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Biomedical subjects

T Kudo

Publications and source records attributed to T Kudo.

At least 811 records · Page 45Linked to original sources
PubMed1975

Enhancement of host immune response to cell surface antigens by a preparation of Streptococcus hemolyticus.

A preparation (OK-432) of a low virulence strain, Su, of Streptococcus hemolyticus (Group A) has been found to possess 2 different effects on tumor cells: a) A direct pharmacological effect like other antitumor drugs, and b) an indirect effect through the enhancement of the host immune response. In order to examine the second effect, 2 different antigen systems were used, Gross (G) cell surface antigens (GCSAs) and the cell surface differentiation antigen PCl. At certain ages, untreated C57BL/6 and BALB/c mice occasionally produce natural antibodies to GCSAs and PCl, respectively. When the mice were injected intraperitoneally (i.p.) with OK-432 at 2 months of age, they produced natural antibodies to GCSAs or to PCl antigen, unlike untreated mice of the same strains at the same ages (negative controls), which produced no antibodies. The specificity of the antibodies was carefully examined by cytotoxicity tests. In addition, the activity of the natural antibodies was not neutralized with OK-432 itself. We have proven that OK-432 enhances the production of natural antibodies to specific cell-surface antigens.

Animals↗
PubMed1975

[Effects of adrenergic agents on secretion of salivary kallikrein in the submandibular gland of the dog].

The effects of sympathetic nerve stimulation and administrations of sympathomimetics on the secretion of salivary kallikrein induced by stimulation of Chorda tympani were examined quantitatively and qualitatively in the dog submandibular gland. Both sympathetic stimulation and administrations of sympathomimetics such as norepinephrine, epinephrine, and isoproterenol caused increased secretion of salivary kallikrein. Among these effects, those of the sympathetic stimulation, norepinephrine, and epinephrine were not completely abolished by pretreatment with phenoxybenzamine or propranolol, but the effect of isoproterenol was abolished by pretreatment with propranolol, and was hardly influenced by pretreatment with phenoxybenzamine. From these results, it would appear that secretion of salivary kallikrein may be mediated through adrenergic alpha- and beta-receptors. On the other hand, in contrast with the activities of the salivary kallikrein secreted by Chorda tympani stimulation or administration of isoproterenol which were not inhibited by SBTI, the activities of the salivary kallikrein secreted by sympathetic stimulation as well as administration of norepinephrine or epinephrine were markedly inhibited by SBTI. From these results, it is concluded that secretion of glandular kallikrein is due either to Chorda tympani stimulation or is mediated through adrenergic beta-receptor, while secretion of plasma kallikrein is mediated through adrenergic alpha-receptor.

Animals↗