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1.
脑梗死患者ACE基因多态性的研究   总被引:3,自引:0,他引:3  
张旭  夏君慧 《现代康复》2000,4(10):1498-1499
目的研究血管紧张素转换酶(ACE)基因插入(I)/缺失(D)多态性与脑梗死(CI)的关系。方法用聚合酶链式反应(PCR)技术分别检测235例CI患和158例对照人群ACE基因型和基因频率。结果CI组与对照组D:I等位基因频率之比差异显(P<0.001)。DD基因型CI组明显高于对照组。DD基因型CI相对危险性增高。结论ACE基因缺失多态性与CI发生显相关同时有脑卒中和高血压家族史的DD型AC  相似文献   

2.
为了探讨血管紧张素Ⅰ转换酶(ACE)基因第16内含子插入/缺失(I/D)多态性与冠心病(CAD)的关系,应用聚合酶链反应测定了79例冠心病(CAD)及68名正常人ACE基因第16内含子I/D多态性。结果显示,CAD病人ACE基因I型、ID型和DD型频率分别为28%(22/79)、29%(23/79)和43%(34/79),而正常人则分别为41%(28/68)、32%(22/68)和26%(18/68)。两组的DD基因型及D等位基因型均差异显著(P<0.05)。提示DD基因型可能为CAD发生的危险因素之一  相似文献   

3.
ACE基因多态性与胰岛素依赖性糖尿病肾病   总被引:1,自引:0,他引:1  
目的探讨ACE基因多态性与糖尿病肾病的关系。方法用扩增片段长度多态度性的方法,对42例胰岛素依赖性糖尿病(IDDM)患者和相应例数的正常人,进行了ACE基因多态性分析。结果IDDM患者和正常人之间ACE基因插入(I)/缺失(D)多态性频率差异不显著,IDDM伴肾病组D等位基因频率明显高于IDDM不伴肾病组(P<005),DD基因型也有相同趋势(P<01)。结论ACE基因缺失型(D)等位基因和缺失型基因型(DD)与IDDM合并肾病的发病可能有关。  相似文献   

4.
目的从分子生物学的角度探讨血管紧张素I转换酶(ACE)基因型变化及高血压参与临床急性脑血管病(ACVD)的分子生物学机理的可能性。方法对203例ACVD患者和51例对照组的外显子16片段进行PCR扩增,检测扩增的DNA条带,进行统计分析。结果有高血压史伴ACE基因的脑梗死(AI)发生率显著高于ACE基因阴性的患者。结论ACE基因多态性与ACVD无关,但高血压史伴ACE基因多态性是AI发生的致危因素之一,DD型ACE基因的患者中高血压的有无之比为10:2。  相似文献   

5.
脑卒中的危险因素分析及其与ACE基因的关系   总被引:4,自引:0,他引:4  
目的:为分析脑卒中的危险因素及其与血管紧张素转换酶插入/缺失(ACEI/D)多态性的关系。方法:用PCR方法分析117例脑缺血、19例脑出血ACEI/D多态性和100例原发性高血压患者。用SASS分析软件分析脑卒中的危险因素。结果:DD基因型频率和D等位基因频率比较:脑卒中组显著高于正常对照组;有脑卒中家族史脑缺血患者显著高于无家族史者。高血压组与正常对照组相比,无显著差别。脑出血组的高血压的发生  相似文献   

6.
人类血管紧张素Ⅰ转化酶(ACE)基因有三种类型:插入纯合型(II),缺失纯合型(DD),插入/缺失杂合型(I/D)[1]。文献报道血清ACE水平与ACE基因型有相关性,并与心血管病及糖尿病早发肾病有关[2]。我们参考有关文献建立了ACE基因多态性检测方法,初步探讨了不同基因型血清ACE水平及与临床的关系。1 材料与方法11 研究对象 正常组86例,男50例女36例均为体检健康者。冠心病(CAD)组40例,男18例女22例;慢性肾功能不全组(CRF)61例,男38例女24例,均为门诊及住院确诊病…  相似文献   

7.
血管紧张素Ⅰ转换酶基因对脑卒中发病分子机理探讨   总被引:1,自引:0,他引:1  
裘秀兰  王欣波 《现代康复》2000,4(10):1504-1504
目的从分子生物学的角度探讨血管紧张素Ⅰ转换酶(ACE)基因型变化及高血压参与临床急性脑血管病(ACVD)的分子生物学机理的可能性。方法对203例ACVD患和51例对照组的外显子16片段进行PCR扩增,检测扩增的DNA条带,进行统计分析。结果有高血压史伴ACE基因的脑梗死(AI)发生率显高于ACE基因阴性的患。结论ACE基因多态性与ACVD无关,但高血压史伴ACE基因多态性是AI发生的致危因素  相似文献   

