长沙地区汉族人群载脂蛋白H基因多态性的研究

目的 探讨长沙地区汉族人群载脂蛋白H(apolipoproteinH，apoH)基因多态性的分布规律。方法 采用PCR-单链构象多态(single conformation polymorphism，SSCP)技术和DNA直接测序法检测100例长沙地区汉族正常人的apoH基因8个外显子的多态标记，并与其他人种进行比较。结果 发现长沙地区汉族人群apoH基因的4种位点多态性，其中3号外显子G341A(Ser88Asn)多态位点GG、GA和AA基因型频率分别为0.900、0．090和0．010，G和A等位基因频率分别为0．945和0．055；7号外显子G817T(Leu247Val)多态GG、GT和TT基因型频率分别为0．610、0．340和0．050，G和T等位基因频率分别为0．780和0．220；8号外显子G1025C(Try316Ser)多态GG、GC基因型频率分别为0．880和0．120，G和C等位基因频率分别为0．940和0．060；8号外显子C1080T多态CC、CT基因型频率分别为0．930和0．070，C和T等位基因频率分别为0．965和0．035。结论 长沙地区汉族人群apoH基因存在4种位点多态性，不同多态位点基因频率分布与其他人种比较有显著性差异。     

长沙地区汉族人群apoB基因多态性与脑梗死的关系研究

目的探讨湖南长沙地区汉族人群载脂蛋白B(apolipoprotein B,apoB)G12669A、C7673T多态性与脑梗死的关系。方法采用聚合酶链反应-限制性片段长度多态性分析法分别检测130例脑梗死患者和100例正常对照的apoB基因G12669A、C7673T多态等位基因频率。结果湖南长沙地区汉族人群存在apoB基因G12669A、C7673T多态性,脑梗死组中apoB基因G12669A、C7673T多态等位基因频率G/A为0.904/0.096,C/T为0.881/0.119,在正常对照G/A为0.955/0.045,C/T为0.960/0.040;脑梗死组apoB基因G12669A多态A等位基因频率及C7673T多态T等位基因频率均显高于正常对照组(P<0.05,P<0.01)。结论apoB G12669A多态A等位基因可能是湖南长沙地区汉族人群脑梗死发病的遗传易感因素。     

G10631A和C521T基因多态性与脑梗死相关性

目的探讨肾素-血管紧张素系统G10631A及C521T基因多态性与脑梗死患病风险的相关性。方法选择2016-05—2019-05郑州人民医院神经内科收治的100例脑梗死患者为脑梗死组,并选择同期100名健康志愿者为对照组。采集2组受试者静脉血样,采用酚/氯仿法提取DNA,采用限制性片段长度多态性分析技术检测G10631A及G521T的单核苷酸多态性。结果脑梗死组患者G10631A的AA基因型及A等位基因频率均高于对照组(χ2=8.672、10.172,P<0.05),脑梗死组患者C521T的TT基因型及T等位基因频率均高于对照组(χ2=8.665、22.118,P<0.05),G10631A的AA基因型、C521T的TT基因型可增加脑梗死发生率(OR=2.039、2.031,P<0.05)。脑梗死组患者A-T单体型出现频率高于对照组(χ2=16.127,P<0.05),但脑梗死组G-C单体型出现频率低于对照组(χ2=17.368,P<0.05)。结论肾素-血管紧张素系统G10631A的AA基因型及A等位基因、G521T的TT基因型及T等位基因和A-T单体型可能是脑梗死的遗传易感因素。     

MMP-2、MMP-9基因多态性与缺血性脑卒中临床分型及预后

目的探讨基质金属蛋白酶2(Matrix Metalloproteinase-2,MMP-2)基因C1306T、C735T和MMP-9基因C1562T多态性位点与缺血性脑卒中的关系。方法采用限制性片段长度多态性分析技术,检测缺血性脑卒中组232例和健康对照组235例MMP-2基因C1306T、C735T和MMP-9基因C1562T多态的分布。结果缺血性脑卒中组和对照组MMP-2 C1306T基因型和等位基因频率分布无统计学意义。在动脉粥样硬化性血栓性脑梗死组MMP-9 C1562T的CT+TT基因型频率和T等位基因频率、MMP-2 C735T的CC基因型频率和C等位基因频率明显高于对照组(P<0.05),而在脑栓塞组、腔梗组差异无统计学意义(P>0.05)。多因素Logistic回归分析,MMP-2、MMP-9不同基因型别与缺血性脑卒中预后无显著相关性(P>0.05)。结论 MMP-2 C735T的C等位基因、MMP-9 C1562T的T等位基因是动脉粥样硬化性血栓性脑梗死的遗传易感基因之一。MMP-2、MMP-9基因多态性与缺血性脑卒中预后无关。     

