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Introduction: Urological complications after kidney transplantation may lead to graft loss. In this study, we retrospectively reviewed urological complications in 1,223 kidney transplantations that were performed at our institution. Materials and Methods: The occurrence of urological complications such as urine leakage, ureteral obstruction and vesicoureteral reflux (VUR) according to the different way of urinary tract reconstruction, ureteroneocystostomy (U-C) and ureteroureterostomy (U-U), was studied. Results: Urological complications were encountered in 92 (7.5%) cases, including urine leakage (n = 43, 3.5%), ureteral obstruction (n = 35, 2.9%) and VUR (n = 14, 1.1%). 75 cases (7.9%) were in the U-C group and 17 cases (6.2%) in the U-U group. 91 recipients were successfully treated, and 1 patient lost the graft due to kidney pelvis and ureteral necrosis. There was no recipient loss due to these complications. For recipients with urological complications, the 1- and 3-year survival rates were 90 and 88% for recipients and 87 and 82% for grafts, respectively. Conclusions: After U-U, the same number of overall incidences of urological complications is observed as after U-C; however, a decrease in the number of incidences of urine leakage is apparent. Therefore, U-U is a good first option with a greater success rate of resolving ureteral stenosis with endourology and no risk of VUR. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The authors carried out a descriptive analysis of acute chemical intoxication in a large petrochemical corporation with 38,000 employees, located in a suburban district of Shanghai, China, to determine the chemicals involved and the primary causes of the incidents. Between 1977 and 1997, 350 cases of acute chemical-intoxication were recorded, resulting in a total of 541 workers with symptoms. Of these, 483 were male and 58, female, with over half the victims under 30 years old. Two hundred and seventy-five cases were serious enough to necessitate hospital admission. There were 266 cases of chemical irritation or inhalation responses (49.2%), 215 cases of mild chemical poisoning (39.7%), 31 cases of moderate poisoning (5.7%), and 29 cases resulting in critical injury (5.4%), including eight deaths (1.5%). The main causes of injury reported by patients were lack of training about safety (63%) and equipment failure (23%). The chemicals involved were asphyxiating gases (302 cases; 55.8%), irritating gases (111 cases; 20.5%), and other toxins. Intervention strategies for the prevention of acute chemical exposures were suggested to the corporation.

Mannose-terminal glucocerebrosidase prepared by exoglycosidase digestion of human placental glucocerebrosidase is reported effective in the treatment of patients with type 1 Gaucher's disease [Barton et al. (1991); N Engl J Med 324:1464-1470]. However, the amount of enzyme that is necessary for therapeutic effect is much higher than would be predicted from in vitro activity measurements. We have investigated the fate of infused enzyme following intravenous administration in Sprague-Dawley rats. In this model system, the enzyme is rapidly cleared from the plasma compartment by receptor-mediated endocytosis via the mannose-specific receptor present on reticuloendothelial cells. Enzyme activity measured in rat liver biopsy specimens at various times post-infusion revealed a rapid initial loss of approximately one-half of the maximum delivered enzyme in the first hour followed by a slower decay with a half-life of approximately 6-8 h. The loss in enzyme activity is paralleled by a loss in enzyme protein when analyzed by Western blots. There is no evidence for return of enzyme activity or inactive enzyme protein to the plasma. Incomplete integration into the lysosomal membrane was demonstrated by the use of differential extraction of purified rat liver lysosomes to distinguish between lumenal and membrane bound enzyme. Immunoelectron microscopy of rat liver following infusion of mannose-terminal glucocerebrosidase confirmed localization of the delivered enzyme primarily within the lumen of the lysosomes of Kupffer cells and to a lesser extent associated with the lysosomal membrane. Enzyme activity was stable in isolated rat liver lysosomes preloaded with mannose-terminal glucocerebrosidase and incubated in the absence or presence of ATP. Acidification of the lysosomes to pH 3 results in a rapid loss of enzyme activity and protein; however, the relationship between the in vitro loss and the loss in enzyme activity in intact liver is not clear. We conclude from these studies that rapid intracellular degradation of administered glucocerebrosidase is the prime factor responsible for the high dose required for effective treatment of Gaucher's disease.