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Biomedical subjects

H Ishida

Publications and source records attributed to H Ishida.

At least 1,009 records · Page 56Linked to original sources
PubMed1980

Specific changes in the cholinergic system in guinea-pig vas deferens after denervation.

A small rapid phase (1st phase) was distinguished from a concomitant phase (2nd phase) in contraction of guinea-pig vas deferens. The vas deferens 4 days after denervtion exhibited supersensitivity to stimulants. The supersensitivity in the 2nd phase of contraction was nonspecific, but that in the 1st phase was specific to muscarinic cholinergic agonists. The increase in sensitivity resulted in a shift of the dose-response curve to lower concentrations without significant change in the maximal response. Muscarinic cholinergic receptors in the vas deferens, determined by measuring binding of [3H]quinuclidinyl benzilate, changed after denervation. The maximal binding sites increased from 115 to 165 fmol/mg of protein with no significant change in the dissociation constant. The affinity of the receptor for agonist also did not change significantly. Studies on [3H]WB4101 binding indicated no significant change in alpha adrenergic receptors after denervation. Thus, specific supersensitivity of the cholinergic mechanism mediated by muscarinic acetylcholine receptors occurred after denervation of guinea-pig vas deferens. This increased sensitivity is discussed in relation to the amount of receptor.

Acetylcholine↗
PubMed1979

Effects of estrogens on the testosterone levels of peripheral and spermatic vein blood in patients with prostatic cancer.

The mean testosterone levels of peripheral and spermatic vein blood in 16 patients with prostatic cancer who did not have estrogen therapy were 418.2 plus or minus 30.8 ng./dl. (mean plus or minus standard error) and 39.7 plus or minus 5.6 micrograms/dl., respectively. There were 13 patients with prostatic cancer who received estrogen therapy with daily doses of 30 mg. hexesterol or 300 mg. diethylstilbestrol diphosphate and who had decisive decreases of testosterone levels in peripheral (90.1 plus or minus 23.2 ng./dl.) and spermatic vein blood (3.3 plus or minus 1.2 migrogram/dl.). The rate of reduction of testosterone by estrogen therapy was one-tenth in the spermatic vein blood, while that in the peripheral blood was one-fifth. These data indicate that continuation of oral estrogens of these doses is sufficient to suppress the testicular androgens. On the other hand, the spermatic testosterone concentration was about 40 times higher than the peripheral testosterone concentration in patients receiving estrogen treatment. This result suggests that testosterone still is secreted from the testes under large therapeutic doses of estrogens.

Adult↗
PubMed1979

Studies on pituitary-gonadal endocrine function in XYY men.

Serum luteinizing and follicle-stimulating hormones and testosterone levels were studied in 11 patients with 47-XYY chromosomes and a comparison was made to normal men and patients with other testicular diseases, including Klinefelter's syndrome. Serum follicle-stimulating hormone levels in patients with XYY chromosomes were elevated significantly in comparison to those in normal men but lower than those in men with Sertoli cell only syndrome and Klinefelter's syndromes. Serum luteinizing hormone levels were somewhat elevated and serum testosterone levels were somewhat low in comparison to normal men, although the difference was not significant. Results of the short-term human chorionic gonadotropin stimulation test suggested almost normal Leydig cell reserve capacity in patients with XYY chromosomes.

Adolescent↗
PubMed1979

Induction by parathyroid hormone of ornithine decarboxylase in rabbit costal chondrocytes in culture.

The activity of ornithine decarboxylase (ODC) in rabbit costal chondrocytes in culture markedly increased after addition of parathyroid hormone (PTH), reaching a maximum 4 to 5 h after PTH addition. The effect of PTH was dose-dependent both in the presence and absence of fetal calf serum. Addition of cycloheximide or actinomycin D prevented the induction of ODC by PTH. Calcitonin, 1,25-dihydroxyvitamin D3, and vitamin A had no stimulatory effect on the activity of ODC, and did not inhibit the induction of ODC by PTH, when added with PTH.

Animals↗