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    The Effects of Interferon ?2b on Chemically-induced Peritoneal Fibrosis and on Peritoneal Tissue MMP-2 and TIMP-2 Levels in Rats
    (Field House Publishing Llp, 2010) Ucar, E.; Borazan, A.; Semerci, E.; Binici, D. N.; Yaldiz, M.; Aysal, A.; Altug, E.
    This study investigated the effect of interferon alpha 2b on chlorhexidine gluconate (CH)-induced peritoneal fibrosis (PF) in rats and assessed peritoneal tissue levels of metalloproteinase (MMP)-2 and tissue inhibitors of metalloproteinases (TIMP)-2. Wistar albino rats (n = 8 per group) were treated as follows: control group, 3 ml/day of 0.9% saline intraperitoneally for 28 days; CH group, 0.1% CH (200 g [3 ml]/day) in 15% ethanol and 0.9% saline intra-peritoneally for 28 days; CH + interferon (IFN) group, CH (as above) plus pegylated IFN-alpha 2b 1.5 mu g/kg per week subcutaneously on days 0, 7, 14, 21 and 28; IFN group, pegylated IFN-alpha 2b (as above). Parietal peritoneum samples were obtained from the left anterior abdominal wall after 35 days. Parietal thickness, degree of vascular proliferation and inflammation, and MMP-2 and TIMP-2 levels were determined. The mean peritoneal thicknesses of the control, CH, CH + IFN and IFN groups were 7.02 +/- 3.89, 156.86 +/- 29.13, 59.88 +/- 22.1, 9.27 +/- 2.03 mu m, respectively. Pegylated IFN-alpha 2b decreased CH-induced expression of MMP-2 in the parietal peritoneum, but had no effect on TIMP-2 levels. Further studies are needed to determine the optimal dosage and duration for pegylated IFN-alpha 2b treatment.
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    Öğe
    GENOMIC DAMAGE IN PATIENTS WITH TYPE-2 DIABETES MELLITUS
    (Medecine Et Hygiene, 2013) Binici, D. N.; Karaman, A.; Coskun, M.; Ogiu, A. Uyanik; Ucar, F.
    Genomic damage in patients with type-2 diabetes mellitus: DNA damage seems to play a role in the pathogenesis of type-2 diabetes mellitus (DM2) and its complications. Several in vitro assays have been used to measure the DNA damage. In the present study, we aimed to investigate the frequency of sister chromatid exchange (SCE) and micronuclei (MN) in DM2 patients compared with healthy controls. SCE and MN tests were carried out with the blood-cell cultures from 50 DM2 patients and 30 healthy, age- and sex-matched control subjects. The mean age of the DM2 patients was 58.12 +/- 13.39 years, with a mean duration of the diabetes of 5.40 +/- 4.32 years. The mean level of HbA1c of the DM2 patients was 8.93 +/- 2.56. Patients with DM2 showed a higher frequency of SCE compared with controls (7.11 +/- 1.14 and 4.96 +/- 0.92, p<0.001). Furthermore, the SCE frequency was positively correlated with the plasma HbA1c level (p< 0.05), but there was no significant correlation between the duration of diabetes and SCE. On the other hand, our result showed a MN frequency significant increase in DM2 patients (3.45 +/- 1.01 per 1000 cells) relative to that of the control group (1.79 +/- 0.67 per 1000 cells) (p<0.001), but there was no significant correlation between the duration of diabetes, HbA1c and MN. In conclusion, these results suggest that DM2 is a condition with genomic instability characterized by an increased level of SCE and MN. Hyperglycemia-induced oxidative stress may be the underlying factor of the increased SCE and MN frequency.