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    Free radical-induced damage in experimental peripheral nerve injection injury
    (Thieme Medical Publ Inc, 2003) Saray, A; Apan, A; Kisa, U
    Peripheral nerve injury secondary to injection of therapeutic agents is well-documented. Until recently, the precise mechanism of injury has been obscure; even today, the treatment of these nerve injection injuries remains controversial. The aim of this study was to determine the involvement of ischemia-reperfusion injury in the development of peripheral nerve injection injury. Wistar rats were randomized into three groups. Sciatic nerve was used as the standardized nerve injection injury model. Two commonly used agents, lidocaine HCl 1 percent and phenol 5 percent, were tested for their comparative effects on the sciatic nerve. Lidocaine and phenol were injected,into the sciatic nerves of the rats in Groups 1 and 2, respectively. Physiologic saline was used in the controls (Group 3). All the agents were injected intrafascicularly. The effects of nerve injection injury were assessed by measuring thiobarbituric acid reactive substance (TBARS) levels and obtaining walking-track analyses (WTA). Nerve injection caused significant increases in TBARS levels, which were correlated with the severity of the injury. The TBARS levels were related to the severity of injury caused by the tested agents; TBARS levels in phenol-injected nerves were significantly higher than those of lidocaine-injected nerves. Patterns of alterations in TBARS levels also paralleled the changes in print-length factor. Injection of lidocaine and phenol resulted in near-normal walking tracks at 8 and 12 weeks, respectively, while saline injection caused only transient impairment in walking tracks. These findings indicate that reactive oxygen species are involved in the pathogenesis of experimental peripheral nerve injection injury. Indices of free oxygen radical damage correlate with the progression of functional alterations after nerve injection injury.
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    Investigation (in vivo and in vitro) of booster dose requiremet for long-term protection against hepatitis B virus infection
    (Elsevier Science Bv, 2002) Saygun, O.; Eyigun, C.P.; Avci, I.Y.; Kisa, U; Pahsa, A.
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    Testicular tissue nitric oxide and thiobarbituric acid reactive substance levels: evaluation with respect to the pathogenesis of varicocele
    (Springer, 2004) Kisa, U; Basar, MM; Ferhat, M; Yilmaz, E; Basar, H; Caglayan, O; Batislam, E
    The aim of the present study is to evaluate tissue nitric oxide (NO) and thiobarbituric acid reactive substance (TBARS) levels in testicular tissue, and to determine their relationship with seminal parameters in order to explain possible effects on varicocele pathophysiology.Ten adult male Wistar rats at 8 weeks old underwent partial left renal vein ligation. A sham operation was performed on control rats in a second group of another ten rats. All animals were killed 4 weeks after surgery. The testes were removed and histological changes were observed by light microscopy with haematoxylin and eosin stain on half of each testis. The rest of testis was used for the evaluation of testicular tissue NO and TBARS levels. Epididymal aspirated seminal plasma was used for semen analysis and morphological analysis was carried out according to Kruger's criteria. Statistical analysis was performed by using Mann-Whitney U-tests and Spearman rank correlations between the two groups for NO and TBARS levels and for seminal parameters. Testicular tissue NO and TBARS levels (mean+/-SEM) were 62.8+/-10.1 mumol/g protein and 4.7+/-0.3 nmol/g protein in group 1. These parameters were 16.9+/-2.2 mumol/g protein and 3.1+/-0.2 nmol/g protein in the group 2 controls. There were significant differences between these parameters (P-NO=0.000, P-TBARS=0.001). Although a positive and significant correlation between testicular tissue NO and TBARS levels was found (r(s)=0.739, P=0.014), there was only a strong negative correlation between NO levels and sperm motility in group 1 (r(s)=-0.815, P=0.004). We found that this effect of NO on sperm motility was independent from TBARS levels after regression analysis (r(2)=-0.687, beta=0.825, P=0.034). Although there were statistically significant differences in seminal parameters between the two groups, there was no difference between them in the histopathological examination. We found that sperm motility was significantly related to testicular tissue NO levels only. Thus, we suggest that NO is an important mediator in the pathogenesis of varicocele. TBARS and other substances have been effective via NO pathways.