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1.
Common polymorphisms and cardiovascular factors in patients with myocardial infarction of Costa Rica
Salazar-Sánchez L Chaves L Cartin M Schuster G Wulff K Schröder W Herrmann FH 《Revista de biología tropical》2006,54(1):1-11
Eight common polymorphisms of known myocardial infarction (MI) risk factors (factor V Leiden (FVL), factor V HR2 (FVHR2), factor II 20210G > A (FII), factor VII IVS7 (FVII IVS7), factor VII Arg353Gln (FVII), factor XIII Va134Leu (FXIII), Methylenetetrahydrofolate reductase C677T (MTHFR), Angiotensin Converting Enzyme (ACE)) and environmental risk factors were analyzed in a MI patients of Costa Rica. This case-control study included 186 MI subjects, 95 of them < or = 45 years and 201 age and sex matched controls. With the use of PCR method the polymorphisms were detected and through interviews additional information was collected. Hypercholesterolemia and smoking were associated with a significant risk in younger patients. High fibrinogen level was an important risk factor and interaction with smoking was detected. Mainly, the genotype 34LeuLeu of FXIII showed significant protective effect, (OR 0.32, 95% CI 0.13-0.80) while the other polymorphisms showed no significant difference between the cases and the controls. Carriers of FVII (OR 2.75, 95% CI 1.07-7.02) and FXIII (OR 4.20, 95% CI 2.03-8.67) polymorphisms showed interaction with fibrinogen in the statistical analysis. It was concluded that there was an important interaction between the common risk factors and the polymorphisms (FVII; FXIII) in the development of MI. This is one of the first reports in a Latin-American population dealing with these molecular markers and MI. 相似文献
2.
Kariz S Milutinović A Bregar D Terzić I Terzić R Lovrecić L Herova M Hruskovicova H Peterlin B Petrovic D Zorc-Pleskovic R 《Collegium antropologicum》2007,31(2):503-507
In this study we investigated the association of the interleukin-1 receptor antagonist gene variable number tandem repeat (IL1RN VNTR) polymorphism and of the inhibitor of kappa B-like protein (IKBL) gene polymorphism with myocardial infarction (MI) in a group of patients with type 2 diabetes. The IL1RN VNTR and the IKBL+ 738T > C gene polymorphisms were tested in 374 Caucasians: 151 cases with MI and 223 subjects with no history of coronary artery disease. The IL1RN VNTR polymorphism was not a risk factor for MI in Caucasians with type 2 diabetes (genotype 22 vs. the rest: odds ratio (OR) 1.6; 95% confidence interval (CI) = 0.8-3.5; p = 0.2). We also failed to demonstrate that IKBL+ 738T > C gene polymorphism was associated with MI in patients with type 2 diabetes (OR = 0.9; 95% CI = 0.3-2.6; p = 0.9). We provide evidence that the IL1RN VNTR and the IKBL + 738T > C gene polymorphisms are not risk factors for MI in Caucasians with type 2 diabetes. 相似文献
3.
Yang Y Ruiz-Narvaez E Kraft P Campos H 《Human biology; an international record of research》2007,79(6):637-647
We assessed the effect of APOE polymorphisms -491 A/T, C112R (APOE*4), and R158C (APOE*2) and saturated fat intake on plasma lipid levels and risk of myocardial infarction (MI) in 1,927 case subjects and 1,927 population-based control subjects matched for age, sex, and residence, all living in the Central Valley of Costa Rica. A significant gene-diet interaction (p = 0.0157) was observed. High saturated fat intake was associated with a 49% increased risk of MI (OR = 1.49; 95% CI, 1.16-1.92) among wildtype subjects. In contrast, high saturated fat intake was associated with a 2.2-fold increased risk of MI among carriers of APOE*2 (OR = 3.17; 95% CI, 1.58-6.36) and with a 1.6-fold increase among carriers of the -491T and APOE*4 variants together (OR = 2.59; 95% CI, 1.38-4.87). Consistently, a high fat diet elicited a greater response in LDL cholesterol among carriers of APOE*2 (+ 17%) and APOE*4 (+ 14%) compared to noncarriers (+6%). The frequency of APOE variants was similar in case and control subjects, although APOE*4 homozygotes were at increased risk of MI compared to noncarriers (OR = 2.26; 95% CI, 1.03-4.98). This study supports the hypothesis that the APOE*2 and APOE*4 variants increase susceptibility to MI in the presence of high saturated fat and could explain inconsistent findings on the effects of these variants on MI in various populations. 相似文献
4.
