Talk:Inclusion body myositis

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General Comments[edit]

My father has IBM and is not a good news, I'd like to share info and experience about it. pino --— Preceding unsigned comment added by (talkcontribs) 5 May 2005 17:53‎

My Mom was just recently diagnosed with this disease. We are going to put her on a nutritional detoxification program to see if it restores some of the lost neurological functionality that may be causing the inclusion bodies to be formed. We'll see how she's doing in a few months. -Brent --— Preceding unsigned comment added by (talkcontribs) 25 June 2005 11:32‎

  • I completed a big edit of this article, snipping away some spurious material and improving legibility. --Agamemnon2 08:32, 15 September 2005 (UTC)

can inclusion body myositis kill you? i dont know and i need to know because im doing a project on it. --— Preceding unsigned comment added by (talkcontribs) 20 February 2007 02:29‎

Clean up[edit]

This Article needs a clean up badly to conform to Wiki standards. I am surprised the conservative Ghouls who prowl Wiki slapping Citation needed tags everywhere, have not found the site yet? The referencing system needs stanardizing, use Diberri's here I have converted those references I can find, other tagged.

Too many blog sites used as references, they are not WP:RS. This Article appears to be based on only four RS references! With 850 studies on the Pubmed list for the condition, a few more need to be referenced. There has been many more (about 100, since Nov. 2006). Added some more recent ref's but text needs update.

I will move the out of date piece to this page where it belongs, as discussion. When citing a study in the Article, one can only say what the authors say. A reveiw is needed to quote other conclusions, editors can not make their own conclusions in the Article but can discuss it on the Talk page. Jagra (talk) 04:30, 3 April 2008 (UTC)

Recent (November 2006) Research Advance.[edit]

Published online before print October 31, 2006 Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0603386103

MyoD expression restores defective myogenic differentiation of human mesoangioblasts from inclusion-body myositis muscle.

Roberta Morosetti *, Massimiliano Mirabella *, Carla Gliubizzi *, Aldobrando Broccolini *, Luciana De Angelis ¶, Enrico Tagliafico ||, Maurilio Sampaolesi **, Teresa Gidaro *, Manuela Papacci *, Enrica Roncaglia ||, Sergio Rutella , Stefano Ferrari ||, Pietro Attilio Tonali *, Enzo Ricci *, and Giulio Cossu **

,*Department of Neurosciences and Interdisciplinary Laboratory for Stem Cell Research and Cellular Therapy, Catholic University, Largo A. Gemelli 8, 00168 Rome, Italy; Fondazione Don Carlo Gnocchi, 00194 Rome, Italy; Institute of Cell Biology and Tissue Engineering, San Raffaele Biomedical Science Park, 00128 Rome, Italy; ¶Department of Histology and Embriology, University "La Sapienza," 00161 Rome, Italy; ||Department of Biomedical Sciences, University of Modena and Reggio Emilia, 41100 Modena, Italy; **Stem Cell Research Institute, San Raffaele Hospital, 20132 Milan, Italy; Institute of Hematology, Catholic University, 00168 Rome, Italy; and Department of Biology, University of Milan, 20133 Milan, Italy Edited by Tullio Pozzan, University of Padua, Padua, Italy, and approved September 19, 2006 (received for review April 28, 2006)

This is how to reference it on this page, you do not need to type all that stuff above, anyone clicking on the PMID number will instantly see the Article Abstract PMID 17077152 and can then click on the free full Article.

This is a highly selective layman's translation and synopsis. Please refer to the original article for confirmation of the information presented here.

Synopsis: This research reports the isolation and characterization of mesoangioblasts, [ME - so - angie - OH - blasts] vessel-associated stem cells, obtained from the diagnostic muscle biopsies of patients with inflammatory myopathies (IM). Mesoangioblasts represent a distinct type of mesoderm progenitor cells that eventually develop (differentiate) into a variety of mesoderm tissues including skeletal, cardiac and smooth muscle. The number of mesoangioblast cells isolated, their rate of growth and lifespan, their marker expression, and their ability to differentiate into smooth muscle do not differ between mesoangioblasts from normal patients and IM mesoangioblasts. IBM mesoangioblasts show the same ability to divide that is observed in normal muscle suggesting that the disease has not reduced their proliferation potency. Nevertheless, although IBM mesoangioblasts can normally differentiate into smooth muscle cells (SMCs), their differentiation into skeletal muscle seems markedly impaired, because no skeletal myotubes are seen arising from IBM mesoangioblasts after laboratory stimulation. Thus, mesoangioblasts isolated from IBM, fail to differentiate into skeletal myotubes (developing skeletal muscle fibers characterized by their tubular appearance).

IBM mesoangioblasts were found to express high levels of genes known to inhibit the generation of new muscle (myogenesis) such as TGFbeta-1, SFRP-2 (secreted frizzled-related protein 2), and BHLHB3 (basic helix-loop-helix domain containing class B3 transcription factor).

