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Biomedical subjects

T Kudo

Publications and source records attributed to T Kudo.

At least 721 records · Page 40Linked to original sources
PubMed1981

Inhibition of development of methylnitrosourea-induced rat colon tumors by indomethacin treatment.

This study deals with the nonsteroid antiinflammatory drug indomethacin, a prostaglandin synthesis inhibitor, in the treatment of carcinogen-induced colonic tumors in rats. CD-Fischer rats were given an intrarectal instillation of methylnitrosourea (2 mg, three times a week for the first to the fifth week) in order to produce colonic tumors. Thereafter, a long-term treatment with an i.p. injection of indomethacin (2.5 mg/kg body weight, three times a week) was started at the 11th week, before the tumors developed. At autopsy, after the 15-week treatment with indomethacin, the colonic tumor incidence was significantly lower in treated rats than in vehicle-treated or untreated control rats. However, the 10-week cessation of treatment following this effective dosage led to a rapid development of tumors. In another experimental group of rats in which tumors were detected endoscopically, when treatment was initiated late, at the 26th week, for 10 weeks, tumor incidence and number were not altered. The data suggested that indomethacin inhibited the development of colonic tumors but did not reject or kill the growing tumors. It is postulated that indomethacin treatment may effectively prevent the development of colonic cancer in patients at high risk of colonic adenomatosis and carcinomatosis.

Adenocarcinoma↗
PubMed1980

Enzyme-linked immunosorbent assay for measuring serum IgE.

Serum IgE was measured by a sandwich method using polystyrene beads coated with anti-IgE gamma-globulin and peroxidase labelled anti-IgE gamma-globulin. The method was simple, and as sensitive as the radioimmunoassay.

Enzyme-Linked Immunosorbent Assay↗
PubMed1980

[Mechanism of substance P-induced salivary secretion in the rat: effect of substance P on autonomic nervous system and prostaglandin synthesis (author's transl)].

Salivary flow and amylase secretion induced by substance P(SP) administered intraventricularly were considerably less than that by SP given intravenously (i.v.). Salivary flow induced by SP (i.v.) was partially inhibited by baclofen, atropine, d-tubocurarine, alcuronium, phenylephrine and PGE2, while it was enhanced by arachidonic acid and indomethacin. Salivary amylase secretion induced by SP given i.v. was enhanced markedly by isoproterenol, phenoxybenzamine, phentolamine and No. 865-123 (an adrenergic neuron blocking agent), and moderately by baclofen, PGE2 and arachidonic acid, while it was not influenced by propranolol. The enhancements of amylase secretion by adrenergic alpha-blockers were completely inhibited by propranolol. The in vitro examination using rat brain synaptosomes showed that SP promoted markedly the synthesis of PGs, especially of PGE2. These results suggest that the SP-receptor has a nicotinic receptor-like property and may be closely related to adrenergic alpha-receptors situated postsynaptically and presynaptically and to postsynaptic PGE2-receptors. From these results, it is concluded that SP-induced salivary flow and amylase secretion are modulated by the promotion of PGs synthesis in the autonomic nervous system.

Amylases↗