In situ hybridization of hepatitis B DNA in hepatitis B-associated glomerulonephritis.

Renal tissues from 43 of 49 children with hepatitis B virus-associated glomerulonephritis (HBV-GN) were examined for HBV DNA by in situ hybridization (ISH) assay within the last 10 years. HBV DNA was identified in 41 of the 43 cases (95.3%). HBV DNA was distributed generally in the nucleus and cytoplasm of epithelial cells and mesangial cells of glomeruli, and epithelial cells of renal tubules. HBV DNA also existed simultaneously in renal interstitial tissues in some of these cases. The positive results from HBV DNA ISH correlated well with HBV antigen assays. The analyses implied that the more extensive the existence of HBV DNA in the nephron unit and interstitial tissue, the more severe the clinical manifestation. The duration of proteinuria in cases with HBV DNA in renal tubules was much longer than in those with no HBV DNA in renal tubules. The persistence of the HBV genome or genes in the kidney could lead to the expression of viral antigens in renal tissues and might cause cellular pathological alteration. This would support utilization of antiviral therapy, such as cytokines, in the treatment of HBV-GN.

Inhibition of collagen production by traditional Chinese herbal medicine in scleroderma fibroblast cultures.

The in vitro effect of one traditional Chinese herbal medicine (Japanese name: "Keishi-bukuryo-gan"), which has been empirically used in scleroderma patients in China and Japan, on collagen production in fibroblast cultures was studied. Fibroblasts from 3 scleroderma patients and 2 normal controls were incubated with various concentrations of "Keishi-bukuryo-gan" and collagen production was then determined by a radiochemical method. "Keishi-bukuryo-gan" significantly and selectively inhibited collagen synthesis in a dose-dependent manner, with a tendency of a stronger effect on scleroderma fibroblasts than control cells. The results may explain the clinical usefulness of this medicine, and it may become a promising new agent for the treatment of scleroderma.

rpt-1, an intracellular protein from helper/inducer T cells that regulates gene expression of interleukin 2 receptor and human immunodeficiency virus type 1.

The Rpt-1 (for regulatory protein, T-lymphocyte, 1) gene, selectively expressed by resting but not by activated CD4+ inducer T cells, encodes an intracellular protein (rpt-1, Mr 41,000) that down-regulates gene expression directed by the promoter region of the gene encoding interleukin 2 receptor alpha chain and by the long terminal repeat of human immunodeficiency virus type 1. The data reported here suggest that rpt-1 levels may be inversely correlated with activation of CD4+ T cells and human immunodeficiency virus replication leading to clinical symptoms of the acquired immunodeficiency syndrome.