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    Association between serotonin 2A receptor (HTR2A), serotonin transporter (SLC6A4) and brain-derived neurotrophic factor (BDNF) gene polymorphisms and citalopram/sertraline induced sexual dysfunction in MDD patients
    (NATURE PUBLISHING GROUP, 2020) Oz, Merve Demirbugen; Baskak, Bora; Uckun, Zuhal; Artun, Nazan Yuce; Ozdemir, Hatice; Ozel, Tugba Kizil; Ozguven, Halise Devrimci
    Sexual dysfunction (SD) is a troublesome adverse effect of selective serotonin reuptake inhibitors (SSRIs). A variety of mechanisms might be involved in the occurrence of SD but the exact mechanism is still not clear. Genetic variations among patients treated with SSRIs are strong determinants of intolerance and poor compliance. The present study aimed to determine the relationship between serotonin-2A receptor (HTR2A) gene -1438A/G and 102T/C polymorphisms, serotonin transporter gene (SLC6A4) 5-HTT-linked polymorphic region (5-HTTLPR) insertion/deletion variant and brain-derived neurotrophic factor (BDNF) gene Val66Met polymorphisms and the occurrence of SD adverse effect in major depressive disorder patients treated with citalopram (CIT) or sertraline (SERT). The result from this investigation revealed that the -1438A/G and 102T/C polymorphisms appear to be associated with the SD induced by CIT. It was also demonstrated that patients receiving SERT, carrying T allele of HTR2A or L allele of 5-HTTLPR more likely to experience SD. Most important overall finding of the study is the combined effects of -1438A/G, 102T/C, and 5-HTTLPR polymorphisms. In a logistic regression model, the occurrence of SD increased with the number of risky alleles. As compared with subjects receiving SERT with few risky (<= 2) alleles, those with had 5-6 alleles had an increased SD risk. After all, according to these findings, -1438A/G, 102T/C, and 5-HTTLPR polymorphisms could be considered as promising pharmacogenetic biomarkers in CIT/SERT treatment in major depressive disorder (MDD) patients to avoid the occurrence of SD.
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    Effects of Acute and Chronic Electroconvulsive Shocks on Glycogen Synthase Kinase 3β Level and Phosphorylation in Mice
    (Lippincott Williams & Wilkins, 2013) Basar, Koray; Eren-Kocak, Emine; Ozdemir, Hatice; Ertugrul, Aygun
    Objectives Glycogen synthase kinase 3 beta (GSK-3 beta) is recently proposed as a novel target in the treatment of mood disorders. Recent evidence has suggested that acute and chronic administration of antidepressants led to inhibition of GSK-3 beta via phosphorylation of Serine9 residue. Acute electroconvulsive shock (ECS) has been reported to increase GSK-3 beta phosphorylation transiently. In this study, the changes in the level of GSK-3 beta and its phoshorylated form (phospho-Ser9-GSK-3 beta) following chronic ECS (cECS) were investigated in mice. Methods Mice were given daily ECS via bilateral corneal electrodes for 10 consecutive days in the chronic group and a single ECS in the acute group. Electrodes were applied without stimulation in corresponding sham groups. Immunoblotting for GSK-3 beta and phospho-Ser9-GSK-3 beta was performed with the frontal cortex and hippocampus samples, extracted 10 minutes after single ECS, and 24 hours after the last ECS in the chronic group. The optical densities of the bands obtained were compared between the active treatment and sham groups for each condition separately. Results The level of phospho-Ser9-GSK-3 beta was not different following chronic ECS, but significantly higher following acute ECS, compared with the corresponding sham group, in the hippocampus and frontal cortex. The level of GSK-3 beta was similar to sham following both acute and chronic ECS, in both regions. Conclusions The transient increase in GSK-3 beta phosphorylation observed following acute ECS in the mice hippocampus and frontal cortex was not found to persist 24 hours following chronic ECS. The mechanism of action of ECS does not seem to involve persistent change in the level and phosphorylation of GSK-3 beta.
