Browsing by Author "Serdaroglu A."

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    Histologic and morphologic effects of valproic acid and oxcarbazepine on rat uterine and ovarian cells
    (2010) Cansu A.; Erdogan D.; Serdaroglu A.; Take G.; Coskun Z.K.; Gurgen S.G.
    Purpose: To determine the histologic and morphologic effects of valproic acid (VPA) and oxcarbazepine (OXC) on rat uterine and ovarian cells. Methods: Fifty-six female prepubertal Wistar rats (21-24 days old and weighing between 47.5 and 58.1 g) were divided equally into four groups, which were given drinking water (controls), 300 mg/kg/day of VPA, 100 mg/kg/day of OXC or VPA + OXC via gavage, for 90 days. Ovaries and uteri of rats on proestrous and diestrous phases of estrous cycle were extirpated and placed in a fixation solution. The tissue specimens were assessed with apoptosis (TUNEL) staining protocols, eosinophil counting, and electron microscopic techniques. Results: In uteri, apoptosis in stroma, mitochondrial swelling, and cristolysis were observed in the VPA group, and OXC led to negative effects on epithelial cell and intracellular edema. In ovaries, both drugs increased apoptosis and intracytoplasmic edema. Organelle structure disruption was also observed in the OXC group. More conspicuous degenerative modifications were determined in the VPA + OXC group. In uteri, the number of TUNEL-positive luminal epithelial cells was 7.20 ± 1.32 in controls, and significantly increased to 29.60 ± 1.58, 34.20 ± 2.53, and 54.80 ± 2.04 in VPA, OXC, and VPA + OXC groups, respectively (p < 0.001). The highest number of TUNEL-positive glandular epithelium cells was observed in the VPA + OXC group; however, the number of TUNEL-positive stroma cells was highest in the VPA group. The highest number of eosinophils in stroma was in the VPA group. Conclusion: VPA and OXC trigger apoptotic and degenerative effects on rat uterine and ovarian cells. VPA also prevents implantation of embryo to the uterus and causes abortion via endometrial eosinophil infiltration. © 2009 International League Against Epilepsy.
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    Methylphenidate has dose-dependent negative effects on rat spermatogenesis: Decreased round spermatids and testicular weight and increased p53 expression and apoptosis
    (2011) Cansu A.; Ekinci Ö.; Ekinci Ö.; Serdaroglu A.; Erdǒan D.; Co̧kun Z.K.; Gürgen S.G.
    In the present study, we aimed to evaluate the possible effects of methylphenidate on rat testes. Forty-two Wistar rats were randomly distributed into three experimental groups of 14 rats each. For 90 days, each group via gavage received the following: group 1 = tap water (control group), group 2 = 5 mg/kg/day of ritalin (methylphenidate, MPH), and group 3 = 10 mg/kg/day of ritalin. After sacrificing the animals, the body weights as well as the absolute and relative testicular weights were measured. Testes were sampled, fixed, and processed and, by histopathological examination, quantitative morphometric analysis of Sertoli cells, spermatocytes, and spermatids was performed in stages II, V, and XII. Immunohistochemistry was performed for transforming growth factor (TGF)-β1 and p 53, and the apoptotic index was assessed through the TUNEL method. Group 2 had a reduction of round spermatids in stage II. Group 3 had reduction in both stage II and stage V spermatids, as well as lower testicular weight. The p 53 expression was increased in group 3. In groups 2 and 3, the TGF-β1 expression was reduced and the apoptotic index by TUNEL was increased. Body weights remained stable on either group. Our results showed that methylphenidate might negatively affect spermatogenesis not only by reducing testicular weight and amount of round spermatids but also by increasing apoptotic death and p 53 activation. The findings of the study, however, must be cautiously interpreted. © SAGE Publications 2011.
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    Therapeutic implications of etiology-specific diagnosis of early-onset developmental and epileptic encephalopathies (EO-DEEs): A nationwide Turkish cohort study
    (W.B. Saunders Ltd, 2024) Kanmaz S.; Tekgul H.; Kayilioglu H.; Atas Y.; Kart P.O.; Yildiz N.; Gumus H.; Aydin K.; Olculu C.B.; Dogan D.E.T.; Per H.; Canpolat M.; Gulec A.; Yildirim N.; Turk E.; Celik N.; Ozturk S.; Kumandas S.; Kilic B.; Topcu Y.; Ozpinar E.; Coskun A.; Arslan M.; Akkoyunlu D.S.; Cine N.; Uzan G.S.; Gunay C.; Akyol D.; Ersoy O.; Direk M.C.; Komur M.; Kirkgoz H.; Karaoğlu P.; Ibis I.B.P.; Cerci C.; Orak A.; Oktay S.; Ayanoglu M.; Yildirim M.; Bektas O.; Serdaroglu E.; Yilmaz S.B.; Cankurt I.; Hirfanoglu T.; Arhan E.; Gencpinar P.; Dundar N.O.; Teber S.; Serin H.M.; Yilmaz S.; Tosun A.; Polat M.; Yilmaz U.; Unalp A.; Kara B.; Okuyaz C.; Yis U.; Hiz S.; Aktan G.; Gokben S.; Unay B.; Serdaroglu A.; Cansu A.
    Objective: To evaluate the etiology-specific diagnosis of early-onset developmental epileptic encephalopathies (EO-DEEs) in a nationwide Turkish cohort to determine the implications for therapeutic management. Methods: The cohort comprised 1450 patients who underwent EO-DEE. The utility of genetic testing was assessed with respect to the initial phases of next generation sequencing (NGS) (2005–2013) and the current NGS era (2014–2022). A predefined four-stepwise diagnostic model was evaluated using cost-effectiveness analysis. The diagnostic and potential therapeutic yields of the genetic tests were subsequently determined. Results: Gene-related EO-DEEs were identified in 48.3 % (n = 701) of the cohort: non-structural genetic (62.6 %), metabolic genetic (15.1 %), and structural genetic (14.1 %). The most common nonstructural genetic variants were SCN1A (n = 132, 18.8 %), CDKL5 (n = 30, 4.2 %), STXBP1 (n = 21, 2.9 %), KCNQ2 (n = 21, 2.9 %), and PCDH19 (n = 17, 2.4 %). The rate of ultra-rare variants (< 0.5 %) was higher in the NGS era (52 %) than that in the initial phase (36 %). The potential therapeutic yields with precision therapy and antiseizure drug modification were defined in 34.5 % and 56.2 % in genetic-EO-DEEs, respectively. The diagnostic model provided an etiology-specific diagnosis at a rate of 78.7 %: structural (nongenetic) (31.4 %), genetic (38.5 %), metabolic (6.1 %), and immune-infectious (2.8 %). Based on a cost-effectiveness analysis, the presented diagnostic model indicated the early implementation of whole-exome sequencing for EO-DEEs. Significance: In the present cohort, the higher rate (48.3 %) of gene-related EO-DEE diagnoses in the NGS era provides a potential therapeutic management plan for more patients. © 2024 British Epilepsy Association