No abstract

In RCC, serum VEGF165 level was significantly correlated to tumor stage and grade. Increased levels were correlated to adverse survival. Although, VEGF did not remain as an independent prognostic factor in multivariate analysis the levels of VEGF165 in serum was found useful for the identification of patients with potentially progressive disease especially for those with vein invasion.

Abstract. To test the possible role of superoxide radicals in the diabetogenic action of streptozotocin, blood glucose levels were measured in mice after a single high-dose (150 mg/kg body weight) or multiple low-dose (40 mg/kg for 5 days) injections of streptozotocin. Pre-treatment 6 h before streptozotocin with 250–300 mg/kg superoxide dismutase coupled to polyethylene glycol reduced the hyperglycaemic response in mice injected with a single dose of streptozotocin. The blood glucose levels after multiple low doses of streptozotocin were not affected by superoxide dismutase-polvethvlene glycol. Enzymatically inactive superoxide dismutase did not affect the development of hyperglycaemia. The results suggest that superoxide radicals may play a role in the diabetogenic action of streptozotocin injected as a high-dose single bolus.

SummaryTo investigate pituitary effects on the vitamin K-dependent coagulation factors, female rats were hypophysectomized (hypox) and treated with growth hormone (GH), cortisone, thyroxine, vitamin K, or saline. After 11 days of treatment, the prothrombin time, platelet count, and factors II, VII, IX, and X were determined. The prothrombin time was 52.9 ± 1.2% for control rats and 39.1 ± 0.8% for hypox rats (mean ± SEM; p<0.001). All factors decreased after hypophysectomy, reaching significance for factor VII (from 264 ± 23% to 131 ± 9%; p <0.001) and factor IX (from 28.4 ± 2.2% to 17.1 ± 2.5%; p<0.01) while the platelet count was unaffected. When hypox rats were treated with GH, the prothrombin time increased to 50.9 ± 1.0% (p <0.001) and factor VII to 299 ± 10% (p<0.001). Factor II, IX, and X were slightly increased after GH substitution but not after cortisone, thyroxine, or vitamin K treatment. To summarize, GH is of importance for normal hemostasis in the female rat.

The present study examined the possibility to enhance lung cancer cell cytotoxicity and apoptosis of the anticancer drug cisplatin by exposure with adenylate cyclase (AC) toxin from Bordetella pertussis. A malignant mesothelioma cell line (P31) and a small-cell lung cancer cell line (U1690) were exposed to increasing concentrations of cisplatin and AC toxin, alone or in combination. Cytotoxicity was determined by a fluorescein-based assay and apoptosis by flow cytometry quantification of annexin V binding. Caspase-3, -8, and -9 activities were measured by enzyme activity assays. The cytotoxicity of AC toxin was time and dose dependent with an LD50 value at 72 h of 3 and 7 mg/L for P31 cells and U1690 cells, respectively. Cisplatin showed a similar time- and dose-dependent cytotoxicity, which was increased in the presence of a low toxic concentration (1 mg/L) of AC toxin. Furthermore, cisplatin caused a dose-dependent increase of annexin V binding cells of both cell lines after 24-h incubation, which was also enhanced in combination with AC toxin. AC toxin (1 mg/L) increased cisplatin-induced caspase-3, -8, and -9 activities in U1690 cells. Only minor increases of caspase-8 and -9 were noted for P31 cells. The present results, together with the knowledge that bacterial toxins decrease side effects of traditional cancer treatment, suggest a possibility to use them to enhance the therapeutic effect of cancer chemotherapy with reduced clinical adverse effects.