[CT findings of Crohn's disease of the small intestine].
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Adolescent↗
Biomedical subjects
N Yahata
Publications and source records attributed to N Yahata.
Membranous glomerulonephritis with nephrotic syndrome associated with chronic lymphocytic leukemia.
A 66-year-old woman was admitted to our hospital for evaluation of edema of the extremities. Laboratory findings suggested that she had nephrotic syndrome and chronic lymphocytic leukemia (CLL). Renal biopsy (with PAM staining) showed a spike formation in the capillary wall. Immunofluorescent staining revealed deposition of immunoglobulin G (IgG) and the third component of complement in the glomerular basement membrane. Electron microscopy showed fibrillary deposits in the subepithelium. These findings indicated membranous glomerulonephritis (MGN). In addition, focal segmental sclerosis and interstitial lymphocytic infiltration were observed in the renal biopsy specimen. In CLL patients nephrotic syndrome occurs rarely. Even if the complication occurs, MGN is not frequent. Both diseases are suspected to occur in association with each other, and immunologic abnormality contributes to their coexistence. Although administration of prednisolone and endoxan improved leukocytosis, proteinuria was not sufficiently improved with combination therapy.
Aged↗
Dehydroepiandrosterone inhibits B16 mouse melanoma cell growth by induction of differentiation.
BACKGROUND: Low serum concentrations of dehydroepiandrosterone (DHEA) and its sulfate are associated with an increased incidence of various human malignancies. DHEA has chemopreventive and antiproliferative effects in experimental studies. Accordingly, the effects of DHEA on B16 mouse melanoma cells were studied. MATERIALS AND METHODS: The effects of DHEA on cell number and melanin production of the melanoma cells were measured. Specific DHEA receptor was detected by a cytosol binding assay. Protein kinase C (PKC) activity of the melanoma cells was detected by phosphorylation of PKC specific substrate. RESULTS: DHEA dose-dependently inhibited the growth of melanoma cells and enhanced melanin production, which indicated the induction of differentiation. There was a [3H]DHEA specific binding protein in the melanoma cell cytosol. Although DHEA did not promote the translocation of PKC from the cytosolic to the membrane fraction, the total PKC activity was upregulated by treatment with DHEA. CONCLUSIONS: DHEA inhibited the growth of B16 mouse melanoma cells by the induction of differentiation, possibly related to PKC upregulation mediated by DHEA receptor.
Animals↗