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Browsing by Author "Tacoy, Gulten"

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    Effect of Dobutamine Stress Echocardiography on Serum Heart Fatty Acid Binding Protein Levels
    (2017) Akinci, Sinan; Balcioglu, Akif Serhat; Tacoy, Gulten; Tavil, Yusuf; Guslbahar, Ozlem; Ozdemir, Murat; https://orcid.org/0000-0001-5250-5404; 28597800; AAD-5564-2021
    Objective Heart fatty acid binding protein (HFABP) is a low-molecular-weight free protein that is abundant in the intracytoplasmic space of myocytes. Due to its unique features, serum HFABP levels may increase in myocardial ischaemia. The aim of this study was to evaluate the effect of myocardial ischaemia induced by dobutamine stress echocardiography (DSE) on serum HFABP levels. Methods and results A total of 30 consecutive patients with suspected myocardial ischaemia underwent DSE examination. HFABP levels were measured immediately before and 1 hour after DSE. HFABP rose significantly in individuals in the DSE positive group (1.66 +/- 1.18 ng/ml vs 2.65 +/- 1.34 ng/ml, P = 0.004), but remained unchanged in the DSE negative group (1.61 +/- 0.77 ng/ml vs 1.85 +/- 0.76 ng/ml, P = 0.066). Conclusion Serum HFABP levels increased significantly at 1 hour in the presence of ischaemia induced by DSE in patients with stable clinical coronary syndromes. No such increase was evident in the absence of ischaemia.
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    The role of oxidative DNA damage and GSTM1, GSTT1, and hOGG1 gene polymorphisms in coronary artery disease risk
    (2016) Okyay, Kaan; Kadioglu, Ela; Tacoy, Gulten; Ozcagli, Eren; Akboga, Mehmet K.; Cengel, Atiye; Sardas, Semra; 0000-0001-6134-8826; 27182613; AAK-7355-2020
    Objective: Atherosclerotic coronary artery disease (CAD) appears to be a multifactorial process caused by the interaction of environmental risk factors with multiple predisposing genes. Therefore, in this study we aimed to determine the role of oxidative DNA damage and some variations in glutathione S-transferase (GSTM1 and GSTT1) and DNA repair (hOGG1) genes in CAD risk. Methods: A case-control study was conducted on 59 individuals who had undergone coronary angiographic evaluation. Of these, 29 were patients diagnosed with CAD (mean age = 61.5 +/- 10.3) and 30 were controls examined for reasons other than suspected CAD and who had angiographically documented normal coronary arteries (mean age = 60.4 +/- 11.6). Basal DNA damage as well as pyrimidine and purine base damage were evaluated in peripheral blood lymphocytes using the modified comet assay. Polymerase chain reaction-restriction length polymorphism (PCR-RFLP)-based assay was used for genotyping. Results: Basal DNA damage levels in patients [9.16 (3.26)] were significantly higher than those in controls [7.59 (3.23); p=0.017], and basal DNA and pyrimidine base damage levels were significantly correlated with disease severity based on Gensini scoring (r=0.352, p= 0.006; r= 0.318, p=0.014, respectively). However, no significant differences were observed in terms of oxidized DNA bases between patients and controls. The frequencies of studied genotypes (GSTM1, GSTT1, and hOGG1) were similar between groups. Conclusion: The results of this study pointed out the role of DNA damage in CAD and its severity. However, GSTM1, GSTT1, and hOGG1 gene polymorphisms seemed to have no effect on individual susceptibility for disease progression.

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