Person: KAHVECİ, NEVZAT
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KAHVECİ
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NEVZAT
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Publication The effect of cdp-choline on hippocampal tcamkii, pcamkii and pcreb levels in rem-sleep deprived rats(Wiley, 2019-12-01) Süyen, Güldal; Çakır, Aysen; ÇAKIR, AYŞEN; CANSEV, MEHMET; Öcalan, Buşra; Koç, Cansu; KOÇ, CANSU; KAHVECİ, NEVZAT; Kahveci, Nevzat; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; 0000-0002-6097-5585; 0000-0003-2918-5064; 0000-0003-0841-8201; AAA-4754-2022; A-6819-2018; M-9071-2019; AAG-7070-2021Publication The effect of uridine on inflammatory mediators in rem sleep deprived rats(Wiley, 2023-01-01) Esmerce, Büşra Öcalan; Çakır, Aysen; Çilingir, Sümeyye; Suyen, Güldal; Kahveci, Nevzat; Esmerce, Büşra Öcalan; ÇAKIR, AYŞEN; KAHVECİ, NEVZAT; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; 0000-0001-7729-7373; HMR-2796-2023; A-6819-2018; AAG-7070-2021Publication Heat shock proteins(Türk Cerrahi Derneği, 2009-10-01) Özürk, Ersin; Kahveci, Nevzat; Özlük, Kasım; Yılmazlar, Tuncay; Özürk, Ersin; KAHVECİ, NEVZAT; Özlük, Kasım; YILMAZLAR, AHMET TUNCAY; Uludağ Üniversitesi/Tıp Fakültesi/Genel Cerrahi Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; 0000-0003-0841-8201; FRI-7780-2022; JJX-0104-2023; AAG-7070-2021; CKK-3621-2022Heat shock proteins (HSP) are a group of proteins that have a molecular weight less than 100 kDa and whose production is induced by heat (42-46 degrees C) shock. Infection, inflammation, some toxins such as ethanol, arsenic, trace metals and ultraviolet light, hunger, hypoxia, lack of nitrogen (in plants) and dehydration are the factors that could induce HSP production. HSPs are classified into four main groups according to their molecular weights; HSP 90 family, HSP 70 family, HSP 60 family and the small HSP family. They have functions mainly in cytoprotection, neurodegenerative pathologies, signal transduction pathways and cancer immunology.Publication Melatonin treatment affects leptin and nesfatin-1 levels but not orexin-a levels in rem sleep deprived rats(Kafkas Univ, Veteriner Fakultesi Dergisi, 2023-09-01) Çakır, Aysen; ÇAKIR, AYŞEN; Sehzade, Sevda; Koç, Cansu; KOÇ, CANSU; Kahveci, Nevzat; KAHVECİ, NEVZAT; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; 0000-0002-6097-5585Sleep contributes to the energy balance of body. This study aims to investigate how rapid eye movement (REM) sleep deprivation (SD) or recovery sleep affects rat weight and the serum levels of Nesfatin-1, Orexin-A, and Leptin; additionally, seeks to determine the impact of melatonin administration on these parameters. Male, Sprague Dawley rats were randomized into two groups (n=9). REMSD was induced using the modified multiple platform method (MMPM). Melatonin was used as a treatment (20 mg/kg). Study Group I was created to investigate the effectiveness of the treatment during REMSD. Study Group II was established to analyze the possible therapeutic role of melatonin and recovery sleep after REMSD-induced damage. The rats' weights were recorded during the experiments. Blood samples were collected from all rats via decapitation after experiments. The levels of serum Nesfatin-1, Orexin-A, and Leptin were analyzed using the ELISA method. REMSD affected weight of the rats and altered the levels of serum Nesfatin-1 and Leptin. Melatonin administration influenced weight gain and affected Nesfatin-1 and Leptin levels. REMSD or melatonin did not affect Orexin-A levels. REMSD and melatonin play significant roles in the body's energy balance. This study will contribute to elucidating the role of SD in metabolic processes and will play a role in assessing the impact of melatonin, a commonly used treatment in human and veterinary medicine.Publication Proteomics analysis of CA1 region of the hippocampus in pre-, progression and pathological stages in a mouse model of the alzheimer's disease(Bentham Science, 2019-01-01) Gürel, Buşra; Cansev, Mehmet; Koç, Cansu; Öçalan, Buşra; Çakır, Ayşen; Aydın, Samı; Kahveci, Nevzat; Ulus, İsmail Hakkı; Şahin, Betül; Başar, Merve Karayel; Baykal, Ahmct Tarık; CANSEV, MEHMET; KOÇ, CANSU; Öçalan, Buşra; ÇAKIR, AYŞEN; Aydın, Sami; KAHVECİ, NEVZAT; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Bilim Dalı; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Bilim Dalı; 0000-0002-6097-5585; 0000-0003-0841-8201; 0000-0002-3405-3640; 0000-0001-7729-7373; AAG-7070-2021; AAA-4754-2022; A-6819-2018; AAL-1786-2020; M-9071-2019; N-9927-2019; CCT-7508-2022Background: CA1 subregion of the hippocampal formation is one of the primarily affected structures in AD, yet not much is known about proteome alterations