Person: OKTAY, NİHAL ŞEHKAR
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OKTAY
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NİHAL ŞEHKAR
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Publication Metadata only Is sialic acid a promising marker for periodontal diseases?(WOLTERS KLUWER MEDKNOW PUBLICATIONS, 2020) KURU, LEYLA; Oktay, S.; Bal, O. Ozoner; Kuru, L.; Yarat, A.; Noyan, U.Objective: Periodontal diseases are inflammatory chronic infections. Sialic acid (SA) is an acute phase reactant by itself. The aim of this study is to investigate the relationship between salivary and serum SA levels and clinical parameters in different forms of periodontal diseases. Subject and Methods: Systemically healthy subjects were included in the study; patients with chronic gingivitis (CG) (n = 10), chronic periodontitis (CP) (n = 10), and aggressive periodontitis (AgP) (n = 10), and ten volunteers with healthy periodontium as the control group. Total SA levels were determined by Warren's thiobarbituric acid method in whole saliva, parotis saliva, and serum samples of subjects before and 3 months after nonsurgical periodontal treatment. Full mouth clinical parameters including plaque index, gingival index, probing depth, and bleeding on probing were also recorded. Results: Before treatment, in both periodontitis groups salivary and serum SA levels were higher than those of controls (P = 0.001). Both salivary and serum SA levels decreased significantly in the patient groups after treatment (P < 0.001). Multiple comparisons of baseline clinical parameters in all groups revealed significant differences (P = 0.001) and these parameters decreased significantly on the 90th day (P < 0.01). There were positive correlations between SA levels and periodontal indices of the CG, CP, and AgP groups (P < 0.05). Conclusion: Our results suggest that SA level in both saliva and serum may be a potentially useful marker to determine inflammatory changes and investigate different forms of periodontal diseases.Publication Metadata only Overpressure blast injury-induced oxidative stress and neuroinflammation response in rat frontal cortex and cerebellum(ELSEVIER SCIENCE BV, 2018) OKTAY, NİHAL ŞEHKAR; Toklu, Hale Z.; Yang, Zhihui; Oktay, Sehkar; Sakarya, Yasemin; Kirichenko, Nataliya; Matheny, Michael K.; Muller-Delp, Judy; Strang, Kevin; Scarpace, Philip J.; Wang, Kevin K. W.; Tumer, NihalBackground & aim: Overpressure blast-wave induced brain injury (OBI) and its long-term neurological outcome pose significant concerns for military personnel. Our aim is to investigate the mechanism of injury due to OBI. Methods: Rats were divided into 3 groups: (1) Control, (2) OBI (exposed 30 psi peak pressure, 2-2.5 ms), (3) Repeated OBI (r-OBI) (three exposures over one-week period). Lung and brain (cortex and cerebellum) tissues were collected at 24 h post injury. Results: The neurological examination score was worse in OBI and r-OBI (4.2 +/- 0.6 and 3.7 +/- 0.5, respectively) versus controls (0.7 +/- 0.2). A significant positive correlation between lung and brain edema was found. Malondialdehyde (index for lipid peroxidation), significantly increased in OBI and r-OBI groups in cortex (p < 0.05) and cerebellum (p < 0.01-0.001). The glutathione (endogenous antioxidant) level decreased in cortex (p < 0.01) and cerebellum (p < 0.05) of r-OBI group when compared with the controls. Myeloperoxidase activity indicating neutrophil infiltration, was significantly (p < 0.01-0.05) elevated in r-OBI. Additionally, tissue thromboplastin activity, a coagulation marker, was elevated, indicating a tendency to bleed. NGF and NF-kappa B proteins along with Iba-1 and GFAP immunoreactivity significantly augmented in the frontal cortex demonstrating microglial activation. Serum biomarkers of injury, NSE, TNF-alpha and leptin, were also elevated. Conclusion: OBI triggers both inflammation and oxidative injury in the brain. This data in conjunction with our previous observations suggests that OBI triggers a cascade of events beginning with impaired cerebral vascular function leading to ischemia and chronic neurological consequences.Publication Metadata only The effect of vitamin U on the lung tissue of pentyleneterazole-induced seizures in rats(SPRINGER, 2018) YARAT, AYŞEN; Oktay, Sehkar; Bayrak, Gamze; Alev, Burcin; Ipekci, Hazal; Ustundag, Unsal Veli; Turkyilmaz, Ismet Burcu; Pisiriciler, Rabia; Emekli-Alturfan, Ebru; Tunali-Akbay, Tugba; Yanardag, Refiye; Yarat, AysenThe aim of this study is to investigate the therapeutic effects of vitamin U (Vit U) on lung tissue of pentyleneterazole (PTZ)-induced seizures in rats. Sprague Dawley male rats were randomly divided into four groups as follows: control (0.9% NaCl given, intraperitoneally); Vit U (50 mg/kg/day, for 7 days by gavage); PTZ; (60 mg/kg one dose, intraperitoneally); and PTZ + Vit U (in same dose and time). At the end of the experiment, lung tissues were taken and examined biochemically and cytologically. Lipid peroxidation (LPO), glutathione (GSH), sialic acid (SA), and nitric oxide (NO) levels, and superoxide dismutase (SOD) and catalase (CAT) activities were determined in lung homogenates. Imprinted lung samples were stained with May Grunwald-Giemsa stain and microscopically examined for the presence of collagen fibers, macrophage, leucocyte, and epithelial cells. PTZ administration significantly increased GSH level and CAT activity and significantly decreased SOD activity compared to the control group. Vit U administration significantly increased GSH level and CAT activity compared to the control group. GSH and NO levels significantly decreased in PTZ + Vit U group compared to the PTZ group. In cytologic analysis, increased collagen fibers, macrophages, leucocytes, and epithelial cells were observed in PTZ group compared to the control group, and Vit U administration decreased these cytological parameters compared to the PTZ group. The findings of this study support the possible protective role of using Vit U as an add-on therapy in order to prevent lung tissue injury which may occur during seizures in epilepsy.