Fakülteler / Faculties
Permanent URI for this communityhttps://hdl.handle.net/11727/1395
Browse
7 results
Search Results
Item Hyperviscosity in Renal Transplant Recipients(2015) Tutal, E.; Uyar, M. Erkmen; Uyanik, S.; Bal, Z.; Guliyev, O.; Toprak, S. K.; Ilhan, O.; Sezer, S.; Haberal, M.; 0000-0002-3462-7632; 0000-0001-7717-5827; 26036545; AAJ-8097-2021; H-9131-2012; IAO-2608-2023; AAZ-5795-2021; ABC-8182-2021Objective. The resistance of blood to flow is called plasma viscosity. Increased blood viscosity has been described in patients with coronary and peripheral arterial disease. In this study, we evaluated the influence of clinical and laboratory findings on plasma viscosity in renal transplant recipients. Methods. Eighty-one kidney transplant recipients (37.8 +/- 11.3 years old, 50.38 +/- 16.8 months post-transplantation period, 27 female) with normal graft functions were enrolled. The biochemical and clinical parameters in the 1st year after transplantation were retrospectively recorded, and graft function was evaluated by means of the yearly decline in eGFR. Plasma viscosity was measured and searched for the association with cross-sectionally analyzed cardiovascular parameters including body composition analyses, ambulatory blood pressure monitoring (ABPM) data, and pulse-wave velocity. Results. Patients were divided into 2 groups according to the median value of serum viscosity. Patients with high viscosity had higher serum low-density lipoprotein (P = .042) and C-reactive protein (P = .046) levels than lower viscosity group. In ABPM, daytime (P = .047) and office systolic (P = .046) blood pressure levels and left ventricular mass index (LVMI; P = .012) were significantly higher in patients with hyperviscosity. Patients with high viscosity had higher hip circumference (P = .038) and fat mass (P = .048). Estimated glomerular filtration rate decline was significantly higher in high-viscosity patients than in patients with low viscosity levels (12.9% vs 17.2%; P = .001) at 2 years' follow-up. Conclusions. We suggest that the hyperviscous state of the renal transplant recipients may arise from the inflammatory state, hypertension, and increased fat mass and increased LVMI. Hyperviscosity is also closely related to renal allograft dysfunction.Item Brain-Derived Neurotrophic Factor Levels in Children with Asthma and Isolated Chronic Cough(2016) Guc, Belgin Usta; Asilsoy, Suna; Cihan, Fatma Goksin; https://orcid.org/0000-0002-9432-3008; HOH-3400-2023; AAM-7975-2020Studies show that neurogenic inflammation is implicated in the pathogenesis of chronic cough. Neurotrophins (NTs) regulate the synthesis of neuropeptides, which cause neurogenic inflammation. There is growing evidence suggesting their involvement in airway inflammation. The role of the brain-derived neurotrophic factor (BDNF), a member of the NT family, is not clear in chronic cough. The aim of this study was to evaluate the role of BDNF in children with nonspecific isolated chronic cough and to compare the differences between patients with asthma and healthy controls. In this case-control study, we included 30 patients with chronic cough (5-15 years) as the patient group. As the control group, 28 asthma patients under control, 30 children with asthma attacks, and 30 healthy children were included. Serum BDNF levels were measured by ELISA in all groups. The median of BDNF levels was 708.12 pg/mL (155-974) in the patient group, 952.94 pg/mL (220-1,018) in the controlled asthma group, 852.09 pg/mL (355-1,036) in the uncontrolled asthma patients, and 572.65 pg/mL (213-818) in the healthy children group. There were differences in the patient group and control groups regarding the BDNF levels (for the patient group and the controlled asthma group, P = 0.0014; for the patient group and the uncontrolled asthma patients, P = 0.0009; for the patient group and healthy children group, P = 0.05). The BDNF levels of asthma patients were statistically different from healthy children (P = 0.0001). Neurogenic inflammation was implicated in the pathogenesis of chronic cough. In patients with chronic cough, high BDNF levels may support the presence of asthma.Item Optogenetic Spreading Depression Elicits