NOS3基因多态性与血脂、缺血性脑卒中的相关性研究

目的为了探索NOS3基因G894T多态性与缺血性脑卒中的关联,以及与血脂的关系。方法聚合酶链式反应-限制性片段长度多态性(PCR-RFLP),琼脂糖凝胶电泳检测100例缺血性脑卒中患者和对照组80例健康志愿者的NOS3基因G894T多态性。自动生化分析仪检测血脂指标。结果 (1)卒中组与对照组相比GT(27/100和22/120)和TT(7/100和2/120)基因型分布频率较高(P 0. 05)。T等位基因分布在卒中组(20. 5%)也显著高于对照组(10. 83%)(P 0. 01);(2)卒中组中TT基因型携带者血脂水平TC和LDL-C显著高于GG和GT基因型患者,而其他血脂水平无显著差异;(3)关联分析显示TT基因型与卒中患病风险具有相关性(P 0. 05)。结论 NOS3基因多态性与缺血性脑卒中发病存在关联,TT基因型携带者患病风险高于GG基因型携带者。     

血管紧张素原基因M235T及α-内收蛋白基因G460T多态性与脑梗死的关系

目的 探讨血管紧张素原(AGT)基因M235T及α-内收蛋白基因G460T多态性与脑梗死的关系.方法 采用PCR-限制性片段长度多态性(RFLP)方法检测396例脑梗死患者(脑梗死组)和360名健康体检者(正常对照组)AGT基因M235T及α-内收蛋白基因G460T基因型及等位基因频率,分析其与脑梗死的关系.结果 (1)脑梗死组AGT MM基因型频率明显低于正常对照组,MT基因型频率明显高于正常对照组(均P ＜0.05);两组间等位基因频率差异无统计学意义.(2)两组间α-内收蛋白G460T基因型及等位基因频率差异无统计学意义.(3)脑梗死组MM+ GG频率显著少于正常对照组(P＜0.05).结论 AGT基因MT基因型可能与脑梗死发病有关;α-内收蛋白基因G460T多态性可能与脑梗死的发病无关;MM +GG基因型组合可能为脑梗死发病的保护因素.     

蒙古族脑卒中患者5,10-亚甲基四氢叶酸还原酶、内皮型一氧化氮合酶、β-1肾上腺素能受体和G蛋白β3亚单位基因多态性的研究

目的 研究蒙古族脑卒中患者5,10-亚甲基四氧叶酸还原酶(MTHFR)基因C677T、内皮型一氧化氮合酶(eNOS)基因G894T、β-1肾上腺素能受体(ADRB1)基因G1165C、G蛋白β3亚单位(GNB3)基因C825T位点的多态性.方法 用PCR方法检测68例蒙古族脑卒中患者和107名健康对照者上述4个基因位点的多态性.用Logistic回归分析基因多态性与脑卒中的关系.结果 脑卒中组eNOS基因G894T位点T等位基因频率显著高于正常对照组(P<0.01);两组MTHFR基因C677T位点、ADRB1基因G1165C位点、GNB3基因C825T位点基因型及等位基因频率比较差异无统计学意义.Logistic回归分析显示eNOS基因G894T位点GT基因型是脑卒中发病的独立危险因素(OR为4.550,95%CI为1.324～15.633,P<0.05).结论 eNOS基因G894T GT基因型是蒙古族脑卒中患者发病的独立危险因素;MTHFR基因C677T位点、ADRB1基因G1165C位点、GNB3基因C825T位点多态性与蒙古族脑卒中无明显关系.     

