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作 者:叶冬青[1] 胡以松[1] 李向培[2] 杨仕贵[1] 张国庆[1]
机构地区:[1]安徽医科大学流行病与卫生统计学系教研室 [2]安徽省立医院风湿科
出 处:《中华风湿病学杂志》2004年第4期196-201,共6页Chinese Journal of Rheumatology
基 金:国家自然科学基金资助项目(30371247);安徽省自然科学基金项目(98437231);教育部科学技术研究重点资助项目(03056);安徽省教育厅重点科研资助项目(2002kj175ZD)
摘 要:目的探讨基质衍生因子1-3'A(stromalcell-derivedfactor1-3'A,SDF1-3'A)、趋化性细胞因子受体2-64I(chemoattractantcellreceptor2-64I,CCR2-64I)190位点、单核趋化蛋白1(monocytechemoattractantprotein-1promoter-2518polymorphism,-2518MCP-1)基因多态性及其交互作用与系统性红斑狼疮(SLE)的相关性。方法以143例SLE病人和157名健康对照为对象进行病例对照研究。应用聚合酶链反应—限制性内切酶片段长度多态性(polymerasechainreaction/restrictionfragmentlengthpolymor-phism,PCR-RFLP)方法确定SDF1-3'A和-2518MCP-1基因多态性,应用突变特异性扩增系统(amplifica-tionrefractorymutationsystem,ARMS)确定CCR2-64I基因多态性。结果-2518MCP-1、CCR2-64I、SDF1-3'A等位基因及基因型频率在SLE和健康对照组之间差异无显著性。但-2518MCP-1A/G基因型对照组高于病例组(χ2=4.11,P=0.04)。基因间交互作用分析发现,当SDF1-3'A、-2518MCP-1、CCR2-64I基因型分别为G/G、A/G和G/G时,对SLE发病可能具有保护作用(P<0.05)。其他基因型间均未见交互作用(P>0.05)。结论单个-2518MCP-1、CCR2-64I、SDF1-3'A基因多态性与SLE易感性无关联,但他们之间可能存在交互作用。Objective To investigate the influence of stromal cell-derived factor 1-3'A (SDF1-3'A),chemoattractant cell receptor 2-64I (CCR2-64I),the monocyte chemoattractant protein-1 promoter -2518 polymorphism(-2518MCP-1) and the gene-gene interaction on systemic lupus erythematosus(SLE).Methods The polymorphisms of SDF1-3'A,CCR2-64I and -2518MCP-1 were determined by polymerase chain reaction/restriction fragment length polymorphism(PCR-RFLP) and amplification refractory mutation system (ARMS) respectively.The case-control study was used to explore the association between gene polymorphism and SLE.Results There was no significant difference in distribution of allelic and genotype frequency of SDF1-3'A,CCR2-64I and -2518MCP-1 between SLE and control.But compared with SLE patients,the genotype frequency of A/G of -2518MCP-1 was higher in control.The analysis of gene-gene interaction showed that there was a significant protection effect when the genotype of SDF1-3'A,CCR2-64I and -2518MCP-1 was G/G,A/G and G/G respectively.Conclusion There is no direct effect of SDF1-3'A,CCR2-64I and -2518MCP-1 polymorphism on SLE ,but it is possible that there is gene-gene interaction.
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