8.
目的 探讨国人血管紧张素转化酶(ACE)基因的插入/缺失(I/D)多态性与心肌梗死的关系。方法 应用多聚酶链反应方法检测ACE基因多态性。结果 心肌梗死患者ACE基因DD型频率(0.38)及D等位基因频率(0.58)均明显高于对照组。结论国人ACE基因DD型与心肌梗死有关,可能是发生心肌梗死的重要因素之一。  相似文献   

9.
人群血管紧张素转换酶基因多态性与原发性高血压的关系   总被引:3,自引:0,他引:3  
通过病例对照研究,了解中国人血管紧张素转换酶(ACE)基因插入/缺失(I/D)多态性的分布,探讨其与原发性高血压的关系。对社区人群病例对照研究中确诊的112例原发性高血压患者和相同数量的性别、年龄相匹配的健康人,测定他们的空腹血浆脂质并且测量他们的身高,体重,腰围,臀围及坐位血压,应用聚合酶链反应(PCR)检测ACE基因多态性。结果发现病例组和对照组ACE I/D多态性基因构成有显著性差异(X^2  相似文献   

10.
ACE基因插入缺失多态性与糖尿病肾病病情发展的关系   总被引:8,自引:1,他引:7  
目的:探讨非胰岛素依赖型糖尿病(NIDDM)肾病(DN)病情进展与血管紧张素转换酶(ACE)基因插入缺失(ID)多态性的关系。方法:用PCR方法分别检测了92例不同程度蛋白尿的NIDDM患者的ACE基因型。结果:随着DN蛋白尿程度加重,DD型频率逐渐增高(微白蛋白尿期17%,显性蛋白尿期25%,肾功能不全期46%),而II型频率逐渐下降(在3组分别为33%、29%和8%),DI型在3组分布无显著性差异;在肾功能不全期组,DD型频率(46%)显著高于肾功能正常期组(20%),I型频率(8%)显著低于肾功能正常期组(32%),DI型频率在2组无显著性差异。结论:DD型NIDDM患者发生DN后,病情进展较快,DD型是DN恶化的促进因素;II型为保护性因素。  相似文献   

11.
目的 探讨血管紧张素转化酶(ACE)基因插入/缺失(I/D)多态性与老年人原发性高血压及合并糖尿病患者的关系.方法 应用聚合酶链反应(PCR)技术对60名正常对照组,105例老年高血压患者,38例老年高血压合并糖尿病患者进行ACE基因I/D多态性检测.结果 老年高血压患者中的DD基因型频率(0.352)和等位基因频率(0.543),老年高血压合并糖尿病患者的DD基因型频率(0.421)和等位基因频率(0.579)均明显高于正常对照组的0.133和0.250,而老年高血压组与老年高血压合并糖尿病组患者的DD基因型频率和D等位基因频率之间的差别无显著性.结论 ACE基因缺失型是老年高血压的危险因素,但ACE基因缺失不是糖尿病的危险因素之一.  相似文献   

12.
血管紧张素转换酶基因多态性及血清水平与脑梗死的关系   总被引:2,自引:0,他引:2  
目的研究血管紧张素转换酶(ACE)基因多态性及血清ACE水平与脑梗死之间的相互关系及可能机制。方法对84例脑梗死患者和74例健康对照者用聚合酶链反应(PCR)技术和琼脂糖凝胶电泳法分别进行ACE基因插入/缺失(I/D)多态性测定。分析比较脑梗死组与健康对照组之间ACE基因多态性的分布差异。结果脑梗死组DD基因型频率(50%)和D等位基因频率(64%)与健康对照组(分别为28%、4600)比较增高,差异有统计学意义(分别为P〈0.01,P〈0.05)。ACE基因多态性与血清ACE水平有关,ACE水平依次为:DD型〉ID型〉Ⅱ型,三者相互之间差异有统计学意义(P〈0.01)。结论ACE基因多态性与血清ACE水平和脑梗死有关,其DD型基因和D等位基因是脑梗死的危险因素。  相似文献   

13.
The relationship between angiotensin-converting enzyme (ACE) gene polymorphism and type I aortic dissection was examined in 205 unrelated hypertensives. A total of 94 patients underwent emergency repair due to type I aortic dissection, confirmed by computed tomography, and the remaining 111 were controls. Polymerase chain reaction was used to confirm that ACE gene polymorphism was due to insertion (I) or deletion (D) of a 287 base pair (bp) DNA sequence within intron 16. The genotype distribution and allele frequency of ACE I/D polymorphism between patients and controls were not statistically significant. When the frequency of at least one D allele carrier (DD or ID genotype) was compared with the II homozygous genotype, there was also no significant difference between the study groups. The findings revealed no association between ACE I/D polymorphism and aortic dissection. We conclude that I/D mutation of the ACE gene does not seem to be a risk factor for aortic dissection.  相似文献   

