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1.
Pasalić D Marinković N Grsković B Ferencak G Bernat R Stavljenić-Rukavina A 《Molecular biology reports》2009,36(4):775-780
Human C-reactive protein (CRP) is a reactant involved in the acute phase response and one of the many molecular factors involved
in pathogenesis of coronary artery disease (CAD). CRP gene variants potentially mediate CRP plasma concentrations and the
development of CAD. 220 Croatian subjects with angiographically confirmed CAD and 132 control subjects were included in the
study. CRP gene polymorphisms 1059G/C and -717G/A were determined by RFLPs, using MaeIII and KspI endonuclease, respectively. Plasma concentrations of CRP and homocysteine were determined by immunoturbidimetry and FPIA,
respectively. CRP 1059G/C gene variants were significantly associated with CAD (OR = 0.50; 95% CI = 0.27, 0.94; P = 0.032). Wild GG genotype and rare allele C carrier genotypes were 184 and 22 in CAD(+) group, and 101 and 24 in CAD(−)
group, respectively. Multivariate analysis with age, gender, BMI, smoking status, hypertension and diabetes as covariates
showed that 1059C carriers had lower CRP concentrations in CAD(−) (P = 0.010) and CAD(+) subjects (P = 0.028). This allele was also significantly associated with lower plasma homocysteine concentrations in both groups (P = 0.018 for CAD(−) and 0.002 for CAD(+). There was no significant difference between CAD(+) and CAD(−) subjects in absolute
frequencies for CRP -717A/G gene variant, but multivariate analysis showed that carriers of the rarer G allele had significantly
higher CRP plasma concentrations in CAD(−) subjects (P = 0.031) and higher homocysteine concentrations in CAD(+) group (P < 0.001). Atherosclerosis is an inflammatory disease resulting from different genetic and environmental factors. Results
presented here support the contribution of CRP genetic variations in the development of CAD. 相似文献
2.
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
3.
Kurnaz O Akadam-Teker AB Yilmaz-Aydoğan H Tekeli A Isbir T 《Molecular biology reports》2012,39(4):4351-4358
In coronary artery disease (CAD), a potentially reversible factor leading to cardiac death is left ventricular hypertrophy
(LVH). The 3′untranslated region (3′UTR) 188CT polymorphism of lectin-like oxidized low-density lipoproteins receptor-1 (LOX-1)
gene has been associated with an increased risk for CAD. We aim to investigate, in a Turkish population, whether 3′UTR188CT
variation could affect the development of LVH in CAD patients. In a population-based case–control study, we compared 83 cases
with CAD and 99 healthy controls for this polymorphism. The LOX-1 3′UTR188CT genotypes were determined by PCR–RFLP technique.
LOX-1 3′UTR188 TT genotype was associated with significantly increased systolic blood pressure (P = 0.047) and risk of LVH (P = 0.014, OR: 3.541) when compared with the C allele carriers. In addition, the TT genotype was positively associated with
decreased levels of HDL-cholesterol in the control subjects (P = 0.031) and increased levels of VLDL-C in the patient group (P = 0.009). The LOX-1 3′UTR188CT gene polymorphism may predispose to the development of LVH in CAD patients, dependent on blood
pressure. 相似文献
4.
Yilmaz A Menevse S Onaran M Sen I Ergun MA Camtosun A Kupeli B Bozkirli I 《Molecular biology reports》2011,38(8):4931-4934
Nephrolithiasis is a complex disease and many gene polymorphisms have been associated with stone formation. In this study
we aimed to investigate another possible relationship between E-cadherin gene (CHD1) 3′-UTR C/T polymorphism and calcium oxalate nephrolithiasis in the Turkish population. Study population was composed of
143 patients with nephrolithiasis and 158 control subjects. CHD1 3′-UTR C/T polymorphism was analysed using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP)
technique. Genotype distribution of the investigated polymorphism was not deviated from Hardy–Weinberg equilibrium (HWE) in
patients and control subjects (P > 0.05). C allele frequency was 85.7 and 85.1% in patients and controls, respectively (P = 0.836). Genotype distributions of the CHD1 3′-UTR C/T polymorphism among patients were also not significantly different from those among control subjects (P = 0.636). Our results showed that there is no association between the CHD1 gene 3′-UTR C/T polymorphism and nephrolithiasis in our population. 相似文献
5.
