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    Evaluation of the Association between Lithium Treatment and GSK-3? Polymorphism in Bipolar Disorder Patients
    (Turkiye Sinir Ve Ruh Sagligi Dernegi, 2018) Altinbas, Kursat; Yesilbas, Dilek; Ince, Bahri; Cansiz, Alparslan; Sılan, Fatma; Özdemir, Öztürk; Guloksuz, Sinan
    Objective: There is a lack of evidence regarding clinical predictors for the treatment response to lithium, which is the main stay treatment option for bipolar disorder. Studies that examined the mechanistic action of lithium revealed that glycogen synthase kinase 3 beta (GSK-3 beta) enzymeinhibition was important in regard to treatment responses. Based on this background, we aimed to investigate the association between responses to lithium treatment and five different polymorphisms of GSK-3 beta. Method: Lithium treatment response scale (LTRS) scores for 100 patients diagnosed with bipolar disorders type I were calculated according to the hospital records. Blood samples were collected and genomic DNA was obtained using the MagNA Pure Compact automatic isolation method. The GSK-3 beta: rs17183904, rs17183897, rs34009575, rs34002644, and rs17183890 polymorphisms were analyzed by real time PCR. Results: In this cohort, the mean age of patients was 41.1 +/- 10.3 years, the mean age of disease onset was 24.5 +/- 8.2, and the mean LTRS score was 4.9 +/- 1.8. There was no statistically significant difference for LTRS scores between groups in terms of gender, marital status, level of education, and the type of first episode. LTRS was significantly higher in only the patients harbouring GSK-3 beta rs17183890 AG genotype (p=0.008, t: 2.71). Interestingly, no differences were found for the remaining polymorphisms. Conclusion: The specific GSK-3 beta polymorphism that associated with lithium-response in our study may help to predict lithium responses and to develop individualized treatment. We presume that our pharmacogenomic findings may also provide important contributions to the clinical practice in regard to future evaluation of the treatment adherence and side effects. To obtain these goals, further genome-wide scanning studies conducted on larger sample cohorts are required.
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    Minor hemoglobins HbA2 and HbF associate with disease severity in bipolar disorder with a likely protective role of HbA2 against post-partum episodes
    (Elsevier, 2013) Ince, Bahri; Guloksuz, Sinan; Altinbas, Kursat; Oral, Esat Timuin; Alpkan, Latif Ruhsat; Altinoz, Meric A.
    Background: There exist studies indicating that bipolar disorder (BD) associates with changes in brain blood flow. Human brain with its high demand to oxygen constitutes 2% of the Loral body weight, while it receives 20% of cardiac output, a and 13;-,Ylobin chains of hemoglobin were recently found in neural tissues, yet no study has questioned blood hemoglobins in BD. Methods: A total of 120 euthymic BD patients (40 males and SO females) were analyzed via high performance liquid chromatography (1-IPLC) to measure minor hemoglobin levels, which were statistically compared with disease characteristics. Results: Minor hemoglobins HbA2 and HbF associated positively with episode density as a measure of disease severity in BD. An increased level of HbA2 meant significantly less postpartum episodes in child bearing women. HbF levels were higher in patients with a positive family history of any psychotic disorder. Sum of HbA2 and HbF correlated with episode density with a stronger significance (p <0001) supporting intermittent hypoxia hypothesis in 130. Limitations: The study was conducted only on euthymic patients to avoid likely bigger exogenous effects such as electro-convulsive therapy and diverse drug regimes, yet larger comparative studies are needed to support our current findings. Conclusions: Higher HbA2 and HbF in more severe bipolar disorder may be compensations against intermittent hypoxias in BD. HbA2 increases following myocardial angina and in mountain dwellers, which may indicate protective roles in extreme conditions. HbF increase may act more as a maladaptation or emerge via haplotypal associations of BD genes and gamma-globin locus at 11p15.5. (C) 2013 Elsevier B.V. All rights reserved,