Zielinska-Blizniewska H Sitarek P Milonski J Dziki L Przybylowska K Olszewski J Majsterek I 《Molecular biology reports》2012,39(5):5449-5457
Nasal polyps are strongly associated with a risk of chronic rhinosinusitis development as well as other obstruction including
asthma and allergy. The following study tested the association of the 140A/G polymorphism of lactoferine (LF) encoding gene
and the −33C/G polymorphism of osteoblast-specific factor-2 (OSF-2) encoding gene with a risk of chronic rhinosinusitis with nasal polyps in a Polish population. One hundred ninety five patients
of chronic rhinosinusitis with nasal polyps as well as 200 sex, age and ethnicity matched control subjects without chronic
sinusitis and nasal polyps were enrolled in this study. Among the group of patients 63 subjects were diagnosed with allergy
and 65 subjects with asthma, respectively. DNA was isolated from peripheral blood lymphocytes of patients as well as controls
and gene polymorphisms were analyzed by restriction fragments length polymorphism polymerase chain reaction (RFLP-PCR). We
reported that the 140A/G LF (OR 4.78; 95% CI 3.07–7.24), the −33C/G OSF-2 OR 3.48; 95% CI 2.19–5.52) and the −33G/G OSF-2 (OR 16.45; 95% CI 6.71–40.30) genotypes were associated with an increased risk of chronic rhinosinusitis with nasal polyps
among analyzed group of patients. Moreover, the group of patients without allergy or asthma indicated the association of the
−33C/G (OR 3.72; 95% CI 2.24–6.19 and OR 15.11; 95% CI 5.91–38.6) and −33G/G (OR 3.73; 95% CI 2.24–6.19 and OR 14.07; 95%
CI 5.47–36.16) genotypes of the OSF-2 as wells as 140A/G (OR 3.89; 95% CI 2.40–6.31 and OR 3.62; 95% CI 2.45–5.34) genotype of OSF-2 with an increased risk of chronic rhinosinusitis with nasal polyps. Finally, it was also found that the selected group of
patients with allergy or asthma indicated a very strong association of the −33C/G (OR 2.40; 95% CI 1.23–4.69 and OR 2.40;
95% CI 1.23–4.69, respectively) and −33G/G (OR 16.01; 95% CI 5.77–44.41 and OR 17.90; 95% CI 6.53–49.05, respectively) genotypes
of the OSF-2 as wells as 140A/G (OR 3.22; 95% CI 1.74–6.11 and OR 3.25; 95% CI 1.75–6.04, respectively) genotypes with an increased risk
of chronic rhinosinusitis with nasal polyps. Thus, our results suggest that LF and OSF-2 gene polymorphisms may have deep impact on the risk of rhinosinusitis nasal polyps’ formation which may also depend on asthma
or allergy. Our results showed that the 140A/G polymorphism of LF gene and the −33C/G polymorphism of the OSF-2 gene may be associated with the risk of chronic rhinosinusitis with nasal polyps in a Polish population. 相似文献
5.
Liping Hou Shufeng Chen Hongjiang Yu Xiangfeng Lu Jianhong Chen Laiyuan Wang Jianfeng Huang Zhongjie Fan Dongfeng Gu 《Human genetics》2009,125(1):11-20
The human PLA2G7 gene encodes lipoprotein-associated phospholipase A2 (Lp-PLA2), an emerging risk factor for cardiovascular diseases. In the present study, seven single nucleotide polymorphisms (SNPs)
in the PLA2G7 gene were genotyped in 827 patients with coronary heart disease (CHD), of which 512 were patients with myocardial
infarction (MI), and 947 age- and gender-matched controls in a Chinese Han population. Plasma Lp-PLA2 activity was measured in 416 randomly selected controls and 689 randomly selected CHD patients, including 423 MI patients.