Saedi M Vaisi-Raygani A Khaghani S Shariftabrizi A Rezaie M Pasalar P Rahimi Z Pourmotabbed T 《Molecular biology reports》2012,39(1):555-562
The Matrix metalloproteinas-9 functional promoter polymorphism 1562C>T may be considered an important genetic determinant
of early-onset coronary artery disease (ECAD). In this study, association between MMP-9 1562C>T allele with plasma MMP-9 activity,
homocysteine and lipid–lipoproteins level and ECAD in Iranian subjects was investigated. This case–control study consisted
of 53 ECAD patients (age < 55 years) and unrelated late-onsets CAD (age > 70 years) who angiographically had at least 50%
stenosis. MMP-9 1562C>T polymorphism was detected by PCRRFLP, plasma MMP-9 activity, serum lipid and homocysteine levels were
determined by gelatin gel zymography, enzyme assay and by HPLC, respectively. The presence of MMP-9 1562C>T allele was found
to be associated with ECAD (OR = 3.2, P = 0.001). The ECAD patients with MMP-9 1562C>T allele had higher MMP-9 activity (P = 0.001), LDL-C (P = 0.045), TC (P = 0.02) and homocysteine (P = 0.01) levels than the LCAD subjects. MMP-9 1562C>T allele is a risk factor for ECAD. The carriers of this allele have high
levels of MMP-9 activity, LDL-C, TC and homocysteine (P = 0.01), thus, are more likely to develop myocardial infarction and CAD at young age (less than 55 years). 相似文献
6.
Vaisi-Raygani A Rahimi Z Tavilani H Vaisi-Raygani H Kiani A Aminian M Shakiba E Shakiba Y Pourmotabbed T 《Molecular biology reports》2012,39(3):2723-2731
We have previously shown that angiotensin-converting enzyme (ACE) gene D allele is an independent risk factor for early onset
coronary artery disease (CAD). Little is known about the concomitant presence of the ACE gene D allele and paraoxonase (PON1)
codon 192 arginine (Arg) on the severity of CAD. Regarding the high rate of CAD among Iranians the aim of present study was
to examine the hypothesis of synergistic effects between ACE-D and PON1-Arg alleles on predisposition and the severity of
CAD in our population. The PON1 192 and ACE insertion/deletion (I/D) genotypes were detected by PCR-RFLP and PCR, respectively
in 414 individuals undergoing their first coronary angiography. Patients were placed into one of two groups: CAD and control
without CAD or diabetes. We mentioned the synergistic effects of both genes and not ACE gene alone is a risk factor for CAD.
We found that PON1 Arg 192 and ACE D allele act synergistically to increase the risk of CAD (OR 1.3, P = 0.044). Our results showed a significant correlation between the possession of both PON1 192 Arg and the ACE D allele and
the extent of CAD in CAD patients and CAD subjects without diabetes, represented by the increased frequency of three-vessel
disease with OR 2.7, P = 0.046; χ2 = 4, P = 0.046 and OR 2.4, P = 0.051; χ2 = 3.8, P = 0.051, respectively. We found that PON1 Arg 192 and ACE D alleles act synergistically to increase the risk of CAD in CAD
patients and CAD subjects without diabetes from west of Iran, who have high frequency of three-vessel disease. Our data suggest
that PON1 192 Arg and the ACE D allele in combination with each other can be important independent risk factor for severity
of CAD in patients carrying both PON1 192 Arg and the ACE D allele in a west population of Iran. 相似文献
7.
