Person: YALÇIN, MURAT
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YALÇIN
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MURAT
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Publication The effect of centrally injected arachidonic acid on respiratory system(Wiley, 2015-09-01) Erkan, Leman Gizem; Güvenç, Gökçen; Altınbaş, Burçin; Yalçın, Murat; Erkan, Leman Gizem; Güvenç, Gökçen; Altınbaş, Burçin; YALÇIN, MURAT; Uludağ Üniversitesi/Veteriner Fakültesi; 0000-0002-1413-3651; 0000-0002-5600-8162; 0000-0002-9534-736X; IYS-2646-2023; AAR-6815-2021; AAG-6956-2021; CNS-3398-2022Publication Centrally and peripherally injected nesfatin-1-evoked respiratory responses(Elsevier, 2019-09-01) Çiftçi, Kübra; Güvenç, Gökçen; Kaşıkçı, Esra; Yalçın, Murat; Çiftçi, Kübra; Güvenç, Gökçen; Kaşıkçı, Esra; YALÇIN, MURAT; Bursa Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı; 0000-0002-1413-3651; 0000-0002-5600-8162; AAR-6815-2021; AAG-6956-2021; HHG-0105-2022; CZB-8484-2022Nesfatin-1, which is an anorexiogenic peptide, plays a crucial role as a neurotransmitter and/or neuromodulator in the central nervous system for cardiovascular control and energy balance etc. It is expressed abundantly in multiple brain nuclei including central respiratory control areas such as nucleus tractus solitarius, nucleus ambiguous, dorsal vagal complex, dorsal motor nucleus of the vagus nerve, and hypothalamus. To date, no previous studies have been found to report nesfatin-1-evoked respiratory effects. Therefore, the present study was designed to investigate the possible impacts of centrally and/or peripherally injected nesfatin-1 on respiratory parameters in either 12h-fasted or fed-ad libitum rats.Intracerebroventricular (ICV) administration of nesfatin-1 provoked significant hyperventilation by increasing tidal volume (TV), respiratory rate (RR) and respiratory minute ventilation (RMV) in both the 12h fasted and the fed-ad libitum Sprague Dawley rats in dose- and time- dependent manner. Moreover, the hyperventilatory effects of centrally injected nesfatin-1 were more potent in the fed-ad libitum rats. Intravenous injection of nesfatin-1 induced a significant rise in RR and RMV, but not in TV, in the fed-ad libitum rats.In conclusion, these findings plainly report that both centrally and/or peripherally injected nesfatin-1 induces significant hyperventilatory effects in the 12h-fasted and the fed-ad libitum rats. These hyperventilatory effects of nesfatin-1 might show a discrepancy according to the food intake of the rats and the delivery method of the peptide.Publication Central histaminergic system mediates prostaglandin cascade induced cardiovascular effects(Federation Amer, 2013-04-01) Yalçın, Murat; Altınbaş, Burçin; Topuz, Bora Burak; Yılmaz, Mustafa Sertaç; Savcı, Vahide; Aydın, Sami; YALÇIN, MURAT; Altınbaş, Burçin; Topuz, Bora Burak; YILMAZ, MUSTAFA SERTAÇ; SAVCI, VAHİDE; Aydın, Sami; Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Fizik Bölümü; 0000-0002-5600-8162; 0000-0001-9496-1475; AAG-6956-2021; IYS-2646-2023; KHD-9454-2024; AAH-1571-2021; EBJ-3864-2022; CCT-7508-2022Publication Block et al. fluorinated analogs of organosulfur compounds from garlic ( allium sativum ): Synthesis, chemistry and anti-angiogenesis and antithrombotic studies (vol 22, artn 2081, 2027)(Mdpi, 2023-02-01) Block, Eric; Bechand, Benjamin; Gundala, Sivaji; Vattekkatte, Abith; Wang, Kai; Mousa, Shaymaa S.; Godugu, Kavitha; Mousa, Shaker A.; Yalçın, Murat; YALÇIN, MURAT; Bursa Uludağ Üniversitesi/Veteriner Fakültesi.; 0000-0002-4668-1687; 0000-0002-7996-0658; 0000-0002-5602-4015; 0000-0002-5600-8162; 0000-0002-9294-015X; P-7203-2014; H-5438-2016; AAG-6956-2021; A-7151-2017; D-3989-2014Publication Nanotetrac targets integrin αvβ3 on tumor cells to disorder cell defense pathways and block angiogenesis(Dove Medical Press Ltd, 2014-01-01) Davis, Paul