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1.
内皮细胞型一氧化氮合酶基因多态性与血管性疾病的关系   总被引:4,自引:0,他引:4  
内皮细胞型一氧化氮合酶基因是动脉粥样硬化性血管病的易感基因,该基因的多态性与颈动脉粥样硬化斑块,缺血性卒中,心血管病,高血压病以及糖尿病肾病等血管性疾病的发生和发展有一定的相关性。  相似文献   

2.
内皮型一氧化氮合酶(eNOS)基因被列为冠心病(CHD)的一个候选易感基因。本文对与冠心病关系较为密切的三种eNOS基因多态性:4b/a、T786C和G894T的研究进展作一综述,对进一步认识冠心病的发病机制具有重要意义。  相似文献   

3.
内皮细胞型一氧化氮合酶基因是动脉粥样硬化性血管病的易感基因,该基因的多态性与颈动脉粥样硬化斑块、缺血性卒中、心血管病、高血压病以及糖尿病肾病等血管性疾病的发生和发展有一定的相关性。  相似文献   

4.
内皮型一氧化氮合酶基因多态性与脑梗死的研究   总被引:1,自引:0,他引:1  
内皮型一氧化氮合酶基因的错义突变(Glu298Asp)导致一氧化(NO)合成减少,而后者对血管内皮起到保护作用。NO产生的减少使血管内皮功能降低,进而使颈动脉粥样斑块形成的易感性增加,从而引起脑梗死。本文就NO合酶及NO的生物学特性及与颈动脉粥样硬化和脑梗死的相关性研究作一综述。  相似文献   

5.
冠状动脉粥样硬化性心脏病(cronary atherosclerotic heart disease,CHD)简称冠心病,是指冠状动脉发生粥样硬化引起管腔狭窄或闭塞,导致心肌缺血缺氧或坏死引起的心脏病.吸烟、肥胖、高血压及代谢综合征等均已成为广为人知的几个冠心病重要危险因素.但也有患者没有这些危险因素存在,并且在一些个体中,常有明显的冠心病家族史,说明冠心病是环境与遗传危险因素动态相互作用所致的.目前已有诸多冠心病基因多态性研究,包括内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS).在近年的荟萃分析中显示,某些遗传变异可能为特定群体冠心病发病的危险因素之一.  相似文献   

6.
目的 探讨内皮型一氧化氮合酶 (eNOS)基因多态性与急性心肌梗死 (AMI)的相关性。方法 依据eNOS基因外显子 7G894T位点设计引物 ,通过巢式聚合酶链反应 (PCR)扩增目的片段 ,限制性内切酶消化目的片段 ,琼脂糖凝胶电泳 ,紫外透射分析仪检测 ,计数 10 7例AMI病人及 81例健康者基因型及突变基因频率 ,通过χ2 检验有无统计学意义。结果 eNOS基因外显子 7的 894位点有 3种基因型 :GG、GT、TT。AMI组 10 7例中2 5例发生G894T突变 ,纯合子TT 9例 ,杂合子GT 16例。对照组 81例中 13例发生G894T突变 ,均为杂合子。两组等位基因纯合子突变具有非常显著统计学意义 ,x2 =5 4 2 9,P <0 0 5 ,两组等位基因总突变率 (纯合子 +杂合子 )无明显统计学意义 ,x2 =1 5 2 9,P >0 0 5。结论 eNOS基因 894位点TT型突变与AMI发病密切相关 ,是AMI发病的危险因子  相似文献   

7.
目的 研究我国青岛地区人群内皮型一氧化氮合酶( eNOS) G894T基因多态性与冠状动脉病变的关系.方法 选择100例冠心病患者为研究对象,行多层螺旋CT冠脉成像并计算冠脉钙化积分(CACS),根据CACS分组.应用基因芯片技术对患者的基因型和等位基因进行分析并比较.结果 CACS不同者,基因型分布和等位基因频率不同,差异具有显著性(P<0.01).Logistic回归分析显示eNOS基因G894T多态性、吸烟是冠状动脉病变的危险因素.多元线性回归示eNOS基因GT +TT型、高血脂、吸烟是影响CACS的主要因素,标准回归系数(Beta)分别为0.476,0.217,0.191 (P <0.05).结论 吸烟是冠状动脉病变的独立危险因素,eNOS基因G894T多态性、高血脂、吸烟共同参与冠状动脉病变的发生,eNOS基因G894T可能是冠状动脉病变的遗传易感基因.  相似文献   

