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Background: The purpose of the present paper was to investigate the expression level of thymidine phosphorylase (TPase) in superficial bladder cancer tissues obtained by transurethral resection, and determine whether its expression correlates with tumor recurrence. Methods: From March 1998 to December 2001, 99 patients with superficial bladder cancer were diagnosed and treated at eight affiliated hospitals. Tissue specimens obtained by transurethral resection of superficial bladder cancer (TURBT) were applied to immunohistochemical study using anti-TPase antibody as well as pathological diagnosis. The data were subjected to statistical analysis. Results: Using MoAb 654-1 as the primary antibody, TPase was clearly stained in human bladder cancer tissues. The maximum TPase level measured by enzyme-linked immunosorbent assay (ELISA) method in normal bladder tissues was 18.7 U/mg protein. The TPase activity was 2.8-fold higher in tumors than in normal bladder samples (P = 0.037). The TPase positivity rates determined by immunohistochemical and ELISA methods were distinctly correlated (P = 0.046). For the recurrence-free rates in pT1 tumors treated by TURBT alone (n = 46), there were no statistically significant differences between Tpase-positive or -negative cases. Conclusions:The TPase expression determined by ELISA and immunohistochemistry is significantly up-regulated in superficial bladder tumors compared with normal bladder samples. However, TPase expression by immunohistochemistry is not a predictive index of recurrence-free rate for superficial bladder cancer treated with TURBT alone.

Two unrelated boys with mild persistent proteinuria and underexcretory-type hyperuricemia of more than 9.0 mg/dl (535 μmol/l) are described. The proteinuria was detected at age 10 and 6 years, respectively. The fractional excretion of uric acid in both was low at 2–3%, when the creatinine clearance was decreased by about 50%. Tissue examination revealed focal interstitial fibrosis in both patients and medullary urate crystals in one patient in whom medullary tissue was obtained on biopsy. An immunofluorescence study was negative for immunoglobulins, complements and fibrin. Treatment of hyperuricemia did not prevent further deterioration of their renal function. One of them underwent a renal transplantation and then his serum uric acid level returned to the normal range. Neither patient had a family history of hyperuricemia, gout or inherited progressive renal disease. Both patients are likely to be sporadic cases of familial nephropathy with gout, an autosomal dominant disease, due to a new mutation. Hyperuricemia due to diminished uric acid clearance may be a risk factor or predictor for the development of progressive renal disease in some subjects.

SUMMARYThe eflect of administration of FK506 at 1 mg/kg body weight for 14 days on rat lymphoid tissues, especially the thymus. and recovery after discontinuation of treatment, were investigated by the immunoperoxidase technique and flow cytofluoromciry using monoclonal antibodies 0X6. OX7. OX8. OX18 and W3/25. reactive with rat lymphocytes. Marked reduction of the thymic medulla upon treatment was clearly demonstrated by staining with OX18 and OX6. Changes produced by FK506 were also observed in the cortical area ofthe thymus, and were especially marked in the subcapsular area and around blood vessels. Eventually, the thymic cortex appeared patchy, this change heing maximal 14 days after the start of administration. Obvious restitution of the thymic medulla was evident about 14 days after withdrawal of FK506. Flow cytometrJc analysis of the Ihymus showed that the jwrcentages of cells labelled positively with OX7. OX8 and W3/25 were increased with FK306 treatment, and recovered to the normal levels soon after withdrawal. Furthermore, the peak of fiuorescence intensity of OX7*. 0X8' and W3/25+ cells showed a temporary shift to the right during r-K506 treatment; however, the peak of fluoreseence intensity of OX 18 ' cells showed a temporary shift to the left. Treatment with FK506aiso produced a significant change in 'H-thymidine uptake by thymocyte. These results suggest that FK506 may inhibit the proliferation, maturation and difl'erentiation of thymocytes. However, thymocytes prepared from FK506-treated rats and labelled with FITC behaved similarly to rat thymocytes in normal recipient rats. This suggests that during FK506 treatment thymocytes may retain their potential for peripheral mobilization.

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