This study was carried out in 52 non-diabetic, 62 diabetic patients with coronary artery disease (CAD) and 55 controls. A
Gly to Ser change RAGE gene was analyzed by PCR-RFLP techniques. GlyGly genotype frequency is higher in non-diabetics versus
controls (P < 0.001). GlySer frequency is higher in diabetics than controls and non-diabetics (P < 0.001). Ser allele frequency is respectively increased in the order of diabetics > Controls > non-diabetics. These results
reveals none association between Gly82Ser and the development of disease in non-diabetic patients. In diabetics with Ser allele,
higher prevalence of left-ventricule-hypertrophy was observed, but the significant difference between Gly82Ser and left-ventricule-hypertrophy
only found in the whole patient group. As a result Ser allele has much more importance in the development of left-ventricule-hypertrophy
than other cardiovascular risk factors. In this study we found the presence of Gly allele contributes to the CAD in non-diabetics
and Ser allele may contribute to disease in diabetics. 相似文献
8.
9.
The first step in the activation of blood coagulation factor XIII (FXIII) is the proteolytic cleavage of the potentially active A subunit (FXIII-A) by thrombin at Arg37-Gly38. Both fibrin formation and FXIII-A Val34Leu polymorphism influence the rate of proteolytic activation of purified factor XIII, however their relative importance and interaction in determining the time of onset and the rate of FXIII activation in whole plasma have not yet been explored. In the present study it was shown that in plasma, fibrin formation preceded the truncation of FXIII-A by thrombin, the activation process took place exclusively on the surface of newly formed fibrin and activated FXIII remained associated with the fibrin clot. The time of fibrin formation closely correlated with the time of FXIII activation, while there was no significant relationship between the time of FXIII activation and FXIII-A Val34Leu genotype. However, in the case of Leu34 variant the lag phase between fibrin formation and FXIII-A truncation was significantly shorter than in the case of Val34 variant. The results suggest that in whole plasma the onset of FXIII activation is determined by fibrin formation, while the rate of activation is modulated by Val34Leu polymorphism. 相似文献
10.
Growth differentiation factor (GDF)-15 belongs to a member of the transforming growth factor-β cytokine superfamily, and elevated
GDF-15 concentrations are linked to increased risk of cardiovascular diseases and future adverse cardiac events in apparently
healthy elderly women, acute coronary syndrome, and chronic heart failure. However, its genetic mechanisms are still unknown.
We investigated whether GDF-15 −3148C>G variant (SNP, rs4808793) is associated with a predisposition to coronary artery disease
(CAD) and its severity in a Chinese population. We studied 418 consecutive patients, including 192 with coronary stenosis
≥50% or previous myocardial infarction and 226 controls without documented CAD. Coronary artery disease cases and controls
were genotyped for SNP rs4808793 by using the ligase detection reaction method. The three genotypes CC, CG, and GG were present
in rs4808793. No differences were found in genotype distribution and allele frequencies of rs4808793 between subjects with
and without CAD, or when grouped according to sex. Logistic regression did not reveal any increased risk of CAD in subjects
carrying the CG, GG genotype, or G allele at rs4808793 compared with individuals carrying the CC genotype or C allele; this
finding was the same when subjects were grouped by sex (all P > 0.05). Rs4808793 does not affect main anthropometric and metabolic characteristics, nor did there exists any association
between rs4808793 and the severity of coronary lesions (all P > 0.05). Our data do not support an association of rs4808793 with CAD or its severity in a Chinese population. 相似文献
11.