14.
OBJECTIVES: Presence of the D allele or homozygosity for the deletion (D) allele of the angiotensicen-converting enzyme (ACE) insertion/deletion (I/D) polymorphism has been discussed as potent risk factor for coronary artery disease (CAD) and myocardial infarction (MI). The D allele is associated with higher levels of circulating ACE and therefore may predispose one to cardiovascular damage. DESIGN AND METHODS: The study presented here was performed to investigate the association between the ACE genotype and ACE levels. The study group was comprised of 118 angiographically verified CAD patients. 65 patients were MI (+) and 53 patients were MI (-) in this group. A total of 70 healthy individuals were taken as controls. Genomic DNA of 188 subjects was extracted from whole blood. The polymerase chain reaction was used for ACE genotyping, and ACE levels were measured by ELISA. RESULTS: The D allele was found to be significantly more frequent in patients with MI (+) compared with controls (P = 0.024). ACE levels were significantly higher in both MI (-) and MI (+) groups with CAD patients than in controls (P < 0.005). Plasma ACE level was higher in all three groups in the DD genotype compared to II genotype. In groups I and III, this was statistically significant (P < 0.0001, P < 0.01). CONCLUSIONS: It was shown that the I/D polymorphism in the gene for ACE is a genetic risk factor for CAD patients who have a history of MI. ACE insertion/deletion gene polymorphism is also associated with plasma ACE levels in CAD patients with a history of MI.  相似文献   

15.
血管紧张素转换酶基因多态性与肝肾综合征相关研究   总被引:4,自引:2,他引:4  
目的 探讨血管紧张素转换酶 (ACE)基因插入 /缺失 (I/ D)多态性与失代偿性肝硬化并发肝肾综合征 (HRS)之间的关系。方法 应用聚合酶链反应方法扩增 5 6例失代偿性肝硬化并发 HRS患者及 6 0例正常对照组 ACE基因上 DNA片断 ,根据 I/ D判断其多态性 ;同时各例均采血测丙氨酸转氨酶、天冬氨酸转氨酶、血清肌酐 (SCr)及尿素氮 (BU N)等指标 ,并测定肾小球滤过率 (GFR) ,比较不同基因型间上述指标的差异显著性。结果  HRS患者各基因型及等位基因频率与对照组间差异均无显著性 (P均 >0 .0 5 ) ;I等位基因频率均显著高于 D等位基因频率 (P均 <0 .0 1)。正常对照组中 3种基因型频率间差异无显著性 (P>0 .0 5 ) ;HRS组中 II基因型频率显著高于 ID型及 DD型 (P均 <0 .0 5 )。 II基因型的 BU N与 SCr均显著高于 ID型及 DD型(P均 <0 .0 5 ) ,GFR显著低于 ID型及 DD型 (P均 <0 .0 5 )。结论  ACE基因多态性与失代偿性肝硬化并发HRS的发生率有关 ,II基因型可能为失代偿性肝硬化易并发 HRS的遗传学方面因素 ;失代偿性肝硬化并发HRS患者中 ,II基因型个体的肾功能衰竭程度重于 ID型及 DD型。  相似文献   

16.
目的 探讨血管紧张素转化酶(ACE)基因插入/缺失(I/D)多态性、血管紧张素Ⅱ-1型受体(AT1R)基因A1166C多态性与原发性高血压(EH)的相关性,以及多种危险因素与EH的关系.方法 选取125例健康者(对照组)和148例EH患者(EH组)作为研究对象作问卷调查、医学体检和血液生化项目检测,应用聚合酶链反应(PCR)技术检测研究对象ACE基因的I/D多态性;应用PCR、限制性内切酶酶切的方法检测AT1R基因A1166C多态性,并用Logistic回归筛选高血压的危险因素.结果 EH组和对照组的DD基因型频率和D等位基因频率差异均不显著.EH组的AC基因型频率23.0%,C等位基因频率11.5%,均显著高于对照组的12.8%和6.4%.EH组ACE基因DD型+AT1R基因AC型联合基因型频率7.4%,显著高于对照组的1.6%.多因素Logistic回归结果表明,EH的危险因素主要有BMI、EH家族史和DD+AC联合基因型.结论 ACE基因D等位基因可能与EH发病无关联;AT1R基因A1166C多态性可能是EH的重要遗传因素;DD+AC联合基因型对EH的发病有显著的联合促进作用.  相似文献   