J.; Lin, Hung-Yun; Sudha, Thangirala; Yalçın, Murat; Tang, Heng-Yuan; Hercbergs, Aleck; Leith, John T.; Luidens, Mary K.; Ashur-Fabian, Osnat; Incerpi, Sandra; Mousa, Shaker A.; YALÇIN, MURAT; Uludağ Üniversitesi/Tıp Fakültesi/Radyasyon Onkolojisi Anabilim Dalı; 0000-0002-5600-8162; AAG-6956-2021The extracellular domain of integrin alpha v beta 3 contains a receptor for thyroid hormone and hormone analogs. The integrin is amply expressed by tumor cells and dividing blood vessel cells. The proangiogenic properties of thyroid hormone and the capacity of the hormone to promote cancer cell proliferation are functions regulated nongenomically by the hormone receptor on alpha v beta 3. An L-thyroxine (T-4) analog, tetraiodothyroacetic acid (tetrac), blocks binding of T-4 and 3,5,3'-triiodo-L-thyronine (T-3) by alpha v beta 3 and inhibits angiogenic activity of thyroid hormone. Covalently bound to a 200 nm nanoparticle that limits its activity to the cell exterior, tetrac reformulated as Nanotetrac has additional effects mediated by alpha v beta 3 beyond the inhibition of binding of T-4 and T-3 to the integrin. These actions of Nanotetrac include disruption of transcription of cell survival pathway genes, promotion of apoptosis by multiple mechanisms, and interruption of repair of double-strand deoxyribonucleic acid breaks caused by irradiation of cells. Among the genes whose expression is suppressed by Nanotetrac are EGFR, VEGFA, multiple cyclins, catenins, and multiple cytokines. Nanotetrac has been effective as a chemotherapeutic agent in preclinical studies of human cancer xenografts. The low concentrations of alpha v beta 3 on the surface of quiescent nonmalignant cells have minimized toxicity of the agent in animal studies.Publication The mediation of central cyclooxygenase and lipoxygenase pathways in orexin-induced cardiovascular effects(Elsevier, 2021-03-01) Altınbaş, Burçin; Güvenç-Bayram, Gökçen; Yalçın, Murat; YALÇIN, MURAT; Altınbaş, Burçin; Güvenç-Bayram, Gökçen; Bursa Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı; 0000-0002-1413-3651; 0000-0002-5600-8162; 0000-0002-9534-736X; IYS-2646-2023; AAR-6815-2021; AAG-6956-2021Previously it was reported that central orexin (OX) and arachidonic acid (AA) signaling pathways played an active role in the control of the cardiovascular system. It was also reported that they have exhibited their cardiovascular control role by using similar central or peripheral mechanisms. However, there has been no study demonstrating the interaction between OX and AA signaling pathways in terms of cardiovascular control. The current study was designed to investigate the possible mediation of the central cyclooxygenase (COX) and lipoxygenase (LOX) pathways in OX-induced cardiovascular effects in the rats.Intracerebroventricular injection of OX increased blood pressure and heart rate in a dose-dependent manner in normotensive male Sprague Dawley rats. Moreover, the microdialysis study revealed that intracerebroventricular injected OX caused a time-dependent increase in the extracellular total prostaglandin concentrations in the posterior hypothalamus. Interestingly, central pretreatment with a non-selective COX inhibitor, ibuprofen, or a non-selective LOX inhibitor, nordihydroguaiaretic acid, partially reversed pressor and tachycardic cardiovascular responses evoked by central administration of OX.In summary, our findings show that the central treatment with OX causes pressor and tachycardic cardiovascular responses along with an increase in posterior hypothalamic extracellular total prostaglandin concentrations. Furthermore, our results also demonstrate that central COX and LOX pathways mediate, at least in part, centrally administered OX-evoked pressor and tachycardic responses, as well.Publication The effect of centrally and peripherally injected cdp-choline on plasma nesfatin-1 level in rats(Ankara Univ Press, 2019-01-01) Usta, Hikmet