SUMMARYBackground: Increased insulin resistance is the major pathogenic mechanism in the development of nonalcoholic steatohepatitis. Aim: To investigate the therapeutic effect of metformin, a well-known insulin-sensitizing agent, in the treatment of non-alcoholic steatohepatitis. Methods: Thirty-six patients with non-alcoholic steatohepatitis were randomized into two groups. The first group was given lipid and calorie-restricted dietary treatment alone, and the second group was given metformin 850 mg b.d. plus dietary treatment, for 6 months. The changes in biochemical, sonographic and histological parameters were compared.

Cyclophosphamide (CP) has potential urotoxicity such as hemorrhagic cystitis (HC). 2-Mercaptoethane sulfonate (mesna) has been widely used as an effective agent against CP-induced cystitis, but significant HC has still been encountered clinically. In recent studies, mesna was shown to be more effective if combined with antioxidants. The purpose of this study was to evaluate the effects of antioxidants, alpha-tocopherol, beta-carotene and melatonin on CP-induced bladder damage in rats, even if used without mesna administration. Male Sprague-Dawley rats weighing 180-210 g were divided into 5 groups. Four groups received a single dose of CP (100 mg/kg) intraperitoneally with the same time intervals. Group 2 received CP only, group 3 received beta-carotene (40 mg/kg/day), group 4 received alpha-tocopherol (40 mg/kg/day) and group 5 received melatonin (10 mg/kg/day) both before and the day after CP injection. Group 1 served as control. Bladder histopathology, as well as malondialdehyde (MDA) and iNOS levels, and excretion of nitrite-nitrates (NO(x)) in urine were evaluated. CP injection resulted in severe histological changes and macroscopic hematuria. alpha-Tocopherol and melatonin showed meaningful protection against bladder damage. Protection by beta-carotene was also significant but weaker. MDA levels increased significantly with CP injection and all antioxidants ameliorated this increase in bladder tissue. CP also elevated the NO(x) level in urine and iNOS activity in bladder. Only melatonin was able to decrease these parameters. In conclusion, there is no doubt that oxidants have a role in the pathogenesis of CP-cystitis. Antioxidants, especially melatonin and alpha-tocopherol, may help to ameliorate bladder damage induced by CP.

Most FLLs are benign ones such as hemangiomas and cysts, which can be readily and practically characterized only by using visual assessment of DWIs without requiring time-consuming conventional and dynamic contrast-enhanced imaging sequences. Some benign lesions that are falsely interpreted as malignant can be further characterized by using conventional and contrast-enhanced MR studies.

Although histopathologic scores in treatment groups were found to be lower than in group VII, the difference was statistically significant only in group V (p < 0.001). In evaluation of oxidative stress, we found that MDA levels decreased and SOD levels increased in treatment groups in comparison with levels in group VII. Probiotic treatment alone reduced bacterial translocation. Probiotic-antibiotic combination therapy was shown to improve histopathologic scores and oxidative parameters.

Nitric oxide produced by inducible nitric oxide synthase is an important mediator in the pathogenesis of cyclophosphamide induced cystitis. Hyperbaric oxygen has a beneficial effect on repairing bladder damage rather than on bladder protection.