8.
目的 探讨内皮型一氧化氮合酶(eNOS)基因G894T多态性和内皮素-2(endothelin-2,ET-2)基因A985G多态性与老年高血压的关系.方法 测定高血压患者和年龄、性别相匹配的对照者的身高、体重、血脂、血糖等指标.采用基因芯片技术测定(230例高血压患者和186例健康人)的eNOS和ET-2基因多态性,并对测定的基因型和等位基因频率进行病例对照研究.应用logistic回归分析性别、体重指数、血脂、血糖及基因型对高血压的影响. 结果 高血压组eNOS基因G894T中GG、GT、TT基因型频率及G、T等位基因频率与对照组相比差异显著(分别为χ2=13.698及χ2=13.075,P均<0.05);高血压组ET-2基因A985G中AA、AG、GG基因型频率及A、G等位基因频率与对照组相比差异显著(分别为χ2=19.358及χ2=20.452,P均<0.05).Logistic回归分析显示性别、体重指数、血糖、血总胆固醇及eNOS、 ET-2基因型是高血压发病的危险因素,OR值分别为0.052、1.121、 1.323、4.006、0.294、3.423(P<0.01).结论 性别、体重指数、血糖、血总胆固醇是高血压的独立危险因素;eNOS 基因G894T和ET-2基因A985G可能是老年高血压发病的易感基因.  相似文献   

9.
目的探讨内皮型一氧化氮合酶(eNOS)基因G894T多态性与老年钙化性心瓣膜病(SCVD)的关系。方法采用基因芯片技术测定老年钙化性心瓣膜病的患者(132例)和无瓣膜钙化的对照患者(108例)的eNOSG894T多态性,并对两组检测结果进行基因频率比较,应用二分类logistic回归分析该基因多态性对瓣膜钙化的影响。结果SCVD组GT+TT基因型、T等位基因频率均明显高于对照组,差异具有统计学意义(基因型c^2=8.486,P=0.004;等位基因c^2=9.425,P=-0.002);二分类多自变量logistic回归分析显示,eNOS G894T多态性、总胆固醇水平、低密度脂蛋白水平、空腹血糖水平、体质量指数、收缩压水平以及高血压病史、冠心病病史、高血脂病史均与SCVD独立相关,差异有统计学意义(P〈0.05),为SCVD的危险因素。结论eNOSG894T可能是SCVD的遗传易感基因。  相似文献   

10.
一氧化氮合酶基因多态性与糖尿病血管并发症   总被引:2,自引:0,他引:2  
一氧化氮合酶 (NOS)有 3种亚型 ,即内皮细胞型、诱导型和神经型。NOS基因是与糖尿病并发症有关的重要候选基因 ,NOS基因存在多态性 ,ecNOS 4b 4a基因多态性可能与糖尿病肾病 (DN)的发生相关 ,而与糖尿病视网膜病变 (DR)的发生无关。iNOS基因 (CCTTT) 1 4 等位基因是DR、DN和糖尿病并发冠心病的保护性基因。对nNOS基因的研究较少  相似文献   

11.
目的探讨内皮型一氧化氮合酶(eNOS)Glu298Asp基冈多态性与冠心病的关系。方法以89例冠心病患者为病例组(男性62例,女性27例),均行冠状动脉造影确诊,对照组78例(男性44例,女性34例)均行冠状动脉造影排除冠心病,运用基因芯片技术方法检测eNOS Glu298 Asp基因的多态性,对比分析冠心病组及对照组eNOS Glu298 Asp基因型及等位基因的差异。结果eNOS Glu298 Asp基因型分布冠心病组与对照组比较差异无统计学意义(P=0.495),D等位基因频率冠心病组(10.11%)与对照组(10.27%)相比差异无统计学意义(P=0.965)。结论eNOS Glu298 Asp基因变异与冠心病的发病可能无相关性。  相似文献   