载脂蛋白M基因多态与脑梗死的相关性

目的 探讨中国北方汉族人群载脂蛋白M(ApoM)基因多态与脑梗死的关系.方法 采用聚合酶链反应(PCR)扩增基因组DNA直接测序法结合PCR-限制性片段长度多肽(RFLP)方法检测560例脑梗死和550名健康对照的ApoM基因多态,发现1号内含子rs805264、5号内含子rs707922及rs707921 3个单核苷酸多态位点.结果 脑梗死组ApoM基因rs805264位点GA+AA型及A等位基因频率、rs707922位点GT+TT型及T等位基因频率、rs707921位点CA+AA型及A等位基因频率均明显高于对照组.ApoM基因rs805264、rs707922和rs707921 3个多态位点存在显著连锁不平衡,三座位等位基因G-G-C紧密连锁,A-T-A紧密连锁(χ2=2595.03,P<0.01).3个位点的每对之间均存在强连锁不平衡(D′=0.972～0.992).Logistic回归分析显示,A-T-A单体型与脑梗死明显相关(OR= 1.780, 95% CI 1.333～ 2.376,P<0.01).结论 ApoM基因rs805264位点GA基因型及A等位基因、rs707922位点GT基因型及T等位基因、rs707921位点CA基因型及A等位基因与脑梗死密切相关.ApoM基因A-T-A单体型可能与脑梗死遗传致病有关.     

广东汉族人群缝隙连接蛋白37基因多态性与动脉粥样硬化性脑梗死的关系

目的探讨广东汉族人群缝隙连接蛋白37(Cx37)基因多态性与动脉粥样硬化性脑梗死的关系。方法应用SNaPshot技术,检测250例动脉粥样硬化性脑梗死患者(病例组)和200例健康人(对照组)的Cx37基因rs1764391多态位点的基因型和等位基因频率。结果病例组与对照组Cx37基因的多态位点rs1764391的基因型分布无统计学意义(P=0.217);病例组的T等位基因频率高于对照组(22.4%vs 17.7%,P=0.085);病例组中,TT+CT基因型(T等位基因携带者)的颈总动脉内膜-中膜厚度大于CC基因型,差异有统计学意义(P=0.032)。结论广东汉族人群Cx37基因的多态位点rs1764391与动脉粥样硬化性脑梗死无关,T等位基因增加颈总动脉内膜-中膜厚度。     

载脂蛋白(a)基因增强子DH Ⅲ多态性与湖南地区汉族人群动脉粥样硬化血栓性脑梗死的相关性

目的研究载脂蛋白(a)基因DHⅢ增强子-1230A/G多态性与湖南地区汉族人群动脉粥样硬化血栓性脑梗死的关系。方法应用聚合酶链式反应-限制性片段长度多态性技术及DNA序列测定法检测湖南地区汉族人群134例动脉粥样硬化血栓性脑梗死患者、110名健康对照者的载脂蛋白(a)基因DHⅢ增强子-1230A/G多态,同时用免疫比浊法检测所有研究对象的血浆脂蛋白(a)水平。结果在动脉粥样硬化血栓性脑梗死组载脂蛋白(a)基因DHⅢ增强子-1230 A/G多态G等位基因频率(0.728)明显高于对照组(0.618;P=0.01);GG型频率(0.500)明显高于对照组(0.400;P0.05)。动脉粥样硬化血栓性脑梗死组各基因型血浆脂蛋白(a)水平均明显高于对照组,差异具有统计学意义(P0.05)。结论载脂蛋白(a)基因DHⅢ增强子-1230 A/G多态性可能与中国湖南地区汉族人群动脉粥样硬化血栓性脑梗死有关;G等位基因可能是动脉粥样硬化血栓性脑梗死的危险因素之一。     

Apolipoprotein H gene polymorphisms and risk of primary cerebral hemorrhage in a Chinese population

BACKGROUND AND PURPOSE: Apolipoprotein H (ApoH) has been implicated in several physiologic pathways including lipid metabolism, coagulation and the production of hypertension, which are related to the pathogenesis of primary cerebral hemorrhage (PICH). The gene coding for ApoH is polymorphic, with the occurrence of several common alleles in the general population. This genetically determined variation can effect lipid metabolism and the production of hypertension. We determined the distribution of ApoH gene polymorphisms in Chinese people and investigated whether these polymorphisms were associated with increased risk of PICH in a Chinese population. METHODS: We studied polymorphisms of the ApoH gene by the polymerase chain reaction-single strand conformation polymorphism technique and DNA sequencing in 140 PICH patients and 100 healthy control subjects. Serum antiphospholipid antibodies and lipid levels were also examined in all subjects. RESULTS: Four polymorphisms of the ApoH gene have been identified in Chinese people. No difference in genotype frequencies of G817T (Leu247Val) polymorphism, G1025C (Try316Ser) polymorphism and C1080T polymorphism was observed between PICH patients and control subjects (p > 0.05). The G341A (Ser88Asn) polymorphism correlated significantly with PICH. The frequencies of the A allele were significantly higher in PICH patients than in controls, especially in PICH patients with hypertension and a family history of stroke. CONCLUSIONS: Our results suggest that the G341A (Ser88Asn) polymorphism might be associated with increased risk of PICH in a Chinese population. The association appeared to be mediated by the generation of hypertension.     

