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Biomedical subjects

N Yokoe

Publications and source records attributed to N Yokoe.

13 recordsLinked to original sources
PubMed1983

Effect of a protein-bound polysaccharide PS-K on the complement system.

A protein-bound polysaccharide from mycelia of Coriolus versicolor PS-K, clinically used as an immunomodulator, has been shown to restore the decreased cellular immune response and to exhibit host-mediated antitumor activity. In this experiment, PS-K was found to increase serum complement level in guinea pig and in human without malignancy, when hemolytic assay of complement was performed using sensitized sheep erythrocytes for the classical pathway activity and unsensitized rabbit erythrocytes for the alternative pathway activity. Assay of complement components revealed increase in C3 level in guinea pig, but no significant changes in C1q, C4, C3, properdin, C3 activator, and C1-inhibitor in human, while C5 and C9 were depressed. Conversion of beta 1C to beta 1A was observed in the 7th day's plasma of these patients by crossed immunoelectrophoresis. Biosynthesis of guinea pig C3 was accelerated by administration of PS-K, but that of C4 was not affected. These evidences suggested that PS-K might potentiate immune response of the host by elevating serum complement level, in addition to the activation of the complement system.

Animals↗
PubMed1979

Lipid peroxidation and lysosomal enzymes in D-galactosamine hepatitis and its protection by vitamin E.

Role of lipid peroxidation on lysosomal instability in liver tissue was investiaged in an experimental model of D-galactosamine hepatitis in rats fed on vitamin E (V.E) deficient diet. Administration of D-galactisamine to V.E deficient rats resulted in a sudden increase of serum glutamic oxaloacetic transaminase (sGOT), glutamic pyruvic transaminase (sGPT), lipid peroxide value, as well as beta-glucuronidase and acid phosphatase activity examined as markers of lysosomal enzymes, when compared with control rats fed on V.E supplemented diet. Lipid peroxide in the liver tissue also showed significant increase in V.E deficient rats. In contrast, beta-glucuronidase and acid phosphatase in the liver tissue were found to decrease in V.E deficient rats by the administration of D-galactosamine, indicating that the enzymes in the lysosome were entirely released outside the liver cells as a result of cell destruction. It is concluded that the increase of lipid peroxide causes the instability of lysosomal membranes and releases various kinds of hydrolytic enzymes to lead further to cell damage. V.E might act on inhibiting lipid peroxidation to stabilize lysosomal membranes.

Acid Phosphatase↗
PubMed1979

Cold activation of complement and kinin.

Differences between serum and plasma complement, which now is called as the cold activation of complement, was investigated in relation with the phenomenon reported as the cold promoted activation of factor VII, to which kallikrein and Hageman factor are known to participate. Despite the presence of several similarities in these two phenomena, it is concluded that the cold activation of complement is not related to the coagulation nor the kinin system. Evidence that tranexamic acid, a potent antiplasmin compound, provided an inhibitory effect on the cold activation of complement, suggested that the phenomenon could not be explained by a single mechanism, and plasmin might be involved in the phenomenon in a limited case.

Cold Temperature↗
PubMed1979

Effect of a streptococcal preparation on the complement system.

Streptococcal preparation OK-432 (Picibanil), clinically being used as an immunopotentiator, has been shown to activate the complement system either through the classical or the alternative pathway in vitro [15]. In this experiment, OK-432 was found to increase serum complement level in guinea pigs, and in human without malignancy, when investigated by hemolytic assay using sensitized sheep erythrocytes (EA) for the classical pathway activity and unsensitized rabbit erythrocytes (RaE) for the alternative pathway activity. Assay of complement components revealed a significant increase in C3, but decrease in Clq, while no specific tendency was observed in C4, C5, C9, properdin, C3 activator and Cl-inhibitor. These evidences suggested that OK-432 might potentiate immune response of the host by elevating serum complement level, in addition to activate the complement system.

Aged↗
PubMed1978

Hemorrhagic necrosis of the intestinal mucosa associated with disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC), experimentally induced by endotoxin, caused severe hemorrhagic necrosis of the intestinal mucosa in dogs. Microscopic observation showed tortuous thrombus formation in the microcirculation of the villi. Ligation of the pancreatic and bile ducts, or administration of heparin protected the mucosa from hemorrhagic necrosis, while systemic administration of tranexamic acid increased the intestinal mucosal lesion. Local pretreatment of the intestinal mucosa by Trasylol or tranexamic acid reduced the degree of hemorrhagic necrosis. It is concluded that intravascular coagulation in the microcirculation of the intestinal mucosa, as well as pancreatic proteases, play a role in the pathogenesis of hemorrhagic necrosis in the intestine associated with DIC.

Animals↗