Ayşin; Güvenç, Gökçen; Savcı, Vahide; SAVCI, VAHİDE; Yalçın, Murat; YALÇIN, MURAT; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Veteriner Fakültesi.; 0000-0002-1413-3651; 0000-0002-5600-8162; KHD-9454-2024; AAG-6956-2021; AAR-6815-2021Nesfatin-1 has a role in appetite control and energy balance. The activity of the cholinergic system also is able to affect feeding behavior. Moreover, the central cholinergic system interacts with central nesfatinergic systems. The main goal of the study was to determine the effect of intracerebroventricular (icv) and intravenous (iv) administrated CDP-choline (0.5 ve 1 mu mol; icv ve 250 mg / kg; iv) on levels of plasma nesfatin-1 in the homogeneous number of male and female fasted and the satiated Wistar albino rats. The polyethylene cannula was inserted into the carotid artery and jugular vein of the rats anesthetized with sevoflurane (2-4%/100% O-2) to collect blood samples and to make iv injection, respectively. For icy treatment, the lateral ventricle of rats was cannulated with guide cannula. The basal levels of plasma nesfatin- I in the satiated rats were higher than those observed in the fasted animals. While 0.5 and 1 mu mol dose of icy and/or 250 mg/kg dose of iv injected CDP-choline increased the level of plasma nesfatin-1 in the satiated rats, plasma nesfatin-1 level of the fasted animals decreased after the same dose and route of CDP-choline injection. The current findings show that CDP-choline can influence the level of plasma nesfatin-1 in the rats. The effect of the drug was different according to the food intake of the rats. These data might suggest a potential role in CDP-choline on plasma nesfatin-1 concentration.Publication Lead-induced endothelial cell dysfunction: Protective effect of sulfated non-anticoagulant low molecular weight heparin(Korean Soc Environmental Risk Assessment & Health Science, 2021-04-12) Motawei, Shimaa M.; Sudha, Thangirala; Godugu, Kavitha; Mousa, Shaker A.; Yalçın, Murat; YALÇIN, MURAT; Bursa Uludağ Üniversitesi/Veteriner Fakültesi.; 0000-0002-5600-8162; AAG-6956-2021Objective The aim of this investigation is to determine the potential protective effect and mechanism of a novel non-anticoagulant heparin-derived product on lead (Pb) mediated endothelial cells (ECs) toxicity. Pb is known to have detrimental effects on human health by affecting the function of all systems of the human body due to its toxicity on ECs. Altered activities of the protective substances secreted by the vascular endothelium such as EC's tissue factor pathway inhibiter (TFPI), nitric oxide and other protective factors might increase the risk for vascular disorders. Heparin and its sulfated non-anticoagulant low molecular weight heparin (S-NACH) are known to enhance TFPI release from ECs, which is a protective mechanism for the ECs against thrombo-inflammation. Methods We examined 3-100 mu M Pb-induced dysfunction on ECs and the potential protective effect of 1-10 mu M S-NACH in returning the ECs' normal function. Methods included an in vitro tube formation assay and an in vivo Matrigel plug angiogenesis model in mice. Results We found that Pb-induced EC dysfunction by inhibiting EC viability. The cytotoxic effect of 3-100 mu M Pb on ECs inhibited angiogenesis in a dose-dependent manner. Pb disrupted ECs' normal physiological function by hindering the release of its endogenous vascular protective mediators TFPI-1 and TFPI-2. The impairment effect of 3-30 mu M Pb on ECs' release of both TFPIs was effectively reversed to normal levels by S-NACH in a concentration-dependent manner and combatted the harmful Pb effects on physiological angiogenesis. Conclusions Our data indicate that S-NACH, which is devoid of bleeding side effects, can effectively reverse potentially high-risk Pb-mediated endothelial cytotoxicity by reversing the physiological release of endogenous EC TFPIs.Publication A new protocol for collagen-induced local arthritis model