Ahmet Var Ozan Ütük Sinem Akçalı Tamer Şanlıdağ Bekir S. Uyanık Gönül Dinç 《Molecular biology reports》2009,36(8):2235-2243
Single point mutations in the genes coding for hemostatic factors were shown to be major inherited predisposing factors for
venous thromboembolism. However, their contribution in the development of non-diabetic coronary artery disease [nDCAD] remains
controversial. Angiographically demonstrated nDCAD patients (n = 86) and healthy controls (n = 90) were included in the study. Genotype analysis of hemostatic gene polymorphisms were assessed by using CVD strip assay,
based on allele specific oligonucleotide probes. The carrier frequency of factor V (FV) H1299R, prothrombin G20210A, glycoprotein
(Gp) IIIa L33P, plasminogen activator inhibitor-I (PAI-1) 4G/5G, 4G/4G, 5G/5G, methylenetetrahydrofolate reductase (MTHFR)
A1298C and β-fibrinogen −455 G > A were similar between patients and controls. In contrast, frequency of FV Leiden was significantly
higher among patients (12.5%) than controls (5%, OR: 7.94; 95%CI: 1.9–49.6) and FXIII V34L was significantly lower among patients
(23.7%) than controls (40%, OR: 0.24; 95%CI: 0.1–0.89). In addition, the frequency of the MTHFR C677T polymorphism was 32.5%
among patients compared with 42.5% in controls, of which the T/T genotype was significantly lower among patients (5%) than
controls (17.5%, OR: 0.06; 95%CI: 0.01–0.58). No difference was observed in prevalence of prothrombin G20210A, FV H1299R,
Gp IIIa L33P, PAI-1 4G5G, MTHFR A1298C, β fibrinogen 455 G > A mutations between patients and controls. However, lower frequency
of FXIII Val34Leu and MTHFR C677T polymorphisms may decrease, while FV Leiden polymorphism may increase development of nDCAD. 相似文献
12.
Asad Vaisi-Raygani Zohreh Rahimi Haidar Tavilani Tayebeh Pourmotabbed 《Molecular biology reports》2010,37(4):2083-2091
We have previously shown that butyrylcholinesterase-K (BCHE-K, G1615A/Ala539Thr) variant increases the risk of coronary artery
disease (CAD). In addition, we have found that the presence of APOE-ε4 allele augments the risk of CAD in patients with type
II diabetes mellitus (T2DM/CAD). Here we explored the concomitant presences of two alleles of the BCHE-K and APOE-ε4 in increasing
the risk of CAD or diabetes in T2DM patients with or without CAD and CAD patients without T2DM. This case–control study comprised
631 subjects undergoing their first coronary angiography. They were matched and randomly assigned into four groups: type II
diabetic patients with no sign of CAD (T2DM), type II diabetic patients with CAD/ND (T2DM/CAD), CAD patients with no sign
of diabetes (CAD/ND), and healthy individuals (NCAD/ND). BCHE-K variant and APOE genotypes were detected by PCR-RFLP and serum
lipid level was measured enzymatically. We found that BCHE-K and APOE-ε4 allele act synergistically to increase the risk of
CAD in both T2DM, non-diabetic and total CAD (TCAD = T2DM/CAD + CAD/ND) individuals. The level of synergy 1.5 and 1.2 fold
are higher in CAD patients (OR = 4.5; P = 0.011) with T2DM than the non-diabetic CAD patients (OR = 3.07; P = 0.024) and TCAD patients (OR = 3.74; P = 0.018), respectively. The CAD subjects with and without T2DM and TCAD patients carrying both APOE-ε4 allele and BCHE-K
had significantly lower plasma HDL-C (P values = 0.008, 0.047, and 0.036, respectively) and higher plasma LDL-C (P values = 0.025, 0.048, and 0.04, respectively), than that of the control carriers both APOE-ε4 and BCHE-K. We have found
that BCHE-K and APOE-ε4 allele not only act synergistically to increase the risk of CAD, particularly in T2DM subjects in
population from western Iran, who have high levels of LDL-C and low levels of HDL-C, suggesting that a specific therapeutic
intervention should be considered for these particular groups of patients. 相似文献
13.
