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Objective To report the oncologic outcomes of upper tract urothelial carcinoma treated with laparoscopic nephroureterectomy and pluck method for distal ureter resection. Materials and methods Between May 2004 and November 2015, 118 patients with upper urinary tract urothelial carcinoma received laparoscopic radical nephroureterectomy with endoscopic bladder cuff excision at our institution. The medical records were reviewed retrospectively for clinical and pathological results. Cox regression analyses were performed on factors related to oncological outcomes. Results The median follow-up was 26 months. Bladder recurrence was found in 27 patients (22.9%), extravesical retroperitoneal recurrence in four patients (3.4%), and metastases in 17 patients (14.4%). Multivariate analyses showed that male sex was associated with higher bladder recurrence [odds ratio (OR) = 2.2; 95% confidence interval (CI), 1.02–4.78; p = 0.045)], tumor size had significant correlation with locoregional recurrence (OR = 1.29; 95% CI, 1.07–3.43; p = 0.029), tumor stage was significantly correlated with subsequent metastasis (OR = 2.08; 95% CI, 1.21–3.56; p = 0.008) and overall survival (OR = 1.84; 95% CI, 1.06–3.22 ; p = 0.031), and tumor size correlated significantly with cancer-specific survival (OR = 2.57; 95% CI, 1.16–5.72; p = 0.021). Conclusions Tumor size and tumor stage were significantly associated with survival (cancer-specific and overall survival) in patients receiving nephroureterectomy with pluck method.

BackgroundOur prior study showed that resveratrol could suppress infarct volume and exert neuroprotective effect on rats subjected to focal cerebral ischemia (FCI) injury. Recently, it has been reported in some literature that resveratrol protects the spinal cord, kidney, and heart from ischemia-reperfusion injury through upregulation of nitric oxide (NO). Therefore, this study was designed to investigate the role of nitric oxide on the neuroprotective mechanisms of resveratrol on rats after FCI injury.MethodsThe FCI injury was induced by the middle cerebral artery (MCA) occlusion for 1 hour and then a 24-hour reperfusion followed in the anesthetized Long-Evans rats. Resveratrol was intravenously injected after 1 hour MCA occlusion.ResultsTreatment of resveratrol (0.1 and 1 μg/kg) decreased the lactate dehydrogenase (LDH) in plasma and malondialdehyde (MDA) in FCI injury brain tissue, whereas the level of NO in plasma was increased. In addition, resveratrol downregulated protein and mRNA expression of inducible nitric oxide synthase (iNOS), and upregulated protein and mRNA expression of endothelial nitric oxide synthase (eNOS), while the expression of protein and mRNA of neuronal nitric oxide synthase (nNOS) was unchanged. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, the nonselective NOS inhibitor) or L-N5-(1-iminoethyl)-ornithine (L-NIO, the eNOS selective inhibitor) completely blocked the effect of resveratrol in decreasing infarction volumes.ConclusionsThis study demonstrated the important role of NO in the neuroprotective effect of resveratrol in FCI injury.Clinical RelevanceIschemic brain damage is the major cause of permanent disability in young adults. It has been suggested that up to 80% of all strokes result from ischemic damage in the middle cerebral artery area. The potential for clinical application of pharmacological agents has generated enormous interest in identifying the underlying intracellular signaling pathways and to develop therapeutic strategies that can benefit ischemic stroke injury in patients. This study explored the possible involvement of nitric oxide in neuroprotective effect of resveratrol on focal cerebral ischemia injury.

Background Antioxidants effectively reduce ischemia-reperfusion (IR) injury. The cardioprotective effects of luteolin, a flavonoid that exhibits antioxidant properties and is widely available in many fruits and vegetables, were examined in rats subjected to myocardial IR injury. Methods and results Rats were subjected to myocardial ischemia or reperfusion injury to evaluate the antiarrhythmic effects of luteolin. Myocardial infarct size was determined histochemically with triphenyltetrazolium chloride staining of the left ventricle. Luteolin was administered intravenously 15min before occlusion of the coronary artery. The incidence and duration of ventricular tachycardia and ventricular fibrillation and mortality during myocardial ischemia were significantly reduced by luteolin (10µg/kg). Similarly, luteolin (1µg/kg) reduced ventricular arrhythmias and mortality during the reperfusion phase. Pretreatment with luteolin decreased plasma lactate dehydrogenase and nitric oxide (NO) levels. Luteolin (10µg/kg) significantly reduced the myocardial infarct size, as well as malondialdehyde production in tissue samples of myocardial IR injury. Luteolin also downregulated inducible NO synthase protein and mRNA expression, but did not significantly alter neuronal NO synthase or endothelial NO synthase expression. Conclusions Luteolin is capable of protecting the myocardium against IR injury. The actions of luteolin are at least partly mediated through downregulation of NO production and its own antioxidant properties.