Lp-PLA2 activity in CHD and MI cases was significantly higher (233.42 ± 57.66 and 234.27 ± 59.51 nmol ml−1 min−1, respectively) than in controls (211.47 ± 58.61 nmol ml−1 min−1). After adjusting for traditional risk factors by logistic regression, the odds ratios for CHD and MI per 1 standard deviation
increment of Lp-PLA2 activity were 1.27 (95% CI, 1.07–1.50) and 1.27 (95% CI, 1.05–1.54), respectively. Both single SNP analysis and haplotype
analysis showed that the V279F and I198T polymorphisms were significantly associated with the reduced Lp-PLA2 activity, but neither was associated with increased CHD risk. Both univariate and multivariate analyses, adjusting effects
of conventional factors, indicated that the rs13210554 T allele increased the risk of MI in this Chinese Han population. In
summary, an independent association of increased plasma Lp-PLA2 activity with CHD and MI existed in this Chinese Han Population. Although V279F and I198T mutations significantly decreased
the activity of Lp-PLA2, only the promoter rs13210554 polymorphism was associated with MI. Lp-PLA2 activity appears to influence the CHD and MI risk in Chinese Han population.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
6.
APOC3/A5 haplotypes, lipid levels, and risk of myocardial infarction in the Central Valley of Costa Rica 总被引:6,自引:0,他引:6
Ruiz-Narváez EA Yang Y Nakanishi Y Kirchdorfer J Campos H 《Journal of lipid research》2005,46(12):2605-2613
Genetic variation in the APOC3 and APOA5 genes has been associated with plasma triglyceride concentrations and may affect the risk of myocardial infarction (MI). To assess whether APOC3/A5 haplotypes are associated with risk of MI, we examined three single-nucleotide polymorphisms (SNPs) in APOC3 (3238C>G, -455T>C, and -482C>T) and six SNPs in the APOA5 gene (-1131T>C, c.-3A>G, c.56C>G, IVS3+476G>A, c.553G>T, and c.1259T>C) in incident cases (n = 1,703) of a first nonfatal MI matched for gender, age, and area of residence with population-based controls (n = 1,703). Conditional logistic regression models, adjusted for potential environmental confounders, were used for analysis. The common APOC3*222 haplotype was more frequent in cases than in controls (17.4% and 13.7%, respectively, P < 0.001) and was associated with increased risk of MI [odds ratio (OR) = 1.27; 95% confidence interval (95% CI), 1.09, 1.48] compared with APOC3*111 wild-type haplotype. This association was independent of the APOA5 SNPs. Although the APOC3 3238G, APOA5 -1131C, APOA5 c.-3G, and APOA5 c.1259C alleles were associated with higher triglyceride plasma concentrations, these effects could not explain the associations with MI in this population. In summary, this study supports the hypothesis that haplotypes in the APOC3 gene but not in the APOA5 gene increase susceptibility to MI. 相似文献
7.
