Tıp Fakültesi / Faculty of Medicine
Permanent URI for this collectionhttps://hdl.handle.net/11727/1403
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Item Role of the MyD88 Dependent Pathway in Degenerative Disc Disease(2023) Akgun, Mehmet Yigit; Akyol, Sibel; Ozlen, Fatma; Alizada, Orkhan; Cetintas, Semih Can; Turk, Okan; Hanci, Murat; 0000-0003-0942-9906; 37144651; E-1210-2019AIM: To define the substantial role of the TLR4 signaling pathway in the MyD88-dependent pathway, and to evaluate the results of TLR4 activation in nucleus pulposus cells. Moreover, we aim to associate this pathway with intervertebral disc degeneration and magnetic resonance imaging (MRI) findings. Additionally, the clinical differences among patients and the effects of their drug use will be evaluated. MATERIAL and METHODS: Eighty-eight adult male patients with lower back pain and sciatica underwent MRI studies, which showed degenerative changes. Disc materials were obtained intraoperatively from those who underwent surgery for lumbar disc herniation. These materials were kept in freezers at -80 degrees C without any delay. Then, the collected materials were examined using enzyme-linked immunosorbent assays. RESULTS: Modic type I degeneration had the highest values of all markers, whereas Modic type III degeneration had the lowest values. These results verified that this pathway plays an active role in MD. Moreover, contrary to the current knowledge on which Modic type inflammation is more dominant, we showed that it is the Modic type I phase. CONCLUSION: The most intense inflammatory process was observed in Modic type 1 degeneration, and the MyD88-dependent pathway was found to play a key role. While the most intense molecular increase was detected in Modic type 1 degeneration, the lowest levels were observed in Modic type III degeneration. It has been observed that the use of nonsteroidal anti-inflammatory drugs affects the inflammatory process through the MyD88 molecule.Item Effect of Smoking on Peripheral Blood Lymphocyte Subsets of Patients With Chronic Renal Failure(2016) Birben, Ozlem Duvenci; Akcay, Sule; Sezer, Siren; Sirvan, Sale; Haberal, Mehmet; 0000-0002-8360-6459; 0000-0002-3462-7632; 27805522; AAB-5175-2021; AAJ-8097-2021Objectives: Smoking is known to suppress the immune system. It is also known that chronic renal failure affects the immune system. However, the number of studies investigating the effects of chronic renal failure and smoking together is limited. In our study, we examined whether smoking affects the diminished response of the immune system in patients with chronic renal failure. Materials and Methods: We compared peripheral blood lymphocyte subsets in smoking and nonsmoking patients with chronic renal failure. We also used the Fagerstrom Test for Nicotine Dependence to evaluate its correlation with the lymphocyte subset count in patients who are current smokers. Results: Our study included 126 patients with chronic renal failure. According to their smoking habits, patients were divided into 2 groups: smokers and nonsmokers. The average age of patients who were smokers was 53.2 +/- 1.5 years, with average age of nonsmokers being 59.2 +/- 2.2 years. The average duration of smoking in smokers was 30.7 +/- 2.7 pack-years. We found that the percentage of cluster of differentiation 16-56 cells (natural killer cells) and lymphocyte percentage were significantly lower among smokers in our study (P < .05). We compared the lymphocyte subset panel to pack-years and found that the rate of cluster of differentiation 16-56 cells decreased as smoking duration increased. Conclusions: Our study revealed that smoking suppresses the immune system, as measured by lymphocyte subsets, in patients with chronic renal failure, similar to that shown in healthy smokers. According to our findings, patients with chronic renal failure, where infection is the primary reason for mortality and morbidity, must be questioned for smoking and referred to smoking cessation clinics. Because of its immunosuppressive