12.
13.
目的 采用Meta分析的方法评估内皮型一氧化氮合酶(eNOS)基因G894T多态性与心肌梗死(MI)相关性.方法 按照文献纳入标准制定检索策略后,采用计算机检索PubMed、中国期刊全文数据库和万方数据库中1995年至2012年12月30日间发表的探讨eNOS基因G894T多态性与MI相关性的病例-对照研究,由两名作者独立提取数据及评价方法学质量后,采用RevMan 5.1软件进行Meta分析.结果 最终纳入13个病例-对照研究,共计2264例MI患者,2774例健康对照人群.基于随机效应模型的Meta分析结果显示,eNOS G894T多态性能够显著增加MI的患病风险[T vs.G:OR=1.51,95%CI:1.21~1.89;TT vs.GG:OR=1.99,95%CI:1.21~3.26;GT vs.GG:OR=1.34,95%CI:1.07~1.68;(GT+TT) vs.GG:OR=1.47,95%CI:1.14~1.88;TT vs.(GG+GT):OR=1.80,95%CI:1.13~2.86].亚组分析结果表明这一相关性存在于亚洲人群与急性心肌梗死(AMI)之间,而与非亚洲人群无相关性,与混合MI(AMI和陈旧性MI)间可能存在相关性,漏斗图提示有发表偏倚存在.结论 基于当前的证据,eNOS G894T多态性与MI存在相关性,特别是亚洲人群与AMI.但当前证据尚不能确定eNOS G894T多态性是否是MI的独立危险因素,以及eNOS G894T多态性与陈旧性MI、与非亚洲人群AMI的相关性.  相似文献   

14.
BACKGROUND: Reduced or impaired synthesis of nitric oxide promotes the proliferation of vascular smooth muscle cells, and thus may induce the neointimal formation leading to coronary in-stent restenosis. Recent reports have suggested that the Glu298Asp polymorphism in exon 7 of the endothelial nitric oxide synthase gene is associated with coronary spasm and acute myocardial infarction. In this study, we have examined the implication of this polymorphism with regard to coronary restenosis after Palmaz-Schatz stent deployment. METHODS: Eighty-nine lesions in 85 consecutive patients were treated with Palmaz-Schatz stents, and were prospectively followed up for 6 months. The lesions were classified into a restenosis group (% diameter stenosis=50%) and a non-restenosis group. Assessment was made using an automated quantitative angiographic system. We performed polymerase chain reaction-restriction fragment length polymorphism analysis to detect the missense Glu298Asp variant in exon 7 of the endothelial nitric oxide synthase gene. RESULTS: Coronary risk factors and angiographic findings of stenotic lesions did not differ between the groups. Univariate analyses showed that the missense Glu298Asp variant was the only statistically significant predictor of restenosis (odds ratio, 4.27; P=0.025). In addition, multiple logistic regression analysis revealed the missense Glu298Asp variant as the only independent predictor for in-stent restenosis (odds ratio, 3.90; P=0.036). CONCLUSIONS: The missense Glu298Asp variant may be an independent risk factor for in-stent restenosis.  相似文献   

15.
BACKGROUND: Coronary spasm seems to be associated with coronary nitric oxide deficiency. OBJECTIVES: We investigated whether the Glu298Asp polymorphism in the endothelial nitric oxide synthase (eNOS) gene is a definite risk factor for coronary spasm and whether diffuse spasm involving normal-looking coronary artery correlates significantly with the Glu298Asp polymorphism, in contrast with focal spasm superimposed on an atherosclerotic plaque. METHODS: A polymerase chain reaction followed by restriction fragment length polymorphism analysis was performed in 118 control participants and in 102 patients with variant angina and a similar degree of atherosclerotic burden. Patients with coronary spasm were divided into diffuse spasm and focal spasm subgroups according to morphological criteria. RESULTS: There was a significantly higher incidence of the Glu298Asp polymorphism in the coronary spasm group than in the control group (21.5% compared with 8.5%, P=0.006). Multiple logistic regression analysis using risk factors and the Glu298Asp polymorphism showed that the most important predictive factor for coronary spasm was the Glu298Asp polymorphism (odds ratio 2.83, 95% confidence interval 1.25-6.41, P=0.009). The diffuse spasm subgroup had a significantly higher frequency of the Glu298Asp polymorphism than the control group (25.9% compared with 8.5%, P=0.002). However, the focal spasm subgroup did not differ from the control group in the frequency of Glu298Asp polymorphism. CONCLUSION: The Glu298Asp polymorphism in the eNOS gene is a definite risk factor for coronary spasm, especially for diffuse coronary spasm. This result supports the notion that diffuse coronary spasm is significantly associated with endothelial dysfunction, in contrast to focal spasm.  相似文献   

