中国脑血管病杂志2011，Vol.8Issue(5)：230-234,5.DOI:10.3969/j.issn.1672-5921.2011.05.002
血栓调节蛋白-33G/A基因多态性与脑梗死的关系
Relationship between thrombomodulin promoter-33G/A polymorphism and cerebral infarction
摘要
Abstract
Objective To investigate the correlation between cerebral infarction and thrombomodulin (TM) promoter-33G/A (TM-33G/A) mutation. Methods A total of 130 patients with cerebral infarction in the First People's Hospital in Kunming area, Yunnan province from December 2009 to July 2010 and 120 controls (patients with depression, anxiety, dizziness, and encephalitis) admitted to the hospital at the same time period were included in the study. A polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay was used to detect the TM-33G/A polymorphism of the included subjects. Multivariate Logistic Regression was used to analyze the correlation between cerebral infarction and TM33G/A polymorphism. Results ①In 130 patients with cerebral infarction, GG genotype was 99, GA genotype was 30, AA genotype was 1, and the G/A point mutation rate was 23.85％. In 120 patients in the control group, GG genotype was 106, GA genotype was 13, AA genotype was 1, and the G/A point mutation rate was 11.67％. There was significant difference between the two groups (P ＜0.05 ). ②Multivariate Logistic Regression analysis revealed that, in addition to history of smoking, hypertension, increased iow-density lipoprotein cholesterol, and increased fasting glucose, the TM-33G/A polymorphism was also an independent risk factor for cerebral infarction (OR, 2. 175, 95％ CI: 1. 049 -4. 511, P = 0. 037). Conclusion TM-33G/A polymorphism may be one of the risk factors for cerebral infarction.关键词
脑梗死/血栓调节蛋白/基因/多态性,限制性片段长度Key words
Brain infarction/ Thrombomodulin/ Genes/ Polymorphism, restriction fragment length引用本文复制引用
武岭,唐慧,侯晓艳,孟强..血栓调节蛋白-33G/A基因多态性与脑梗死的关系[J].中国脑血管病杂志,2011,8(5):230-234,5.基金项目
云南省科技计划资助项目(2010ZC211) （2010ZC211）
