Tıp Fakültesi / Faculty of Medicine

Permanent URI for this collectionhttps://hdl.handle.net/11727/1403

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Subject: search.filters.subject.Pathogenesis

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    Investigation of SCGB3A1 (UGRP2) Gene Arrays in Patients with Nasal Polyposis
    (2014) Palali, Mehmet; Ozcan, K. Murat; Ozdas, Sibel; Koseoglu, Sabri; Ozdas, Talih; Erbek, Selim S.; Yildirim, Erol; Ensari, Serdar; Dere, Huseyin; https://orcid.org/0000-0003-4825-3499; 24710847; B-7604-2019
    The aim of the current study is to investigate the potential relationship between polymorphisms and nasal polyposis (NP) pathogenesis in the SCGB3A1 (UGRP2) gene, which is a member of the secretoglobin gene super family. Genotypic variations were studied by performing DNA sequencing in blood samples of 80 patients with NP and 70 healthy individuals to evaluate nucleotide changes and their positions that might be in the SCGB3A1 gene (promotor, splicing points, and exon distributions). In the SCGB3A1 gene, three single-nucleotide changes labeled IVS1-89 T > G, c. -183 G > T, IVS1-189 G > A were identified. IVS1-89 T > G and IVS1-189 G > A belong to the first intronic region of the gene, whereas c. -183 G > T was observed in the promoter region of the gene. The IVS1-89 T > G nucleotide change was observed in the patient and control groups, whereas c. -183 G > T and IVS1-189 G > A nucleotide changes were observed in the control group only. SCGB3A1 (IVS1-89) genotype frequencies between patients with NP and control group were not significantly different (p = 0.311). There was a statistically significant difference in the control group in comparison to patients with NP in terms of SCGB3A1 (c. -183 GT) and SCGB3A1 (IVS1-189 GA) frequency (p = 0.0045 and p = 0.009, respectively). The findings of the current study suggest that SCGB3A1-183 T and SCGB3A1 IVS1-189 A alleles might have a protective effect against NP, and that SCGB3A1 (-183 GT and IVS1-189 GA) genotypes should be studied in future population-based studies.
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    Association of Interleukin-10 Gene Promoter Polymorphisms with Obstructive Sleep Apnea
    (2016) Ozdas, Sibel; Ozdas, Talih; Acar, Mustafa; Erbek, Selim S.; Koseoglu, Sabri; Gokturk, Gokhan; Izbirak, Afife; https://orcid.org/0000-0003-4825-3499; 26139223; B-7604-2019
    Interleukin-10 (IL) is an anti-inflammatory cytokine that regulates normal sleep patterns, and recent studies have reported that it is a potential useful biomarker to identify presence and severity of sleep apnea syndrome (OSAS). Promoter polymorphisms of IL-10 gene have been associated with altered expression levels, which contributes to OSAS. The aim of this study was to determine the prevalence of -1082 G/A, -819 C/T, and -592 C/A promoter polymorphisms of IL-10 gene in individuals with OSAS and controls. An open-label study was performed in the Otorhinolaryngology and Sleep Disorders Outpatient Clinics. One hundred four cases with OSAS were included as the study group, and 78 individuals without OSAS were included as the controls. DNAs were extracted from peripheral blood leukocytes, and the sites that encompassed those polymorphisms were identified by DNA sequencing analyses. Data were analyzed with SNPStats and multifactor dimensionality reduction (MDR) software. The prevalence of OSAS was higher in males in the study group when compared to controls (P = 0.0003). The IL-10-1082 G/A, -819 C/T, and -592 C/A SNPs, and their minor alleles were associated with a significantly increased risk for OSAS compared to the controls (P E, 0.05 for all). Furthermore, ATA haplotype frequency was significantly higher in the study group compared to the control group, but the GCC haplotype frequency was lower (P = 0.0001 and P = 0.0001). As indicated in MDR analysis, combinations of IL-10 gene were associated with OSAS in single-, double-, and triple-locus analyses. The prevalences of the IL-10 gene promoter polymorphisms were different in OSAS patients and the controls in Turkish population. IL-10 gene polymorphisms may lead to altered inflammatory cascade, which might contribute to OSAS. Further studies on larger cohorts are needed to validate our findings.
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    Investigating the Role of IL-33 in the Pathogenesis of Behcet's Disease
    (2017) Cerci, Pamir; Altiner, Seda; Inal, Ali; Kose, Kenan; Keskin, Goksal; Olmez, Umit; 0000-0002-0690-2529; 28412856; J-8056-2012
    Objectives: Behcet's disease (BD) is an inflammatory disease, characterized by oral aphthous lesions, recurrent uveitis, skin lesions, and genital ulcerations. Increased release of several cytokines may play a role in the inflammatory stages of BD. IL-33, a member of the IL-1 cytokine superfamily, plays an important role in inflammation. We analyzed serum IL-33 concentration in BD patients to assess its possible role in the pathophysiology of this disease. Methods: The study included 54 BD patients, 31 with active BD and 23 with inactive BD as well as 18 matched healthy controls. Serum IL-33 levels were measured using an enzyme-linked immunosorbent assay (ELISA). Results: The mean serum IL-33 levels were 4.84 +/- 2.81 pg/ml in the BD patients (6.16 +/- 2.94 pg/ml in the active stage and 2.86 +/- 0.54 pg/ml in the inactive stage) and 2.88 +/- 0.42 pg/ml in the healthy controls. Serum IL-33 levels were significantly higher in patients with BD compared with the healthy controls (p < 0.01). In active Behcet patients with arthritis the mean serum IL-33 level was higher but this finding was not statistically significant (p = 0.122). Conclusion: IL-33 may play a significant role of in the pathogenesis of BD.