脂蛋白脂酶基因和对氧磷酶1基因联合作用与脑梗死发病的相关性

目的 探讨脂蛋白脂酶(LPL)、对氧磷酶1(PONl)基因联合作用与脑梗死发病的相关性.方法 选取LPL基因2个SNP和PON1基因2个标签SNP,采用聚合酶链反应(PCR)和限制性片段长度多态性(RFLP)技术,对705例脑梗死患者和431例对照组人群进行检测,应用UNPHASED软件、等位基因条件分析的方法,分析基因的联合作用与脑梗死的相关性.结果 LPL基因rs328位点G等位基因分布在动脉粥样硬化性脑梗死组与对照组差异显著(x2=4.83,P=0.034,OR=1.47,95％CI=1.03～2.13);rs326位点G等位基因分布在动脉粥样硬化性脑梗死组与对照组差异显著(x2=3.597,P=0.047,OR=1.64,95％CI =1.12～1.84);PON1基因上的rs2299262位点与LPL基因上的rs328位点联合作用与脑梗死的发病具有相关性(x2=6.26,df =2,P=0.043).结论 LPL基因rs328位点G等位基因携带者患大动脉粥样硬化性脑梗死的风险高于非携带者.LPL基因rs326位点G等位基因携带者患大动脉粥样硬化性脑梗死的风险高于非携带者.PON1基因上的rs2299262位点与LPL基因上的rs328位点联合作用与脑梗死的发病具有相关性.     

脑出血患者脂蛋白脂酶Ser447Ter基因多态性的研究

目的探讨脂蛋白脂酶(LPL)Ser447Ter基因多态性与脑出血关系。方法应用聚合酶链式反应-限制性片段长度多态性技术(PCR-RFLP)对313例脑出血患者和351例正常对照者脂蛋白脂酶(LPL)Ser447Ter基因多态性进行研究。结果在脑出血组中,LPLSer447Ter3种基因型频率分别为CC85.6%、CG14.1%和GG0.3%。LPLSer447Ter基因型和等位基因频率的分布在脑出血组与对照组之间无显著性差异(P>0.05);而LPLSer447TerCG+GG基因型携带者甘油三酯(TG)、载脂蛋白B(ApoB)和脂蛋白(a)[LP(a)]水平低于GG基因型携带者(P<0.05)。结论研究未发现LPLSer447Ter基因多态性与脑出血存在相关关系。     

内皮源性一氧化氮合酶基因多态性与缺血性脑卒中相关性研究

目的通过病例对照研究,探讨内皮源性一氧化氮合酶(eNOS)基因多态性与缺血性脑卒中的关系。方法采用聚合酶链反应(PCR)和限制性片断长度多态性(RFLP)技术,对452例缺血性脑卒中患者和153例健康对照人群的eNOS基因rs3918181位点进行基因多态性检测。结果大动脉粥样硬化型脑梗死组的基因型与等位基因频率与正常对照组比较P>0.05,无统计学意义。腔隙性脑梗死组eNOS基因AA AG基因型频率明显高于对照组,相对于GG基因型,暴露于AA AG基因型人群的OR值为1.644(95%CI 1.124～2.405)。腔隙性脑梗死A等位基因频率也显著高于对照组,相对于G等位基因,A等位基因OR值为1.419(95%CI 1.061～1.898)。结论内皮源性一氧化氮合酶(e-NOS)基因rs3918181位点多态性与腔隙性脑梗死相关;A等位基因可能增加中国汉族人罹患腔隙性脑梗死的风险。     