Angiotensinogen and angiotensin-I converting enzyme gene polymorphisms and the risk of coronary artery disease in Chinese 总被引:2,自引:0,他引:2
Y.-L. Ko S.-M. Wang Y.-S. Ko Po-Hsien Chu Ming-Sheng Teng Nye-Jan Cheng Wei-Jan Chen Tsu-Shiu Hsu Chi-Tai Kuo Chen-Wen Chiang Ying-Shiung Lee 《Human genetics》1997,100(2):210-214
The homozygous deletion allele (DD) of the angiotensin-I converting enzyme (ACE) gene and the T235 homozygote of the angiotensinogen
(AGT) gene have been reported to be correlated with an increased prevalence of coronary artery disease (CAD) and myocardial
infarction (MI). The importance of the DD genotype and T235 homozygote as genetic risk factors for CAD in Chinese remains
uncertain. This study included 426 patients who underwent coronary angiography and 180 healthy subjects without clinical evidence
of CAD. Coronary angiography identified 268 patients with CAD (CAD group) and 158 patients without CAD. The healthy subjects
and patients without angiographic evidence of CAD constituted the control group. Three polymorphisms were studied: an insertion/deletion
(I/D) polymorphism of the ACE gene and the T174 M and M235T polymorphisms of the AGT gene. No association was found between
any of the three studied polymorphisms and the risk of CAD or MI in Chinese using univariate or multivariate analysis. In
multivariate analysis, the relative risks were 1.20 (95% confidence interval = 0.91–1.61, P = 0.20) for the DD genotype, 1.05 (95% CI = 0.82–1.35, P = 0.69) for the T174 homozygote, and 1.19 (95% CI = 0.91–1.55, P = 0.20) for the T235 homozygote. Similarly, no significant difference was found in the frequencies of the DD genotype and
the T174 and T235 homozygotes between the control group, the CAD group, the non-MI group, and the MI group when analyzed according
to sex, age, or degree of risk. Our data suggest that neither the DD genotype of the ACE I/D polymorphism nor the T174 and
T235 homozygotes of the AGT gene confer significant risk for CAD or MI in Chinese.
Received: 18 December 1996 / Accepted: 27 February 1997 相似文献
8.
Jayashree Shanker Ganapathy Perumal Arindam Maitra Veena S. Rao B. K. Natesha Shibu John Sridhar Hebbagodi Vijay V. Kakkar 《Journal of genetics》2009,88(3):291-297
Elevated factor VII (FVII) level is a risk factor for coronary artery disease (CAD). We investigated the role of R353Q polymorphism
in the F7 gene in 139 Indian families with CAD, comprising of 222 affected subjects, 105 unaffected subjects and 126 affected sibling
pairs. Plasma per cent FVIIc activity (FVII.c activity) differed significantly across R353Q genotype (P < 0.0001). Frequency of subjects with RR and QQ genotypes were higher in 4th quartile and 1st quartile of FVII.c activity,
respectively (P < 0.0001). F7 R353Q SNP was able to explain up to 7% of variation in FVII.c activity by regression analysis and an additive genetic component
of variance of 28.04% by heritability analysis. Quantitative trait loci analysis showed suggestive linkage evidence of F7 SNP with per cent FVII.c activity (LOD score −1.82; P = 0.002). Individuals with RR and RQ genotypes carried an OR of 2.071 (95% c.i. = 1.506−2.850) and 2.472 (95% c.i. = 1.679−3.641),
respectively, towards CAD risk. There was significant correlation of FVII.c activity with lipid markers, particularly among
those with RR and RQ genotype after covariate adjustment. In conclusion, the F7 R353Q SNP appears to moderately influence plasma FVII.c activity and risk of CAD in Indians. 相似文献
9.
Published data on the association of vascular endothelial growth factor (VEGF) −1154G>A polymorphism with cancer risk is inconclusive.
To derive a more precise estimation of association between VEGF −1154G>A polymorphism and the risk of cancer, we performed
a meta-analysis of 7,071 cancer cases and 7,693 controls from 16 published case–control studies. Our meta-analysis didn’t
reveal an association between VEGF −1154G>A polymorphism and overall cancer risk (GG vs. AA: OR: 1.08, 95% CI: 0.96–1.20;
GA vs. AA: OR: 1.04, 95% CI: 0.93–1.17; recessive model: GG+GA vs. AA: OR: 1.06, 95% CI: 0.95–1.18; dominant model: GG vs.
GA+AA, OR: 1.11, 95% CI: 1.00–1.24). Nevertheless, for non-Caucasians, GG homozygote may have higher cancer risk compared
with either A carriers (OR: 1.58, 95% CI: 1.12–2.23) or AA homozygote (OR: 1.43, 95% CI: 1.17–1.76). No significant heterogeneity
was detected except in the dominant model and “prostate cancer” subgroup analysis. More studies with larger samples are warranted
to confirm these findings. 相似文献
10.