in the extracellular milieu of this region. Objective: In this study, we aimed to identify the protein expression alterations throughout the pre-pathological, progression and pathological stages of AD mouse model.Methods: The CA1 region perfusates were collected by in-vivo intracerebral push-pull perfusion from transgenic 5XFAD mice and their non-transgenic littermates at 3, 6 and 12 were beta months of age. Morris water maze test and immunohistochemistry staining of A performed to determine the stages of the disease in this mouse model. The protein expression differences were analyzed by label-free shotgun proteomics analysis.Results: A total of 251, 213 and 238 proteins were identified in samples obtained from CA1 regions of mice at 3, 6 and 12 months of age, respectively. Of these, 68, 41 and 33 proteins showed statistical significance. Pathway analysis based on the unique and common proteins within the groups revealed that several pathways are dysregulated during different stages of AD. The alterations in glucose and lipid metabolisms respectively in pre-pathologic and progression stages of the disease, lead to imbalances in ROS production via diminished SOD level and impairment of neuronal integrity.Conclusion: We conclude that CA1 region-specific proteomic analysis of hippocampal degeneration may be useful in identifying the earliest as well as progressional changes that are associated with Alzheimer's disease.Publication Can heat shock protein 32 be used for the early diagnosis of acute mesenteric ischemia?(Türk Cerrahi Derneği, 2016-03-01) Berhuni, Sait; Öztürk, Ersin; Oral, Arzu Yılmaztepe; Sarkut, Pınar; Kahveci, Nevzat; Yılmazlar, Tuncay; Özlük, Kasım; Yerci, Ömer; Berhuni, Sait; Öztürk, Ersin; YILMAZTEPE ORAL, ARZU; Sarkut, Pınar; KAHVECİ, NEVZAT; YILMAZLAR, AHMET TUNCAY; Özlük, Kasım; YERCİ, ÖMER; Uludağ Üniversitesi/Tıp Fakültesi/Genel Cerrahi Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Biyokimya Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Patoloji Anabilim Dalı.; 0000-0002-8962-9758; 0000-0003-0841-8201; AAG-7070-2021; A-5841-2017; CEH-4566-2022; JGW-0566-2023; HKB-5363-2023; CKK-3621-2022; JJX-0104-2023; EIS-5114-2022Objective: Acute mesenteric ischemia is a challenging and fatal disease. The aim of this study was to detect the heat shock protein 32 (HSP32) response in intestinal tissue and systemic blood to intestinal ischemia and ischemia/reperfusion to define a tool for the early diagnosis of acute mesenteric ischemia.Material and Methods: Thirty female Wistar albino rats were equally divided into 3 groups. Group 1 rats underwent simple laparotomy and closure (control). In Group 2 rats, 1-hour intestinal ischemia followed by 5-hour reperfusion was performed, and Group 3 rats were subjected to 6-hour intestinal ischemia. The experiment was repeated with a 24-hour waiting period. At the end of the waiting period, blood was withdrawn from the tail veins of the rats and the rats were sacrificed via cardiac puncture. Re-laparotomy was subsequently performed and intestinal tissue and luminal samples were obtained for biochemical and pathological investigations. The HSP32 levels of intestinal tissues, luminal contents and blood levels were compared among the groups.Results: At the end of the 24-hour waiting period, the median tissue HSP32 levels were 0.43 (0-6.6) ng/mL for Group 1, 9.51 (2.5-49.9) ng/mL for Group 2 and 43.13 (6.3-121.3) ng/mL for Group 3 (p= 0.001). The median blood HSP32 levels were 0.11 (0.1-1.4) ng/mL for Group 1, 0.42 (0.1-0.7) ng/mL for Group 2, and 0.25 (0.1-1.2) ng/mL for Group 3 (p= 0.047). The HSP levels in the luminal contents were undetectable.Conclusion: Both ischemia and ischemia/reperfusion significantly raised intestinal tissue HSP32 levels in comparison with the control group. However, this change was not reflected in the circulating blood or luminal contents.Publication Effect of linopirdine on forced swimming test in rats(Nobel İlaç, 2019-01-01) Uzunok, Barış; Kahveci, Nevzat; Suyen, Güldal Güleç; Büyükuysal, M. Çağatay; KAHVECİ, NEVZAT; Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı; 0000-0003-0841-8201; AAG-7070-2021Objective: In this study, we aimed to investigate the effect of Kv7 type voltage-gated potassium channel blocker linopirdin in Forced Swimming Test (FST) in rats.Material and Method: For this purpose, on the second day of the swimming test, rats received %0.9 NaCl (4 mu l) or a Kv7 type voltage-gated potassium channel blocker linopirdine (0.1, 1, 10 mu g/4 mu l) intracerebroventricularly (i.c.v.), 15 min before the test.Results: Linopirdine at a dose of 0.1 mu g/4 mu l significantly decreased immobilisation (p=0.003) and significantly increased swimming (p<0.01) with