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    Evaluation of vascular reactivity of young male hypogonadotrophic hypogonadism patients
    (Springer, 2010) Deniz, Ferhat; Ermis, Necip; Kepez, Alper; Tuerk, Baris; Akkoyunlu, Murat; Kara, Batuhan; Kutlu, Mustafa
    We aimed to study the vascular reactivity of young male hypogonadal hypogonadism patients without any cardiovascular risk factors and compare these findings with the ones of age-matched healthy controls. Study population consisted of 26 young male hypogonadotrophic hypogonadism patients (20.9 +/- A 1.3 years) and 25 age-matched healthy male controls (21.8 +/- A 2.9 years, P = NS). In addition to detailed hormonal analysis, each subject underwent ultrasound study of right brachial artery. Vessel diameter was measured at rest, during reactive hyperemia [endothelium-dependent flow-mediated vasodilation (FMD)] and after sublingual nitroglycerin administration (endothelium-independent vasodilation). Both flow-mediated and endothelium-independent sublingual nitroglycerin mediated dilatation values of patients were higher compared to controls (12.98 +/- A 10.76% vs. 7.92 +/- A 1.96%, P = 0.003 and 21.44 +/- A 10.36% vs. 14.72 +/- A 3.57%, P = 0.023, respectively). Linear regression analysis revealed that only serum HDL levels (relative risk 2.94, 95% CI 0.12-0.66, P = 0.006) and baseline vessel diameter (relative risk -2.77, 95% CI -17.73 to -2.70, P = 0.009) were found to be independently associated with FMD values. Endogenous male sex hormones seem to exert negative effects on vascular reactivity parameters and much of their effects are indirect that is by the way of alteration on lipid profile.
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    Identification of a Novel Deletion in AVP-NPII Gene in a Patient with Central Diabetes Insipidus
    (Assoc Clinical Scientists, 2015) Deniz, Ferhat; Acar, Ceren; Saglar, Emel; Erdem, Beril; Karaduman, Tugce; Yonem, Arif; Cagiltay, Eylem
    Central Diabetes Insipidus (CDI) is caused by a deficiency of antidiuretic hormone and characterized by polyuria, polydipsia and inability to concentrate urine. Our objective was to present the results of the molecular analyses of AVP-neurophysin II (AVP-NPII) gene in a large familial neurohypophyseal (central) DI pedigree. A male patient and his family members were analyzed and the prospective clinical data were collected. The proband applied to hospital for eligibility to be a recruit in Armed Forces. The patient had severe polyuria (20 L/day), polydipsia (20.5 L/day), fatique, and deep thirstiness. CDI was confirmed with the water deprivation-desmopressin test according to an increase in urine osmolality from 162 mOsm/kg to 432 mOsm/kg after desmopressin acetate injection. To evaluate the coding regions of AVP-NPII gene, polymerase chain reactions were performed and amplified regions were submitted to direct sequence analysis. We detected a heterozygous three base pair deletion at codon 69-70 (207_209delGGC) in exon 2, which lead to a deletion of the amino acid alanine. A three-dimensional protein structure prediction was shown for the deleted AVP-NPII and compared with the wild type. The three base pair deletion may yield an abnormal AVP precursor in neurophysin moiety, but further functional analyses are needed to understand the function of the deleted protein.