16.
An endothelial nitric oxide synthase (eNOS) gene polymorphism (Glu298Asp) has been associated with cardiovascular disease. We investigated whether carriage of the polymorphism was associated with functional changes in the endothelium, and how genotype altered the harmful and beneficial impact of environmental influences on the endothelium. Endothelium-dependent, flow-mediated brachial artery dilatation (FMD) and endothelium-independent dilatation response to glyceryl trinitrate were measured using high-resolution ultrasound in 248 subjects (131 female, 117 male, aged 20 to 28) genotyped for the Glu298Asp polymorphism. Vascular function was compared between genotype groups and interactions with the proatherogenic risk factor, smoking, and the antiatherogenic influence of n-3 fatty acids (n-3FA) were investigated. Vascular function was not related to genotype in the group as a whole or within sexes. However, among males, smoking was associated with lower FMD in Asp298 carriers (nonsmokers 0.125+/-0.085 mm versus smokers 0.070+/-0.060 mm, P=0.006) but not in Glu298 homozygotes (nonsmokers 0.103+/-0.090 mm versus smokers 0.124+/-0.106, P=0.5). In the whole group, n-3FA levels were positively related to FMD in Asp298 carriers (reg coeff=0.023 mm/%, P=0.04, r=0.20) but not in Glu298 homozygotes (reg coeff=-0.019 mm/%, P=0.1). These differences between genotype groups were significant in interaction models. The Glu298Asp polymorphism is associated with differences in endothelial responses to both smoking and n-3 FA in healthy young subjects. These findings raise the possibility of genotype-specific prevention strategies in cardiovascular disease.  相似文献   

17.
目的 探讨内皮源性一氧化氮合酶 (e NOS)基因 G894T多态性与脑梗死的关系。方法 取病例组 1 4 8例 ,对照组 1 0 9例 ,各例抽取新鲜静脉血 5 ml,提取 DNA后 ,通过 PCR- RFL P法进行基因分型。结果 病例组和对照组各基因型分布 GG、GT、TT分别是 83.1 % ,1 4 .2 % ,2 .7% ,对照 90 .8% ,9.2 % ,0 .0 0 % (χ2 =3.1 78,P=0 .0 75) ,符合 Hardy- Weinberg平衡 ,两组统计学上无明显差异。但 T等位基因频率在病例组中较对照组明显升高 (P=0 .0 2 7) ,相对危险度 1 .33(95% CI:0 .61 7~ 0 .92 2 )。病例组中 ACE D等位基因频率亦较对照组明显升高 (P=0 .0 1 7)。病例组 T等位基因携带者的血浆胆固醇水平较 GG纯合子患者明显升高 (P=0 .0 2 5) ,而在对照组中并无此差异。结论  e NOS基因 G894T突变可能是国人脑梗死的遗传学危险因素 ,其致病机理可能与 ACE D缺失型及血浆胆固醇水平有协同作用。  相似文献   

18.
19.
目的 探讨天津市汉族人群内皮型一氧化氮合酶(eNOS)基因第14内含子rs3918181位点多态性与原发性高血压(EH)的关系.方法 采用聚合酶链反应-限制性内切酶片段长度多态分析法(PCR-RFLP)对290例EH患者和161名健康对照者的eNOS基因rs3918181位点进行基因多态性分型,同时检测所有研究对象的血脂等危险因素,分析不同基因型与EH发病的关系.结果 两组年龄、体质指数的差异有统计学意义(均为P<0.05).EH组患者的AA、AG和GG基因型分布频率分别为0.293、0.393和0.314,对照组分别为0.180、0.472和0.348,两组相比差异有统计学意义(均为P <0.05);EH组A与G等位基因频率分别为0.490和0.510,对照组分别为0.416和0.584,两组相比差异有统计学意义(均为P <0.05).影响EH的危险因素有年龄、体质指数.结论 eNOS基因rs3918181位点多态性与EH相关.  相似文献   

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