Trigeminal Pain and Anxiety Behavior(2020) Harriott, Andrea M.; Chung, David Y.; Uner, Aylin; Bozdayi, Refik O.; Morais, Andreia; Takizawa, Tsubasa; Qin, Tao; Ayata, Cenk; 33016466Objective Cortical spreading depression (SD) is an intense depolarization underlying migraine aura. Despite the weight of evidence linking SD to the pain phase of migraine, controversy remains over a causal role of SD in cephalgia because of the invasive nature of previous SD induction methods. To overcome this problem, we used a novel minimally invasive optogenetic SD induction method and examined the effect of SD on behavior. Methods Optogenetic SD was induced as a single event or repeatedly every other day for 2 weeks. End points, including periorbital and hindpaw mechanical allodynia, mouse grimace, anxiety, and working memory, were examined in male and female mice. Results A single SD produced bilateral periorbital mechanical allodynia that developed within 1 hour and resolved within 2 days. Sumatriptan prevented periorbital allodynia when administered immediately after SD. Repeated SDs also produced bilateral periorbital allodynia that lasted 4 days and resolved within 2 weeks after the last SD. In contrast, the hindpaw withdrawal thresholds did not change after repeated SDs suggesting that SD-induced allodynia was limited to the trigeminal region. Moreover, repeated SDs increased mouse grimace scores 2 days after the last SD, whereas a single SD did not. Repeated SDs also increased thigmotaxis scores as a measure of anxiety. In contrast, neither single nor repeated SDs affected visuospatial working memory. We did not detect sexual dimorphism in any end point. Interpretation Altogether, these data show a clinically congruent causal relationship among SD, trigeminal pain, and anxiety behavior, possibly reflecting SD modulation of hypothalamic, thalamic, and limbic mechanisms. ANN NEUROL 2020Item Antiproliferative and anti-apoptotic effect of astaxanthin in an oxygen-induced retinopathy mouse model(2019) Kucukoduk, Ali; Helvacıoglu, Fatma; Haberal, Nihan; Dagdeviren, Atilla; Bacanli, Didem; Yilmaz, Gursel; Akkoyun, Imren; 0000-0001-8990-8282; 30851776; P-2877-2014Objective: To evaluate the impact of intravitreal (IV) and intraperitoneal (IP) astaxanthin (AST) injections on neovascular development (ND), retinal morphology, and apoptotic activity in a C57BL/6J mouse model with hyperoxia-induced retinopathy (HIR). Design: C57BL/6J mouse model. Methods: Two negative control groups (n = 6 each; one of which received IV sterile dimethyl sulfoxide [DMSO]) of C57BL/6J-type mice were exposed to room air. The HIR groups included 36 C57BL/6J-type mice exposed to 75% +/- 2% oxygen from postnatal day (PD) 7 to PD 12. On PD 12, these mice were randomized into 6 groups (n = 6 each): 2 HIR control groups (one of which received IV-DMSO), 2 IV-AST groups (10 and 100 mu g/mL), and 2 IP-AST groups (0.5 and 5 mg/kg). We measured ND by counting neovascular tufts in cross sections and examined histological, ultrastructural changes via light and electron microscopy. Apoptosis was detected using terminal deoxynucleotidyl transferase-mediated nick end-labeling. Results: No ND was detected in the negative control groups. ND levels were not significantly different between high- and low-dose AST for either means of administration. However, ND levels were significantly lower in the AST groups, regardless of delivery, compared to the control groups. The means of delivery (IP versus IV) also yielded significant differences in ND. The incidence of mitochondrial dysmorphology and apoptosis were lower in groups receiving AST. Conclusions: AST seems to suppress ND and has anti-apoptotic activity in the HIR mouse model.Item Quantitative Data for Transcutaneous Electrical Nerve Stimulation and Acupuncture Effectiveness in Treatment of Fibromyalgia Syndrome(2019) Yueksel, Merve; Ayas, Sehri; Cabioglu, Mehmet Tugrul; Yilmaz, Derya; Cabioglu, Cagri; 0000-0002-1903-7132; 0000-0002-5078-6529; 30949223Aim. To evaluate the effects of acupuncture and transcutaneous electric nerve stimulation (TENS) applications on the quantitative electroencephalography (qEEG) changes and to evaluate their therapeutic effects