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  1. Home
  2. Browse by Author

Browsing by Author "Sagcan, A"

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    No association of interleukin-6 gene polymorphism (-174 G/C) with premature coronary artery disease in a Turkish cohort
    Sekuri, C; Cam, FS; Sagcan, A; Ercan, E; Tengiz, I; Alioglu, E; Berdeli, A
    Objectives Interleukin (IL-6) may contribute to the inflammatory response by activating endothelial cells and stimulating the synthesis of fibrinogen. It might thus be important in the pathogenesis of inflammation associated with coronary artery disease (CAD). Several studies suggested that the -174 C allele was associated with an increased prevalence of coronary heart disease. The aim of this study was to investigate further the association of the IL-6 -174 G/C allele status with premature CAD. Methods A total of 120 patients and 105 controls were included in the study. The IL-6 -174 G/C polymorphism was genotyped using PCR-restriction fragment length polymorphism. Results The genotype distribution of the -174 G/C polymorphism was not different in premature CAD patients (GG: 53%; GC: 42.6%; CC: 4.3%) and controls (GG: 54.3%; GC: 39%; CC: 6.7%) (P=0.72). The prevalence of the C allele was 25.6% in patients and 26.1% in controls. By multiple regression analysis, family history, smoking, diabetes, and hypertension were independent risk factors of premature CAD, but not IL-6 genotype. Conclusions We conclude that the IL-6 -174 G/C polymorphism is not associated with the risk of premature CAD, and does not contribute to cardiovascular risk stratification.
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    The G894T polymorphism on endothelial nitric oxide synthase gene is associated with premature coronary artery disease in a Turkish population
    Cam, SF; Sekuri, C; Tengiz, I; Ercan, E; Sagcan, A; Akin, M; Berdeli, A
    Introduction: The aim of the present study was to investigate the association between premature coronary artery disease and Glu298Asp polymorphism of the endothelial nitric oxide synthase gene. Materials and methods: The eNOS gene polymorphism was analysed in 115 (mean age, 48.1 +/- 7.9 years) Turkish patients with a diagnosis of premature coronary artery disease and 83 (mean age, 44.6 +/- 1.4 years) control subjects. The Glu298Asp polymorphism of the endothelial nitric oxide synthase gene was determined by polymerase chain reaction and restriction fragment length polymorphism. Results: The patients group showed an increase in the frequency of the T allele compared to controls (0.456 versus 0.169, p=0.0001). There was a significant association between the TT genotype and premature coronary artery disease [eNOS TT vs. TG and GG; OR=17.000 (CI 95% 3.952-73.125, p=0.0001)]. The eNOS T/G genotypes were not associated with the number of affected vessels (p > 0.05). In addition, the family history of premature coronary artery disease, smoking, diabetes, obesity, dyslipidemia and eNOS TT genotype were independent risk factors of coronary artery disease. The patients with eNOS TT genotype had 15 fold risk of coronary artery disease compared with the control group [OR= I 5,356(Cl 95%3.262-77.289, p=0.001)]. Conclusions: These results suggest that premature coronary artery disease is associated with the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene in our population. (c) 2004 Elsevier Ltd. All rights reserved.
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    LACK OF ASSOCIATION BETWEEN MCP-1 GENE POLYMORPHISM (-2518G/A) AND PREMATURE CORONARY ARTERY DISEASE
    Cam, FS; Sekuri, C; Sagcan, A; Ercan, E; Tengiz, I; Alioglu, E; Berdeli, A
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    Effect of the asp298 variant of endothelial nitric oxide synthase on patients with early coronary artery disease in a Turkish population
    Cam, FS; Sekuri, C; Ercan, E; Sagcan, A; Berdeli, A
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    Association between renin-angiotensin system gene polymorphisms and premature coronary heart disease in a Turkish population
    Sekuri, C; Cam, E; Ercan, E; Sagcan, A; Berdeli, A; Ese, E
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    Renin-angiotensin system gene polymorphisms and premature coronary heart disease
    Sekuri, C; Cam, FS; Ercan, E; Tengiz, I; Sagcan, A; Eser, E; Berdeli, F; Akin, M
