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  1. #61

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    23.04.2007
    3,455

    03 2009




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    Guardian; 04.12.2009 18:23.
       

  2. #62
      Igor_Passau
    12.05.2009
    38
    2,990
    "Fuer einen treuen Freund gibt es keinen Preis, nichts wiegt seinen Wert auf"
       

  3. #63
      Natali
    21.04.2007
    880

    27 2010 . , , , (). , , Journal of Medical Microbiology.
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    , . , . , Faecalibacterium prausnitzii . , , Butyricicoccus pullicaecorum, .

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    . Filip Van Immerseel, Ghent University , . " . , . .
       

  4. #64
      Igor_Passau
    12.05.2009
    38
    2,990

    Natali
    27 2010 . , , , (). , , Journal of Medical Microbiology.
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    , . , . , Faecalibacterium prausnitzii . , , Butyricicoccus pullicaecorum, .

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    . Filip Van Immerseel, Ghent University , . " . , . .
    ! !
    "Fuer einen treuen Freund gibt es keinen Preis, nichts wiegt seinen Wert auf"
       

  5. #65
      ˸
    04.01.2010
    62
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  6. #66
      Igor_Passau
    12.05.2009
    38
    2,990

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    "Fuer einen treuen Freund gibt es keinen Preis, nichts wiegt seinen Wert auf"
       

  7. #67
      Igor_Passau
    12.05.2009
    38
    2,990

    . .

    Peripheral neuropathy is one of the most frequently reported neurological extra-intestinal manifestations of the Crohn disease. Former studies have showed sympathetic neuropathy as early manifestation of CD by physical tests. The aim of this study is to examine sympathetic neuropathy in CD by using sympathetic skin response (SSR). We performed SSR on 6 Patients (4 male, 2 female) that were diagnosed as CD. Their age was between 26 till 68 years with the mean of (43.3 +/- 17.1) years. The duration of their disease was at least 4 years (mean: 9.0 +/- 8.4) and none of the patients had any symptoms or signs related to autonomic nervous system dysfunction. Hand and foot latencies in CD patients were prolonged relative to controls and the difference of hand latencies was statistically significant. Two patients demonstrated total abnormal results. In conclusion, there is some sub-clinical sympathetic dysfunction in CD patient. This suggests that SSR can be useful in detecting early autonomic changes in these patients.

    http://www.ncbi.nlm.nih.gov/pubmed/20349555
    "Fuer einen treuen Freund gibt es keinen Preis, nichts wiegt seinen Wert auf"
       

  8. #68

    23.09.2010
    ,
    47
    26,604

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    12. Geboes K. Patholoqy of inflammatory bowel disease (IBD): variability with time and treatment // Colorectal. Dis. 2001. V. 3. . 2-12.

    13. Helits T., Halme L., Lappala*hen M. et al. CARD 15/NOD 2 gene variants are associated with familially occurring and complicated forms of Crohn's disease // Gut. 2003. V. 52. . 558-562.

    14. Lee F.D., Maguire C., Obeidat W. et al. Importance of cryptolytic lesions and pericryptal qranulomas in inflammatory bowel disease // Clin. Pathol. 1997. V. 50. . 148-152.

    15. Peeters M., Geypen B., Claus D. et al. Clustering of increased small intestinal permeability in families with Crohn's disease // Gastroenterology. 1997. V. 113, 3. . 802-807.

    16. Sheehan A.L., Warren B.F., Gear M.W.L. et al. Fat-wrapping in Crohn's disease: patholoqical basis and relevance to surgical practice // Br. J. Surg. 1992. V. 79. . 955-959.

    17. Valdez R., Appelman H., Broun*er M.P. et al. Diffuse duodenitis associated with ulcerative colitis // Amer. J. Surg. Patrol. 2000. V. 24. P. 1407-1413.
       

  9. #69
      Igor_Passau
    12.05.2009
    38
    2,990

     Bacteroidetes

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    http://www.biomedcentral.com/1471-2180/11/7





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    http://old.izvestia.com.ua/?/article...1/12/204518-14
    "Fuer einen treuen Freund gibt es keinen Preis, nichts wiegt seinen Wert auf"
       

  10. #70

    23.09.2010
    ,
    47
    26,604

    ! . ?
    Aryl Hydrocarbon Receptor Activation by TCDD Reduces Inflammation Associated with Crohn's Disease

    Crohn's disease results from a combination of genetic and environmental factors that trigger an inappropriate immune response to commensal gut bacteria. The aryl hydrocarbon receptor (AhR) is well known for its involvement in the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant that affects people primarily through the diet. Recently, TCDD was shown to suppress immune responses by generating regulatory T cells (Tregs). We hypothesized that AhR activation dampens inflammation associated with Crohn's disease. To test this hypothesis, we utilized the 2,4,6-trinitrobenzenesulfonic acid (TNBS) murine model of colitis. Mice were gavaged with TCDD prior to colitis induction with TNBS. Several parameters were examined including colonic inflammation via histological and flow cytometric analyses. TCDD-treated mice recovered body weight faster and experienced significantly less colonic damage. Reduced levels of interleukin (IL) 6, IL-12, interferon-gamma, and tumor necrosis factor-α demonstrated suppression of inflammation in the gut following TCDD exposure. Forkhead box P3 (Foxp3)egfp mice revealed that TCDD increased the Foxp3+ Treg population in gut immune tissue following TNBS exposure. Collectively, these results suggest that activation of the AhR by TCDD decreases colonic inflammation in a murine model of colitis in part by generating regulatory immune cells. Ultimately, this work may lead to the development of more effective therapeutics for the treatment of Crohn's disease. http://toxsci.oxfordjournals.org/con...68.short?rss=1
       

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