Angiotensinogen, one of the most important proteins in the renin–angiotensin system, plays a key role in the progress of coronary heart disease and myocardial infarction (MI). Many studies have investigated the association between angiotensinogen gene M235T polymorphism and MI risk, but the results were inconsistent. We performed a meta-analysis of 22 studies on M235T polymorphism and MI risk published before November 2012. This meta-analysis included a total of 4,606 MI cases and 4,918 controls. Overall, the per-allele odds ratio (OR) of the 235T variant for total MI risk was 1.04 (95 % CI 0.92–1.17). When a recessive model was evaluated, the OR was 1.06 (95 % CI 0.96–1.17) and under a dominant model, the OR was 0.96 (95 % CI 0.82–1.11). Under pairwise comparisons, non-significant associations were found between M235T polymorphism and MI risk (MT vs. MM, OR, 0.96, 95 % CI 0.87–1.06; TT vs. MM, OR, 1.03, 95 % CI 0.83–1.28). Subgroup analyses in the different ethnic groups and different control sources were performed and no significant association was found also. Based on the available evidence, no association between M235T polymorphism and MI risk was observed, even in the sub-analysis concerning different races and control sources. The direction of further research should focus not only on the simple relationship of M235T polymorphism and MI risk, but also on gene–gene and gene-environment interaction. 相似文献
11.
Bo Luan Yaling Han Xiaolin Zhang Jian Kang Chenghui Yan 《Molecular biology reports》2010,37(1):399-403
SDF-1 has been demonstrated to be involved in the pathophysiology of atherosclerosis. This study was aimed to investigate
whether the SDF1-3′A polymorphism (rs1801157) is associated to myocardial infarction (MI) in a sample of Chinese Han population. A total of
560 patients with MI and 532 controls were enrolled in the study. The SDF1-3′A polymorphism was determined by polymerase chain reaction -restriction fragment length polymorphism (PCR-RFLP) analysis. A
significant difference in genotype distribution and allele frequency was observed between patients and controls (P = 0.003 and P = 0.001, respectively). The A allele carriers had a significantly reduced MI risk compared with the GG homozygotes (OR, 0.69;
95% CI, 0.52–0.92; adjusted P = 0.007) in a logistic regression model after controlling conventional risk factors. The present study showed a significant
association between the SDF1-3′A polymorphism and MI in Chinese Han population. 相似文献
12.
Jyosna Khanam Delowar Hossain Bayejid Hosen Mesbah Uddin Asadul Kabir Mohammad Anwarul Bari 《Reports of Biochemistry & Molecular Biology》2020,9(3):366
Background:Myocardial infarction is one of the leading causes of morbidity and mortality worldwide. Oxidative stress plays a vital role in the pathogenesis of atherosclerosis leading to myocardial infarction and Glutathione S-transferases (GSTs) act as detoxifying enzymes to reduce oxidative stress. The aim of the present study was to investigate the associations of the GST (T1 & M1) gene polymorphism with the susceptibility of myocardial infarction in the Bangladeshi population.Methods:A case-control study on 100 cardiac patients with MI and 150 control subjects was conducted. The genotyping of GST (T1 & M1) gene was done using conventional Polymerase Chain Reaction.Results:The percentage of GSTM1 genotypes was significantly (p< 0.01) lower in patients compared to control subjects while the GSTT1 genotypes were not significantly different between the study subjects. The individual with GSTM1 null allele was at 2.5-fold increased risk {odds ratio (OR)= 2.5; 95 % confidence interval (95 % CI)= 1.4 to 4.3; p< 0.01} of experiencing MI while individual with either GSTM1 or GSTT1 genotypes was at lower risk. In the case of GST M1 and GST T1 combined genotype, patients having both null genotypes for GST M1 and GST T1 gene showed significantly (p< 0.01) higher risk of experiencing MI when compared to control subjects (OR= 3.5; 95% CI= 1.7–7.2; p< 0.001). Conclusion:Thus our recent study suggested that GSTM1 alone and GSTM1 and T1 in combination augments the risk of MI in Bangladeshi population. Key Words: Bangladesh, GST (T1 & M1), Myocardial infarction, PCR, Polymorphism 相似文献
13.
