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Biomedical subjects

E Hosoya

Publications and source records attributed to E Hosoya.

At least 55 records · Page 3Linked to original sources
PubMed1983

Protective effects of juzentaihoto, dried decoctum of 10 Chinese herbs mixture, upon the adverse effects of mitomycin C in mice.

In view of the reduction of side effects as well as the enhancement of anti-tumor activities of anticancer drugs, we have been interested in the combined use of Chinese medicines with them. In the present study, we attempted to examine the effects of Chinese prescription, juzentaihoto (JTX), combined with mitomycin C (MMC). JTX is consisted of Astragali radix, Chinnamomi cortex, Rehmanniae radix, Paeonia radix, Cnidii rhizoma, Atractylodis lanceae rhizoma, Angelicae radix, Ginseng radix, Hoelen and Glycyrrhizae radix. In BDF1-mice which were implanted with P-388 leukemic cells, JTX prolonged significantly the average survival days of MMC-treated group. In tumor-free BDF1-mice, JTX improved the leukopenia and the body weight loss which were caused by MMC. Additionally, JTX delayed the appearance of deaths by lethal dosis of MMC. These results indicate that JTX enhances the anti-tumor activity of MMC and lessens the adverse effects of it. JTX may be useful for patients undertaking MMC treatment.

Animals↗
PubMed1981

An experimental study on the enhancing effects of phenylalanine on acupuncture analgesia.

In this preliminary study we examined the enhancing effect of D-phenylalanine on acupuncture anesthesia. We made 4 different kinds of experiments with 3 volunteers. The results show that D-phenylalanine extends the analgesic effect of acupuncture analgesia remarkably, with no exception in 3 cases. According to these facts, we believe that these findings have an important meaning for those who are engaged in acupuncture treatment or research.

Acupuncture Therapy↗
PubMed1978

A new microwave device for rapid thermal fixation of the murine brain.

A microwave applicator was developed to provide rapid thermal fixation of enzymes in the murine brain. Although the power output of the device is only 1.3 kW, whole-brain levels of acetyicholine after microwave fixation are comparable to those observed at a power output of 5 kW, and are markedly higher than those obtained by a conventional method (freezing) of fixation.

Acetylcholine↗
PubMed1977

Effects of repeated morphine administration on copulation and on the hypothalamic-pituitary-gonadal axis of male rats.

Adult male rats were administered morphine twice a day for 45 days and the effects of morphine on the copulation rate, the weight of various organs, and on the hypothalamic-pituitary-gonadal axis were examined. Morphine administered rats showed a loss of weight, hypertrophy of the adrenals, decreased weight of accessory sex organs, low sperm count, and decreased copulation rate. The contents of the luteinizing hormone releasing hormone in the hypothalamus and the luteinizing hormone in the pituitary remained unchanged. Serum luteinizing hormone and testosterone levels decreased, but serum follicle-stimulating hormone levels increased. These results suggest that morphine inhibits the hypothalamic-pituitary-gonadal axis and causes a diminution in the number of fertilizations of the partner females.

Animals↗
PubMed1977

Regional acetylcholine content in mouse brain after morphine tablet implantation.

Implantation of a 75 mg morphine tablet in mice caused a significant decrease in the body weight and hypothermia. After 3 days, the concentration of acetylcholine decreased in all brain regions with the exception of the cerebellum. A significant decrease in acetylcholine content was observed in the midbrain, corpus striatum and the cerebral cortex 3 days after implantation. It is postulated that the decrease in Ach content is due to an increased release of acetylcholine as a result of development of tolerance to morphine.

Acetylcholine↗
PubMed1976

Effects of humoral modulators and naloxone on morphine-induced changes in the spontaneous locomotor activity of the rat.

The s.c. administration of 20 mg/kg of morphine-HCl produced a decrease in the spontaneous locomotor activity (SLMA) of rats. The decrease in SLMA was significantly antagonized by p-chlorophenylalanine (p-CPA). When rats pretreated with p-CPA were given 5-hydroxytryptophan before morphine injection, the marked sedative response to morphine was restored, suggesting that the morphine-induced decrease in SLMA of rats may depend on the release of 5-hydroxytryptamine by morphine. By contrast, the s.c. administration of 5 mg/kg of morphine-HCl produced a significant increase in SLMA of rats. The magnitude of the increase was reduced by atropine, scopolamine or alpha-methyl-p-tyrosine. It appears that both adrenergic and cholinergic mechanisms participate in the increase in SLMA of rats induced by morphine. Both the increase in SLMA produced by 5 mg/kg of morphine and the decrease in SLMA induced by 20 mg/kg of morphine were completely antagonized by the s.c. administration of naloxone-HCl, 0.0625 and 0.25 mg/kg, respectively. Thus, it appears that the receptor with which morphine interacts to produce stimulation is chemically identical with or very similar to the receptor with which morphine combines to induce depression. The former receptors, however, are likely to be located on different neurons from the latter.

5-Hydroxytryptophan↗
PubMed1976

Effect of humoral modulators of morphine-induced increase in locomotor activity of mice.

The effect of humoral modulators on the morphine-induced increase in locomotor activity of mice was studied. The subcutaneous administration of 10 mg/kg of morphine-HC1 produced a marked increase in locomotor activity in mice. The morphine-induced hyperactivity was potentiated by scopolamine and attenuated by physostigmine. In contrast, both methscopolamine and neostigmine, which do not penetrate the blood-brain barrier, had no effect on the hyperactivity produced by morphine. Pretreatment of mice with alpha-methyltyrosine (20 mg/kg i.p., one hour), an inhibitor of tyrosine hydroxylase, significantly decreased the activity-increasing effects of morphine. On the other hand, pretreatment with p-chlorophenylalamine (3 X 320 mg/kg i.p., 24 hr), a serotonin depletor, caused no significant change in the hyperactivity. The study suggests that the activity-increasing effects of morphine are mediated by the release of catecholamines from adrenergic neurons in the brain. And the results are consistent with the hypothesis that morphine acts by retarding the release of acetylcholine at some central cholinergic synapses. It is also suggested from collected evidence that the activity-increasing effects of morphine in mice are mediated by mechanisms different from those which mediate the activity-increasing effects of morphine in rats.

Animals↗