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作 者:华开罗[1] 夏冰[2] 李春[2] 郭秋莎[2] 夏华向[3]
机构地区:[1]武汉大学医学院附属中山医院消化内科,430033 [2]武汉大学中南医院综合医疗科武汉大学医学院消化系病研究中心过敏与免疫相关性疾病重点实验室 [3]香港大学玛丽医院内科
出 处:《胃肠病学》2006年第7期408-411,共4页Chinese Journal of Gastroenterology
摘 要:背景:幽门螺杆菌(H.pylori)感染是消化性溃疡的主要病因。脂多糖(LPS)通过Toll样受体(TLR)4激活核因子(NF)-κB,在抗感染免疫应答中起启动和调节作用。TLR4基因发生Asp299Gly突变可中断TLR4介导LPS信号传导。目的:研究我国湖北省汉族人群TLR4基因Asp299Gly多态性与消化性溃疡和H.pylori感染的关系。方法:采用病例对照研究和聚合酶链反应-限制性片段长度多态性(PCR-RFLP)法,检测126例消化性溃疡患者和264名正常对照者的TLR4等位基因Asp299Gly基因型分布。结果:消化性溃疡者H.pylori阳性率(90.5%)显著高于正常对照组(61.7%)(P<0.0001,OR=5.889,95%CI:3.089~11.216)。在H.pylori感染相关性消化性溃疡组和正常对照组中均未发现TLR4基因Asp299Gly的突变型,其基因型、等位基因以及携带者频率总体分布无显著性差异。结论:本研究未能显示TLR4基因Asp299Gly基因多态性与H.pylori感染、H.pylori相关性消化性溃疡形成有相关性。Helicobacter pylori (H. pylori) is a major cause of peptic ulcer, Toll-like receptor (TLR) 4 is a member of nuclear factor (NF)-KB activators that is known to bind lipopolysaccharide(LPS) through their LPR domain. The Asp299Gly mutation interrupts TLR4-mediated LPS signaling. Aims: To study the distribution of TLR4 gene Asp299Gly polymorphism and to define the relationship between TLR4 genotype and H. pylori-associated peptic ulcer in Chinese population with Han nationality in Hubei province, Methods: One hundred and twenty six patients with peptic ulcer and 264 healthy controls were genotyped by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) method for TLR4 gene Asp299Gly polymorphism. Results: H. pylori infection was detected in 90.5% of 126 patients and 61.7% of 264 healthy controls (P〈0.0001, odds ratio=5.889, 95% CI: 3.089-11.216). The distributions of the genotype and allele frequencies of TLR4 Asp299Gly were not significantly different in the groups studied. All the subjects tested were of TLR4 gene wild type A. Conclusions: The non-synonymous single nucleotide polymorphism Asp299Gly in TLR4 gene is rare and is not associated with H. pylori-associated peptic ulcer in Chinese population with Han nationality in Hubei province.
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