No consensus has been recently reached at the relationship between the α1-antichymotrypsin (ACT) signal peptide −15A/T polymorphism
and Alzheimer’s disease (AD) risk. Thus, our study aimed to better assess this association by performing a meta-analysis,
including 4,212 cases and 4,039 controls from 29 studies. Odds ratios (ORs) with the 95% confidence interval (CI) were used
to assess the strength of relationship between ACT −15A/T polymorphism and AD risk. Overall, a borderline statistically significant
association was detected under recessive model comparison in all subjects (AA vs. AT+TT: OR 1.12, 95% CI 1.01–1.25, P = 0.04). But in subgroup analysis by ethnicity, no significant association was found in Caucasians, Asians, or Africans.
Moreover, after exclusion of one study which affect the heterogeneity, the ACT A allele and AA genotype were statistically
associated with late-onset AD (LOAD) risk (AA vs. TT: OR 1.25, 95% CI 1.06–1.48, P = 0.007, A vs. T: OR 1.12, 95% CI 1.03–1.21, P = 0.008), especially in Caucasians. In conclusion, our study suggests that the common α1-antichymotrypsin signal peptide
−15A/T polymorphism may not be a major risk factor for AD. However, the polymorphism is capable of increasing LOAD risk. 相似文献
14.
The association between angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism and risk of myocardial infarction (MI) has been extensively studied. However, the results were in controversy. This study aimed to explore the association between ACE I/D polymorphism and risk of MI by using a meta-analysis. We retrieved the following databases to indentify eligible studies: Medline, Embase, ISI, VIP, CBM and Wan Fang database. The latest update was 10th May, 2012. Odds ratio and 95% confidence interval (95% CI) were used to present the strength of the association. A total of 40 case–control studies with 34 993 participants were included. Overall, D allele of ACE I/D polymorphism was significantly associated with an increased risk of MI in genetic comparison models (OR (95% CI): 1.41 (1.22–1.64) for DD vs. II; 1.11 (1.01–1.21) for ID vs. II; 1.23 (1.10–1.37) for D carriers vs. II; 1.28 (1.15–1.43) for DD vs. I carriers and 1.06 (1.02–1.10) for D carriers vs. I carriers). Subgroup analyses, according to ethnicities and countries of participants also indicated that D allele was significantly associated with an increased risk of MI in Asians (especially for Chinese) and Caucasians (especially for English, French, Germans and Italians) (OR (95% CI) of DD vs. ID + II: 2.11 (1.65–2.70) for Asians and 1.15 (1.05–1.27) for Caucasians). In conclusion, this meta-analysis indicated that D allele of ACE I/D polymorphism was a possible risk factor for MI incidence for both Asians and Caucasians. 相似文献
15.
《Cytokine》2014,65(3):646-651
Controversial results regarding the association of eNOS gene (NOS3) polymorphisms with myocardial infarction (MI) have been reported. This study investigated the relationship of the −786T>C (rs2070744), 894G>T (rs1799983) and 4a4b polymorphisms of the NOS3 gene with the presence of MI in the Tunisian population. In addition, we also examined the association of NOS3 gene haplotypes with MI in Tunisian subjects.A total of 303 patients with MI and 225 controls were included in the study. The 894G>T and −786T>C single nucleotide polymorphisms were analyzed by PCR-RFLP, and 4a4b polymorphism just for PCR.There was significant linkage disequilibrium between the three NOS3 polymorphisms (p < 0.0001). The genotype distribution and allele frequency of NOS3 4a4b, but not −786T>C and 894G>T, polymorphism was significantly different between MI patients and controls. The univariate logistic regression analysis showed a significant association of the 4a4b polymorphism and MI according to co-dominant, dominant and recessive models (co-dominant model OR: 4.38, 95%CI: 1.24–15.41; p = 0.021, dominant model OR: 1.66, 95%CI: 1.14–2.42); p = 0.007, and recessive model OR: 3.85, 95%CI: 1.10–13.47; p = 0.035). The multivariate analysis, adjusted for traditional cardiovascular risk factors, revealed that the NOS3 4a4a genotype was an independent predisposing factor to MI, according to the models considered. In addition, a haplotype 7 (C-T-4a), (OR = 12.05, p = 0.010) was a risk factor of MI after controlling for classical risk factors.These finding suggest that the 4a4b polymorphism of the NOS3 gene was associated with MI in Tunisian patients. 相似文献
16.
