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Item Antineuronal antibodies and 8-OHdG an indicator of cerebellar dysfunction in autism spectrum disorder: a case?control study(2019) Kilicaslan, Fethiye; Ayaydin, Hamza; Celik, Hakim; Kutuk, Meryem Ozlem; Kandemir, Hasan; Koyuncu, Ismail; Kirnit, AdnanObjectives: Autism spectrum disorder (ASD) is a neurodevelopmental disorder, that starts in early childhood and presents with deficiencies in social-communicational domains along with restricted and repetitive behaviours/interests. While genetic factors are dominant in its pathogenesis, many factors, including neurological, environmental and immunological have been identified. Furtheremore, although cerebellar dysfunction in the etiology of autism has been shown in different studies, the possible causes of the dysfunction and the role of neuroinflammation among these causes have not been clarified yet. Anti-Yo, anti-Hu, anti-Ri and anti-Amphiphysin antibodies have been found to be associated with cerebellar degeneration. The aim of the present study was to compare anti-Yo, anti-Hu, anti-Ri and anti- Amphiphysin antibodies and 8-OHdG values in blood using the ELISA method between ASD patients and healthy children to demonstrate the role of neuroinflammation as a potential cause of cerebellar dysfunction and DNA damage and evaluate the relationship between Childhood Autism Rating Scale (CARS) scores in children diagnosed with ASD and these parameters. Methods: Thirty-five consecutive children between the ages of 3 and 12 referred to the Child and Adolescent Psychiatry Outpatient Clinic of Harran University Hospital and diagnosed with ASD according to the DSM-5 diagnostic criteria were included in the study. The children did not have any chronic physical disorders and were treatment naive. Thirty-three healthy children between the ages of 3 and 12 without any physical or psychiatric disorders were included as the healthy control group. For psychiatric evaluation, a sociodemographic form and to measure the severity of autism, CARS was used. In the study, anti-Yo, anti-Hu, anti-Ri and anti-Amphiphysin antibodies and 8-OHdG values in blood were investigated using the ELISA method. Results: Thirty-five cases with autism (62.9% males) and thirty-three healthy controls (72.7% males) were included in the present study (p?=?0.385). The median age was 6.0 in the ASD group and 7.0 in the control group (p?=?0.146). Among ASD patients, anti-Ri antibody positivity was detected, while no anti-Ri antibody positivity was found in the control group (p?=?0.002). In the ASD group, the anti-Hu and 8-OHdG values were found to be significantly higher than those of the controls (p?Item The role of oxidative DNA damage and GSTM1, GSTT1, and hOGG1 gene polymorphisms in coronary artery disease risk(2016) Okyay, Kaan; Kadioglu, Ela; Tacoy, Gulten; Ozcagli, Eren; Akboga, Mehmet K.; Cengel, Atiye; Sardas, Semra; 0000-0001-6134-8826; 27182613; AAK-7355-2020Objective: Atherosclerotic coronary artery disease (CAD) appears to be a multifactorial process caused by the interaction of environmental risk factors with multiple predisposing genes. Therefore, in this study we aimed to determine the role of oxidative DNA damage and some variations in glutathione S-transferase (GSTM1 and GSTT1) and DNA repair (hOGG1) genes in CAD risk. Methods: A case-control study was conducted on 59 individuals who had undergone coronary angiographic evaluation. Of these, 29 were patients diagnosed with CAD (mean age = 61.5 +/- 10.3) and 30 were controls examined for reasons other than suspected CAD and who had angiographically documented normal coronary arteries (mean age = 60.4 +/- 11.6). Basal DNA damage as well as pyrimidine and purine base damage were evaluated in peripheral blood lymphocytes using the modified comet assay. Polymerase chain reaction-restriction length polymorphism (PCR-RFLP)-based assay was used for genotyping. Results: Basal DNA damage levels in patients [9.16 (3.26)] were significantly higher than those in controls [7.59 (3.23); p=0.017], and basal DNA and pyrimidine base damage levels were significantly correlated with disease severity based on Gensini scoring (r=0.352, p= 0.006; r= 0.318, p=0.014, respectively). However, no significant differences were observed in terms of oxidized DNA bases between patients and controls. The frequencies of studied genotypes (GSTM1, GSTT1, and hOGG1) were similar between groups. Conclusion: The results of this study pointed out the role of DNA damage in CAD and its severity. However, GSTM1, GSTT1, and hOGG1 gene polymorphisms seemed to have no effect on individual susceptibility for disease progression.Item Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats(2016) Aydin, Mehtap; Aydin, Sevtap; Sahin, Tevfik Tolga; Bacanli, Merve; Taner, Gokce; Basaran, Arif Ahmet; Basaran, Nursen; 27994910Background: The increases of free radicals have been proposed to be involved in the pathogenesis of sepsis, which leads to multiple-organ dysfunction syndromes. The uses of antioxidants as a complementary tool in the medical care of oxidative stress-related diseases have attracted attention of researchers. Resveratrol (RV) has suggested being antioxidant, anti-proliferative, and anti-inflammatory effects in various experimental models and clinical settings. Aims: This study was undertaken to evaluate the protective effects of RV on oxidative DNA damage induced by sepsis in the liver and kidney tissues of Wistar albino rats. Study Design: Animal experimentation. Methods: Four experimental groups consisting of eight animals for each was created using a total of thirty-two male Wistar albino rats. Sham group was given 0.5 mL of saline intra-peritoneal (ip) only following laparatomy. Sepsis group was given 0.5 mL saline ip only following the induction of sepsis. RV-treated group was given a dose of 100 mg/kg ip RV in 0.5 mL saline following laparatomy. RV-treated sepsis group was given 100 mg/kg ip RV in 0.5 mL saline following the induction of sepsis. A model of sepsis was created by cecal ligation and puncture technique. In the liver and kidney tissues, oxidative stress parameters (malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPX)) and a proinflammatory cytokine (tumor necrosis factor alpha (TNF-alpha)), were evaluated spectrophotometrically and DNA damage was determined by the alkaline single cell gel electrophoresis (comet assay) technique using formamidopyrimidine DNA glycosylase protein. Results: In the RV-treated sepsis group, the levels of MDA and TNF-alpha were lower and GSH levels, SOD and GPX activities were higher than in the septic rats (p<0.05). RV treatment significantly reduced the sepsis-induced oxidative DNA damage in the liver and kidney cells (p<0.05). Conclusion: It is suggested that RV treatment might reduce the sepsis-induced oxidative DNA damages in sepsis-related diseases; however, there is a need for more studies to clear up the protective mechanisms of RV against sepsis.