Browsing by Author "Alioglu, E"
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Item Why fear can be fatal?Tuncer, E; Yavuz, V; Turk, UO; Alioglu, EItem LACK OF ASSOCIATION BETWEEN MCP-1 GENE POLYMORPHISM (-2518G/A) AND PREMATURE CORONARY ARTERY DISEASECam, FS; Sekuri, C; Sagcan, A; Ercan, E; Tengiz, I; Alioglu, E; Berdeli, AItem Decreased erythropoietin levels after cardiac ischemiaErcan, E; Duman, C; Sonmez, G; Tengiz, I; Alioglu, E; Turk, U; Sekuri, C; Cam, SItem Polymorphisms of the methylenetetrahydrofolate reductase, vascular endothelial growth factor, endothelial nitric oxide synthase, monocyte chemoattractant protein-1 and apolipoprotein E genes are not associated with carotid intima-media thicknessAlioglu, E; Turk, U; Cam, S; Abbasaliyev, A; Tengiz, I; Ercan, EBACKGROUND: Single nucleotide polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR), vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), monocyte chemoattractant protein-1 (MCP-1) and apolipoprotein E (ApoE) genes appear to be a genetic risk factor for atherosclerosis. Common carotid intima-media thickness (cIMT) provides information on the severity of atherosclerosis.OBJECTIVE: To investigate the relationship between cIMT and gene polymorphisms associated with atherosclerosis in Turkish patients with coronary artery disease (CAD).METHODS: Sixty-two patients with angiographically diagnosed stable CAD were divided into two groups according to their cIMT values (group 1: n=35, cIMT of 1 mm or greater; group 2: n=27, cIMT of less than 1 mm). MTHFR 677 C/T, VEGF-460 C/T, eNOS 894 G/T, MCP-1-2518 A/G and ApoE (E2, E3 and E4) gene polymorphisms (where A is adenine, C is cytosine, G is guanine and T is thymine) were analyzed by polymerase chain reaction and restriction fragment length polymorphism. Evaluations of cardiovascular risk factors and coronary atherosclerotic lesions were performed in all patients. Serum homocysteine and high-sensitivity C-reactive protein were measured and compared between the two groups.RESULTS: Serum high-sensitivity C-reactive protein (P=0.04) and homocysteine (P=0.006) levels were higher in group 1 than in group 2. The ratio of multivessel CAD and previous myocardial infarction was significantly higher in group 1 than in group 2 (P=0.014). In the study population, no significant difference in cIMT was observed according to the polymorphisms studied. Only hyperhomocysteinemia (OR 1.17 [95 % CI 1.01 to 1.35], P=0.033) and previous myocardial infarction (OR 3.76 [95 % CI 1.10 to 12.81], P=0.034) maintained a significant correlation with cIMT on multiple logistic regression analysis.CONCLUSION: cIMT is increased in patients with hyperhomocysteinemia, inflammation and extended CAD. MTHFR 677 C/T, VEGF-460 C/T, eNOS 894 G/T, MCP-1-2518 A/G and ApoE single nucleotide polymorphisms were not associated with increased cIMT.Item The relationship between paraoxanase gene Leu-Met (55) and Gln-Arg (192) polymorphisms and coronary artery diseaseTaskiran, P; Cam, SF; Sekuri, C; Tuzun, N; Alioglu, E; Altintas, N; Berdeli, AObjectives: Paraoxonase (PON1) is a high-density lipoprotein (HDL)-associated esterase that hydrolyses lipoperoxides. PON1 serves as a protective factor against oxidative modification of LDL, suggesting that it may play an important role in the prevention of atherosclerotic process. Research has focused on two polymorphisms: leucine (L allele) to methionine (M allele) substitution at codon 55, and glutamine (A allele) to arginine (B allele) substitution at codon 192. Study design: We examined amino acid changes at codon 55 and 192 in the PON1 gene by polymerase chain reaction and using restriction enzymes in 120 patients (92 men, 28 women; mean age 48.2 +/- 4.3 years) with premature coronary artery disease (CAD) and in 102 healthy subjects (80 men, 22 women; mean age 46.8 +/- 5.2 years) with no history of CAD and a normal electrocardiogram. Results: Distribution of genotypes in the patient and control groups at codon 55 was 6.7% and 4.9% for MM, 46.7% and 29.4% for LM, 46.7% and 65.7% for LL, respectively. The frequencies of genotypes at codon 192 were as follows: 4.2% and 2% for RR, 40% and 35.3% for QR, and 55.8% and 62.8% for QQ, respectively. While the frequency of PON1 55M allele was higher in the CAD group (0.3 vs. 0.2), PON1 192R allele frequency did not differ (0.2). There was a significant relationship between the PON1 M/L55 polymorphism and CAD (p=0.017), whereas the R/Q192 polymorphism was not associated with CAD (p=0.445). Conclusion: These data suggest that the PON1 M/L55 polymorphism shows a significant relationship with CAD and the Q/R192 polymorphism is not a major risk factor causing susceptibility to CAD in our population.Item G protein β3 subunit gene polymorphism in Turkish hypertensivesAlioglu, E; Ercan, E; Tengiz, I; Yildiz, A; Türk, UO; Saygi, S; Çam, FS; Berdeli, AObjective: G protein is one of the most important regulators of intracellular signaling pathways. C825T polymorphism of G protein (33 subunit is associated with increased intracellular signal transduction. The 825T allele has been found associated with a variety of cardiovascular risk factors, including hypertension. The aim of the present study was to investigate the association between the C825T polymorphism of the G protein beta 3 subunit and essential hypertension in Turkish population. Methods: This cross-sectional, case-controlled study included 209 patients with essential hypertension (Patient group) and 82 subjects with normal blood pressure (Control group). The G protein 133 subunit C825T gene polymorphism was determined by polymerase chain reaction. Hypertension was defined according to JNC VII criteria. Statistical analysis was performed using Chi square and unpaired t tests. Logistic regression analysis was used to study association between hypertension and genotypes. Results: We found that the frequencies of the G protein 133 subunit C825T polymorphism in hypertensive and control groups were 17.7%, 59.3%, 23.0% and 32.9%, 48.8%, 18.3%, (CC, CT, TT) respectively (chi(2)=7.963, p=0.019). In the multivariate logistic regression analysis CT genotype had 2.2 (OR=2.262, 95% CI 1.228-4.167, p=0.009), and TT genotype had 2.3 times (OR=2.335, 95% CI 1.089-5.008, p=0.029) greater risk of hypertension compared to CC genotype. Conclusion: It seems that the G protein (33 subunit C825T gene polymorphism is associated with systolic and diastolic blood pressure. Furthermore, the study indicates that the G protein 133 subunit may be a susceptible gene to essential hypertension. (Anadolu Kardiyol Derg 2008; 8: 337-5)Item No association of interleukin-6 gene polymorphism (-174 G/C) with premature coronary artery disease in a Turkish cohortSekuri, C; Cam, FS; Sagcan, A; Ercan, E; Tengiz, I; Alioglu, E; Berdeli, AObjectives 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.