in patients with fibromyalgia syndrome (FMS). The study included 42 patients with FMS and 21 healthy volunteers. The patients were randomly assigned to two groups (n=21 in each) to undergo either TENS or acupuncture application. In both acupuncture and TENS groups, baseline electroencephalography (EEG) recording was performed for 10min and, then, TENS or acupuncture was performed for 20min, followed by another 10min EEG recording. Baseline qEEG findings of FMS patients in the TENS and acupuncture groups were similar. Delta and theta powers over the frontal region of FMS patients were lower than controls. Theta powers of right posterior region were also lower than controls. In the TENS group, after the treatment, an increase was observed in the alpha power of the left anterior region as well as a decrease in pain scores. In the acupuncture group, an increase was determined in the alpha power of the right and left posterior regions as well as a decrease in pain score after the treatment. The power of low- and moderate-frequency waves on resting EEG was decreased in the patients with FMS. Decreased pain and increased inhibitor activity were found on qEEG after TENS and acupuncture applications. In conclusion, both TENS and acupuncture applications seem to be beneficial in FMS patients.Item Therapeutic Potential of Apigenin, a Plant Flavonoid, for Imatinib-Sensitive and Resistant Chronic Myeloid Leukemia Cells(2014) Solmaz, Soner; Gokbulut, Aysun Adan; Cincin, Birsu; Ozdogu, Hakan; Boga, Can; Cakmakoglu, Bedia; Kozanoglu, Ilknur; Baran, YusufDespite the presence of many therapeutic regimens like imatinib and other tyrosine kinase inhibitors, the development of resistance, intolerance, and side effects makes chronic myeloid leukemia (CML) therapy challenging. Thus, there is a need to discover novel drugs for CML patients. In this study, we attempted to assess apigenin, a common plant dietary flavonoid, in terms of its cytotoxic, apoptotic, and cytostatic effects on imatinib-sensitive and resistant Philadelphia-positive CML cells. We analyzed apigenin's effects on cell proliferation, apoptosis, caspase-3 activity, loss of mitochondrial membrane potential, and cell cycle progression in K562 and K562/IMA3 cells. Furthermore, we described genes and gene networks that are modulated in CML in response to apigenin. Results of our study revealed that apigenin has cytotoxic and apoptotic effects on both cell types. We also displayed that apigenin induced G2/M arrest in K562 cells while arresting K562/IMA3 cells in S phase especially at the highest apigenin concentration. The expression analysis identified a set of genes that were regulated by apigenin in K652 and K562/IMA3 cells. Association of modulated genes with biological functional groups identified several networks affected by apigenin including cell survival, proliferation, cell death, cell cycle, and cell signalling pathways.Item Biphasic ROS production, p53 and BIK dictate the mode of cell death in response to DNA damage in colon cancer cells(2017) Kutuk, Ozgur; Aytan, Nurgul; Karakas, Bahriye; Kurt, Asli Giray; Acikbas, Ufuk; Temel, Sehime Gulsun; Basaga, Huveyda; 0000-0001-9854-7220; 28796811; AAH-1671-2019Necrosis, apoptosis and autophagic cell death are the main cell death pathways in multicellular organisms, all with distinct and overlapping cellular and biochemical features. DNA damage may trigger different types of cell death in cancer cells but the molecular events governing the mode of cell death remain elusive. Here we showed that increased BH3-only protein BIK levels promoted cisplatin-and UV-induced mitochondrial apoptosis and biphasic ROS production in HCT-116 wild-type cells. Nonetheless, early single peak of ROS formation along with lysosomal membrane permeabilization and cathepsin activation regulated cisplatin-and UV-induced necrosis in p53-null HCT-116 cells. Of note, necrotic cell death in p53-null HCT-116 cells did not depend on BIK, mitochondrial outer membrane permeabilization or caspase activation. These data demonstrate how cancer cells with different p53 background respond to DNA-damaging agents by integrating distinct cell signaling pathways dictating the mode of cell death.