    Introduction Experimental and clinical studies demonstrated that the renin-angiotensin system (RAS) affects the pathogenesis of atherosclerosis and prognosis of coronary heart disease (CHD). The aim of this study was to investigate the genotype distribution and the allele frequencies of three RAS genes polymorphisms and their effects on premature CHD in a Turkish population. Materials and methods One-hundred and fifteen Turkish patients with premature CHD and 128 controls were included into the study. Angiotensin-converting enzyme (ACE), angiotensin II type 1 (AT(1)) receptor and angiotensinogen (AGT) gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results The patients group showed an increased frequency of the ACE D allele compared with controls (65% vs. 35%, p=0.0001). There was a significant association between the DD genotype and premature CHD (ACE DD vs. ID and II; odds ratio [OR]=2.82 [CI 95% 1.33-2.91, p=0.002]). Also, we observed increased premature CHD risk associated with higher frequencies of the AGT MM genotype in patients when compared with controls (AGT MM VS. TT and MT OR=1.92 [Cl 95% 1.11-3.33, p=0.018]). We found a significant association between AT(1)-receptor AA genotype and decreased risk of premature CHD (AT1R AA vs. AC and CC, OR= 0.57[CI 95% 0.34-0.95, p=0.03]). Conclusions We demonstrated that increased premature CHD risk is associated with higher frequencies of the ACE DD and AGT MM genotypes. These findings indicate a synergistic contribution of ACE DD and AGT MM polymorphisms to the development of premature CHD. Also, our results suggest that family history, smoking, diabetes, hypertension, obesity and ACE DD genotype were independent risk factors for premature CHD.
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    No association of IL-6 gene polymorphism (474 G/C) with premature coronary artery disease
    Sekuri, C; Cam, FS; Tengiz, I; Sagcan, A; Ercan, E; Akin, M; Berdeli, A
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    Association between the eNOS (Glu298Asp) and the RAS genes polymorphisms and premature coronary artery disease in a Turkish population
    Berdeli, A; Sekuri, C; Cam, FS; Ercan, E; Sagcan, A; Tengiz, I; Eser, E; Akin, M
    Background: The renin-angiotensin system (RAS) and endothelial nitric oxide (NO) affect the pathogenesis of atherosclerosis and prognosis of coronary artery disease (CAD). Previous epidemiologic data suggested that genetic factors are more likely to affect young rather than old people. Our objective was to investigate the association between the polymorphisms of eNOS (Glu298Asp) and the RAS genes and premature CAD in a Turkish population. Methods: A total of 115 Turkish patients with premature CAD and 83 controls were included in the study. ACE I/D, AT1R A/C, AGT T/M and eNOS Glu298Asp gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results: It was found that increased premature CAD risk is associated with higher frequencies of the ACE DD [OR: 2.600 (CI 95% 1.395-4.847,p=0.002)], AGT MM [OR=2.407 (Cl 95% 1.267-4.573,p=0.007)] and eNOS 894TT [OR-17.000 (CI 95% 3.952-73.125,p<0.001)] genotypes. Carriers of ACE DD+eNOS 894TT (p=0.002), AGT MM+eNOS 894TT (p=0.001), ATIR AA+eNOS 894TT and ATIR non-AA+eNOS 894TT (p=0.002) genotypes were significantly associated with the risk of premature CAD.
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    Effect of monocyte chemoattractant protein-1 (MCP-1) gene polymorphism in Turkish patients with premature coronary artery disease
    Cam, FS; Sekuri, C; Sagcan, A; Ercan, E; Tengiz, S; Aliogiu, E; Berdeli, A
    Objectives. It has been suggested that monocyte chemoattractant protein-1 (MCP-1) is important in the initiation of atherosclerosis and crucial in monocyte recruitment into the subendothelial lesions. Recent studies have demonstrated that MCP-1 -2518 A>G polymorphism is associated with susceptibility to coronary artery disease (CAD). Since there are conflicting reports on the possible association of MCP-1 -2518 A>G polymorphism with CAD, we investigated the role of this polymorphism in Turkish patients with premature CAD. Material and methods. Genomic DNA was collected from 171 premature CAD patients and 151 healthy individuals. MCP-1 -2518 A>G polymorphism was genotyped using the PCR-RFLP method. Results. There were no differences between genotype distribution and allele frequencies in the premature CAD and control groups (AA: 49.7%; AG: 40.3%; GG: 10.0% in premature CAD groups and AA: 53.7%; AG: 34.4%; GG: 11.9% in controls; p = 0.53). The prevalence of the G allele was 0.302 in patients and 0.291 in controls. Conclusions. Our data demonstrate that MCP-1 -2518 A>G polymorphism is not associated with premature CAD in Turkish patients. Further studies are needed to elucidate the role of this polymorphism in the pathogenesis of CAD in various populations.

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