NOS1基因多态性与腔隙性脑梗死相关性研究

目的:探讨神经元型一氧化氮合酶基因( NOS1)多态性与腔隙性脑梗死发病的关系。方法:本研究共纳入385例腔隙性脑梗死患者和313例对照组人群，以位于NOS1基因的rs9658281和rs2682820位点为遗传标记，采用聚合酶链式反应-限制性片断长度多态性(PCR-RFLP)技术检测NOS1基因的多态性。结果:Cocaphase 分析表明腔隙性脑梗死组rs9658281位点G等位基因频率较对照组显著增高(x2 =4.135，P=0.042，OR=1.422，95％ CI 1.013～1.997)，这种差异在女性患者更加明显(x2=9.522，P=0.002，OR=2.502，95％ CI 1.398～4.479)。卡方检验表明腔隙性脑梗死组rs9658281位点的GG基因型频率较对照组显著增高(x2=5.862，P=0.015，OR=1.579，95％ CI 1.091～2.286)，这种差异在女性更加明显(x2=13.641，P＜0.0001，OR=3.501，95％CI 1.800～6.810)。经过多因素回归分析调整了传统危险因素的影响后，两组间的差异仍有显著性(P=0.014)。腔隙性脑梗死组和对照组的rs2682820位点的基因型、等位基因频率差异无显著性（P＞0. 05）。结论:NOS1基因rs9658281位点G等位基因与腔隙性脑梗死的发病可能有关。     

南京地区汉族腔隙性脑梗死患者蛋白激酶Cη基因多态性的研究

目的:探讨南京地区汉族腔隙性脑梗死患者蛋白激酶Cη(PRKCH)基因rs3783799位点和rs2230500位点的单核昔酸多态性(SNPs).方法:采用PCR和连接酶反应(LDR)技术,检测272例南京地区汉族腔隙性脑梗死患者(腔梗组)和296例非腔隙性脑梗死患者(对照组)PRKCH基因的SNPs.比较两组基因型分布和等位基因频率,并对PRKCH基因rs3783799位点和rs2230500位点进行配对连锁不平衡分析及单倍体型分析.结果:腔梗组PRKCH基因rs3783799位点基因型分布[G/G型268例(98.5%),G/A型4例(1.5%)]及A等位基因频率(0.7%)与对照组[G/G型292例(98.6%),G/A型4例(1.4%);0.7%]比较的差异无统计学意义;腔梗组PRKCH基因rs2230500位点基因型分布[G/G型266例(97.8%),G/A型6例(2.2%)]及A等位基因频率(1.1%)与对照组[G/G型290例(98.0%),G/A型6例(2.0%);1.0%]比较的差异亦无统计学意义.单倍体型分析显示,两位点配对单倍体型G/G分布频率在腔梗组为98.9%,在对照组为98.6%,两组间比较的差异无统计学意义.结论:PRKCH基因rs3783799位点和rs2230500位点基因多态性可能与南京地区汉族人群腔隙性脑梗死的发病无关.     

GAS6基因内含子834+7G/A位点多态性与脑梗死的相关性研究

目的 探讨粤西地汉族人群中GAS6基因(生长停滞特异性基因6)内含子834+7G/A位点的单核苷酸多态性(SNP)与脑梗死的相关性.方法 应用聚合酶链反应—限制性内切酶片段长度多态性分析方法 (PCR- RFLP)检测180例梗死患者和150例对照组的GAS6基因内舍子SNP 834+7G/A的基因型.结果 病例组G等位基因携带者的频率为97.8％,AA基因型的频率为2.2％,而在对照组分别为92.0％和8.0％,两组相比较差异有统计学意义(x2=5.920,P=0.015),G等位基因携带者发生脑梗死的风险是AA基因型的3.933倍(OR =3.933,95％ CI:1.117～13.848,P=0.033).结论 GAS6基因内舍予SNP834+7G/A的基因多态性与粤西地区汉族人脑梗死相关,G等位基因携带者增加脑梗死的发病风险,而AA基因型可能对脑梗死有保护作用.     

