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Contrast media (CM) is known to have nephrotoxic adverse effects. Epigallocatechin-3-gallate (EGCG) is the most abundant and active catechin in green tea, and has strong antioxidant and anti-inflammatory properties. This study investigated whether EGCG can reduce contrast-induced nephrotoxicity (CIN), alone or with glycerol (GLY)-induced renal damage, and to understand its mechanisms of protection against toxicity, using models of GLY and CIN in rats. The rats were separated into eight groups (n?=?6 in each), as follows: Healthy, GLY, CM, GLY?+?CM, CM?+?EGCG 50?mg/kg (po), GLY?+?CM?+?EGCG 50?mg/kg (po), CM?+?EGCG 100?mg/kg (po), and GLY?+?CM?+?EGCG 100?mg/kg (po). Both doses of EGCG protected against CM-induced renal dysfunction, as measured by serum creatinine and blood urea nitrogen (BUN). In addition, EGCG treatment markedly improved CIN-induced oxidative stress, and resulted in a significant down-regulatory effect on tumor necrosis factor (TNF)-α and nuclear factor (NF)-κB mRNA expression. Moreover, histopathological analysis showed that EGCG also attenuated CM-induced kidney damage. Considering the potential clinical use of CM and the numerous health benefits of EGCG, this study showed the protective role of multi-dose EGCG treatment on CIN and GLY-aggravated CIN through different mechanisms.  相似文献   
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Gastrointestinal perforation (GIP) is one of the most serious complications occurring after liver transplantation (LT), especially in pediatric patients. This study aimed to determine the risk factors affecting mortality in pediatric patients with GIP after LT. GIP developed in 37 (10%) of 370 pediatric patients who underwent LT at our institute. Patients were divided into two groups: alive (n = 22) or dead (n = 15), and both groups were compared in terms of demographic and clinical parameters using univariate analysis. There was no statistically significant difference between groups in either demographic or clinical parameters, except for perforation site (P = 0.001) and median follow‐up (P = 0.001). Stomas arose in 17 (45.9%) patients: 76% of patients with stomas and 45% of those without survived (P = 0.052). Kaplan‐Meier analysis indicated that patients with stomas had a significantly higher overall survival (P = 0.029) and that patients with duodenal and colonic perforation had a significantly lower overall survival. Multivariate analysis showed that re‐perforation was an independent risk factor for mortality (P = 0.035; OR: 17.674; 95% CI for OR: 1.233‐253.32). Although there are many options for management of GIP, including primary repair, resection plus anastomosis, and resection plus end or loop ostomy, gastrointestinal diversion is still the best option.  相似文献   
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Tumor Biology - Concomitant administration of chemotherapy and radiotherapy is currently recognized as the standard of treatment in locally advanced inoperable non-small cell lung cancer (NSCLC)....  相似文献   
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Tumor Biology - Mucosal melanoma (MM) is a rare type of cancer that differs significantly from cutaneous melanoma. In this study, we aimed to evaluate clinical and demographical characteristics,...  相似文献   
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International Urology and Nephrology - To compare the heart rate increase side effect of different antimuscarinic drugs used in overactive bladder (OAB). Overall 341 patients were consecutively...  相似文献   
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Prolonged status epilepticus may directly cause selective neuronal necrosis due to excitotoxic mechanisms, as observed in experimental models and described in case reports. A 36-year-old woman presented with right hemiplegia and aphasia following a generalised tonic-clonic status epilepticus of two hours duration. Accompanying serial MRI with advanced imaging techniques, EEG and histopathology of the cortical tissue of the patient were all compatible with excitotoxic neuronal necrosis. In this histopathologically-proven rare case of status epilepticus-induced excitotoxic neuronal injury, the observation of delayed cortical laminar necrosis on MRI, together with paroxysmal lateralised epileptiform discharges on the EEG, suggests that these changes may be an early sign of impending and ongoing excitotoxic neuronal injury and delayed cell death caused by glutamate release due to excessive neuronal firing in status epilepticus.  相似文献   
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