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Biomedical subjects

Y Harada

Publications and source records attributed to Y Harada.

At least 811 records · Page 45Linked to original sources
PubMed1981

IgE biosynthesis and IgE-bearing cells in atopic and normal peripheral blood.

The authors investigated the number of IgE-bearing cells in atopic and normal peripheral blood as well as IgE produced in vitro by mononuclear cells. The significant correlation between IgE produced in vitro and IgE in plasma (r = 0.91, P less than 0.001) or the number of IgE-bearing cells (r = 0.44, P less than 0.03) was observed. The data suggest that increased plasma IgE level in atopic patients is due mainly to conditions favoring increased production of IgE. The catabolic rate of IgE did not seem to exert an important effect on plasma IgE level.

Adolescent↗
PubMed1981

Reduced resistance to Pseudomonas septicaemia in diabetic mice.

Antibacterial resistance in a diabetic state was studied using experimental Pseudomonas infection in streptozotocin (SZ) induced diabetic mice. The results obtained were as follows: (1) there was no difference in acute death rate between normal and diabetic mice when infected with Pseudomonas aeruginosa. However, a significant increase in the number of bacteria in the kidney and liver occurred at a later stage of infection in diabetic mice. (2) Active immunization with a phenolized vaccine resulted in 100% survival in either normal or diabetic mice; otherwise challenge was lethal. However, the organs examined in diabetic vaccinated mice contained distinctly increased numbers of bacteria as compared with normal vaccinated mice 7 days after infection. (3) There were no significant differences in antibody titre between normal and diabetic ice after infection, but passive protection with immune serum from diabetic vaccinated mice was less effective than that from vaccinated mice. Furthermore, immune serum from normal vaccinated mice exerted protective action less efficiently in diabetic recipients than in normal recipients. (4) The bactericidal effect of peripheral whole blood was apparently lower in diabetic mice than in normal mice. (5) Treatment with insulin restored such reduced resistance to Pseudomonas infection in diabetic mice. These findings suggest that the decreased resistance to Pseudomonas infection in diabetic mice should be ascribed to impaired function of antibody, abnormalities in phagocytic cells and disturbed microcirculation caused by the insulin-deficient state.

Animals↗
PubMed1980

Analgesic action of intrathecal and intracerebral beta-endorphin in rats: comparison with morphine.

beta-Endorphin and morphine were given into the nucleus reticularis gigantocellularis (NRGC), spinal subarachnoid space and third ventricle of rats, and the antinociceptive effects were assessed by the tail-pinch method. The NRGC was 4-5 times as sensitive to beta-endorphin as was the spinal subarachnoid space and third ventricle, while the NRGC was 13-19 times as sensitive to morphine as were the other regions. Thus, it would appear that beta-endorphin has more sites of action for the production of analgesia than does morphine.

Analgesics↗
PubMed1980

Potentiation of anti-aggregating activity of PGI2 by 7-ethoxycarbonyl-6,8-dimethyl-4-hydroxymethyl-1(2H)-phthalazinone (EG-626) in rabbit platelets in vitro.

Anti-aggregating activity of 7-ethoxycarbonyl-6,8-dimethyl-4-hydroxymethyl-1(2H)-phthalazinone (EG 626) was tested using rabbit platelets in vitro. EG-626 alone, when added before, prevented platelet aggregation induced by ADP, as did PGI2, papaverine and dipyridamole. Spontaneous disaggregation was also accelerated when EG-626 was added after the maximal aggregation induced by ADP. EG-626 alone also inhibited platelet aggregation induced by collagen and arachidonic acid. ID50s of these agents in ADP-induced aggregation were 7-9 nM for PGI2, 223 microM for EG-626, 266 microM for papaverine and 957 microM for dipyridamole. When EG-626 was used in combination with PGI2, a threshold dose (50 microM) of EG-626 potentiated the antiaggregation effect of subthreshold dose (3 nM) of PGI2 upto 100% inhibition in collagen-induced platelet aggregation. The marked potentiating effect of EG-626 was accompanied by an accumulation of cyclic AMP in the platelets. These effects might be due to inhibition of phosphodiesterase. Papaverine and dipyridamole, other phosphodiesterase inhibitors, also potentiated the anti-aggregating activity of PGI2. The activity of papaverine, however, was one eighth of EG-626 and that of dipyridamole was much less. The most effective combination of PGI2 and EG-626 to induce 50% inhibition was obtained with 20% of ID50 of each agent, whereas that of PGI2 and papaverine or dipyridamole was 39 or 41%, respectively.