血浆纤溶酶原激活物抑制剂-1基因启动子区4G/5G多态性与脑血管疾病的关系

目的 探讨血浆纤溶酶原激活物抑制剂-1基因启动子区4G/5G多态性与脑血管疾病之间的关系.方法 应用PCR技术和琼脂糖电泳对30例脑出血患者、90例脑梗死患者(其中腔隙性脑梗死30例,小面积脑梗死30例,大面积脑梗死30例)进行了API-1基因启动子4G/5G多态性的检测和分析,并与30例非脑血管疾病者对照比较.结果 对照组、脑出血组、脑梗死组基因型频率及等位基因频率分布比较均有统计学差异(P＜0.05).对照组与脑出血组间基因型频率及等位基因频率比较均无统计学差异(P＞0.05).对照组与脑梗死组间基因型频率及等位基因频率比较均有统计学差异(P＜0.05),脑梗死组4G/4G基因型频率(44.4%)较对照组(20%)高;脑梗死组4G等位基因频率(63.3%)较对照组(38.8%)高,比较均有统计学差异(P＜0.05).脑梗死组各亚型基因型频率及等位基因频率比较均无统计学差异(P＞0.05).性别在各组不同基因型中分布:对照组及脑出血组性别在不同基因型分布比较无统计学差异(P＞0.05).脑梗死组性别在不同基因型分布比较有统计学差异(P＜0.05),4G/4G基因型中男性占25%;女性占65%,比较有统计学差异(P＜0.05).腔隙性脑梗死组及小面积脑梗死组性别在不同基因型中分布比较均无统计学差异(P＞0.05).大面积脑梗死组性别在不同基因型中分布比较有统计学差异(P＜0.05),4G/4G基因型男性占21.4%;女性占78.6%,比较有统计学差异(P＜0.05).结论 PAI-1基因启动子区4G/5G多态性在怀化市正常人群中大致分布为:4G/4G占20%;4G/5G占63.3%;5G/5G占16.7%.PAI-1基因启动子区4G/5G多态性与脑出血无关.PAI-1基因启动子区4G/5G多态性与缺血性脑卒中有关,4G/4G基因型可能是缺血性脑卒中的一个独立危险因素,尤其可能与女性大面积脑梗死密切相关.PAI-1基因启动子区4G/5G多态性与缺血性脑卒中的梗死面积无关.     

屏氧酶-1基因多态性与腔隙性脑梗死

目的探讨屏氧酶-1(PON-1)基因192位G ln-Arg(Q/R192)多态性与腔隙性脑梗死的关系。方法采用聚合酶链式反应(PCR)限-制性片段长度多态性方法测定109例腔隙性脑梗死患者(腔隙性脑梗死组)和339名健康普查者(对照组)PON-1Q/R192基因多态性,并进行基因型的比较。结果在腔隙性脑梗死人群中PON-1Q/R192 3种基因型频率分别为QQ 15.6%、QR 52.3%、RR 32.1%。PON-1Q/R192基因型和等位基因频率分布在腔隙性脑梗死组与对照组之间无显著性差异(P>0.05);各基因型之间血脂水平也无显著性差异(P>0.05)。结论腔隙性脑梗死和非腔隙性脑梗死的PON-1Q/R192的基因多态性无明显差异。     

脂蛋白脂酶Ser447Term多态性和卒中相关危险因素相互作用对缺血性脑卒中发病的影响

目的 本研究旨在探讨脂蛋白脂酶(LPL) Ser447Term多态性与一些常见的卒中危险因素之间的相互影响.方法 检测704个汉族缺血性脑卒中患者的基因型,根据这些患者所具有的卒中相关危险因素将其分为2型糖尿病组、高血压组、吸烟组和高脂血症组.应用聚合酶链反应-限制性片段长度多态性方法对Ser447Term的多态性进行基因分型.结果 卡方(x2)检验结果显示:在有糖尿病史的卒中患者中Ser447Term G等位基因的携带率显著高于无糖尿病史的卒中患者(x2=7.25,P=0.007,OR=1.78,95％ C/I.18～ 2.68).这样的相关性并未在具有其他3个卒中相关的危险因素的患者中观察到.结论 LPL基因多态性与糖尿病的联合作用可能促成缺血性卒中的一个亚组的发病.     