Coagulation factor XIII VaI34Leu polymorphism in patients with small vessel disease or primary intracerebral hemorrhage

BACKGROUND AND PURPOSE: Factor (F) XIII is a transglutaminase which stabilizes fibrin clots by forming cross-links between chains of fibrin. A common Val34Leu polymorphism of FXIII is correlated with the level of activated plasma FXIII. The homozygous 34Val genotype may be associated with an increased risk for thrombosis by forming fibrin fibers more resistant to fibrinolysis. The aim of the study was to investigate the association between the FXIII Val34Leu polymorphism and the risk of ischemic stroke due to small vessel disease (SVD) or the risk of primary intracerebral hemorrhage (PICH). METHODS: 66 patients with SVD stroke and 135 age- and sex-matched controls as well as 64 patients with PICH and their 127 controls were included. The FXIII Val34Leu polymorphism was genotyped using the polymerase chain reaction and restriction enzyme digestion methods. RESULTS: The homozygous 34Val genotype was found significantly more often in patients with SVD stroke than in their controls (62 vs. 42%). On multivariate analysis, the Val/Val genotype was associated with an increased risk of SVD stroke (odds ratio: 2.1, 95% confidence interval: 1.1-3.9). The genotype distribution did not differ significantly between PICH patients and their controls (50 vs. 43%). CONCLUSION: Our results suggest that the Val/Val genotype of FXIII could be associated with an increased risk of SVD stroke.     

Factor XIII Val34Leu polymorphism and the risk of myocardial infarction under the age of 36 years

There are limited and controversial data regarding the impact of factor XIII (FXIII) Val34Leu polymorphism in the pathogenesis of premature myocardial infarction (MI). We examined whether FXIII Val34Leu polymorphism is associated with the development of early MI. We recruited 159 consecutive patients who had survived their first acute MI under the age of 36 years (mean age = 32.1 +/- 3.6 years, 138 were men). The control group consisted of 121 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease (CHD). FXIII Val34Leu polymorphism was tested with polymerase chain reaction and reverse hybridization. There was a lower prevalence of carriers of the Leu34 allele in patients than in controls (30.2 vs. 47.1%, p = 0.006). FXIII Val34Leu polymorphism was associated with lower risk for acute MI after adjusting for major cardiovascular risk factors (odds ratio [OR] = 0.51, 95% confidence interval [CI] 0.27-0.95, p = 0.03). Subgroup analysis according to angiographic findings ("normal" coronary arteries [n = 29] or significant CHD [n = 130]) showed that only patients with MI and significant CHD had lower prevalence of carriers of the Leu34 allele compared to controls after adjusting for major cardiovascular risk factors (OR = 0.42, 95% CI 0.22-0.83, p = 0.01). Our data indicate that FXIII Val34Leu polymorphism has a protective effect against the development of MI under the age of 36 years, particularly in the setting of significant CHD.     

Brain-derived neurotrophic factor gene C-270T and Val66Met functional polymorphisms and risk of schizophrenia: a moderate-scale population-based study and meta-analysis

BACKGROUND: Lines of evidence have suggested that the brain-derived neurotrophic factor (BDNF) gene may be involved in the pathogenesis of schizophrenia. Two common functional polymorphisms C-270T and Val66Met within the BDNF gene were first reported by Kunugi et al. [Kunugi, H., Nanko, S., Hirasawa, H., Kato, N., Nabika, T., Kobayashi, S., 2003. Brain-derived neurotrophic factor gene and schizophrenia: polymorphism screening and association analysis. Schizophr. Res. 62, 281-283.] and pls expand this too: Hong et al. (2003) to be significantly associated with schizophrenia. However, subsequently several studies obtained conflicting results. METHODS: We compared the allele/genotype frequencies of the C-270T and Val66Met polymorphisms and the haplotype frequencies at the two polymorphisms in a moderate independent patient-control sample from the Han Chinese population. Two systematic meta-analyses were performed to assess the collective evidence for association across studies for each of the two polymorphisms. RESULTS: No statistically significant differences were found in allele or genotype or haplotype frequencies between patient and normal control subjects for either of the two polymorphisms. On the other hand, the meta-analysis of all published population-based association studies showed statistically significant evidence for heterogeneity among each of the two polymorphisms. Stratification of the studies by ethnicity of the samples yielded no significant evidence for an association with the polymorphisms in the Caucasian population (for C-270T polymorphism: pooled OR(Caucasian)=0.736, 95% CI=0.476-1.139, p=0.169; for Val66Met polymorphism: pooled OR(Caucasian)=1.027, 95% CI=0.796-1.325, p=0.835), nor in the Asian population (for C-270T polymorphism: pooled OR(Asian)=0.445, 95% CI=0.144-1.373, p=0.159; for Val66Met polymorphism: pooled OR(Asian)=0.962, 95% CI=0.820-1.128, p=0.635). CONCLUSIONS: Our population-based study and meta-analysis demonstrate that the BDNF C-270T and Val66Met polymorphisms do not play major roles in the susceptibility to schizophrenia in either Caucasian or Asian populations. But we can not rule out the possibility that other polymorphisms with the BDNF gene are involved in the pathophysiology of schizophrenia.     