effects, smoking behaviors must be solved preoperatively in transplant candidates.Item Novel inflammatory targets for immunotherapies in pediatric patients with trichotillomania(2020) Kutuk, Meryem Ozlem; Tufan, Ali Evren; Kilicaslan, Fethiye; Mutluer, Tuba; Gokcen, Cem; Karadag, Mehmet; Yektas, Cigdem; Kandemir, Hasan; Buber, Ahmet; Aksu, Gulen Guler; Topal, Zehra; Giray, Asli; Celik, Fatma; Acikbas, Ufuk; Kutuk, Ozgur; 0000-0002-2918-7871; 32113788; AAI-9626-2021Immune dysregulation may be important in the etiology of obsessive-compulsive and related disordersandbody-focusedrepetitivebehaviors, such as Trichotillomania (TTM). The role of inflammation and inflammatory markers in TTM has received relatively little attention. This study was aimed to determine the expression levels of inflammatory markers (i.e. IL-1 beta, IL-1 alpha, IL-4, IL-6, IL-17, TNF-alpha and TGF-5) in peripheral blood mononuclear cells of children with TTM and healthy controls and to evaluate their association with clinical variables. Seventy-seven patients with TTM and 107 healthy controls were enrolled in the study. Peripheral blood was collected in standardized conditions. The mean age of patients and controls did not differ significantly (10.8 +/- 4.4 and 12.0 +/- 3.2 years; respectively). The majority of patients with TTM and controls were females (n = 55, 71.4 % and n = 55, 51.4 %; respectively); with a greater preponderance of females among TTM. Patients with TTM had significantly elevated expression levels of TNF-alpha, IL-6 and IL-17 compared to controls. However, the expression level of IL-4 was significantly reduced in TTM patients compared to controls. Accordingly, we found a proinflammatory state in TTM and those findings may suggest novel treatment options for TTM and further, crossdisciplinary studies focusing on neuro- inflammation in TTM conducted on larger samples are needed.Item Cytokine expression profiles in Autism spectrum disorder: A multi-center study from Turkey(2020) Kutuk, Meryem Ozlem; Tufan, Evren; Gokcen, Cem; Kilicaslan, Fethiye; Karadag, Mehmet; Mutluer, Tuba; Yektas, Cigdem; Coban, Nurdan; Kandemir, Hasan; Buber, Ahmet; Coskun, Seyma; Acikbas, Ufuk; Guler, Gulen; Topal, Zehra; Celik, Fatma; Altintas, Ebru; Giray, Asli; Aka, Yeliz; Kutuk, Ozgur; 0000-0002-2918-7871; 0000-0001-9854-7220; 0000-0003-2735-4805; 32563959; AAI-9626-2021; AAH-1671-2019; G-8832-2015Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder characterized by impairments in communication and social interaction as well as restricted interests and repetitive behaviors. The pathogenesis of ASD is not completely understood, but a growing body of research has demonstrated that the immune response may be a contributing factor in the etiology and/or ontogeny of ASD. The aim of this study was to determine the expression levels of IL-1 beta, IL-1 alpha, IL-4, IL-6, IL-17, TNF-alpha and TGF-beta in peripheral blood mononuclear cells of children with ASD and healthy controls in order to determine the contributions of cytokines to ASD. Within the study timeframe, 195 children with ASDs (80.5% male) and 162 controls (73.6% male) were enrolled. Most children with ASD had a comorbid disorder (n = 114, 58.5%), with the most common diagnoses as Intellectual Developmental Disorder (IDD, n = 64, 32.8%) and ADHD (n = 64, 32.8%). The majority of children with ASD had severe autistic symptoms as evaluated via Childhood Autism Rating Scale (CARS, n = 130, 64.6%). The mean CARS score in the ASD sample was 40.8 (S.D. = 7.6). The patients with ASD were found to have significantly higher levels of IL-6 (p < 0.001) and significantly lower levels of IL-17 (p < 0.05, all Bonferroni corrected). Treatment tended to affect IL-4 levels. Lastly, discriminant function analysis (DFA) revealed that a combination of IL-6, IL-17 and IL-1 alpha correctly classified 56.6% of cases. Despite extensive immunological evidence suggesting immune system aberrations, further research is required to clarify the relationship between immune profiles and ASD symptoms.