载脂蛋白E基因多态性与腔隙性梗死关系的研究

目的:探讨载脂蛋白E(ApoE)基因多态性与腔隙性梗死(lacunarinfarction)的相关性。方法:采用病例对照研究,对105例中老年腔隙性梗死患者和322例健康对照者进行研究。用多聚合酶链式反应(PCR)和限制性片段长度多态性测定ApoE基因多态性。结果:对照组ApoE基因的等位基因频率为e210%、e382.4%和e47.6%;腔隙性脑梗死组的等位基因频率为e28.2%、e384.3%和e47.5%。ApoE各基因型和等位基因频率在腔隙性脑梗死和对照组之间差异无显著性(P>0.05)。结论:未发现ApoE基因多态性与腔隙性梗死存在相关关系。     

Lipoprotein lipase Ser447Ter polymorphism associated with the risk of ischemic stroke: a meta-analysis

Introduction

Previous studies suggested lipoprotein lipase (LPL) Ser447Ter and Asn291Ser polymorphisms were associated with the risk of ischemic heart disease, however, their effects on ischemic stroke were controversial. A meta-analysis was performed to assess the associations between these two LPL polymorphisms and the risk of ischemic stroke.

Methods

The electronic databases PubMed and Embase were used to identify relevant studies by two interviews independently. The pooled odds ratios (ORs) and weighted mean differences (WMD) with 95% confidence interval (CI) were estimated for the risk of ischemic stroke and the plasma lipids in various Ser447Ter genotypes respectively. A fixed or random effect model was selected for pooling data based on homogeneity test.

Results

13 studies including 4,681 ischemic stroke cases and 8,516 controls were involved in this meta-analysis. Overall, LPL Ter447 variant was associated with a significantly reduced risk for ischemic stroke (OR = 0.79, 95% CI: 0.68-0.93) both in Caucasian (OR = 0.87, 95% CI: 0.77-0.97) and East-Asian (OR = 0.65, 95% CI: 0.43-0.99), whereas no significant association of Ser291 variant was observed (OR = 1.25, 95% CI: 0.96-1.63). The Ser447Ter polymorphism may be more important in association with the decreased risk of atherosclerotic stroke (OR = 0.44, 95% CI: 0.32-0.62) which derived from significantly increased high density lipoprotein cholesterol, decreased triglyceride and total cholesterol in Ter447 carriers compared with non-carriers.

Conclusions

This meta-analysis indicated that LPL Ser447Ter polymorphism was associated with a significant reduction in the risk of ischemic stroke, especially atherosclerotic stroke subtype in both Caucasian and East-Asian.     

Assessment of genetic risk for myocardial infarction

Although lifestyle and environmental factors influence the prevalence of myocardial infarction, genetic epidemiological studies have suggested that several genetic variants increase the risk for this condition. We have performed a large-scale association study to identify gene polymorphisms for reliable assessment of the genetic risk of myocardial infarction. The study population comprised 3,483 unrelated Japanese individuals (1,913 men; 1,570 women), including 1,192 subjects with myocardial infarction and 2,291 controls. The genotypes for 164 polymorphisms of 137 candidate genes were determined with an oligonucleotide ligation assay based on analysis of fluorescent microspheres with suspension array technology. Multivariable logistic regression analysis with adjustment for age, sex, body mass index, and the prevalence of smoking, hypertension, diabetes mellitus, and hypercholesterolemia revealed that the 677C-->T (Ala222Val) polymorphism of MTHFR, the 1595C-->G (Ser447Stop) polymorphism of LPL, and the -108/3G-->4G polymorphism of IPF1 were significantly associated with the prevalence of myocardial infarction. A stepwise forward selection procedure demonstrated that IPF1, MTHFR, and LPL genotypes significantly affected the prevalence of myocardial infarction. Combined genotype analysis of these polymorphisms yielded a maximum odds ratio of 2.54 for the combined genotype of TT for MTHFR, CC for LPL, and 3G3G for IPF1. The genotypes for MTHFR, LPL, and IPF1 may prove reliable for assessment of genetic risk for myocardial infarction. Determination of the combined genotype for these genes may contribute to primary, personalized prevention of this condition.     