Catechol-O-methyltransferase gene Val/Met functional polymorphism and risk of schizophrenia: a large-scale association study plus meta-analysis.

BACKGROUND: A common functional polymorphism (Val/Met) in the catechol-O-methyltransferase gene (COMT) that markedly affects enzyme activity has been shown to affect executive cognition and the physiology of the prefrontal cortex in humans. It is hypothesized that the high activity Val allele slightly increases risk for schizophrenia through its effect on dopamine-mediated prefrontal information processing. METHODS: We compared the allele/genotype frequencies of the Val/Met polymorphism in a large independent patient-control sample (862 patient and 928 healthy control subjects) from Han Chinese population, and an update meta-analysis was performed to assess the collective evidence across individual studies. RESULTS: No statistically significant differences were found in allele or genotype frequencies between patient and normal control subjects, although a nonsignificant overrepresentation of the Val allele in schizophrenia patients (odds ratio [OR] = 1.09, 95% confidence interval [CI] = .94-1.26) was suggested. Comparatively, the meta-analysis of all published population-based association studies showed statistically significant evidence for heterogeneity among the group of studies. Stratification of the studies by ethnicity of the samples yielded no significant evidence for an association with the Val allele in Asian population (OR = .96, 95% CI = .85-1.09), nor in European population (OR = 1.06, 95% CI = .95-1.19). CONCLUSIONS: Our data provide minimal evidence that the Val allele is a susceptibility factor for schizophrenia in either European or Asian populations.     

Factor XIII Val34Leu variant and the risk of myocardial infarction: a meta-analysis

Genetic factors are thought to contribute to the pathogenesis of acute myocardial infarction (AMI). A common variant of factor XIII (FXIII), FXIII Val34Leu, may be protective against developing an AMI, but various studies show conflicting results. We performed a meta-analysis to determine whether the FXIII Val34Leu variant is associated with a decreased risk of AMI. One hundred ninety-five articles were reviewed and 12 case-control studies were selected. We included studies involving patients with objectively diagnosed AMIs (WHO criteria), provided that FXIII Val34Leu genotyping data were available. Inclusion decisions, quality assessment, and data extraction were conducted by two reviewers. Hypothesizing that the Leu allele was protective, we performed three analyses with the Val/Val genotype as the reference group. Pooled odds ratios (OR) and their 95% confidence intervals (95% CI) were determined. Prior to pooling, heterogeneity testing was performed using the I(2) statistic. These studies included a total of 8,743 patients, of which 3,663 were AMI patients and 5,080 were healthy controls. Using the random effects methods, protective effects were seen with the Leu/Val genotype alone (OR 0.79, 95% CI 0.68-0.93) and with Leu/Val and Leu/Leu genotypes combined (OR 0.79, 95% CI 0.66-0.93). There was also a protective effect with the Leu/Leu genotype alone, (not statistically significant: OR 0.83, 95% CI 0.61-1.12), likely due to the low frequency of this genotype. These results suggest that there is an association between the factor XIII Leu allele and a modest protective effect against AMI and may provide useful information in profiling susceptibility to myocardial infarction.     

