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    Association of platelet-activating factor acetylhydrolase gene polymorphism with premature coronary artery disease in Turkish patients
    (2006) Şekuri C.; Çam F.S.; Tengiz I.; Ercan E.; Bayturan Ö.; Berdeli A.
    Objective: Platelet-activating factor (PAF) is a phospholipid with multiple actions that is involved in inflammatory diseases as well as in atherogenesis. It is inactivated by a plasma enzyme, PAF-acetylhydrolase (PAF-AH). Deficiency of this enzyme in plasma is caused by a missense mutation in the gene (G994T). The aim of this study was to investigate association of this mutation with premature coronary artery disease (CAD). Methods: One hundred and fifteen unrelated Turkish patients with a diagnosis of premature CAD and 128 unrelated healthy subjects were enrolled in this study. Genotyping was performed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results: The prevalence of the G994T mutation in the patients was 2.60 % (heterozygote), and 0 % in the controls. There was no significant difference in allele frequency and genotype distribution among the study groups. Conclusion: The G9943T mutation in the plasma PAF acetylhydrola se gene is not associated with premature CAD in Turkish subjects.
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    The psychometric properties of the Turkish version of myocardial infarction dimensional assessment scale (MIDAS) [Miyokart enfarktüsü boyutsal degerlendirme ölçegi (MIDAS) türkçe sürümünün psikometrik özellikleri]
    (2011) Yilmaz E.; Eser E.; Şekuri C.; Kültürsay H.
    Objective: The purpose of this study was to describe the psychometric properties of the Myocardial Infarction Dimensional Assessment Scale (MIDAS). Methods: This is a methodological cultural adaptation study. The MIDAS consists of 35-items covering seven domains: physical activity, insecurity, emotional reaction, dependency, diet, concerns over medication, and side effects which are rated on a five-point Likert scale from 1: never to 5:always. The highest score of MIDAS is 100.Quality of life (QOL) decreases as the score of scale increases. Overall 185 myocardial infarction (MI) patients were enrolled in this study. Cronbach alpha was used for the reliability analysis. The criterion validity, structural validity, and sensitivity analysis approach was used for validity analysis. New York Heart Association (NYHA) and the Canadian Cardiovascular Society Functional Classifications (CCSFC) for testing the criterion validity; SF-36 for construct validity testing of the Turkish version of the MIDAS were used. Results: The range of Cronbach alpha values is 0.79-0.90 for seven domains of the scale. No problematic items were observed for the entire scale. Medication related domains of the MIDAS showed considerable floor effects (35.7%-22.7%). Confirmatory Factor analysis indicators [Comparative Fit Index (CFI)=0.95 and Root Mean Square Error of Approximation (RMSEA)=0.075] supported the construct validity of MIDAS. Convergent validity of the MIDAS was confirmed with correlation of SF-36 scale where appropriate. Criterion validity results was also satisfactory by comparing different stages of the NYHA and the CCSFC (p<0.05). Conclusion: Overall results revealed that Turkish version of the MIDAS is a reliable and valid instrument. (Anadolu Kardiyol Derg 2011; 11: 386-401) Copyright 2011 by AVES Yayincilik Ltd.
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    The relationship between levels of plasma homocysteine and presence of coronary artery disease and endothelial dysfunction in type II diabetic patients [Tip II diyabetik hastalarda plazma homosistein düzeyleri ile koroner arter hastaligi ve endotel disfonksiyonu varligi arasindaki i·lişki]
    (Turkiye Klinikleri, 2005) Aliyev E.; Tengiz I.; Ercan E.; Şekuri C.; Tümüklü M.; Akin M.; Nalbantgil I.
    Objective: The causal relationship between hyper-homocysteinemia and cardiovascular morbidity and mortality is not clear. In this study, the relationship between levels of plasma homocysteine and the presence of coronary artery disease and endothelial dysfunction in type II diabetic patients was evaluated. Material and Methods: The study group consisted of 50 type II diabetic patients who underwent exercise stress testing or thallium-201 myocardial perfusion imaging for the diagnosis of CAD. The study group was divided into two groups according to myocardial ischemic signs and angiographic findings: Group I (n= 25), patients with CAD or Group II (n= 25), patients without CAD. Plasma homocysteine levels were compared among these groups. In addition, the study population was divided into two groups according to their plasma homocysteine levels: Group H (n= 23), patients with hyper-homocysteinemia or Group N (n= 27), patients with normo-homocysteinemia. Flow-mediated dilatation (FMD) and nitrate-induced dilatation (NID) as markers of the endothelial functions were compared among these different groups. Results: Male gender was dominant in Group I and patients with hyper-homocysteinemia. Other clinical features such as lipid profiles, haemoglobin A1c, fibrinolytic and inflammatory activation markers did not different among the groups. Plasma homocysteine levels were significantly higher in Group I than in Group II (16.4 ± 5.1 and 9.2 ± 2.2 mmol/L, respectively; p< 0.0001). In the second analysis evaluating the effect of hyper-homocysteinemia on endothelial function, determinations of FMD and NID were similar in Groups H and N. Conclusion: Our findings show what appears to be a synergistic contribution of hyper-homocysteinemia on the development of CAD in type II diabetic patients. The detection of hyper-homocysteinemia may be important for the prediction of risk in diabetic patients. In addition, it may provide new approaches for primary and secondary prevention. Copyright © 2005 by Türkiye Klinikleri.
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    The relationship between paraoxanase gene Leu-Met (55) and Gln-Arg (192) polymorphisms and coronary artery disease [Paraoksonaz geninde Leu-Met (55) ve Gln-Arg (192) polimorfizmleri ile koroner arter hastaligi arasindaki ilişki]
    (2009) Taşkiran P.; Çam S.F.; Şekuri C.; Tüzün N.; Alioglu E.; Altintaş N.; Berdeli A.
    Objectives: 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 were 6.7% and 4.9% for MM, 46.7% and 29.4% for LM, 46.7% and 65.7% for LL, respectively. The frequency 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.