DDAH2C-449G基因多态性与动脉粥样硬化血栓形成性脑梗死的相关性

目的 探讨DDAH2C-449G基因多态性与动脉粥样硬化血栓形成性脑梗死(atherothrombotic infarct of brain)的关系。方法 共纳入345例脑梗死患者和201例对照组人群,以DDAH2C-449G基因为遗传标志,采用聚合酶链式反应(PCR)和限制性片段长度多态性技术(RFLP)检测DDAH2C-449G基因多态性。结果 动脉粥样硬化血栓形成性脑梗死GG基因型、G等位基因频率较对照组高(P<0.05).结论 DDAH2C-449G基因多态性可能与动脉粥样硬化血栓形成性脑梗死发病有关,G等位基因可能是动脉粥样硬化血栓形成性脑梗死的易感基因。     

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。     

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。     

粤西汉族人群血浆谷胱甘肽过氧化物酶基因启动子区-723C/T基因多态性与脑梗死的关系

目的 研究粤西汉族人群谷胱甘肽过氧化物酶(GPX-3)基因启动子区-723C/T基因多态性的分布及其与脑梗死的关系. 方法 检测佛广东医学院附属医院神经科自2007年2月至2008年2月收治的粤西地区汉族脑梗死患者102例(病例组)和同期粤西地区汉族健康体检者101例(对照组)的GPX-3基因启动子区-723C/T基因多态性,比较2组的一般资料、卒中危险因素及-723C/T基因多态性的分布特点,多元Logistic回归分析影响脑梗死发生的危险因素,并对筛选出的危险因素进行分层分析. 结果 与对照组比较,病例组高血压、糖尿病病史比例,血糖水平,-723C/T CC基因型频率及C等位基因频率均较高,差异有统计学意义(P＜0.05);多元Logistic回归分析显示-723C/T基因型、高血压病史、糖尿病史是脑梗死发生的独立危险因素;与没有任何危险因素亦不携带风险基因型者比较,有危险因素又携带CC基因型者脑梗死发病风险明显增加,差异有统计学意义(P＜0.05). 结论 中国粤西地区汉族人群GPX -3基因启动子区-723C/T位点存在多态性,C等位基因是脑梗死的危险因素,CC基因型为脑梗死的易感基因型,也是独立危险因素.     

Association of plasminogen activator inhibitor-1 4G/5G promoter polymorphism with recurrent cerebral infarction in China’s North Jiangsu Province*☆

BACKGROUND： Many international studies have shown that plasminogen activator inhibitor-1 （PAl-l） 4G/5G promoter polymorphism does not increase the risk for cerebral infarction.
OBJECTIVE： Using PCR methodology and agarose electrophoresis to detect PAI-1 4G/5G promoter polymorphism in patients with recurrent cerebral infarction in the North Jiangsu Province of China, and to compare results with healthy subjects and patients with first-occurrence cerebral infarction in the same region.
DESIGN, TIME AND SETTING： Non-randomized, concurrent, control trial. A total of 122 cerebral infarction patients were admitted to Xuzhou Medical College Hospital＇s Department of Neurology and Xuzhou Central Hospital＇s Department of Neurology between July 2003 and August 2006.
PARTICIPANTS： The patients consisted of 63 males and 59 females, aged （62 ± 10） years. They were divided into first-occurrence （n = 58） and recurrence （n = 64） groups. In addition, 50 healthy subjects that underwent physical examination in the outpatient department, including 26 males and 24 females, aged （60 ±12） years, were selected as controls.
METHODS AND MAIN OUTCOME MEASURES： PAl-1 4G/5G promoter polymorphism was detected and analyzed using PCR methodology and agarose electrophoresis.
RESULTS： Significant differences were determined in terms of genotypic frequency and allele frequency of PAI-1 4G/5G promoter polymorphism, in patients with first-occurrence or recurrent cerebral infarction, when compared with healthy subjects （P 〈 0.05）. There was, however, no significant difference between the first-occurrence and recurrence groups （P 〉 0.05）.
CONCLUSION： PAl- 1 4G/5G promoter polymorphism is genetic risk factor for cerebral infarction in China. However, it may be associated with recurrence of cerebral infarction in patients from the North Jiangsu Province of China.     

