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Biomedical subjects

H Katayama

Publications and source records attributed to H Katayama.

At least 343 records · Page 19Linked to original sources
PubMed1981

Promoting effect of testosterone propionate on experimental exocrine pancreatic tumors by 4-hydroxyaminoquinoline 1-oxide in rats.

A single intravenous injection of 4-hydroxyaminoquinoline 1-oxide in a dose of 9 mg/kg induced exocrine adenomas of the pancreas in a significantly higher rate in male than in female rats. Castration following HAQO administration diminished the incidence of the pancreatic tumors in male rats. A combined treatment with castration and weekly injections of testosterone propionate in a dose of 1 mg/rat after HAQO administration resulted in high incidence of the pancreatic tumors in both sexes. From these findings, it is concluded that testosterone can promote the induction of the pancreatic tumors in rats by HAQO.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1981

Cell-mediated immunity in idiopathic membranous nephropathy.

Cell-mediated immunity (CMI) was evaluated in 11 patients with idiopathic membranous nephropathy (MN), 50 patients suffering from chronic proliferative glomerulonephritis (CGN) without renal insufficiency and 24 healthy controls. The following parameters were measured: delayed skin reactivity to purified protein derivative (PPD), circulating lymphocytes, lymphocyte cell-surface markers (En and EAC rosettes) and functional markers (mitogenic responses to Con A and PHA). The MN patients with nephrotic syndrome (NS) had less mean induration of skin reactivity and a smaller proportion reacting to the PPD antigen as compared with the control subjects. In contrast, the intensity of skin reactivity and the frequency of negative reactions in MN patients in remission and CGN were similar to those of the control subjects. During the nephrotic stage of MN the proportion of T lymphocytes decreased with simultaneous increase of the proportion of B lymphocytes. It was also found that the MN patients with NS showed impaired lymphocyte reactivity with lower Con A and PHA responses compared to the normal controls. Conversely, the mean mitogenic responses to the antigens in patients with MN in remission and CGN were similar to those of the control subjects. Thus, the majority of MN patients with NS demonstrated an impaired response in a CMI assay system. The possible significance of these phenomena in the pathophysiology of MN is discussed.

Adult↗
PubMed1980

Purification of rat liver glycerate kinase and studies of its enzymatic and immunological properties.

Glycerate kinase was purified to near homogeneity from rat liver mitochondria. Sephadex G-100 chromatography and sodium dodecyl sulfate-gel electrophoresis showed that the enzyme is a monomer with a molecular weight of 51,000-56,000. Kinetic studies indicated that the reaction proceeds by the "rapid equilibrium random sequential" mechanism, and the Michaelis constants were found to be 0.032 mM and 0.091 mM for D-glycerate and ATP, respectively. The binding of D-glycerate specifically protected the enzyme from thermal inactivation. The dissociation constant of the enzyme.D-glycerate complex was similar to the Michaelis constant, suggesting that the protective effect of D-glycerate may be caused by the specific binding of the substrate to the active site of the enzyme. The antibody to the enzyme was prepared by immunizing a rabbit with the purified rat liver glycerate kinase. Immunological experiments indicated that the cytosol and mitochondrial enzymes are indistinguishable. It was also found by immunological studies that the increase in the cytosol and mitochondrial enzyme activity depending on dietary protein intake was proportional to the increase in enzyme protein. These results support our proposal (Kitagawa, Y., Katayama, H., & Sugimoto, E. (1979) Biochim. Biophys. Acta 582, 260-275) that cytosol and mitochondrial glycerate kinase arise from a common translation product and that dietary protein regulates the distribution of glycerate kinase to the cytosol and mitochondria.

Animals↗
PubMed1980

Detection of sclerosis-inducing glycosaminoglycan in the skin of an amine-induced experimental skin sclerosis.

The presence of sclerosis-inducing glycosaminoglycan in the skin was confirmed in an experimental skin sclerosis induced by a chemical compound. An experimental skin sclerosis was first produced in the mouse with bis(4-amino-3-methylcyclohexyl)methane. Out of glycosaminoglycans isolated from the slightly changed skin of this experimental skin sclerosis, the one having a heparan sulfate-like structure was able to again induce sclerotic skin changes in another mouse. The chemical composition of this sclerosis-inducing glycosaminoglycan was somewhat similar to that of the scleroderma-inducing glycosaminoglycan isolated previously from the urine of patients with systemic scleroderma.

Animals↗