No abstract

The urinary transforming growth factor beta (TGF-β) excretion was measured in 33 patients including 10 with systemic lupus erythematosus (SLE), 8 with focal glomerular sclerosis (FGS), 9 with IgA nephropathy (IgAN), and 6 with membranous nephropathy (MN), and in 7 healthy subjects by enzyme-linked immunosorbent assay using a monoclonal antibody specific for TGF-β₁₊₂₊₃. A significantly increased urinary TGF-β excretion was observed in FGS patients (555.5 ± 458.4 ng/mg Cr) as compared with normal controls (46.9 ± 43.9 ng/mg Cr) (p < 0.05) and a relative increase in SLE patients (96.4 ± 58.2 ng/mg Cr) and a decrease in MN patients (24.8 ± 13.3 ng/mg Cr). In contrast, there was no difference in TGF-β excretion between IgAN patients (54.1 ± 37.4 ng/mg Cr) and normal controls. A correlation between the amount of proteinuria and TGF-β was not found. As has been previously demonstrated in experimental studies, TGF-β may play a similar role in human glomerular diseases. The results obtained in this study raised the possibility that extracellular matrix might be produced by glomerular cells in vivo under the control of TGF-β and that TGF-β might act as a stimulator for the development of glomerulosclerosis.

Blood platelet serotonin content was measured in 30 children with early infantile autism, as defined by Kanner, 30 age-matched normal subjects, and 45 children with various neurological and psychiatric disorders. Serotonin content in the autistic group was 980 +/- 357 ng/mg platelet protein (mean +/- standard deviation), a value significantly higher than that for normal children, 807 +/- 202 ng/mg (p less than .025). Autistic children under school age had higher platelet serotonin concentrations than other older autistic individuals. There was little correlation between age and serotonin levels in the normal children. Elevated serotonin was also seen in some of the non-autistic pathological group, who were disturbed and hyperactive. Elevated serotonin levels are not necessarily a specific biochemical finding for autistic children, but seem to be due to their behavioral distinction.

No abstract

Ulinastatin is a potent protease inhibitor purified from the human urine that has been used clinically to treat acute pancreatitis and circulatory shock. In the current study, we evaluated the therapeutic effects of Ulinastatin in a rat model of crescentic glomerulonephritis (CrGN) and investigated its putative mechanisms. Wistar-Kyoto rats were injected with nephrotoxic serum and received daily intraperitoneal injection of Ulinastatin. Ulinastatin treatment significantly reduced proteinuria and glomerular crescentic formation. Moreover, glomerular infiltration of neutrophils and ED1+ cells (monocytes/macrophages) was significantly suppressed by Ulinastatin. In contrast, the glomerular deposition of heterologous (rabbit) and autologous (rat) antibodies was not changed. Neither serum complement activation nor the anti-rabbit immune response was affected by Ulinastatin administration. Our results suggest that Ulinastatin has preventive effects on rat experimental CrGN, mediated at least in part by inhibiting intraglomerular infiltration of inflammatory cells.