In IBM mesoangioblasts, BHLHB3, is highly over active and this in turn inhibits MyoD function, thus preventing the creation of new muscle (myogenesis). IBM mesoangioblasts did not give rise to differentiated myotubes and did not display any MyoD genetic activity (no MyoD mRNA), and MyoD could not be induced by the researcher's laboratory techniques.

The problem of reduced MyoD function in IBM can be addressed in two ways. First, through cell transplantation. Using a mouse model, the researchers treated [human] IBM mesoangioblasts in the laboratory with a virus (an adenoviral vector) carrying with it the full-length mouse MyoD. So, the researchers took the genetic code for MyoD from mice and used the virsus to put it into these IBM mesoangioblast cells. These treated cells were then transplanted into the muscle of special research mice, significantly restoring normal muscle function. This introduction of MyoD overcomes the BHLHB3 inhibition. It also activates the MyoD that is already present in the cells, irreversibly making the cells generate new muscle.

Second, the researchers examined the effect of using a genetic method to block out the function of the BHLHB3 gene. The IBM mesoangioblasts display increased levels of BHLHB3 messenger RNA (mRNA), the inhibitor of MyoD. Therefore, the researchers used small interfering RNA (siRNA) created specifically to block the action of BHLHB3 in mesoangioblasts from three IBM patients. The siRNA treated cells were able to differentiate into muscle, giving rise to muscle myotubes after 7 days.

Therefore, either by silencing the overactive BHLHB3 gene or by transplanting modified cells in order to over express MyoD, we should be able to restore muscle genesis in the IBM mesoangioblasts, opening the way for new cell-based therapeutic strategies to treat IBM. — Preceding unsigned comment added by Jagra (talkcontribs) 3 April 2008 06:53‎

Comprehensive review:

Dalakas, Marinos C. (2006). Sporadic inclusion body myositis—diagnosis, pathogenesis and therapeutic strategies. NATURE CLINICAL PRACTICE NEUROLOGY, AUGUST, 2006, VOL 2, NO 8, 437-447.

Review: January 2006: Twenty two articles resulted from a conference held on inclusion body myositis (s-IBM) - Inclusion-body myositis: Clinical and pathologic aspects, and basic research potentially relevant to treatment. January 26-28, 2005 in Santa Monica. The TMA funded the Conference and the Muscular Dystrophy Association assisted by funding the printing and distribution of the Conference report. The 22 articles were published in electronic format as an Expedited E-Pub at [1] on December 16, 2005. They appear in print in Neurology Volume 66(2) Supplement 1 January 24, 2006. [2]

On my website, I keep a running review of all of the references in English listed on Pubmed. This incorporates most articles published on IBM. I refer the reader to: [3] for articles that cover from June 2005 to June 2006. Previous articles can be found indexed on my main webpage. Thank you. — Preceding unsigned comment added by Jagra (talkcontribs) 5 April 2008 02:40‎

External links[edit]

Wikipedia's external links policy and the specific guidelines for medicine-related articles do not permit the inclusion of external links to non-encyclopedic material, particularly including internet chat boards and e-mail discussion groups. Because I realize that most normal editors haven't spent much time with these policies, please let me provide 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 for support groups.  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 an "audit" in the remaining links.  Thanks, WhatamIdoing (talk) 05:22, 28 April 2008 (UTC)


There's a suggested order for the sections on pages like this at WP:MEDMOS. The list there does not have to be followed precisely, but if it seems sensible and appropriate, or if it suggests ideas about more information you can include, then please consider the advantages of "standardizing" this article (but only to the extent that it is appropriate). WhatamIdoing (talk) 05:22, 28 April 2008 (UTC)

Lithium study comments[edit]

I have removed the following comment from the Article because it is unsourced. All material must be accompanied by WP:RS citations. A phone call from some (maybe disgruntled) researcher is really for this page not the Article.

Comment: I was contacted by a senior researcher who made the following comment on this press release "The press release states outright that lithium can slow progression of inclusion body myositis. The study referred to did not administer lithium to any patients with IBM; the mistake reflects an exageration in which people claim that a manipulated animal has the disease when it in fact is only a model. In this case, the model is grossly inaccurate, but that is another story, and the press release grossly exagerating; it also claims that "mice genetically engineered to have IBM demonstrated markedly better motor function six months after receiving daily doses of lithium chloride, compared with non-treated mice." In fact, the actual results reported in the publication of this study showed no statistically significant difference in motor function in six-month treated mice."

A couple of other comments the citation is not a 'press release' but a scientific study published in a peer reveiwed journal. They cannot say just anything, and this is what it actually says in the full free text paper;

Suppression of GSK-3 activity using either a specific inhibitor or lithium chloride significantly reduced tau phosphorylation and partially rescued motor impairment. Evaluation of the motor performance suggests that prolonged treatment with LiCl may also benefit motor function because we found that mice maintained on the control diet showed a significant deterioration in performance over the 6-month test period. In contrast, all LiCl-treated mice showed a trend toward improved motor performance compared with the saline-treated control animals, although this did not reach statistical significance (see Fig 4C).

As only part of the result is included in the Article it would be more accurate and useful to include both findings. Jagra (talk) 07:49, 8 July 2008 (UTC)