17.
Angiotensin I-converting enzyme gene polymorphism and drug response.   总被引:3,自引:0,他引:3  
An insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene has been described in chromosome 17q23 of the human genome. Subjects with the genotype DD have markedly higher plasma ACE levels than those with genotype II; although ACE concentration in plasma is not rate-limiting for the production of angiotensin II, it has been suggested that the renin-angiotensin system may have an enhanced role in cardiovascular homeostasis in subjects with DD genotype or D allele. Meta-analysis confirmed the association of the D allele with an increased risk of myocardial infarction and stroke, but these relations are still uncertain with longevity and renal deterioration. Otherwise, I allele seems to be related with an improved response to physical training. The I/D polymorphism of the ACE gene is not a marker for any form of hypertension, though some conflicting results have been described. Nevertheless this polymorphism may have an influence on the antihypertensive response, particularly when using ACE inhibitors (ACEI). For example, blood pressure normalization with captopril in patients suffering from cardiac failure would be more effective in II genotype; conversely, both regression in left ventricular hypertrophy and improvement in diastolic filling would be greater after long-term treatment with enalapril in patients with essential hypertension and DD genotype. Conflicting results were also described using ACEI as a renoprotective therapy. This review therefore supports the justification for further evaluation in appropriately powered studies.  相似文献   

18.
GENSINI, F., et al. ; Angiotensin-Converting Enzyme and Endothelial Nitric Oxide Synthase Polymorphisms in Patients with Atrial Fibrillation. Experimental studies have shown a significant increase in angiotensin-converting enzyme (ACE) expression in atrial tissue of AF patients. ACE regulates the synthesis of endothelial nitric oxide (NO), which modulates autonomic nervous activity involved in the development of AF. The aim of the study was to evaluate the prevalence of ACE insertion/deletion and endothelial NO synthase (eNOS) T-786C, G894T, and 4a/4b polymorphisms in 148 patients with persistent AF, compared with 210 control subjects. ACE insertion/deletion polymorphism genotype distribution and allele frequency were significantly different between patients and controls (   P < 0.0001   and   P < 0.0001   , respectively). ACE DD genotype was significantly associated with the risk of AF   (OR DD/ID + II = 3.24, P < 0.0001)   . Analysis of eNOS polymorphisms showed no significant difference in genotype distribution and allele frequency between patients and controls. The results suggest a possible role of ACE DD genotype as a predisposing factor to AF and a pathophysiological mechanism of ACE inhibition in reducing the incidence of AF in patients with left ventricular dysfunction. (PACE 2003; 26[Pt. II]:295–298)  相似文献   

19.
目的探讨血管紧张素转换酶(ACE)基因多态性与2型糖尿病患者合并视网膜病变的关系。方法采用聚合酶链反应技术检测146例2型糖尿病患者ACE基因内含子16插入/缺失多态性,其中合并视网膜病变组27例,未发生视网膜病变组119例;同时选择200例健康志愿者作为正常对照组。结果合并视网膜病变组的ACE基因DD纯合型频率比未患视网膜病变组显著升高(70%与46%,P=0.042),但两组D等位基因频率比较无显著差异(80%与69%,P>0.05)。多因素分析表明,ACE基因DD基因型多态性与收缩压均为2型糖尿病视网膜病变的独立危险因素。结论ACE基因的DD基因型可增加2型糖尿病患者并发视网膜病变的危险性。  相似文献   

20.
目的探讨血管紧张素转化酶(ACE)基因插入/缺失(I/D)多态性与维吾尔族高血压合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者左心室肥厚(LVH)的关系。 方法选取2015年1月至2016年12月于新疆医科大学第一附属医院高血压科首诊住院,且未服用血管紧张素转换酶抑制剂/血管紧张素Ⅱ受体拮抗剂(ACEI/ARB)类降压药物的维吾尔族高血压合并OSAHS患者,共72例,行多导睡眠呼吸监测、动态血压、心脏彩超等检查,聚合酶链式反应(PCR)和琼脂糖凝胶电泳技术测定ACE基因多态性。根据左心室质量指数分为左心室肥厚组(LVH组,n=24)和非左心室肥厚组(NLVH组,n=48),比较两组间基因型及基因频率的差异,使用多因素Logistic回归分析左心室肥厚的影响因素。 结果高血压合并OSAHS患者LVH组ACE基因型频率分别为:II(37.50%),ID(20.83%),DD(41.67%),等位基因频率分别为:I(48.00%),D(52.00%),与NLVH组[II(47.92%),ID(37.50%),DD(14.58%),I(67.00%),D(33.00%)]比较,差异有统计学意义(χ2=6.75,4.70;均P<0.05);对左心室肥厚影响因素进行多因素Logistic回归分析,呼吸暂停低通气指数(AHI)(OR=6.20,95%CI:1.44~26.77;P<0.05)、DD基因型(OR=4.61,95%CI:1.05~20.31;P<0.05)是维吾尔族高血压合并OSAHS患者发生LVH的独立危险因素。 结论ACE基因I/D多态性与维吾尔族高血压合并OSAHS患者发生LVH有关,其中DD基因型维吾尔族患者更易发生LVH。  相似文献   

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