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    THE DISTRIBUTION OF FV-LEIDEN, PROTHROMBIN AND PLASMINOGEN ACTIVATOR INHIBITOR GENE MUTATIONS IN PATIENTS WITH OBSTRUCTIVE SLEEP APNEA
    (Medecine Et Hygiene, 2014) Balbay, Ege Güleç; Küçük, Enes; Balbay, O.; Annakkaya, Ali Nihat; Sılan, Fatma; Çiçekliyurt, Meliha Merve
    Aim: To investigate Factor V Leiden (FVL), Plasminogen Activator Inhibitor (PAI) or Prothrombin (F2L) gene polymorphisms among OSAS patients. Methods: 62 patients (35 male, 27 female) with the suspected diagnosis of OSAS were included. All patients filled out a questionnaire regarding sleep disturbance and underwent polysomnographic (PSG) examination. Genotypes were determined by a polymerase chain reaction and reverse hybridization. Results: The mean age was 51 +/- 12. 20 of the patients were not OSAS while 42 was OSAS. The distribution of FVL genotypes for 1691 GG, GA and AA is found 95 %, 5% and 0% in control group and 88.1%, 11.9% and 0% in patient groups (p:0.654) respectively. The mutant genotype was not observed for both FVL and F2L G20210A. The distribution of F2L 2021 GG, GA, AA was found 95%, 5% and 0% in control group while 97.6%, 2.4% and 0% in patient group (p:0.545) respectively. The genotype frequencies of the OSAS patients for PAT were 45.5% for wild, 45% for heterozygote, and 10% for homozygote mutant genotype in control group and 31% for wild, 47.6% for heterozygote, and 21.4% for homozygote mutant genotype in patient group (p:0.413). No significant associations with these three polymorphism were observed for OSAS and the data was shown as odds value for FVL, F2L respectively; ORFVL=2.5 (95% CI: 0.280-23.573), ORF2L =0.463 (95% CI: 0.027-7.811). Conclusion: Although FVL mutation was insignificantly high in OSAS patients, it may be an important risk factor in known hypercoagulabi-
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    Erdosteine protects rat testis tissue from hypoxic injury by reducing apoptotic cell death
    (Wiley, 2014) Güven, Aysel; İçkin, Meletm; Uzun, O.; Bakar, Coşkun; Balbay, Ege Güleç; Balbay, O.
    The purpose of this study was to examine the effects of hypobaric hypoxia on testis morphology and the effects of erdosteine on testis tissue. Caspase-3 and hypoxia-inducible factor 1 expressions were detected by immunohistochemistry. Adult male Wistar rats were placed in a hypobaric hypoxic chamber. Rats in the erdosteine group were exposed to the same conditions and treated orally with erdosteine (20mgkg(-1) daily) at the same time from the first day of hypoxic exposure for 2weeks. The normoxia group was evaluated as the control. The hypoxia group showed decreased height of spermatogenic epithelium in some seminiferous tubules, vacuolisation in spermatogenic epithelial cells, deterioration and gaps in the basal membrane and an increase in blood vessels in the interstitial area. The erdosteine group showed amelioration of both epithelial cell vacuolisation and basal membrane deterioration. Numbers of hypoxia-inducible factor 1-immunostained Sertoli and Leydig cells were significantly higher in the hypoxia group than in the erdosteine group. The number of seminiferous tubules with caspase-3-immunostained germ cells was highest in the hypoxia group and decreased in the erdosteine and normoxia groups respectively. Based on these observations, erdosteine protects testis tissue from hypoxic injury by reducing apoptotic cell death.
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    A neglected etiology of bronchiectasis: External compression due to hiatal hernia
    (Wolters Kluwer Medknow Publications, 2020) Balbay, E. G.; Unlu, E. N.; Annakkaya, A. N.; Balbay, O.; Kos, M.; Safak, A. A.
    Aim: To investigate the incidence of bronchiectasis supposed to be made by the external compression of hiatal hernia (HH) to bronchi. Materials and Methods: The thorax computed tomography (CT) scans of patients which were carried out in Duzce University Hospital between February 2014 and August 2015 were retrospectively evaluated. The repeated scans in the same patient were excluded. Results: A total of 4388 patients were included in the study. A total of 98 HH cases were detected of which 58 (59.2%) were female. The mean age was 73.30 +/- 9.14 (45-90). The rate of HH according to small, moderate and large size was 45 (45.9%), 9 (9.2%), 44 (44.9%), respectively. The rate of hiatal hernia accompanied by bronchiectasis were similar in both males and females (P = 0.078). The prevalence of bronchiectasis was significantly high in large hernias with 81.4% rate (P = 0.009). Bronchiectasis rate was 12.343 times (OR: 12.343, 95% CI: 1.479-103.027, P = 0.009) higher in the large HH group compared to small and moderate HH groups. Hiatal hernia accompanied by bronchiectasis was 88.1% anatomically near to HH. Conclusions: Thus, hiatal hernia may cause bronchiectasis due to external compression rather than lymphadenopathy or the tumor as an etiology of bronchiectasis and should be considered in the differential diagnosis.