encyclopedic material, particularly including internet chat boards and e-mail discussion groups. Here's some specific information from the guidelines:
- This page, which applies to all articles in the entire encyclopedia, says that links "to social networking sites (such as MySpace or Fan sites), discussion forums/groups (such as Yahoo! Groups), USENET newsgroups or e-mail lists" are to be avoided.
- This page deprecates ""helpful" external links, such as forums, self-help groups and local charities."
- This medical-specific page reinforces the pan-Wiki rules, with a note that "All links must meet Wikipedia's external links guidelines, which in particular exclude discussion forums."
Wikipedia is an encyclopedia, and while it may occasionally be useful to patients or their families, it is not a web directory. Please do not re-insert links that do not conform to the standard rules. Any editor, BTW, is welcome to read all of the rules and perform another "audit" in the remaining links. Thanks, WhatamIdoing (talk) 03:36, 28 April 2008 (UTC)
Pred of death
doi:10.1111/j.1572-0241.2008.01836.x - steroids increase mortality, thiopurines do not. JFW | T@lk 10:11, 26 May 2008 (UTC)
HLA - B27
add info about HLA-B27 please! —Preceding unsigned comment added by 128.125.28.127 (talk) 01:39, 1 June 2008 (UTC)
Thrombosis
Risk of thrombosis increased, especially during flare. I can hear a trial approaching, especially with one of the oral antithrombotics. In fact, perhaps this might also show a disease modifying effect! doi:10.1016/S0140-6736(09)61963-2 JFW | T@lk 10:04, 21 February 2010 (UTC)
What kind of inflammatory bowel disease is this?
Before any reinsertion, I think it needs to be specified what kind of inflammatory bowel disease (if even IBD) is referred to in the following study, since it appears to consist of multiple types with different pathogenesis. Mikael Häggström (talk) 16:20, 25 October 2010 (UTC)
- Research[1] has shown that IL-23 is overexpressed in tissues taken from mouse models of IBD. The group showed that knocking out IL-23 (heterodimer of IL-12p40 and IL-23p19) sharply reduced inflammation of the bowel, both in terms of cells and proinflammatory cytokine production. Also, they found that a novel group of CD4+ T lymphocytes, Th17 T cells, are highly unregulated in bowels of diseased mice. Taken together, the group shows that IL-23 but not IL-12 (a heterodimer of IL-12p40 and IL-12p35) drives innate and T cell mediated intestinal inflammation.
- ^ Hue S, Ahern P, Buonocore S; et al. (2006). "Interleukin-23 drives innate and T cell-mediated intestinal inflammation" ([dead link] – Scholar search). J. Exp. Med. 203 (11): 2473–83. doi:10.1084/jem.20061099. PMC 2118132. PMID 17030949.
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Pregnancy
doi:10.1136/gut.2010.222893 - large cohort of pregnancy on thiopurines; they seem to be safe. JFW | T@lk 12:51, 5 January 2011 (UTC)
Evolutionary Considerations
Prototype to material that should be considered when discussing causes of IBD This source is a primary source that I believe is relevant to the discussion on IBD etiology. The interpretation has not been reviewed by another article.
New research headed by Towfique Raj has shown that variation in a group of genes can put a person at risk for developing inflammatory bowel disease. These susceptibility gene variants were shown to have experienced positive selection 1200-1600 years ago[1] . Four of these genes (RF1, PLEK, DEXI, CD86) are involved in regulation of transcriptional response against viral and bacterial agents[1] . Several of these genes (TMEM116, UHRF1BP1, IRF1, DEXI, RNASET2, CD86, PLEK) were shown to be expressed differentially when their primary dendritic cells were exposed to mycobacterium tuberculosis infection[1] . Three of these genes (FUT2, SH2B3, IRF1) have been correlated with local pathogenic diversity[1] .
From the agricultural revolution onward, humanity has been exposed to a plethora of bacterial and viral vectors due to increasing population density and changing lifestyle. Taken together, the data suggests that the high bacterial and viral exposure experienced by humans in this time led to increased selection for an overactive immune system. While adaptive in this setting, modern medicine and hygiene have changed environmental conditions for humans. It is possible that low pathogen exposure increases susceptibility to inflammatory bowel disease as a result of an imbalance in the immune system.
1. Towfique Raj, Manik Kuchroo, Joseph M. Replogle, Soumya Raychaudhuri, Barbara E. Stranger, Philip L. De Jager. Common Risk Alleles for Inflammatory Diseases Are Targets of Recent Positive Selection. The American Journal of Human Genetics, 2013; DOI: 10.1016/j.ajhg.2013.03.001
LiZhang1312 (talk) 14:30, 14 October 2013 (UTC)
![]() | This article was the subject of an educational assignment in 2013 Q3. Further details were available on the "Education Program:Case Western Reserve University/ANTH 302 Darwinian Medicine (Fall 2013)" page, which is now unavailable on the wiki. |
- ^ a b c d e Raj, Towfique (3/1/2013). "Common Risk Alleles for Inflammatory Bowel Disease are Targets of Recent Positive Selection". The American Journal of Human Genetics. 92 (4): 517–529. doi:http://dx.doi.org/10.1016/j.ajhg.2013.03.001. Retrieved 14 October 2013.
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