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    Effects of ammonia and allopurinol on rat hippocampal NMDA receptors
    (Wiley, 2010) Yonden, Zafer; Aydin, Mehmet; Kilbas, Aynur; Demirin, Hilmi; Sutcu, Recep; Delibas, Namik
    Ammonia is considered to be the main agent responsible for hepatic encephalopathy which progressively leads to altered mental status. N-methyl-D-aspartate (NMDA) is an ionotropic glutamate receptor, which is involved in synaptogenesis, memory and neurotoxicity. The aim of this study was to investigate the effects of ammonia intoxication and allopurinol, a xanthine oxidase (XO) inhibitor, on NMDA receptor subunits, NR2A and NR2B, in the hippocampus of rats. Thirty-six male rats were divided into three groups (n = 12/group) as follows: (1)control group (phosphate buffered saline (PBS) solution); (2)ammonia group (ammonium acetate, 2.5 mmol/kg), (3)ammonia + allopurinol group (ammonium acetate, 2.5 mmol/kg, allopurinol, 50 mg/kg). Each rat received intraperitoneal injection for 28 days. Western Blotting technique was used for detecting NR2A and NR2B expressions. Both NR2A and NR2B subunit expressions decreased 27 and 11%, respectively, in ammonia group with respect to the control group. Ammonium acetate decreased significantly in NR2A subunit expressions in the hippocampus (p < 0.01). Administration of ammonia + allopurinol caused statistically significant increases in NR2A subunit expressions compared to the ammonia group (p < 0.001). The down-regulation of NMDA receptors caused by ammonium acetate suggest that these receptors may play role in the process of hepatic encephalopathy and using allopurinol may have some protective effects in ammonia toxicity. Copyright (C) 2010 John Wiley & Sons, Ltd.
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    Galectin-3: A biochemical marker to detect paroxysmal atrial fibrillation?
    (Canadian Soc Clinical Investigation, 2016) Selcoki, Yusuf; Aydin, H. Ibrahim; Celik, Tugrul H.; Isleyen, Ahmet; Erayman, Ali; Demircelik, M. Bora; Demirin, Hilmi
    Purpose: Atrial fibrillation (AF) is the most common form of arrhythmia. AF leads to electrical remodelling and fibrosis of the atria; however, the mechanism(s) remain poorly understood. Galectin-3 is a potential mediator of cardiac fibrosis. The present study aimed to examine the relationship between serum galectin-3 levels and paroxysmal AF. Methods: Forty-six patients with paroxysmal AF and preserved left ventricular systolic function, and 38 age-and gender-matched control subjects, were involved in the study. Serum galectin-3 levels were analyzed with an enzyme-linked immunosorbent assay (ELISA). Results: Serum galectin-3 levels (median 1.38 ng/mL; 1.21 ng/mL-1.87 ng/mL; p < 0.001) were significantly elevated in patients with paroxysmal AF compared with the control. Left atrial diameter was significantly higher in patients with paroxysmal AF (41.2 +/- 3.0 mm vs. 39.6 +/- 3.3 mm). Left atrial diameter was found to be significantly correlated with serum galectin-3 levels in patients with paroxysmal AF (r= 0.378, p = 0.001). Conclusion: Serum galectin-3 levels are significantly elevated and significantly correlated with left atrial diameter in patients with paroxysmal AF.