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    Effect of bevacizumab on acetic acid–induced ulcerative colitis in rats
    (Academic Press Inc., 2017) Özsoy, Zeki; Özsoy, Şeyma; Gevrek, Fikret; Demir, Emre; Benli , İsmail; Daldal, Emin; Yenidoğan, Erdinç
    Background The aim of this study was to examine the effect of intraperitoneally administered bevacizumab on colitis induced by acetic acid. Methods An experimental model of acetic acid–induced colitis was introduced in rats. After the induction of colitis, bevacizumab was administered intraperitoneally at two different daily doses of low (2.5 mg/kg) or high (5 mg/kg) concentration. Control groups were included for colitis and bevacizumab. After 7 d, the rats were sacrificed, and colonic tissues were harvested for macroscopic and microscopic examination of colonic damage. Tumor necrosis factor alpha, interleukin 1 beta (IL-1?), IL-6, myeloperoxidase, malondialdehyde, glutathione, and superoxidismutase values were measured biochemically. Results There was no statistically significant macroscopic improvement in damage to the colon tissues (P > 0.05). The severity of inflammation was significantly reduced (0.98 ± 0.22) in the low-dose bevacizumab–treated rat group compared with the control group (P < 0.001). The decrease in the inflammation score in the high-dose bevacizumab–treated rat group was not statistically significant (1.40 ± 0.33). In addition, although there was no significant change in the myeloperoxidase levels biochemically, IL-6 and malondialdehyde levels decreased in the low-dose treatment group (P = 0.014, P = 0.002, respectively). A significant decrease was found at both treatment doses in IL-1? (P < 0.001, P = 0.010), tumor necrosis factor alpha (P < 0.001, P = 0.015), superoxidismutase (P = 0.046, P = 0.011), and glutathione (P = 0.012 and P < 0.001) levels. Conclusions Both treatment doses of bevacizumab were observed to have a protective effect in an experimental colitis model, and the dosage of 2.5 mg/kg bevacizumab was found to have a more prominent effect. © 2017 Elsevier Inc.
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    Öğe
    eNOS and VEGF Variants Might Increase the Risk of Pancreatic Cancer
    (Pleiades Publishing Inc, 2021) Hasan Dagmura; Yigit, Serbulent; Gumusay, Ozge; Nursal, Ayse Feyda; Daldal, Emin; Karakus, Nevin
    Background: Endothelial nitric oxide synthase (eNOS) is essential in chronic inflammation and carcinogenesis. The association between variants in vascular endothelial growth factor (VEGF) and several cancers still remains uncertain. We studied whether there is a relation between eNOS/VEGF variants and risk of pancreatic cancer (PC). Materials and Methods: This prospective case-control study included 76 PC patients (28 women and 48 men) and 100 healthy controls. Blood samples from all participants were genotyped for eNOS variable number tandem repeat (VNTR) and VEGF insertion/deletion (I/D) variants by PCR. Results: There was a significant difference between groups for the eNOS intron 4 VNTR genotype distributions (p = 0.01). eNOS 4a/4b and 4b/4b genotypes were higher in patients with PC group compared to controls while eNOS 4a/4b genotype was more prevalent in control group than in patient group. Significant differences were observed between groups for the VEGF I/D variant genotype and allele frequencies (p < 0.00, and p < 0.00). VEGF I/D variant I/I genotype and I allele increased in patient group than controls. A statistically significant association was observed when the patients were compared with the controls according to D/D + D/I versus D/D (p < 0.00, OR: 0.094, 95% CI: 0.03-0.22). Conclusions: We provided evidence that eNOS VNTR and VEGF I/D variants might influence the development of PC.