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
14.
Al-Daghri NM Al-Attas OS Alokail MS Alkharfy KM Hussain T 《Molecular biology reports》2011,38(6):3703-3708
Patients with type 2 diabetes (T2D) are more susceptible to develop cardiovascular complications than non-diabetic subjects.
Several studies have indicated a role of adiponectin gene in the increased coronary artery disease (CAD) risk in T2D patients.
The data however is limited and have been inconsistent. In this study we examined the association of SNP45T>G and SNP276G>T
of adiponectin gene with CAD risk in T2D patients in a Saudi population. A total of 418 type 2 diabetic patients were randomly
recruited in this study from the RIYADH COHORT. Of the total diabetes patients, 123 were also diagnosed to have CAD, while
the rest were control subjects. Anthropometric, clinical and biochemical parameters were measured by standard procedures.
Genotyping of polymorphisms was carried out by PCR–RFLP analysis. Genotype distribution of SNP45T>G was significantly (P = 0.005) different between control and CAD subjects, while the distribution of SNP276G>T genotypes was comparable between
the subjects. The SNP45T>G was significantly associated with risk of CAD [OR (95% CI), 4.7 (1.6–13.5), P < 0.003] but not SNP276G>T [OR (95% CI), 1.02 (0.53–1.9), P > 0.05]. The association of SNP45T>G with CAD risk remained significant even after adjusting for potential confounding factors
[OR (95% CI), 7.2 (1.1–45.9), P < 0.05]. The SNP45T>G of adiponectin gene is an independent risk factor for CAD in T2D patients in a Saudi population. These
findings support a role for adiponectin gene in the increased CAD risk in diabetes patients and are consistent with genetic
heterogeneity in the association between adiponectin gene and coronary artery disease. 相似文献
15.
Esteghamati A Mansournia N Nakhjavani M Mansournia MA Nikzamir A Abbasi M 《Molecular biology reports》2012,39(4):3791-3797
The relation of Two single nucleotide polymorphisms (SNPs) at the adiponectin locus (+45T/G and +276G/T) with coronary artery
disease (CAD) is controversial. The aim of the present study was to evaluate the genetic influence of the adiponectin gene
polymorphisms in the development of CAD among patients with Type 2 diabetes (T2D). The adiponectin genotypes were detected
by polymerase chain reaction and restriction analysis (PCR-RFLP) in our patients. Two adiponectin gene (ADIPOQ) SNPs (i.e.
SNPs +45T>G and +276G>T) were genotyped in 114 Type 2 diabetic subjects with CAD, and 127 Type 2 diabetic patients without
CAD. Demographic and anthropometric data along with plasma biochemistry including lipids, glycemic indices, and adiponectin
were collected. There was a significant difference in the distribution of genotypes of +45T/G and +276G/T between CAD and
non-CAD individuals (P < 0.05). Based on our results SNP+276G>T is associated with decreased risk of CAD after adjustment for potential confounding
factors [adjusted OR = 0.39 (95%CI: 0.22–0.68); P = 0.001]. Similar findings were not observed for the +45T>G SNP. Two haplotypes 45T-276T and 45G-276T were associated with
a decreased risk of CAD [adjusted OR = 0.47 (95% CI: 0.32–0.94); P = 0.03 and adjusted OR = 0.33 (95% CI: 0.13–0.83); P = 0.02 respectively]. No significant difference was observed between HOMA-IR, BMI, waist circumference, history of hypertension,
HbA1C, and lipid concentrations regarding the two SNPs. In conclusion, these findings suggest that T allele of +276G>T SNP
is significantly associated with decreased risk of CAD in T2D Patients. Also Haplotype analysis showed that two haplotypes
45T-276T and 45G-276T were associated with a decreased risk of CAD. 相似文献
16.
