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Biomedical subjects

Y Wada

Publications and source records attributed to Y Wada.

At least 1,045 records · Page 58Linked to original sources
PubMed1982

Cytoplasmic estrogen receptors of rat mammary glands during pregnancy and puerperium.

The variation of cytoplasmic estrogen receptor in the mammary gland during pregnancy and puerperium was studied to determine the role of estrogens in the mechanism of lactation. Cytosol estrogen receptors from rat mammary glands were incubated with 3H-estradiol, and the free estradiol was removed using dextran-coated charcoal. The maximum number of binding sites in the cytosol was estimated from saturation curves and Scatchard analysis. During pregnancy the number of binding sites was relatively low (2.5 to 3.8 pmoles per mg protein), but increased after delivery to 7.8 pmoles per mg protein. The number of estrogen binding sites in the mammary glands of lactating rats five days after delivery was at the same level as on the day of delivery. However, at ten days after delivery the number of binding sites increased markedly to 58.9 pmoles per protein. The number of estrogen-binding sites in the mammary glands of lactating rats was decreased by castration and by the injection of testosterone or 2-bromoergocriptine. There appeared no competition by testosterone, progesterone or cortisol with estrogen receptors in the mammary gland.

Animals↗
PubMed1982

Protein from macrophages inhibiting polymerization of actin.

The crude cytoplasmic extracts of macrophages showed a low actin-polymerization activity as compared with the purified actin preparations. This suggested that an actin-polymerization inhibitor should exist in the crude cytoplasmic extracts of macrophages. Thus, the isolation of actin-polymerization inhibiting protein from the crude extract was attempted. The protein with a high actin-polymerization inhibiting activity had a molecular weight of 65,000 daltons as determined by polyacrylamide gel electrophoresis in dodecyl sulfate, a Stokes radius of 33.8 A as measured by gel filtration and a sedimentation coefficient of 4.9 S as determined by analytical centrifugation. The actin-polymerization inhibiting activity was much higher in 0.1 M KCl than in 0.6 M KCl. It was not affected by either the presence or the absence of free Ca2+. It was considered that the protein is responsible for the large proportion of unpolymerized actin in the crude extract of macrophages.

Actins↗
PubMed1982

Theoretical approach to the epidemiology of onchocerciasis in Guatemala.

The data collected by the Onchocerciasis Research and Control Project in Guatemala were theoretically analyzed. First, Muench's simple catalytic model was applied to the age distribution of the microfilaria-positive rate in each village to obtain the force of infection. The intensity of infection, expressed by force of infection, with Onchocerca volvulus in humans of individual villages was found to be clearly associated with the distribution and abundance of the vector, Simulium ochraceum. By comparing the values of the force of infection between males and females in a village, it can be decided whether humans were infected mainly outside the village or inside. The greater force of infection found in males was considered to be attributable to the more frequent visit of males than females to the mountainous areas where the density of S. ochraceum is higher. On the other hand, the force of infection of males was nearly equal to that of females when the S. ochraceum density was high inside the villages, suggesting the occurrence of within-village infection. Through further theoretical considerations, a mathematical model for the relation between the biting density of vectors and the microfilaria-positive rate of humans in a village was proposed, and the critical density of vectors for maintaining the endemic of onchocerciasis was estimated.

Adolescent↗
PubMed1982

[Anti-inflammatory effects of acemetacin (author's transl)].

It has been previously reported that acemetacin (ACM), the carboxymethyl ester of indomethacin (IND), is almost completely metabolized to IND in vivo. In the present study, the anti-inflammatory effects of ACM were compared with those of IND. ACM showed inhibitory effects on vascular permeability induced by phenylquinone. ACM inhibited carrageenin, kaolin, and nystatin edema dose-dependently and the ED30 in the carrageenin edema test was 2.8 Mg/kg. Inhibitory effects of ACM on carrageenin edema was not influenced by adrenalectomy or repeated administration of ACM. ACM also inhibited ultraviolet erythema at 5 mg/kg. Furthermore, ACM significantly inhibited granuloma formation at 2.5 mg/kg/day. The ED30 for the therapeutic effect on established adjuvant arthritis was 0.33 mg/kg/day. These anti-inflammatory effects of orally administered ACM were equivalent to or somewhat weaker than those of IND at an equimolar dose. Platelet aggregation was inhibited when ACM was given orally to rats and the activity of ACM was similar to that of IND. On the other hand, the effects of locally administered ACM on carrageenin and kaolin edema were markedly less potent than those of IND. In addition, inhibitory effects on prostaglandin synthesis and platelet aggregation in vitro were significantly weaker than those of IND. These results that the observed anti-inflammatory effects orally administered ACM are not due to its inherent action, but due to its metabolite, IND.

Animals↗
PubMed1982

Effects of fluorocarbon infusion on microcirculation during cardiopulmonary bypass.

A pulsatile pump was used to effect a three-hour cardiopulmonary bypass in 15 mongrel dogs. During the bypass, Fluosol-DA (35%) infusion was used in lieu of homologous blood transfusions. The greater omentum was chosen as a model of extraorganic microcirculation, and its reaction to the infusion was observed. The omentum's microcirculation was not adversely affected by the Fluosol-DA (35%): no sludging, microthrombi, arteriovenous fistulas, plasma skimming, stasis, or other adverse findings were observed. The animals' oxygen consumption did not decrease, and the resistance of the systemic blood vessels, did not increase during the experiment, suggesting that the fluorocarbon infusion had no untoward effects on the microcirculation.

Animals↗
PubMed1981

Structural analysis of human hemoglobin variants with field desorption mass spectrometry.

Tryptic hydrolyzates of normal and abnormal human globin chains were analyzed with mass spectrometry, using field desorption ionization technique. All the peptides, including core peptides, were detected as protonated molecular ions in field desorption mass spectra. Since the technique makes it possible to determine the mass number of each peptide, it is very useful for structural analysis of human hemoglobin variants, even those with electrophoretically and chromatographically silent mutations.

Adult↗
PubMed1981

[Irritative effects of acemetacin and indomethacin on the gastrointestinal tracts of rats (author's transl)].

It has previously been reported that acemetacin, a carboxymethyl ester of indomethacin, is converted to indomethacin almost completely by in vivo enzymatic attack, and thus its pharmacological effects are considered to be derived from its active metabolite, indomethacin. Gastric erosions of a slight degree were observed after a single oral administration of acemetacin, whereas indomethacin induced very severe gastric erosions 3 to 5 hours after dosing. On the other hand, the degree of intestinal lesions induced by acemetacin which became apparent 24 hours after dosing were about the same as that induced by indomethacin. The same results were obtained following repeated administration of the drugs. In an in vitro study, indomethacin was found to cause a significant mucosal loss of the isolated rat's small intestine, while there were no changes observed in case of an acemetacin treatment. Indomethacin also markedly inhibited the prostaglandin formation in the gastric mucosa of the rat treated with a single oral dose of the drug. In this test, the inhibitory effect of acemetacin on prostaglandin formation was found to be about half as potent as that of indomethacin. From these data, the less gastric damaging effects of acemetacin as compared to indomethacin can be explained by the fact that acemetacin does not have direct irritative effects on the mucous membrane. Furthermore, it could be due in part to the different abilities of these two drugs to inhibit prostaglandin formation in the gastric mucosa.

Animals↗