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Stem cell articles.

I wrote a whole big page only for the server to get backed up, and lost everything! AGR! lol

Here is a current article that is interesting to read. I don't bother reading anying but the allogeneic (donor) stem cell related parts. I believe since host vs graft disease (the worst risk of doing donor vs your own stem cells) was virtually eliminated (in the words of Dr. Burt) through his current methods (which also involve new treatments to stop/prevent hvgd), that the future will now be pointed towards soley allogeneic. Maybe not in the short term, but as other countries catch on.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3108654/
I also found a German Trial (that i just now lost in the last draft err!) that stated 10 of 11 patients followed up at 3 years were all crohns free. The other one of the 11 had died, not related to crohns. I think it was from "complications" - who knows what they are since it was not a US trial - it was done in Germany, published in 2008. I am trying to find up to date info as of 2011 on these patients, but its a little harder trying to find that info in Germany.



To get in contact with the coordinator of Dr. Burts crohns section, for stem cell trials, email Kristen - k-katsenes@northwestern.edu
 
This is part of that article i lost

"German study pooled 11 CD patients, 6 of whom had active disease and 4 who were taking medication. Of the original 11 patients, 1 died and the remaining 10 found that their CD became inactive following allogeneic HSCT for other medical reasons. Patients were followed up at a median interval of 34 months, and their CD remained in remission.

Allogeneic HSCT alters the genetic mechanisms responsible for the exaggerated immune responses to luminal antigens and has been used on this basis. Its full benefit is not solely its ability to switch the genetic pool of T-cells available completely. It also stimulates donor lymphocyte-induced recipient T-cell aplasia, a process called graft-versus-autoimmunity. The donor lymphocytes attack the recipient's aberrant T-cells, resulting in complete depletion of the former immune system. This is the presumed mechanism of allogeneic HSCT's superior, long-lasting effect when compared with autologous HSCT in treating hematologic malignancy concomitant with autoimmune disease. An allogeneic transplantation should be considered if the immune hyperactivity is presumed to result from underlying genetic abnormality manifested in bone marrow-derived cells. In comparison with autologous HSCT, the abnormality is presumed to be secondary to proliferation of aberrant peripheral T-cells hypersensitive to luminal antigen".
 
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