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目的:研究基因单核苷酸多态性与缺血性脑卒中的关系,寻找缺血性脑卒中发病的遗传易感基因。资料来源:应用计算机检索Medline1980-2005年期间有关纤维蛋白原基因多态性与缺血性脑卒中的文献,检索词“stroke,PlasmaFibrinogen,polymorphism”,并限定文章语言种类为英文。同时计算机检索中国科技期刊全文数据库1995-2005年期间纤维蛋白原基因多态性与缺血性脑卒中的文献,并限定文章语言种类为中文。检索词“缺血性脑卒中,纤维蛋白原,基因多态性”,还通过与作者通信以获得全文等形式获得全文资料。资料选择:纳入文献只限于病例对照研究型论著,排除观察对比研究、经验总结、个案报告等文献。资料提炼:共检索到50余篇关于纤维蛋白原基因多态性与缺血性脑卒中的文献,20篇符合纳入标准,排除30余篇文献。资料综合:血浆纤维蛋白原水平受遗传和环境因素的共同作用,纤维蛋白原基因多态性对血浆纤维蛋白原水平起重要的调控作用,纤维蛋白原通过参与动脉粥样硬化和辅助血小板的聚集及改变血液流变学状态,促进血栓的形成使缺血性脑卒中的发病率增高。但是纤维蛋白原基因多态性的确切作用机制和分子功能还有待于进一步研究。结论:关于纤维蛋白原单核苷酸多态性与缺血性脑卒中的关系尚有争议,还需进一步的研究。
Objective: To study the relationship between single nucleotide polymorphism and ischemic stroke in order to find genetic predisposition genes for ischemic stroke. DATA SOURCES: The computer-based search of the literature on the association between gender and menopausal women during the Medline period 1980-2005 was conducted. The term “stroke, Plasma Fibrinogen, polymorphism” was searched and the language of the article was defined as English. At the same time, we searched the literature of China’s sci-tech periodical full-text database for fibrinogen gene polymorphism and ischemic stroke during 1995-2005, and defined the article’s language type as Chinese. The term “ischemic stroke, fibrinogen, genetic polymorphisms” was also obtained by communicating with authors for full text and other forms of full text information. Data selection: The inclusion of the literature is limited to case-control research articles, excluding observation of comparative studies, lessons learned, case reports and other literature. DATA EXTRACTION: A total of more than 50 articles on the polymorphisms of fibrinogen and ischemic stroke were retrieved, of which 20 met the inclusion criteria and excluded more than 30 articles. DATA SYNTHESIS: Plasma fibrinogen levels are influenced by both genetic and environmental factors. Fibrinogen polymorphisms play an important regulatory role in plasma fibrinogen levels. Fibrinogen, through its involvement in atherosclerosis and secondary platelet aggregation And change the state of blood rheology and promote the formation of thrombus to increase the incidence of ischemic stroke. However, the exact mechanism of action of fibrinogen gene polymorphism and molecular function remains to be further studied. Conclusion: The relationship between single nucleotide polymorphism of fibrinogen and ischemic stroke remains controversial and needs further study.