Browsing by Author "Yeşil H."

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    Montelukast is effective in preventing of ovarian hyperstimulation syndrome; an experimental study
    (Studio K Krzysztof Molenda, 2015) Eskicioğlu F.; Turan G.A.; Sivrikoz O.N.; Cengiz H.; Akan Z.; Şahin N.; Yilmaz O.; Yeşil H.; Vatansever S.
    Objectives: To determine the efficacy of montelukast in comparison with cabergoline in the prevention of ovarian hyperstimulation syndrome (OHSS) in rats. Material and methods: An experimental OHSS model was formed in 35 female Wistar rats. Rats (22 days old) were randomized into 5 groups, each containing 7 animals. The control group received no therapy; the mild OHSS group was administered pregnant mare serum gonadotropin (PMSG) 10 IU for 4 days, hCG 10 IU on the 5th day; the severe OHSS group received PMSG 10 IU for 4 days, hCG 30 IU on the 5th day. The montelukast group: received montelukast 10 mg/kg/day and the cabergoline group was administered cabergoline 100μg/kg/day via oral gavage for 6 days (days 22-27), in addition to those of severe OHSS. All groups were sacrificed on 28th day. Body weight, ovarian diameter and weight, vascular permeability, vascular endothelial growth factor (VEGF), semiquantitative VEGF receptor-1, and VEGF receptor-2 (VEGFR-2) immunohistochemistry were evaluated. Results: Ovarian diameter and VEGF expression were significantly lower in the montelukast and cabergoline groups than in the severe OHSS group. While montelukast was more effective in limiting vascular permeability in the severe OHSS, cabergoline was superior to montelukast with respect to the limiting effect on increased body weight and VEGFR-2 expression. Conclusions: The VEGF/VEGFR-2 interaction plays an important role in OHSS pathogenesis. Montelukast limits VEGF expression, and cabergoline reduces both VEGF and VEGFR-2 expressions; they are both effective therapies for the prevention of severe OHSS.
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    Central nervous system metastatic epithelial ovarian cancer. Clinical parameters and prognostic factors: A multicenter study of Anatolian Society of Medical Oncology
    (S.O.G. CANADA Inc., 2017) Seber S.; Turkmen E.; Harputoǧlu H.; Yeşil H.; Arpaci E.; Menekse S.; Pilanci K.; Oruç Z.; Taskovlu B.Y.; Gumusay O.; Aksoy A.; Karaagac M.; Ozarslan E.; Yetisyigit T.
    Central nervous system (CNS) metastasis is a rare event in the course of late stage epithelial ovarian cancer (EOC); however its incidence is increasing in parallel with prolonged survival of patients. Objective: The authors assessed the clinical parameters and potential prognostic features in patients with CNS metastatic disease. Materials and Methods: Clinical data of the 33 patients from the participating centers were retrospectively collected and analyzed. Median age at the time of CNS metastasis was 57 years. Median time from the diagnosis of primary EOC until CNS metastatic disease was 22 months. Nearly half (45.5%) of the patients had single CNS metastatic lesions and all patients in the study group except two received radiotherapy as palliative treatment. Median overall survival (OS) from the time of CNS metastasis was 15 months (0-66). At univariate analysis only number of brain metastatic lesions (p = 0.001) and presence of extracranial disease (p = 0.004) were strongly associated with OS whereas multimodal treatment, size of metastatic lesions, platinum sensitivity, age, grade, and disease stage at presentation were not. Development of CNS metastasis carries a poor prognosis, however patients with single metastatic lesions and only intracranial metastatic disease can have prolonged survival after appropriate palliative management of their disease.
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    The relation of oxidative stress and apoptosis to histopathologic alterations in the lungs as a result of global cerebral ischemia
    (Taylor and Francis Ltd, 2019) Yeşil H.; Tuğlu İ.
    Heart attack and oxygen deficiency may cause necrosis in the brain and other tissues. We investigated the histopathological effects of nitric oxide (NO) on ischemia/reperfusion in lung and hippocampus using a rat brain bilateral occlusion ischemia model. Male rats were assigned to sham (SH), ischemic preconditioning (PC), global ischemia (GI) and ischemic reperfusion (IR) groups. Before ischemia was induced, blood was drawn to induce hypovolemic hypotension and for blood gas testing. After sacrifice, samples of hippocampus were harvested. Sections were examined using hematoxylin and eosin (H & E) staining and immunostaining using primary antibodies for GFAP, S100β, iNOS, eNOS and the TUNEL method. Following ischemia, we found evidence of gliosis induced oxidative stress and apoptosis in the hippocampus. No significant differences were detected between the SH and PC groups. In the GI and IR groups, apoptosis and necrosis were observed in the hippocampus. Lung sections were stained with H & E and Masson’s trichrome (MT) and immunostained for iNOS and eNOS. The TUNEL method was used to detect apoptosis. Interstitial edema, vascular congestion, intra-alveolar hemorrhage, perivascular edema, neutrophil infiltration and disruption of alveoli were observed after global ischemia and ischemic reperfusion. Inflammatory cells were detected in the connective tissue. The IR and GI groups exhibited significantly more apoptotic cells than the SH or PC groups. Free radicals, such as nitric oxide (NO), that appear following ischemia and reperfusion in the brain may also injure the lungs. Increased NO in both lung and brain tissue suggests that apoptosis in these organs can be induced by reactive nitrogen species. © 2019, © 2019 The Biological Stain Commission.