基质金属蛋白酶-9基因多态与急性脑梗死

目的 探讨基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)基因多态及血清水平与急性脑梗死的关系.方法 对2006年1月至2007年5月期间在我院神经内科住院的急性脑梗死患者101例和我院体检中心健康体检者114名进行研究,采用ELISA法测定血清MMP-9水平,同时采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法 分析MMP-9基因启动子C-1562T多态.结果 脑梗死患者组48 h内血清MMP-9水平为(138.9±121.8)ng/ml,而对照组为(18.4±4.6)ng/ml,两组差异有统计学意义(t=9.93,P=0.00).脑梗死组CT基因型患者外周血MMP-9水平为(113.3±66.6)ng/ml.而CC基因型患者外周血MMP-9水平为(148.6±104.9)ng/ml,两者相比差异无统计学意义(t=1.22,P=0.21).脑梗死组CT+TT基因型频率13.9%,对照组为13.2%,两者比较差异无统计学意义(χ2=0.02,P=0.88),T等位基因频率在脑梗死组为6.9%,对照组为7.5%,两者比较差异也无统计学意义(χ2=0.04,P=0.83).结论 MMP-9基因启动子-1562位点的多态与MMP-9基因表达和脑梗死没有明确的关系.MMP-9基因启动子C-1562T的多态与缺血性脑血管疾病的关系有待进一步研究.     

GNB3基因C825T多态性与缺血性脑卒中的关系

目的 了解G蛋白β亚基（GNB3）基因C825T多态性与北京地区缺血性脑卒中发病之间的关系。方法 利用PCR和分子杂交技术对北京地区294例缺血性脑卒中患者及280例非脑卒中患者的C825T多态性进行检测和分析。结果 C825T多态性位点在两组人群中的分布均符合Hardy-weinberg遗传平衡定律,缺血性脑卒中患者中CC、CT、TT三种基因型频率分布依次为30.27%、49.98%、20.75％,非脑卒中患者中为33.21%、47.50、19.29％,两组人群中825T等位基因频率分别为0.452和0.430,均无显著性差异。结论 GNB3基因C825T多态性与北京地区缺血性脑卒中发病无关。     

Interaction of CTSD and A2M polymorphisms in the risk for Alzheimer's disease

The proteins cathepsin D, encoded by CTSD gene, and alpha2-macroglobulin, encoded by A2M gene, are involved in the biochemical pathway leading to deposition of beta-amyloid. In these proteins two amino acid polymorphisms (CTSD-Ala/Val C-->T and A2M-Ile/Val A-->G) have been associated with an increased risk for Alzheimer's disease (AD), but conflicting results have been reported. We studied the association and the mutual interactions of the CTSD-C/T and A2M-A/G polymorphisms with sporadic AD in 100 patients with late-onset AD and 136 healthy elderly subjects as controls. The CTSD-T allele and the CTSD-C/T genotype are significantly more frequent in AD than in controls. The odds ratio (OR) for CTSD-T subjects is 1.93 [95% confidence interval (CI)=1.01-3.72], and 2.07 (95% CI=1.01-4.21) after adjustment for age, sex and APOE epsilon4+ status, while no significant association was found for the A2M-A/G polymorphism. The coexistence of the CTSD-T with the A2M-G allele synergistically increased the OR for AD to 2.69 (95% CI=1.13-6.34) [2.82 (95% CI=1.12-7.17) after adjustment], and to 3.29 (95% CI=1.33-8.16) if estimated for the allelic combination. Our data suggest that the CTSD-T allele of the CTSD-C/T polymorphism is associated with an increased relative risk for late-onset AD and, more interestingly, the combination of CTSD-T with the A2M-G allele seems to increase this risk.     

中国人内皮型一氧化氮合酶基因G894T多态性与脑梗死相关性的Meta分析

目的综合评价中国人内皮型一氧化氮合酶基因G894T(Glu298Asp)多态性与脑梗死的关系。方法搜集国内外公开发表的有关中国人内皮型一氧化氮合酶基因G894T多态性与脑梗死关系的研究文献,剔除不符合要求的文献,应用Meta分析软件RevMan5.1,对各研究结果进行异质性检验及数据合并,应用RevMan5.1和Stata11.0评估发表偏倚。结果共有11篇文献纳入Meta分析,累计病例组1768例,对照组1818例。合并基因型(GT+TT)/GG的OR值为1.46,95%CI为1.24～1.73(P<0.00001),合并基因型TT/GG的OR值为2.18,95%CI为1.32～3.61(P=0.002),合并基因型GT/GG的OR值为1.41,95%CI 1.18～1.67(P=0.0001),合并等位基因T/G的OR值为1.65,95%CI 1.28～2.12(P=0.0001)。结论中国人内皮型一氧化氮合酶基因G894T(Glu298Asp)多态性与脑梗死的发病具有相关性。携带基因型TT、GT及等位基因T可增加患脑梗死的风险。