Powell BL Wiltshire S Arscott G McCaskie PA Hung J McQuillan BM Thompson PL Carter KW Palmer LJ Beilby JP 《Human genetics》2008,124(3):263-270
PARL (presenilin-associated rhomboid-like) is a mitochondrial protein involved in mitochondrial membrane remodelling, and
maps to a quantitative trait locus (3q27) associated with metabolic traits. Recently the rs3732581 (Leu262Val) variant was
found to be associated with increased levels of plasma insulin, a finding not replicated in a larger cohort. The aim of the
current study was to investigate the associations between rs3732581 and levels of plasma insulin, metabolic syndrome (MetS)
and its components, and cardiovascular disease. The CUPID population consisted of 556 subjects with angiographically proven
CAD and the CUDAS cohort consisted of 1,109 randomly selected individuals from Perth, Western Australia. Samples were genotyped
using mutation-specific PCR. No significant associations were observed between rs3732581 and levels of plasma insulin, glucose,
BMI or MetS in either population. However, carriers of the minor allele had significantly lower mean intima-media thickness
(IMT) [0.69 mm, 95% CI (0.69, 0.70 mm); P = 0.004], compared with major allele homozygotes [mean IMT = 0.71 mm, 95% CI (0.70, 0.72 mm)] in the CUDAS population. Further
analysis using a recessive model showed homozygous carriers of the minor allele were predisposed to CAD [OR 1.55, 95% CI (1.11,
2.16); P = 0.01]. Despite the functional evidence for a role of PARL in regulating insulin levels, no association with rs3732581 was
found in the current study. Additionally, there were no associations with glucose levels, BMI or MetS. There were significant
effects of the variant on mean IMT and risk of CAD. A role for PARL in metabolic conditions cannot be excluded and more comprehensive
genetic studies are warranted. 相似文献
17.
Ahmed W Malik M Saeed I Khan AA Sadeque A Kaleem U Ahmed N Ajmal M Azam M Qamar R 《Molecular biology reports》2011,38(4):2541-2548
A case–control association study on 229 Myocardial Infarction (MI) patients and 217 healthy controls was carried out to determine
the role of tissue-plasminogen activator (t-PA) (Alu-repeat insertion (I)/deletion (D)) and plasminogen activator inhibitor
(PAI-1) (4G/5G insertion/deletion) polymorphisms with MI in the Pakistani population. In MI patients the genotype distribution
of the PAI-1 gene was not found to be different when compared with the unaffected controls (P > 0.05, χ2 = 1.03). The risk allele 4G was also not associated with MI (P > 0.05, χ2 = 0.46, odds ratio (OR) = 1.1 (95% confidence interval (CI) = 0.84–1.43), P > 0.05). Similarly, the genotype frequencies of t-PA I/I, I/D and D/D were not different from the unaffected controls (P > 0.05, χ2 = 1.60), and the risk allele “I” was not found to be associated with MI (P > 0.05, χ2 = 1.35, OR = 0.86 (95% CI = 0.66–1.11), P > 0.05). However, when the data were distributed along the lines of gender a significant association of the 4G/4G PAI-1 genotype
was observed with only the female MI patients (P < 0.05, z-test = 2.21). When the combined genotypes of both the polymorphisms were analyzed, a significant association of
MI was observed with the homozygous DD/4G4G genotype (P < 0.01, z-test = 2.61), which was specifically because of the female samples (P = 0.01, z-test = 2.53). In addition smoking (P < 0.001, χ2 = 13.52, OR = 3.45 (95% CI = 1.77–6.94)), diabetes (P < 0.001, χ2 = 22.45, OR = 8.89 (95% CI = 2.96–29.95)), hypertension (OR = 7.76 (95% CI = 2.88–22.68), P < 0.001) family history (P < 0.001, χ2 = 13.72, OR = 3.7 (95% CI = 1.71–8.18)) and lower HDL levels (P < 0.05) were found to be significantly associated with the disease. In conclusion the PAI-1 gene polymorphism was found to
have a gender specific role in the female MI patients. 相似文献
18.
