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    Expression of cyclin A, cyclin E and p27 in normal, hyperplastic and frankly malignant endometrial samples
    (Informa Healthcare, 2013) Gezginc, S. T.; Celik, C.; Dogan, N. U.; Toy, H.; Tazegul, A.; Colakoglu, M. C.
    Cellular growth is under the control of certain molecules such as cyclins and cyclin dependent kinases. Dysregulation of these proteins disrupt cell cycle and may trigger malignant transformation. Cyclins and kinase inhibitors also play essential roles in endometrial cellular proliferation. But the exact roles of these mediators in the disease process is not clear. We evaluated expression of cyclin A, cyclin E and p27 in normal, hyperplastic and malignant endometrial samples assuming different expression patterns in physiological and pathological processes. A total of 75 patients with histopathological diagnosis of normal proliferative, hyperplastic or malignant endometrial samples were evaluated with different cellular proliferation markers, cyclin A, cyclin E and p27. For cyclin E, endometrial cancer samples had higher rate of immunoreactivity than normal proliferative and hyperplastic endometrial samples. Staining properties for cyclin A were comparable for three groups. However, p27 immunoreactivity decreased progressively as lesions progress from proliferative benign endometrium to frank carcinoma. Further large-scale studies with clinical follow-up will reveal the exact role of cyclins on endometrial carcinogenesis.
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    In vitro vasoactive effects of dexmedetomidine on isolated human umbilical arteries
    (Comenius Univ, 2019) Arun, O.; Taylan, S. B.; Duman, I; Oc, B.; Yilmaz, S. A.; Tekin, A.; Celik, C.
    OBJECTIVE: We aimed to investigate the vasoactive effects of dexmedetomidine on isolated human umbilical arteries and possible mechanisms involved. METHODS: Human umbilical artery strips were suspended in Krebs-Henseleit solution and dose-response curves were obtained for cumulative dexmedetomidine before and after incubation with different agents; propranolol, atropine, yohimbine, prazosin, indomethacin, verapamil. Effects of calcium on cumulative dexmedetomidine-induced contractions were also studied. RESULTS: Cumulative dexmedetomidine resulted in dose dependent contraction responses. Incubation with propranolol (Emax: 93.3 +/- 3.26 %), atropine (Emax: 92.0 +/- 6.54 %), or indomethacin (Emax: 94.25 +/- 2.62 %), did not attenuate dexmedetomidine-elicited contractions (p > 0.05). There were significant decreases in the contraction responses of cumulative dexmedetomidine with yohimbine (Emax: 12.1 +/- 11.9 %), prazosin (Emax: 28.8 +/- 4.6 %) and verapamil (Emax: 11.2 +/- 13.6 %) (p < 0.05). In Ca+2 free medium contraction responses to cumulative dexmedetomidine was insignificant (Emax: 5.20 +/- 3.42 %). Addition of cumulative calcium to the Ca+2 free medium resulted in concentration dependent increase in contractions (Emax: 64.83 +/- 37.7 %) (p < 0.05). CONCLUSION: Dexmedetomidine induces vasoconstriction in endothelial-free umbilical arteries via both, alpha(1)- and alpha(2)-adrenergic receptors and also extracellular Ca+2 concentrations play a major role. beta-adrenergic receptors, muscarinic cholinergic receptors, and inhibition of cyclooxygenase enzyme are not involved in this vasoconstriction (Fig. 3, Ref. 36). Text in PDF www.elis.sk.