Published data on the association between prothrombin G20210A polymorphism and coronary artery disease (CAD) risk are inconclusive.
To derive a more precise estimation of the relationship, a meta-analysis was performed. A total of 42 case–control studies
including 15,041 cases and 21,507 controls were included in this meta-analysis. Overall, significantly elevated CAD risk was
associated with prothrombin G20210A polymorphism (OR, 1.22; 95% CI 1.07–1.40; P = 0.003) when 39 eligible studies were pooled into the meta-analysis. In the subgroup analysis, borderline statistically
increased risk was found for myocardial infarction in 22 case–control studies (OR, 1.27; 95% CI 1.00–1.61; P = 0.05). When stratified by ethnicity, significantly elevated risk was found in Europeans (OR, 1.19; 95% CI, 1.02–1.38; P = 0.02). However, no statistical differences were found among Americans and Asians. In summary, this meta-analysis indicated
that prothrombin G20210A allele is a low-penetrant risk factor for developing CAD in Europeans. 相似文献
17.
Some studies have shown that IL-18 was associated with aetiology and progression of asthma. However, the association between
single-nucleotide polymorphisms −607C/A (rs1946518) and −137G/C (rs187238) located in the IL-18 gene promoter and asthma risk
was still controversial and ambiguous. To derive a more precise effect on the association between these polymorphisms and
asthma risk, we performed a meta-analysis based on the currently available evidence of the literature. A total of 5 studies
with 1411 cases and 1525 controls for −607C/A polymorphism and 5 studies with 1883 cases and 6645 controls for −137G/C polymorphism
were identified to perform a meta-analysis, up to October 2010. Summary ORs and corresponding 95% CIs for IL-18 polymorphisms
and asthma were estimated using fixed- and random-effects models when appropriate. Heterogeneity and publication bias were
evaluated. We found that individuals carrying AC/CC genotype of −607C/A polymorphism were associated with an increased asthma
risk in recessive model (OR = 1.278; 95% CI, 1.073–1.522). However, no significant association was observed between −137G/C
polymorphism and asthma risk under different contrast models. There was no evidence of publication bias. The present meta-analysis
suggested that IL-18 −607C/A polymorphism in promoter region was associated with asthma risk. 相似文献
18.
Many epidemiological studies have explored the relationships between three genetic polymorphisms of genes encoding homocysteine-metabolizing enzymes (methionine synthase [MTR] A2756G, methionine synthase reductase [MTRR] A66G, and N(5),N(10)-methylenetetrahydrofolate reductase [MTHFR] A1298C) and risk of coronary heart disease (CHD), but no conclusive results were obtained. Therefore, we performed a meta-analysis of 23 case-control studies. Odds ratio (OR) and 95% confidence interval (95% CI) were used to examine the strength of the associations. Among those primary studies, 22 studies were for Europeans, and one study focused on the MTR A2756G polymorphism in Asians. The results of combined analyses of the MTR A2756G polymorphism suggested that the G allele was associated with increased risk of CHD and myocardial infarction (MI) especially for Europeans (GG vs. AA for CHD: OR [95% CI]=1.63 [1.18-2.25], p(z)(-test)=0.001, p(heterogeneity)=0.274; GG+AG vs. AA for MI: OR [95% CI]=1.44 [1.08-1.93], p(z)(-test)=0.014, p(heterogeneity)=0.611). In addition, the G allele was also associated with higher risk CHD based on population-based case-control studies (PCC) (GG vs. AA: OR [95% CI]=1.75 [1.24-2.49], p(z)(-test)=0.002, p(heterogeneity)=0.316). The results suggested that the MTRR A66G polymorphism was not associated with risk of CHD for Europeans (AA vs. GG: OR [95% CI]=1.07 [0.59-1.94], p(z)(-test)=0.831, p(heterogeneity)<0.01). The results suggested that the C allele of the MTHFR A1298C polymorphism might be associated with the increased risk of MI for Europeans (CC vs. CA+AA: OR [95% CI]=1.37 [1.03-1.84], p(z)(-test)=0.033, p(heterogeneity)=0.668). However, when subgroup analyses for sources of controls were performed, conflicting results were obtained. The results suggested that the C allele was associated with decreased risk of CHD based on hospital-based case-control studies, but associated with increased risk of CHD based on PCC. This meta-analysis suggests that MTR A2756G polymorphism, but not MTRR A66G and MTHFR A1298C, is associated with risk of CHD for Europeans. Because of limitations and potential bias, more well-designed studies with larger sample size, especially focused on Asians and Africans, should be performed in the future. 相似文献
19.