Four single nucleotide polymorphisms (SNPs, rs2237892, rs2237895, rs2237897, rs2283228) in KCNQ1 are associated with type 2 diabetes mellitus in different ancestral groups. We investigated whether these 4 genetic markers
are determinants of type 2 diabetes and premature coronary artery disease (CAD) in a Chinese population. We studied 398 consecutive
patients, including 180 with coronary stenosis ≥50% or previous myocardial infarction (male <55 years, female <65 years) and
218 controls without documented CAD. CAD cases and controls were genotyped for 4 SNPs by using the ligase detection reaction
method. The 3 genotypes AA, AC, and CC were present in rs2283228 and rs2237895, and the 3 genotypes CC, CT, TT were present
in rs2237897 and rs2237892. No differences were found in genotype distribution and allele frequencies of these 4 SNPs between
subjects with and without type 2 diabetes. Logistic regression showed that the risk of premature CAD in subjects carrying
the CC genotype at rs2237892 was reduced by 90% in relation to individuals carrying the TT genotype (OR = 0.100, 95% CI: 0.018–0.564,
P = 0.009). The association of other 3 SNPs with premature CAD could not be detected, nor did there exist any association of
these 4 SNPs among groups of patients with 0, 1, 2, and 3-vessel disease (all P > 0.05). Our data implicate rs2237892 in KCNQ1 as a protective gene variant against premature CAD and we couldn’t replicate any association of these 4 SNPs with T2DM or
extent of coronary lesions in a Chinese population. 相似文献
19.
Zhu J Yan JJ Kuai ZP Gao W Tang JJ Jia EZ Yang ZJ Wang LS 《Molecular biology reports》2012,39(2):1777-1782
The aim of the present study was to assess the influences of PRKCH gene variants (1425G/A and _15) on the risk of coronary
artery disease (CAD) in a Chinese population. Our study population consisted of 470 CAD patients and 434 control subjects.
The alleles frequencies of the two variants were significantly higher among CAD patients than control subjects (P = 0.001 for 1425G/A and P = 0.001 for _15, respectively). In the CAD group, the A allele carriers of 1425G/A and _15 polymorphisms had higher low-density
lipoprotein cholesterol (LDL-C) levels than homozygote G allele carriers (P = 0.001 and P = 0.021, respectively). In a multiple logistic regression model adjusted for age, sex, body mass index (BMI), etc., a markedly
increased risk of developing CAD was found in subjects carrying GA or AA genotype (P = 0.005 and P = 0.018, respectively). In conclusion, we observed that there was a remarkable association of minor alleles (1425G/A and
_15) in the PRKCH gene with an elevated risk of CAD and increased levels of LDL-C in this Chinese population. 相似文献
20.
Toll-like receptors (TLRs) play roles in innate and adaptive immune responses. Some TLRs are involved in the pathogenesis
of cardiovascular diseases. Coronary artery disease (CAD) has an inflammatory and immunological basis. We investigated whether
TLR8 Met1Val and TLR8-129G>C single nucleotide polymorphisms (SNPs rs3764879 and rs3764880) are associated with CAD in the
Chinese population. We enrolled 412 consecutive patients (185 with coronary stenosis ≥50% or previous myocardial infarction
and 227 controls). Ligase detection reaction was performed to detect SNPs rs3764879 and rs3764880 of TLR8. The SNP at rs3764879
is in complete linkage disequilibrium with rs3764880. No significant difference was found in genotypic or allelic frequencies
of these two common SNPs between CAD cases and controls (P > 0.05, respectively). No associations existed between these two SNPs and the severity of coronary artery stenosis (All P > 0.05). These results do not support an involvement of SNPs rs3764879 and rs3764880 of TLR8 in predisposition to CAD.
Z. Chen and G. Ma contributed equally to this paper. 相似文献