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Biomedical subjects

T Yano

Publications and source records attributed to T Yano.

At least 757 records · Page 42Linked to original sources

Enzyme immunoassay of prostaglandin F2alpha.

An enzyme immunoassay for prostaglandin F2alpha was developed in which the hapten molecule was labeled with alkaline phosphatase protein. After competition between the enzyme-labeled prostaglandin F2alpha and the free prostaglandin F2alpha in their immunoreaction with prostaglandin F2alpha-specific antiserum, the antigen-antibody conjugate was precipitated by the double antibody method, and the activity of precipitated alkaline phosphatase was determined. Calibration curves of enzyme activity versus the amount of added prostaglandin F2alpha were constructed. Under optimal conditions of pH, buffer concentration, incubation time and amount of antibody and enzyme-labeled antigen, prostaglandin F2alpha could be measured quantitatively in the range of 0.5 pmol to 1 nmol. This method was applied for the determinations of prostaglandin F2alpha added to urine.

Animals↗

beta-Galactosidase-linked immunoassay of prostaglandin F2 alpha.

A sensitive and specific enzyme immunoassay for prostaglandin F2 alpha was developed in which prostaglandin F2 alpha was labeled with beta-D-galactosidase. After competitive binding to antibody between enzyme-labeled and free prostaglandin F2 alpha, the immunoreactive product was precipitated by double antibody technique, and the enzyme activity of the precipitate was determined fluorometrically. The procedures allowed determination of 0.03-20 pmol of prostaglandin F2 alpha. The detection limit of 0.03 pmol was comparable with that of previously reported radioimmunoassays. Enzyme immunoassay and radioimmunoassay showed almost the same cross-reactivity with other prostaglandins and metabolites.

Binding, Competitive↗

[A case of thyroid storm associated with diabetic ketoacidosis (author's transl)].

A 31-year-old female was well until few years ago when she was diagnosed as having Graves' disease. Methimazole (MMI) and Lugol's solution were prescribed. But 7 months later, she stopped taking them arbitrarily. Three months later, thirst and general fatigue appeared. Therefore insulin (60u/day) and MMI (30 mg/day) were administered and continued for 40 days. However no remarkable effect was brought about. She was then transferred to the radioisotope ward of Kumamoto Univ. Hospital and was treated with regular insulin only. Ten days later, she fell into thyroid storm associated with diabetic ketoacidosis and was transferred to our ward. We began to administer large volumes of transfusion, regular insulin, MMI, Lugol's solution, propranolol, hydrocortisone and digitalis. In 24 hours, ketoacidosis disappeared and she became alert. For hyperthyroidism, the dosage of MMI was increased to 60 approximately 45 mg/day and was continued for a month; however, her thyroid function did not normalize and agranulocytosis developed. MMI was discontinued, and she was treated with 131I. About a year later, she became euthyroid. Her diabetes mellitus was difficult to control during the hyperthyroid state but it was under good control with monocomponent lente insulin (36u/day) when the euthyroid state was resumed.

Adult↗

Purification and partial characterization of heat-stable enterotoxin of enterotoxigenic Escherichia coli.

Heat-stable enterotoxin was purified from a strain of enterotoxigenic Escherichia coli 53402 A-1 from human intestine. The cells were cultured in Casamino Acids-yeast extract-salts medium, and the purification procedure consisted of protamine sulfate treatment of the culture supernatant, ultrafiltration with an Amicon PM-10 membrane, diethylaminoethyl-cellulose column chromatography, hydroxyapatite column chromatography, Bio-Gel P-10 gel filtration, 90% ethanol extraction, and preparative polyacrylamide gel disc electrophoresis. About 300-fold purification was achieved, with a yield of about 12%. However, the homogeneity of the purified heat-stable enterotoxin was not rigorously demonstrated. The purified heat-stable enterotoxin had an absorption maximum at about 275 nm, and its isoelectric point was about 3.90. The molecular weight of the purified heat-stable enterotoxin was ca. 4,000 by Sephadex G-100 gel filtration. The minimum effective dose of purified heat-stable enterotoxin was about 2.5 ng in the suckling mouse assay. The purified heat-stable enterotoxin gave a positive reaction in not only the suckling mouse assay but also the mouse intestinal loop test and the guinea pig skin permeability test.

Electrophoresis, Polyacrylamide Gel↗

Studies on the metabolism of d-limonene (p-mentha-1,8-diene). IV. Isolation and characterization of new metabolites and species differences in metabolism.

1. The main route of elimination of d-limonene administered orally was via the urine in animals and man, 75-95% of the administered radioactivity being excreted in the urine during 2-3 days. Faecal excretion accounted for less than 10% of the dose in animals during 2-3 days. 2. In addition to six metabolites, namely p-mentha-1,8-dien-10-ol (M-I), p-menth-1-ene-8,9-diol (M-II), perillic acid (M-III), perillic acid-8,9-diol (M-IV), p-mentha-1,8-dien-10-yl-beta-D-glucopyranosiduronic acid (M-V) and 8-hydroxy-p-meth-1-en-9-yl-beta-D-glucopyranosiduronic acid (M-VI) isolated from rabbit urine previously (Kodama et al., 1974), five new metabolites have been isolated from dog and rat urine, and which were characterized as 2-hydroxy-p-menth-8-en-7-oic acid (M-VII), perillylglycine (M-VIII), perillyl-beta-D-glucopyranosiduronic acid (M-IX), p-mentha-1,8-dien-6-ol (M-X) and probably p-menth-1-ene-6,8,9-triol (M-XI). 3. The major metabolite of d-limonene in the urine was M-IV in rat and rabbit, M-IX in hamster, M-II in dog and M-VI in guinea pig and man.

Animals↗

Metabolism of 1-(3-trifluoromethylphenyl)-3-(2-hydroxyethyl) quinazoline-2,4(1H,3H)-dione (H-88). I. Species differences in metabolism.

1. Following oral administration of [14C] H-88 to rat, mouse, quinea-pig and hamster, 40-65% and 5-15% of radioactivity was excreted in urine and faeces respectively during 3 or 4 days. In rabbit, monkey and man, more than 80% of radioactivity was excreted in urine during 2 or 3 days, and faecal excretion was negligible. 2. Rabbit, rat or guinea-pig excreted non-labelled H-88 in urine as unchanged H-88 (M-I), 1-(3-trifluoromethylphenyl) quinazoline-2,4(1H,3H)-dione-3-acetic acid (M-II), H-88 glucuronide (M-III) and 1-(3-trifluoromethylphenyl)-3-(2-hydroxyethyl)-6-hydroxyguinazoline-2,4(1H,3H)-dione (M-IV). 3. The carboxylic acid (M-II) was the major metabolite of H-88 in rat, mouse, guinea-pig and hamster urine and faeces, while the major metabolite in urine of rabbit, monkey and man was H-88 glucuronide (M-III). The 6-hydroxy compound (M-IV) was a major metabolite only in guinea-pig.

Administration, Oral↗