Background
The PlA2 polymorphism of glycoprotein IIIa (GPIIIa) has been previously identified as being associated with myocardial infarction (MI), but whether this represents a true association is entirely unclear due to differences in findings from different studies. We performed a meta-analysis to evaluate whether this polymorphism is a risk factor for MI.Methods
Electronic databases (MEDLINE and EMBASE) were searched for all articles evaluating genetic polymorphisms of GPIIIa. For studies where acute coronary events were recorded in association with genetic analysis, pooled odds ratios (ORs) were calculated using fixed-effects and random-effects models. The primary outcome measure was MI, and a secondary analysis was also performed for acute coronary syndromes (ACS) more generally.Findings
57 studies were eligible for statistical analysis and included 17,911 cases and 24,584 controls. Carriage of the PlA2 allele was significantly associated with MI (n = 40,692; OR 1.077, 95% CI 1.024–1.132; p = 0.004) but with significant publication bias (p = 0.040). The degree of association with MI increased with decreasing age of subjects (≤45 years old: n = 9,547; OR 1.205, 95% CI 1.067–1.360; p = 0.003) and with adjustment of data for conventional cardiovascular risk factors (n = 12,001; OR 1.240, 95% CI 1.117–1.376; p<0.001). There was a low probability of publication bias for these subgroup analyses (all p<0.05).Conclusions
The presence of significant publication bias makes it unclear whether the association between carriage of the PlA2 allele and MI is true for the total population studied. However for younger subjects, the relative absence of conventional cardiovascular risk factors results in a significant association between carriage of the PlA2 allele and MI. 相似文献20.
M. G. Parfenov B. V. Titov M. A. Sudomoina M. Yu. Martynov A. V. Favorov M. F. Ochs E. I. Gusev O. O. Favorova 《Molecular Biology》2009,43(5):873-880
The frequencies of alleles and genotypes for ten functionally significant single-nucleotide polymorphisms were determined
in the FGA, FGB, APOE, LPL, ACE, and CMA1 genes for Russian ischemic stroke (IS) patients and for a control group of Russians similar in gender and age distribution.
The groups showed no significant differences in the frequencies of individual alleles or genotypes for any polymorphism studied.
However, complex analysis of genetic susceptibility by the APSampler algorithm demonstrated that carriership of the APOE (−491A) allele predisposed to IS (p = 0.044, OR 3.8, 95% CI 1.0–15.1). Correspondingly, the APOE (−491T/T) genotype was associated with resistance to IS (p = 0.044, OR 0.26, 95% CI 0.07–1.0). The carriership of FGB (−249C) allele together with this genotype enhanced its protective potential, reducing the p value of the combination twofold (OR 0.17, 95% CI 0.04–0.8). Two more protective combinations were identified: biallelic
APOE (−427C) + LPL (1595G) and triallelic APOE (−491C) + LPL (1595G) + CMA1 (−1903G). In both cases, p = 0.0052, OR 0.18, and 95% CI 0.05–0.66. Altogether, involvement in the formation of IS risk in Russians was evidenced for
alleles of four genes: APOE, FGB, LPL, and CMA1; the APOE involvement was demonstrated for alleles of two polymorphic loci: −491T and −427C. Linkage analysis suggested that these
loci were involved in IS resistance independently of each other. 相似文献