Browsing by Author "Bakan, E."

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Beta-Fibrinogen 455 G/A and Angiotensin Converting Enzyme Ins/Del Polymorphisms in Patients With Lung Cancer
(Yuzuncu Yil Universitesi Tip Fakultesi, 2018) Alp, H.H.; Umudum, F.Z.; Bakan, E.
In our study we have investigated polymorphism due to base change occurring at-455 position of promoter region of β-fibrinogen synthesizing gene in lung cancer patients. In addition, we have also investigated insertion/deletion (I/D) polymorphism in intron 16 of Angiotensin Converting Enzyme (ACE) gene, located on chromosome 17q23. Aim of our study is to determine polymorphisms of β-fibrinogen-455 G/A and ACE I/D in patients with lung cancer and healthy control and to determine whether these polymorphisms contribute to the format ion of lung cancer. In addition, we aimed to clarify whether β-fibrinogen-455 G/A polymorphism effect the level of fibrinogen synthesis in patients with lung cancer. Samples in our study was obtained from 100 patients with lung cancer and 100 healthy volu nteers. Plasma fibrinogen levels were measured with ELISA method. Polymorphism analyses were determined with PCR-reverse hybridization method. Results of our study revealed that fibrinogen levels of patients with lung cancer were significantly higher than healthy control group (p<0.01). No difference was determined for β-fibrinogen-455 G/A and ACE I/D polymorphisms between patients with lung cancer and healthy control group. In both of the groups fibrinogen level was higher in AA genotype compared to GG and GA genotypes in both of the groups (p<0.05) As a result, it can be stated that β-fibrinogen-455 G/A and ACE I/D polymorphisms are not related with formation and prognosis of lung cancer. © 2018, Yuzuncu Yil Universitesi Tip Fakultesi. All rights reserved.
May Supplementation of Coenzyme Q10 Help Prevent Development of Hydatidiform Mole
(7847050 Canada inc, 2017) Kolusari, A.; Cebi, A.; Akgun, E.; Alp, H. H.; Bakan, E.
Objective: The pathological mechanisms of gestational trophoblastic disease have not yet been clearly determined. It is thought that oxidative damage contributes to the process. The aim of this study was to determine the levels of coenzyme Q10 (CoQ10), DNA damage, and lipid peroxidation in patients with hydatidiform mole. Materials and Methods: The authors studied the levels of CoQ10, 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA) by high-performance liquid chromatography (HPLC), and the activity of glutathione peroxidase (GPX) by spectrophotometric method in blood obtained from patients with a complete hydatidiform mole (n=29), healthy pregnant women (n=29), and healthy non-pregnant women (n=29). Results: The 8-OHdG/dG ratio (2.8148 +/- 0.81592) and MDA (10.8341 +/- 4.64875 mu mol) were significantly higher in patients with complete hydatidiform mole, while the ubiquinol-10/ubiquinone-10 ratio (0.2107 +/- 0.15675) and GPX activity (43.4606 +/- 18.31694 mU/ml) were lower (p < 0.001). Conclusion: The authors suggest that both mitochondrial oxidative and oxidative DNA damage play important roles in the pathogenesis of complete hydatidiform mole. Therefore supplementation of CoQ10 prevents recurrent gestational trophoblastic disease.