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作 者:Christoph J.Auernhammer Kathrin Zitzmann Fabian Schnitzler Julia Seiderer Peter Lohse George Vlotides Dieter Engelhardt Michael Sackmann Burkhard G(o|¨)ke Thomas Ochsenkühn
机构地区:[1]Department of Internal Medicine Ⅱ-Grosshadern [2]Department of Clinical Chemistry-Grosshadern
出 处:《World Journal of Gastroenterology》2005年第8期1196-1199,共4页世界胃肠病学杂志(英文版)
基 金:Supported by the Department of Clinical Chemistry - Grosshadem, Ludwig-Maximilians-University
摘 要:AIM: To study the role of the intracellular receptor domain of gp130 in human inflammatory bowel disease (IBD).METHODS: We amplified and sequenced the complete exon 17 of the human gp130 gene in 146 patients with IBD. According to clinical and histopathological signs,the 146 patients with IBD were classified as having Crohn's disease (n = 73) or ulcerative colitis (n = 63),or as indeterminate status (n = 10).RESULTS: No mutations in exon 17 of the gp130 gene could be detected in any of the 146 patients with IBD examined.CONCLUSION: There is no evidence that mutations in exon 17 of the gp130 gene are involved in the pathogenesis of human IBD.AIM: To study the role of the intracellular receptor domain of gp130 in human inflammatory bowel disease (IBD). METHODS: We amplified and sequenced the complete exon 17 of the human gp130 gene in 146 patients with IBD. According to clinical and histopathological signs, the 146 patients with IBD were classified as having Crohn's disease (n = 73) or ulcerative colitis (n = 63), or as indeterminate status (n = 10). RESULTS: No mutations in exon 17 of the gp130 gene could be detected in any of the 146 patients with IBD examined. CONCLUSION: There is no evidence that mutations in exon 17 of the gp130 gene are involved in the pathogenesis of human IBD.
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