respect to the control grup. Linopirdine at the doses of 1 mu g/4 mu l and 10 mu g/4 mu l; i.c.v., significantly decreased immobilisation (p values<0.001) and significantly increased swimming (p=0.003 and p=0.021, respectively), and climbing (p=0.009 and p=0.006, respectively) with respect to the control grup.Conclusion: The results we obtained shows that linopirdine applied through i.c.v way produces similar effects as the anti-depressant drugs in the FST model. Therefore, we believe that drugs that block Kv7 type voltage-gated potassium channels can be considered as antidepressant drug targets.Publication Effects of uridine administration on hippocampal matrix metalloproteinases and their endogenous inhibitors in rem sleep-deprived rats(Elsevier, 2022-10-15) Çakır, Ayşen; Esmerce, Büşra Öcalan; Aydın, Birnur; Koç, Cansu; Cansev, Mehmet; Suyen, Güldal Güleç; Kahveci, Nevzat; ÇAKIR, AYŞEN; ESMERCE, BÜŞRA; KOÇ, CANSU; CANSEV, MEHMET; KAHVECİ, NEVZAT; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; 0000-0002-6097-5585; 0000-0003-0841-8201; A-6819-2018; M-9071-2019; AAG-7070-2021; LGY-8580-2024; N-9927-2019Rapid eye movement (REM) sleep is associated with synaptic plasticity which is considered essential for longterm potentiation (LTP). The composition of extracellular matrix (ECM), in part, plays a role in REM sleepassociated synaptic functioning. The objective of this study was to investigate the effects of uridine administration on levels of matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in rats subjected to REM sleep deprivation (REMSD). REMSD was induced by modified multiple platform method for 96-hour. Rats were randomized to receive either saline or uridine (1 mmol/kg) intraperitoneally twice a day for four days. Rats were then decapitated and their hippocampi were dissected for analyzing the levels of MMP-2, MMP3, MMP-9, TIMP-1, TIMP-2 and TIMP-3 by Western-blotting and the activities of MMP-2 and MMP-9 by Gelatin zymography. REMSD resulted in reduced levels of MMP-3, MMP-9, TIMP-3 and activity of MMP-9 in salinetreated rats, while uridine treatment significantly enhanced their impairment. TIMP-1 was enhanced following REMSD but uridine treatment had no significant effect on TIMP-1 levels. MMP-2, TIMP-2 levels and MMP-2 activity were not affected by either REMSD or uridine administration. These data show that REMSD significantly affects ECM composition which is ameliorated by uridine administration suggesting a possible use of uridine in sleep disorders.Publication Effects of citicoline administration on synaptic proteins in rapid eye movement sleep-deprived rats(Mashhad Univ Med Sciences, 2022-05-01) Çakır, Ayşen; Öcalan, Büşra; Koç, Cansu; Suyen, Güldal Güleç; Cansev, Mehmet; Kahveci, Nevzat; ÇAKIR, AYŞEN; Öcalan, Büşra; KOÇ, CANSU; CANSEV, MEHMET; KAHVECİ, NEVZAT; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; 0000-0002-6097-5585; 0000-0003-2918-5064; 0000-0003-0841-8201; A-6819-2018; LGY-8580-2024; N-9927-2019; AAG-7070-2021; M-9071-2019Objective(s): Sleep has a pivotal role in learning-memory and sleep deprivation (SD) negatively affects synaptic functioning. Cytidine-5-diphosphocholine (Citicoline) has been known to improve learning and memory functions. Our objective was to explore the effects of Citicoline on hippocampal and cortical synaptic proteins in rapid eye movement (REM) sleep-deprived rats.Materials and Methods: Rats (n=36) were randomly divided into 6 groups. Environmental control or sleep deprivation was done by placing the rat on a 13 cm diameter platform (Large Platform [LP] group) or on a 6.5 cm diameter platform (REMSD group), respectively, for 96 hours. Rats randomized for controls (Home Cage [HC] group) were followed up in home cages. Rats in each of the REMSD, LP or HC group were randomized to receive either saline (0,9%NaCl) or Citicoline (600 mu mol/kg) intraperitoneally twice a day for four days. After the experiments, rats were sacrificed; their cerebral cortices and hippocampi were dissected for analyzing the levels of pre-synaptic proteins synaptophysin and synapsin I, and the post synaptic density protein-95 (PSD-95) by Western-blotting.Results: Hippocampal levels of PSD-95, but not the pre-synaptic proteins, were reduced by REM sleep deprivation. Citicoline treatment ameliorated the reduction in PSD-95 levels in REM sleep deprived rats. On the other hand, REM sleep deprivation was not found to be significantly effective on pre-or post-synaptic proteins in cerebral cortex.Conclusion: REM sleep deprivation reduces hippocampal PSD-95 levels which are enhanced by Citicoline treatment. These data propose that Citicoline may ameliorate the adverse effects of SD on hippocampal synaptic functioning.