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   <subfield code="a">10.1007/s00535-010-0368-4</subfield>
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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s00535-010-0368-4</subfield>
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   <subfield code="a">Comparison of the fecal microbiota profiles between ulcerative colitis and Crohn's disease using terminal restriction fragment length polymorphism analysis</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Akira Andoh, Hirotsugu Imaeda, Tomoki Aomatsu, Osamu Inatomi, Shigeki Bamba, Masaya Sasaki, Yasuharu Saito, Tomoyuki Tsujikawa, Yoshihide Fujiyama]</subfield>
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   <subfield code="a">Background: Terminal restriction fragment length polymorphism (T-RFLP) analysis is a powerful tool to assess the diversity of a microbial community. In this study, we performed T-RFLP analysis of the fecal microbiota from patients with ulcerative colitis (UC) and those with Crohn's disease (CD). Methods: Thirty-one patients with UC, 31 patients with CD, and 30 healthy individuals were enrolled. The polymerase chain reaction (PCR) products obtained from the 16S rRNA genes of fecal samples were digested with BslI, and T-RF lengths were determined. Results: The fecal microbial communities were classified into 5 clusters. Twenty-eight of the 30 healthy individuals and 17 of the 18 patients with inactive UC were classified into clusters I, II, and III, but these clusters included a small number of patients with active UC and inactive/active CD. In contrast, 8 of the 13 patients with active UC and the majority of CD patients (12 of the 16 patients with inactive CD, and 11 of the 15 patients with active CD) were included in clusters IV and V. Based on the BslI-digested T-RFLP database, the bacteria showed a significant decrease in the Clostridium family in patients with active UC and inactive/active CD. In contrast, Bacteroides were significantly increased in CD patients. No significant differences were observed between patients with active UC and those with active CD. Conclusion: The fecal microbial communities of IBD patients were different from those of healthy individuals. The gut microbiota of patients with inactive UC tended to be closer to that of healthy individuals, suggesting different roles for the fecal microbiota in the pathophysiology of UC and CD.</subfield>
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   <subfield code="a">Springer, 2011</subfield>
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   <subfield code="a">Inflammatory bowel disease</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">T-RFLP</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Clostridium</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Bacteroides</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Andoh</subfield>
   <subfield code="D">Akira</subfield>
   <subfield code="u">Division of Mucosal Immunology, Graduate School of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Imaeda</subfield>
   <subfield code="D">Hirotsugu</subfield>
   <subfield code="u">Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Aomatsu</subfield>
   <subfield code="D">Tomoki</subfield>
   <subfield code="u">Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Inatomi</subfield>
   <subfield code="D">Osamu</subfield>
   <subfield code="u">Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Bamba</subfield>
   <subfield code="D">Shigeki</subfield>
   <subfield code="u">Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Sasaki</subfield>
   <subfield code="D">Masaya</subfield>
   <subfield code="u">Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Saito</subfield>
   <subfield code="D">Yasuharu</subfield>
   <subfield code="u">Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Tsujikawa</subfield>
   <subfield code="D">Tomoyuki</subfield>
   <subfield code="u">Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Fujiyama</subfield>
   <subfield code="D">Yoshihide</subfield>
   <subfield code="u">Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
   <subfield code="4">aut</subfield>
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  <datafield tag="773" ind1="0" ind2=" ">
   <subfield code="t">Journal of Gastroenterology</subfield>
   <subfield code="d">Springer Japan</subfield>
   <subfield code="g">46/4(2011-04-01), 479-486</subfield>
   <subfield code="x">0944-1174</subfield>
   <subfield code="q">46:4&lt;479</subfield>
   <subfield code="1">2011</subfield>
   <subfield code="2">46</subfield>
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   <subfield code="B">NATIONALLICENCE</subfield>
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   <subfield code="D">Akira</subfield>
   <subfield code="u">Division of Mucosal Immunology, Graduate School of Medicine, Shiga University of Medical Science, Seta Tsukinowa, 520-2192, Otsu, Japan</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
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