Person: ŞAHİNTÜRK, SERDAR
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ŞAHİNTÜRK
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SERDAR
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Publication A novel β-lactam-aminoglycoside combination in veterinary medicine: The couse of ceftiofur and gentamicin to combat resistant Escherichia coli(Hellenic Veterinary Medical Society, 2020-04-01) Cengiz, M.; Şahintürk, P.; Hepbostancı, G.; Akalın, H.; Sonal, S.; CENGİZ, MURAT; ŞAHİNTÜRK, SERDAR; AKALIN, EMİN HALİS; SONAL, SONGÜL; HEPBOSTANCI, G.; Bursa Uludağ Üniversitesi/Veteriner Fakültesi.; Bursa Uludağ Üniversitesi/Tıp Fakültesi.; Bursa Uludağ Üniversitesi/Sağlık Bilimleri Enstitüsü.; 0000-0001-7530-1279; AAU-8952-2020; ABE-5935-2020The focus of this study was to evaluate the efficacy of ceftiofur+gentamicin combination to increase the success of antimicrobial inhibition against resistant Escherichia coli (E.coli) strains isolated from animals. Interaction between drugs was determined using checkerboard method and the fractional inhibitory concentration index was interpreted as synergism, antagonism and indifference. The combination was defined as bactericidal or bacteriostatic based on the minimum bactericidal test results. Mutant prevention concentration test was used to evaluate the resistance tendency suppression potential of the combination. The synergistic effect was detected for all E. coli strains by the checkerboard method; even the strains that were resistant to the individual compounds in the combination. Based on the results of minimum bactericidal concentration test, the combination exhibited bactericidal effect against all E. coli strains. In addition, the individual mutant prevention concentrations of ceftiofur and gentamicin decreased up to 125-fold by using the combination for the inhibition of resistant E. coli strains. The results indicated that killing potential of co-use of the compounds is much stronger than their individual use. The combination achieved to decrease the mutant prevention concentrations and this can reduce the risk of emergence of single mutations during treatment done with suggested doses.Publication [Pyr1]apelin-13 relaxes the rat thoracic aorta via APJ, NO, AMPK, and potassium channels(Aepress Sro, 2021-01-01) Şahintürk, Serdar; Demirel, Sadettin; Özyener, Fadıl; İşbil, Naciye; ŞAHİNTÜRK, SERDAR; DEMİREL, SADETTİN; ÖZYENER, FADIL; İŞBİL, NACİYE; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı; 0000-0002-7612-0055; 0000-0002-3629-5344; 0000-0002-4606-6596; AAH-3460-2021; ACQ-9887-2022; AAH-1641-2021; FBW-7104-2022In this study, the effect and effect mechanisms of [Pyr1]apelin-13, the dominant apelin isoform in the human cardiovascular tissues and human plasma, on vascular contractility were investigated. The vascular rings obtained from the thoracic aortas of the male Wistar Albino rats were placed in the isolated tissue bath system. After the equilibration period, [Pyr1]apelin-13 (10(-9) to 10(-6) M) was applied cumulatively to the aortic rings pre-contracted with phenylephrine in the plateau phase. The protocol was repeated in the presence of specific signaling pathway inhibitors (F13A, L-NAME, dorsomorphin, TEA, U0126, or indomethacin) to determine the effect mechanisms of [Pyr1]apelin-13. [Pyr1]apelin-13 induced a dose-dependent relaxation in the pre-contracted aortic rings. APJ, eNOS, AMPK, and potassium channel inhibition statistically significantly decreased the vasodilator effect of [Pyr1]apelin-13. MAPK and COX inhibition didn't statistically significantly changed the vasodilator effect of [Pyr1]apelin-13. In conclusion, [Pyr1]apelin-13 relaxes the rat thoracic aorta via APJ, NO, AMPK, and potassium channels.Publication Physiological role of K+ channels in irisin-induced vasodilation in rat thoracic aorta(Elsevier Science, 2022-01) Demirel, Sadettin; Şahinturk, Serdar; İşbil, Naciye; Özyener, Fadıl; DEMİREL, SADETTİN; ŞAHİNTÜRK, SERDAR; İŞBİL, NACİYE; ÖZYENER, FADIL; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Bölümü; 0000-0002-7612-0055; 0000-0002-4606-6596; 0000-0002-3629-5344; JAQ-7571-2023; ACQ-9887-2022; FBW-7104-2022; AAH-1641-2021Irisin, an exercise-induced myokine, has been shown to have a peripheral vasodilator effect. However, little is known about the mechanisms underlying its effects. In this study, it was aimed to investigate the vasoactive effects of irisin on rat thoracic aorta, and the hypothesis that voltage-gated potassium (KV) channels, ATPsensitive potassium (KATP) channels, small-conductance calcium-activated potassium (SKCa) channels, largeconductance calcium-activated potassium (BKCa) channels, intermediate-conductance calcium-activated potassium (IKCa) channels, inward rectifier potassium (Kir) channels, and two-pore domain potassium (K2P) channels may have roles in these effects. Isometric contraction-relaxation responses of isolated thoracic aorta rings were measured with an organ bath model. The steady contraction was induced with both 10-5 M phenylephrine and 45 mM KCl, and then the concentration-dependent responses of irisin (10-9-10-6 M) were examined. Irisin exerted the vasorelaxant effects in both endothelium-intact and -denuded aortic rings at concentrations of 10-8, 10-7, and 10-6 M (p < 0.001). Besides, KV channel blocker 4-aminopyridine, KATP channel blocker glibenclamide, SKCa channel blocker apamin, BKCa channel blockers tetraethylammonium and iberiotoxin, IKCa channel blocker TRAM-34, and Kir channel blocker barium chloride incubations significantly inhibited the irisin-induced relaxation responses. However, incubation of K2P TASK-1 channel blocker anandamide did not cause a significant decrease in the relaxation responses of irisin. In conclusion, the first physiological findings were obtained regarding the functional relaxing effects of irisin in rat thoracic aorta. Furthermore, this study is the first to report that irisin-induced relaxation responses are associated with the activity of KV, KATP, SKCa, BKCa, IKCa, and Kir channels.