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    Experimental Chronic Toxoplasmosis Model in Mice: Brain Lesions and Related Behavioral Changes
    (Galenos Yayincilik, 2012) Kocak, Orhan Murat; Atmaca, Hasan Tarik; Terzi, Osman Safa; Buyukkayaer, Seyhan; Ozdemir, Hatice; Uzunalioglu, Tuba; Kul, Oguz
    Objective: In this study, it is aimed to constitute a chronic toxoplasmosis model using toxoplasma gondii (T. gondii) ME49 strain that is supposed to produce tissue cysts, to compare healthy and infected mice in terms of behavioral changes. In addition, the relationship between behavioral changes and brain lesions was questioned. Method: Before experimental application, out of a total of twenty-one 2-month-old Swiss albino mice, T. gondii antibody-free, 14 were infected by intraperitoneal (IP) (n=8) or oral (n=6) inoculation of 2x102 Toxoplasma gondii ME49 oocysts. Four months later, fear-and anxiety-related behavioral changes in infected and healthy control groups were comparatively evaluated with plus-maze test. At the end of the experiment (45 day after inoculation), euthanasia was carried out on all mice and their brains were examined histopathologically and immunohistochemically for the presence of T. gondii tissue cysts. Results: Infected mice had low levels of anxiety, they have entered the open arms more frequently and have spent more time in the open arms of the maze compared to controls. Pathologically, in the infected group, high rates of gliosis, perivascular cell infiltration, meningitis, and neuron necrosis were observed especially in the parietal and temporal lobes, cornu ammonis, amygdala, and thalamus compared to the other parts of the brain. A higher number of tissue cyst formations were positively correlated with the lesion severity in these parts of the brain. Conclusion: It can be suggested that, tissue cysts and neuropathological changes in chronically infected mice brains have direct concern with behavioral manipulation which results from low anxiety levels. (Archives of Neuropsychiatry 2012; 49: 139-144)
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    Influence of CYP2B6 and CYP2C19 polymorphisms on sertraline metabolism in major depression patients
    (Springer, 2016) Yuce-Artun, Nazan; Baskak, Bora; Ozel-Kizil, Erguvan Tugba; Ozdemir, Hatice; Uckun, Zuhal; Devrimci-Ozguven, Halise; Suzen, Halit Sinan
    Background Genetic polymorphisms in CYP2B6 and CYP2C19 may cause variability in the metabolism of sertraline, a widely used antidepressant in major depressive disorder treatment. Objective This study investigates the impact of CYP2B6*4 (785A > G), CYP2B6*9 (516G > T), CYP2B6*6 (516G > T + 685G > A) CYP2C19*2 (685G > A), CYP2C19*17 (-3402C > T) polymorphisms on plasma concentrations of sertraline and N-desmethyl sertraline in major depression patients treated with sertraline [n = 50]. Setting Participants were patients who admitted to an adult psychiatry outpatient unit at a university hospital. These were DSM-IV major depression diagnosed patients with a stable sertraline medication regimen [for at least one month]. Methods CYP2B6*4 (rs 2279343; 785A > G), CYP2B6*9 (516G > T; rs 3745274), CYP2B6*6 (516G > T + 685G > A) CYP2C19*2 (rs 4244285; 685G > A), CYP2C19*17 (rs 11188072; -3402C > T), polymorphisms were analyzed by polymerase chain reaction and restriction fragment length polymorphism. Plasma concentrations were measured by high-performance liquid chromatography in patients treated with SERT. Main outcome measure The distribution of CYP2B6*4, *6, *9 and CYP2C19*2, *17 among patient group and the association between genotype and sertraline metabolism. Results Sertraline, N-desmethyl sertraline, N-desmethyl sertraline/sertraline and dose-adjusted plasma concentrations were statistically compared between individuals with wild-type and variant alleles both for CYP2B6 and CYP2C19 enzymes. The mean N-desmethyl sertraline/sertraline value, was significantly lower in all subgroups with *6 and *9 variant alleles (p < 0.05). Sertraline/C values were significantly higher (p < 0.05) and N-desmethyl sertraline/C values were lower in all subgroups with *6 and *9 variant alleles compared to wild-type subgroup. Conclusion CYP2B6*6 and *9 variant alleles had a significant decreasing effect on sertraline metabolism in major depression patients which might result as variations in sertraline therapy.
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    Magical ideation associated social cognition in adolescents: signs of a negative facial affect recognition deficit
    (W B Saunders Co-Elsevier Inc, 2015) Canli, Derya; Ozdemir, Hatice; Kocak, Orhan Murat
    Background: Studies provide evidence for impaired social cognition in schizotypy and its association with negative symptoms. Cognitive features related to magical ideation a component of the positive dimension of schizotypy have been less investigated. We aimed to assess social cognitive functioning among adolescents with high magical ideation scores, mainly focusing on face and emotion recognition. Methods: 22 subjects with magical ideation scale scores above the cut off level and 22 controls with lowest scores from among 250 students screened with this scale were included in the study. A face and emotion recognition n-back test, the empathy quotient, theory of mind tests and the Physical Anhedonia Scale were applied to both magical ideation and control groups. Results: The magical ideation group performed significantly worse than controls on both face and emotion recognition tests. Emotion recognition performance was found to be affected by memory load, with sadness, among emotions, revealing a difference between the two groups. Empathy and theory of mind tests did not distinguish the magical ideation group from controls. Conclusion: Our findings provide evidence for a deficit in negative emotion recognition affected by memory load associated with magical ideation in adolescents. (C) 2015 Elsevier Inc. All rights reserved.
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    The relationship between the serotonin 2A receptor gene-1438A/G and 102T/C polymorphisms and citalopram/sertraline-induced nausea in major depressed patients
    (Wiley, 2018) Oz, Merve Demirbugen; Uckun, Zuhal; Yuce-Artun, Nazan; Baskak, Bora; Ozdemir, Hatice; Ozel, Tugba Kizil; Suzen, H. Sinan
    Objective: The aim of the present study was to determine the relationship between the polymorphisms of -1438A/G and 102T/C in the 5-HT2A receptor (HTR2A) gene and nausea/vomiting as a side effect induced by sertraline (SERT) or citalopram (CIT) in patients with major depressive disorder. Methods: A total of 128 patients were enrolled, 63 patients received CIT, whereas 65 patients were treated with SERT. Nausea/vomiting were assessed with the UKU Side-effects Rating Scale at baseline and at the end of the second and fourth weeks. Polymerase chain reaction-restriction fragment length polymorphism technique was employed to determine genetic differences. Results: We have found that, in the patients treated with CIT, there was a nominally significant difference in the genotypic distribution associated with -1438A/G polymorphism between patients with and without nausea (X-2 = 6.15, p = 0.041). Moreover, logistic regression analysis revealed a significant association between nausea/vomiting as a side effect and -1438A/G polymorphism. That is, patients with the G allele were at a higher risk for developing nausea/vomiting (p = 0.044, odds ratio = 2.213). The 102T/C polymorphism in the HTR2A gene had no significant effect on the nausea/vomiting as a side effect among participants treated with either CIT or SERT. Conclusion: The present study suggests the association of the HTR2A gene -1438A/G polymorphism with nausea/vomiting as a side effect related to CIT treatment.