Association of plasminogen activator inhibitor-1 4G/5G promoter polymorphism with recurrent cerebral infarction in China’s North Jiangsu Province

BACKGROUND:Many international studies have shown that plasminogen activator inhibitor-l(PAI-1)4G/5G promoter polymorphism does not increase the risk for cerebral infarction.OBJECTIVE:Using PCR methodology and agarose electrophoresis to detect PAl-1 4G/5G promoter polymorphism in patients with recurrent cerebral infarction in the North Jiangsu Province of China,and to compare results with healthy subjects and patients with first-occurrence cerebral infarction in the same region.DESIGN,TIME AND SETTING:Non-randomized,concurrent,control trial.A total of 122 cerebral infarction patients were admitted to Xuzhou Medical College Hospital's Department of Neurology and Xuzhou Central Hospital's Department of Neurology between July 2003 and August 2006.PARTlCIPANTS:The patients consisted of 63 males and 59 females,aged(62±10)years.They were divided into first-occurrence(n=58)and recurrence(n=64)groups.In addition,50 healthy subjects that underwent physical examination in the outpatient department,including 26 males and 24 females,aged (60±12)years,were selected as controls.METHODS AND MAIN OUTCOME MEASURES:PAI-1 4G/5G pmmoter polymorphism was detected and analyzed using PCR methodology and agarose electrophoresis.RESULTS:Significant differences were determined in terms of genotypic frequency and allele frequency of PAI-1 4G/5G promoter polymorphism,in patients with first-occurrence or recurrent cerebral infarction,when compared with healthy subjects(P<0.05).There was,however,no significant differenco between the first-occurrence and recurrence groups(P>0.05).CONCLUSION:PAI=1 4G/5G promoter polymorphism is genetic risk factor for cerebral infarction in China.However,it may be associated with recurrence of cerebral infarction in padents from the North Jiangsu Province of China.     

2型糖尿病患者基质金属蛋白酶-12基因多态性与缺血性卒中的相关性研究

目的探讨2型糖尿病患者基质金属蛋白酶12(MMP-12)基因多态性与缺血性卒中的相关性。方法选择2013年1月至2015年12月在本科治疗的217例2型糖尿病合并缺血性卒中患者作为病例组,按照TOAST分型结果将病例组患者分为大动脉粥样硬化性卒中(LAA)组88例和非大动脉粥样硬化性卒中(n-LAA)组129例,选择同期在我院体检的无缺血性卒中的2型糖尿病患者100例作为对照组,采用聚合酶链反应-限制性内切酶分析(PCR-RFLP)法比较MMP-12(-82 A/G)和MMP-12(-1082 A/G)基因型多态性在各组间的差异。结果病例组和n-LAA组MMP-12(82 A/G)基因型和等位基因与对照组比较,差异均无统计学意义(P0.05)。LAA组(G/G+A/G)基因型频率显著高于对照组(22.73%vs 11.00%,P=0.031);G等位基因频率也高于对照组(18.18%vs 10.05%,P=0.033)。n-LAA组MMP-12(-1082 A/G)基因型和等位基因与对照组比较,差异均无统计学意义(P0.05)。病例组和LAA组(G/G+A/G)基因型频率均显著高于对照组(33.64%vs 22.00%,P=0.036;37.50%vs 22.00%,P=0.020);两组G等位基因频率也均高于对照组(25.58%vs 17.00%,P=0.017;30.68%vs 17.00%,P=0.002)。多因素Logistic回归分析结果显示MMP-12-82A/G等位基因G和MMP-12-1082A/G等位基因G均是2型糖尿病患者发生LAA的危险因素(OR=1.107,95%CI 1.010-1.371,P=0.031;OR=1.285,95%CI 1.142-1.817,P=0.010)。结论对于2型糖尿病患者,MMP-12基因-82位点G等位基因和-1082位点G基因多态性与大动脉粥样硬化性卒中密切相关。