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    Comparing the effects of fluticasone, anti-IgE and anti-TNF treatments in a chronic asthma model
    (Elsevier Doyma Sl, 2018) Ozkars, M. Y.; Keskin, O.; Tokur, M.; Ulasli, M.; Gogebakan, B.; Ciralik, H.; Kucukosmanoglu, E.
    Background: Corticosteroids are used in the treatment of asthma. The aim of this study was to determine the efficacy of anti-IgE and anti-TNF alpha as asthma treatments. Methods: A mouse model of chronic asthma was developed. The fluticasone group was exposed to fluticasone and the anti-IgE and anti-TNF groups were administered anti-IgE or anti-TNF. IL-4, and IgE levels were measured, and histological analysis, pathological analysis and miRNA-126, miRNA-133a analyses were applied. Results: The cell concentration in the BAL fluid decreased in all the treatment groups. The rate of perivascular and peribronchial cell infiltration decreased in the lung in the high-dose anti-IgE and anti-TNF groups. Smooth muscle thickness decreased in the lung tissue in the low dose anti-IgE and anti-TNF groups. Bronchial wall thickness decreased in the lung tissue in the fluticasone + antidgE group. The IL-4 level in BAL fluid decreased in the high-dose anti-IgE, fluticasone + anti-IgE and anti-TNF groups. IgE levels increased in the BAL fluid in the high dose anti-IgE and anti-TNF groups. The lymphocyte level increased in the BAL fluid in the high-dose anti-IgE group. The macrophage level decreased in the BAL fluid in the anti-TNF group. The relative expression of miRNA-126 increased in all groups. The relative expression of miRNA-133a decreased in the placebo and fluticasone groups. The relative expression of miRNA133a increased in the low-dose anti-IgE, high-dose anti-IgE, fluticasone + anti-IgE and anti-TNF groups. Conclusions: The results showed that anti-IgE is successful as a treatment. Fluticasone + antiIgE and anti-TNF were seen to be superior to other therapeutic modalities when used for prophylaxis. (C) 2017 SEICAP. Published by Elsevier Espana, S.L.U. All rights reserved.
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    Reduced gene expression of bikunin as a prognostic marker for renal cell carcinoma
    (Morion LLC, 2014) Bayraktar, E.; Igci, M.; Erturhan, S.; Igci, Y.Z.; Karakok, M.; Gogebakan, B.; Ulasli, M.
    Aim: Experimental and clinical studies showed that bikunin, a Kunitz-type protease inhibitor, found in urine and amniotic fluid has a role in spread of tumor cells by providing a significant reduction in the levels of urokinase-type plasminogen activator (uPA) and its specific receptor urokinase-type plasminogen activator receptor (uPAR). The aim of this study was to investigate expression of bikunin at the mRNA level and screen for mutations in exon sequence in renal cell carcinoma (RCC) tissues. Materials and Methods: Total RNA and DNA were extracted from paired normal and tumor tissues of total 50 RCC (11 papillary, 8 chromophobe, 26 clear cell, and 5 other types) patients (23 females, mean age: 53.55 ± 14.17; 27 males mean age: 62.1 ± 7.92). Bikunin mRNA levels were detected using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Mutational screening was performed by using single strand conformation polymorphism (SSCP) method and nucleotide sequence analysis. Results: There was a statistically significant decrease in the 25 (50%) of tumor tissues comparing to normal tissues in terms of mRNA levels of bikunin (Wilcoxon signed rank test, p = 0.0337). According to the classification based on subtypes of RCC; clear cell RCC samples displayed a reduced gene expression (p = 0.0148). Additionally, the patients with the age above 50 had low bikunin expression. The SNP rs80057939 spanning 4th exon of bikunin was detected in 13 tumor tissues. However, it was not statistically significant (p > 0.05). Conclusion: Decreased bikunin mRNA level in renal cells might be associated with poor prognosis of renal carcinoma. Therefore, gene constructs or exogenous administration of bikunin might be a potential adjuvant therapy for RCC treatment. Copyright © Experimental Oncology, 2014.
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    The role of bronchial epithelial cell apoptosis in the pathogenesis of COPD
    (Springer, 2014) Gogebakan, B.; Bayraktar, R.; Ulasli, M.; Oztuzcu, S.; Tasdemir, D.; Bayram, H.
    There is an increased airway inflammation in the pathogenesis of chronic obstructive pulmonary disease (COPD), and it has been suggested that there may also be problem in the apoptosis and renewal of cells. However, there are limited human airway cell studies, in particular those from larger airways such as bronchi. We cultured primary human bronchial epithelial cells (HBECs) from bronchial explants of smokers (n = 6) without COPD and smokers with COPD (n = 8). Apoptosis was studied by fluorescence activated cell sorting. qRT-PCR was used to assess mRNA expression for proteins involving apoptosis including p21(CIP1/WAF1), p53, caspase-8 and caspase-9. Although there was no difference in the rate of viable cells between cells from smokers and COPDs, the level of early apoptotic cells was significantly increased in COPD cells [mean +/- A standard error of mean (SEM) = 4.86 +/- A 3.2 %, p = 0.015] as compared to smokers (mean +/- A SEM = 2.71 +/- A 1.62 %). In contrast, the rate of late apoptotic cells was significantly decreased in COPD cells (mean +/- A SEM = 9.82 +/- A 5.71 %) comparing to smokers (mean +/- A SEM = 15.21 +/- A 5.08 %, p = 0.003). Although expression of mRNA for p21(CIP1/WAF1) and caspase-9 was similar in both groups, p53 and caspase-8 mRNA expression was significantly greater in COPD cells. These findings suggest that HBEC apoptosis is increased in COPD, and that this involves p53 and caspase-8 pathways.