Animals↗
PubMed1980

Distant metastasis facilitated by BCG: spread of tumour cells injected in the BCG-primed site.

Tumour metastasis in BCG-pretreated mice was studied using a methylcholanthrene-induced fibrosarcoma in C3H/He mice. When tumour cells were injected into the BCG-primed site, distant metastasis occurred in the lungs and the popliteal lymph node, through this tumour did not metastasize in normal mice. Such metastases were increased in proportion to the number of tumour cells injected into the BCG-primed site, and developed soon after tumour challenge. Concomitant immunity developed well in the mice bearing such metastases, but did not inhibit metastatic growth. Experiments using 125I-labelled SRBC or tumour cells revealed that such cells egressed rapidly from the BCG-primed site. When the tumour was inoculated into the contralateral foot to the BCG-primed site, the incidence and the number of metastases was reduced. Furthermore, BCG infection induced an increase of platelet count. I.v. injection of this tumour induced marked thrombocytopenia in normal mice. Administration of pentoxifylline, a methylxanthine derivative before tumour challenge reduced such metastases. These findings suggest that the changes in peripheral blood, such as increased platelet count and increased release of tumour cells from the injection site, facilitated distant metastasis in BCG-pretreated mice.

Animals↗
PubMed1980

Presynaptic inhibition of tooth pulp afferents in the trigeminal nucleus during REM sleep.

In order to find whether presynaptic inhibition of tooth pulp afferents is enhanced in any phase of sleep or wakefulness, the orthodromic mass response of the trigeminal nucleus to electrical stimulation of the ipsilateral tooth pulp and the antidromic mass response of the tooth pulp to stimulation of the trigeminal nucleus were recorded in the cat. Both responses were stable in amplitude during different phases of sleep and wakefulness. However, attenuation of the orthodromic response and augmentation of the antidromic one were sometimes observed during the burst of rapid eye movements during paradoxical sleep, suggesting that presynaptic inhibition is massively enhanced only on those occasions.

Afferent Pathways↗
PubMed1980

Dual effects of a basic anti-inflammatory agent, 2-aminomethyl-4-t-butyl-6-iodophenol hydrochloride (MK-447), on biosynthesis of prostaglandin endoperoxides.

Effects of MK-447 on prostaglandin (PG) endoperoxide formation from arachidonic acid by bovine seminal vesicle microsomes in the presence of cofactors (hemoglobin and tryptophan) were studied by cascade superfusion on rabbit aorta and mesenteric artery and rat stomach and colon. In the presence of hemoglobin (0.2 muM), MK-447 (up to 30 muM) accelerated PG endoperoxide formation, as tryptophan did, whereas higher concentrations of MK-447 lost the acceleration effect and finally inhibited the PG endoperoxide formation. Increased concentration of hemoglobin (2 muM) shifted the dose of MK-447 for peak generation from 30 to 100 muM. Thus, MK-447 shows dual action, acceleration and inhibition, on the PG endoperoxide formation.

Animals↗
PubMed1980

Immunologic features of mice with streptozotocin-induced diabetes: depression of their immune responses to sheep red blood cells.

The immune responsiveness in streptozotocin (SZ)-induced diabetic mice was studied using the immune responses to sheep red blood cells (SRBC) as an indicator system. In SZ-diabetic mice, the weights of such lymphoid organs as the thymus and spleen were significantly decreased with time after SZ administration, whereas the weight of liver was markedly increased. In SZ-diabetic mice, the level of delayed type hypersensitivity (DTH) to SRBC was not lower than that in normal controls in most cases, although the level of DTH was significantly depressed, on occasion, in SZ-diabetic mice. In contrast, antibody-forming activity, measured as the number of plaque-forming cells (PFC), was markedly decreased in SZ-diabetic mice. It seems that antibody production is more profoundly depressed than is DTH in SZ-diabetic mice. The transfer of normal thymus and bone marrow cells into SZ-diabetic mice caused only a partial restoration of PFC activity. When normal spleen cells were transferred into diabetic irradiated mice, proliferation of spleen cells and production of splenic PFC was greatly reduced as compared with normal irradiated mice. Treatment with insulin completely reversed such depression in the transfer system. These findings suggest that the chronic insulin-deficient diabetic state caused a depression and delay in the proliferation and differentiation of lymphoid cells.

Animals↗