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Biomedical subjects

M Miyamoto

Publications and source records attributed to M Miyamoto.

At least 541 records · Page 30Linked to original sources
PubMed1985

Effect of idebenone (CV-2619) on memory impairment observed in passive avoidance task in rats with cerebral embolization.

Effect of idebenone (CV-2619) on memory impairment was studied in rats with cerebral embolization. The cerebral embolization, produced by injecting 2000 microspheres into the internal carotid artery, caused a significant impairment in passive avoidance response. Repeated administrations of idebenone (30 mg/kg/day, i.p.), partially but significantly improved the impairment of the passive avoidance response in the embolized rats. The results suggest that the repeated administration of idebenone exerts an ameliorating effect on memory impairment induced by cerebral embolization.

Animals↗
PubMed1985

Decrease of extracellular fluid in dog submandibular glands during secretion under arterial clamping conditions.

Microscopic observations were made of volume changes in ECF of the dog submandibular glands during resting state and stimulated state without blood supply. The interlobular space, one of the compartments of ECF, decreased significantly during stimulation when blood supply was absent. The results show that the interlobular space plays an important role as a reservoir of fluid in salivary secretion.

Animals↗
PubMed1984

A TRH analog (DN-1417): motor stimulation with rearing related to catecholaminergic mechanisms in rats.

The effect of an analog of TRH, gamma-butyrolactone-gamma-carbonyl-histidyl-prolinamide citrate (DN-1417) on motor activity was studied in rats. Peripheral administration of DN-1417 (0.2-20 mg/kg, i.p.) caused a significant, dose-dependent increase in total spontaneous motor activity, with a definite increase in rearing behaviour. Both increases in spontaneous motor activity and rearing behaviour were markedly inhibited by pretreatment with chlorpromazine (1, 5 mg/kg, i.p.), haloperidol (0.1, 0.5 mg/kg, i.p.), pimozide (1 mg/kg, i.p.) or alpha-methyltyrosine (250 mg/kg, i.p.). Only stimulation of rearing behaviour was selectively attenuated by phenoxybenzamine (5 mg/kg, i.p.) or FLA-63 (25 mg/kg, i.p.) at doses producing no significant effect on spontaneous motor activity. Although propranolol (10 mg/kg, i.p.) and methysergide (10 mg/kg, i.p.) had no effect, atropine (10 mg/kg, i.p.) and mecamylamine (10 mg/kg, i.p.) respectively potentiated and counteracted the effects of DN-1417. Concerning the stimulation of spontaneous motor activity, the nucleus accumbens and lateral hypothalamic area were most sensitive to DN-1417, and the lateral hypothalamic area was the most sensitive site for the stimulation of rearing. Furthermore, DN-1417 (5 X 10(-5) M) significantly enhanced the spontaneous release of [3H]dopamine from the rat nucleus accumbens slices in vitro. These findings indicate that the motor stimulatory action of DN-1417 appears to be mediated primarily via a dopaminergic mechanism by enhancing the release of dopamine from nerve terminals, including the nucleus accumbens in the mesolimbic dopamine system, and, in turn, the rearing may be mediated via noradrenergic mechanism.

Animals↗
PubMed1984

Monoclonal antibodies to rat liver cell membrane glycoproteins.

Monoclonal antibodies were raised against membrane glycoproteins prepared from rat liver using lentil-lectin affinity chromatography. Monoclonal antibodies to rat hepatocytes with three different characteristics were obtained and designated as HAM.1, HAM.2 and HAM.3. The binding characteristics of these three monoclonal antibodies were analysed by flow cytofluorography and indirect radioimmunoassay; HAM.3 recognized a membrane antigen restricted mainly to hepatocytes. However, most rat hepatoma cell lines tested failed to express this antigen. Thus, this antibody might be useful for analysing the molecular nature of a liver-specific antigen or the membrane molecules on the normal and malignantly transformed hepatocytes. All the rat hepatoma cell lines tested were labeled with HAM.1 which recognized a membrane antigen on both hepatocytes and lymphocytes, although the amount of antigen expression was quite low on lymphocytes. HAM.2 was found to recognise the Class 1 (RT-1A) histocompatibility antigen. This antigen was purified from rat liver with a HAM.2-affinity column.

Animals↗
PubMed1984

Major-histocompatibility-complex-restricted male skin graft rejection responses in rats.

Normal DA (RT1a) female rats rejected male skin isografts when preimmunized with RT1-compatible DA, or ACI (RT1a) male bone marrow cells (BMC), but failed to reject them when preimmunized with RT1-incompatible PvG/c (RT1c), F344 (RT1lvl), or BN (RT1n) male BMC--as well as when they were untreated. DA female rats rendered neonatally tolerant to RT1-incompatible PvG/c female tissues failed to reject, not only DA, but also PvG/c male skin grafts when preimmunized with PvG/c male BMC. DA female rats tolerant of PvG/c female tissues that had rejected DA male skin grafts following immunization with DA male BMC failed to reject PvG/c male skin grafts. These results indicate that in rats, unlike mice, male skin graft rejection responses are MHC-restricted, at least in the DA strain.

Animals↗
PubMed1984

The suppression of insulin-specific immune responses by the administration of insulin-derivatized syngeneic cells and soluble lysates from these cells.

The results of this study demonstrated that the i.v. administration of insulin, in the form of a conjugate with either syngeneic spleen cells (SC) or peritoneal exudate cells (PEC), markedly reduced the capacity of recipient mice to develop insulin-specific immune responses, as manifested by diminished in vivo IgE antibody production and by depressed in vitro, lymph node cell proliferation responses, respectively. Furthermore, it was shown that i.v. injection of insulin-PEC conjugates induced the activation of suppressor cells that had the capacity to downregulate insulin-specific IgG plaque-forming cell (PFC) responses. Finally, it was also determined that freezing and thawing of the insulin-PEC conjugates resulted in the release of a soluble tolerogenic molecule and/or membrane preparation that could also markedly depress insulin-specific IgG antibody production.

Animals↗