in balb/c mice(Turkish Soc Immunology, 2018-01-01) Güvenç, Gökçen; Karacay, Mehmet; Çiftçi, Kübra; Akkoç, Ahmet; AKKOÇ, AHMET; Oral, Haluk Barbaros; ORAL, HALUK BARBAROS; Yalçın, Murat; YALÇIN, MURAT; Bursa Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Veteriner Fakültesi/Patoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/İmmunoloji Anabilim Dalı.; 0000-0002-1413-3651; 0000-0002-5090-7917; 0000-0003-0463-6818; 0000-0002-5600-8162; AAR-6815-2021; K-7285-2012; AAG-6956-2021Introduction: Numerous models have been described to study the pathogenesis of rheumatoid arthritis, and to develop new therapies; but each of these models has their own limitations. Nowadays, the collagen-induced arthritis (CIA) mouse model is the most commonly used model for rheumatoid arthritis studies in certain mouse strain like DBA/1 mouse. This study aimed to describe a new protocol for local induction of arthritis in Balb/c mice, including the monitoring of clinical arthritis and the protocols for histological examination of paws of mice.Materials and Methods: For the induction of local arthritis in 40 Balb/c mice, they were immunized intra-articularly with type II collagen and subcutaneous complete Freund's adjuvant in 0 day. As the boost immunization, the animals had same injections on day 14. Mice were divided 4 groups, and they were clinically and histopathologically examined for arthritis on 0, 14, 21 and 30 days of arthritis induction.Results: The first signs ol local arthritis appeared in this model 1 week after boost immunization (day 21). The CIA induced paw clinically showed severe erythema and swelling all around the hindquarter on day 21 and 30. The paw reached almost 4 times thicker than the other paws and histopathological examination confirmed the clinical arthritis on day 21 and 30.Conclusion: Using the protocol described, the investigators may reproducibly and economically induce a high incidence of local CIA in Balb/c mice. The described local CLA model may be used to unravel pathophysiological or immunological mechanisms of arthritis, and can also be used to study the effect of new therapeutics.Publication The involvement of the central cholinergic system in the hyperventilation effect of centrally injected nesfatin-1 in rats(Elsevier, 2021-12-01) Güvenç-Bayram, Gökçen; Yalçın, Murat; YALÇIN, MURAT; Bursa Uludağ Üniversitesi/Veterinerlik Fakültesi.; 0000-0002-1413-3651; 0000-0002-5600-8162; AAG-6956-2021; AAR-6815-2021We recently demonstrated that peripheral and central administration of nesfatin-1 in fasting and satiety states generate hyperventilation activity by increasing tidal volume (TV), respiratory rate (RR), and respiratory minute ventilation (RVM). The present study aimed to investigate the mediation of central cholinergic receptors effective in respiratory control in the hyperventilation activity of nesfatin-1. Besides this, we intended to determine possible changes in blood gases due to hyperventilation activity caused by nesfatin-1 and investigate the mediation of central cholinergic receptors in these changes.Intracerebroventricular (ICV) administration of nesfatin-1 revealed a hyperventilation response with an increase in TV, RR, RMV, and pO(2) and a decrease in pCO(2) in saturated Sprague Dawley rats. ICV pretreatment with the muscarinic receptor antagonist atropine partially blocked the RR, RMV, pO(2), and pCO(2) responses produced by nesfatin-1 while completely blocking the TV response. However, central pretreatment with nicotinic receptor antagonist mecamylamine blocked the respiratory and blood gas responses induced by nesfatin-1.The study's conclusion demonstrated that nesfatin-1 had active hyperventilation effects resulting in an increase in pO(2) and a decrease in pCO(2). The critical finding of the study was that activation of central cholinergic receptors was involved in nesfatin-1-evoked hyperventilation and blood gas responses.