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Biomedical subjects

H Miyata

Publications and source records attributed to H Miyata.

At least 379 records · Page 21Linked to original sources
PubMed1986

Detection of lymphocytic choriomeningitis virus antibody in colonies of laboratory animals in Japan.

Indirect fluorescent antibody method was applied for a detection of lymphocytic choriomeningitis virus (LCMV) antibody in colonies of laboratory animals in Japan. The results showed that the antibody exist in SPF mice (3/152, 2.2%) and conventional mice (30/539, 5.6%) with the titers ranging from 1:10 to 1:160. The antibody was also detected in 2.2% (2/89) of Syrian hamsters, and 2.9% (2/68) of Apodemus agrarius, 21.4% (3/14) of Japanese harvest mice which have been maintained as laboratory colony for several years. However, the antibody was not demonstrated in Mongolian gerbils, Suncus murinus, guinea pigs and rats, thus far. These results indicate that LCMV infection is present in laboratory animals in Japan, and pointed out the importance of microbiological monitoring for LCMV.

Animals↗
PubMed1985

Antigen-specific augmentation of delayed-type hypersensitivity by immune serum factor in mice.

The serum from C3H/He mice immunized with chicken erythrocytes (CRBC) in complete Freund's adjuvant contained a factor able to augment delayed-type hypersensitivity (DTH) antigen specifically, when transferred into naive syngeneic recipient mice before their sensitization with CRBC. This activity in immune serum appeared on Day 4 and reached a peak on Day 8 after immunization, and was enhanced when donor mice were treated with cyclophosphamide (CY) 2 days before immunization. The ability of recipient mice to respond to this factor was enhanced by CY treatment of these mice 4 days before being transferred. This factor could be discriminated from conventional antibodies. Production of this factor in the serum donor and the expression of its activity in transferred recipient was mediated by a T-cell subset which showed a low degree of thymus dependency in ontogenic development.

Animals↗
PubMed1985

Polychlorinated biphenyl poisoning: correlation of sensory and motor nerve conduction, neurologic symptoms, and blood levels of polychlorinated biphenyls, quaterphenyls, and dibenzofurans.

In 1979 in Taiwan, more than 2000 people were poisoned with rice cooking oil contaminated with polychlorinated biphenyls (PCB). One hundred ten patients were studied within one year of the exposure. The blood PCB levels were 39.3 +/- 16.6 ppb. The blood levels of the PCB derivatives, polychlorinated quaterphenyls (PCQ) and polychlorinated dibenzofurans (PCDF), were 8.6 +/- 4.8 and 0.076 +/- 0.038 ppb, respectively. Both the sensory and motor nerve conduction velocities (NCV) of the patients were significantly lower than the control. Abnormal slowing of sensory NCV was found in 43.6% and abnormal slowing of motor NCV was seen in 21.8%. Patients who had higher PCQ blood levels had significantly slower median nerve sensory NCV than those with lower PCQ levels. Patients with higher PCB blood levels had significantly slower peroneal nerve motor NCV than those with lower PCB levels.

Adolescent↗
PubMed1985

PCBs, PCQs and PCDFs in blood of yusho and yu-cheng patients.

Individual blood samples obtained from yusho and yu-cheng patients who had been poisoned by ingesting contaminated cooking oils, from workers occupationally exposed to polychlorinated biphenyls (PCBs) and from unexposed individuals were analyzed for PCBs, polychlorinated quaterphenyls (PCQs) and polychlorinated dibenzofurans (PCDFs) by gas chromatography and mass spectrometry. PCBs were found in the blood of all samples. PCQs were detected in the blood of 54 of 56 living yusho patients 11 years after the outbreak, and in all yu-cheng patients 6 months following poisoning. These facts indicate that the presence of PCQs in the blood was a good mark of past ingestion of the toxic oil. In the yu-cheng cases, PCDFs as well as PCBs and PCQs were detected in all blood samples. These identified isomers have been reported to be remarkably highly toxic compounds, i.e., both the 2,3,7,8-tetrachlorinated and 2,3,4,7,8-pentachlorinated compounds are toxicologically hundreds to thousands of times more toxic than PCB. In view of the high toxicity of PCDFs found in the yu-cheng patients' blood, we must deduce that they are the primary causal agents of yusho as well as of the yu-cheng incident.

Benzofurans↗
PubMed1985

PCBs, PCQs and PCDFs in tissues of yusho and yu-cheng patients.

All five samples of oil involved in the recent yu-cheng outbreak were heavily contaminated with PCBs, PCQs and PCDFs at levels, on the average, of 62, 20 and 0.14 ppm, respectively. The samples not only had roughly one-tenth of the contamination by PCBs, PCQs and PCDFs but also three to four times lower ratios of PCQs and PCDFs to PCBs than samples of oil involved in yusho in Japan. PCBs, PCQs and PCDFs present were all composed of similar congeners to the ones found in the yusho specimens, though some variation of the component ratios of PCBs and PCDFs were observed. On the other hand, five patients with yusho who died 1 to 10 years following poisoning had markedly higher tissue levels of PCDFs and PCQs than did a worker occupationally exposed to PCBs. Taking great differences in the process of the healing and the tissue levels of PCBs, PCQs and PCDFs between the two poisoning cases into consideration, PCDFs and PCQs--especially the former--and not PCBs are deduced to be strongly associated with the development of yusho.

Benzofurans↗
PubMed1984

Antigen-specific augmentation factor involved in murine delayed-type footpad reaction. I. Nature of augmentation factor.

A humoral factor capable of augmenting antigen-specific DTH has been found in the culture supernatant of immune spleen cells and erythrocyte antigen. In this study, a similar factor was identified in the sera of mice sensitized and elicited with heterologous erythrocytes, and the nature of this factor was investigated. Elicitation with antigen was essentially required for the production of the augmentation factor in sensitized mice. The factor showed antigen specificity and antigen-binding capacity. The activity was not assigned to immunoglobulins, as demonstrated by an absorption test with rabbit anti-mouse immunoglobulin-conjugated Sepharose. The activity was stable to heating at 56 degrees C for 30 min, to changes of pH from 3 to 10, and to treatment with trypsin or neuraminidase. The molecular weight of this factor was about 200,000 to 450,000.

Animals↗
PubMed1984

Structural difference between two ATP-binding sites of heavy meromyosin revealed by the dynamic fluorescence quenching technique.

Acrylamide fluorescence quenching of 1,N6- ethenoadenylyl imidodiphosphate (e-AMPPNP) bound reversibly to the ATP binding sites of heavy meromyosin was investigated. In the presence of a 6-fold excess of heavy meromyosin over e-AMPPNP, a modified Stern-Volmer plot was not a linear function of the inverse of the concentration of acrylamide used as a quencher. By analyzing the plot, two Stern-Volmer constants (0.89 M-1 and 13 M-1) were obtained for bound e-AMPPNP. About 94% of bound e-AMPPNP had the Stern-Volmer constant of 0.89 M-1 and 6% of bound e-AMPPNP had the Stern-Volmer constant of 13 M-1. Moreover, in the presence of a 10-fold excess of e-AMPPNP over heavy meromyosin, a curved Stern-Volmer plot was obtained. It was found from this plot that 50% of bound e-AMPPNP had the Stern-Volmer constant of 13 M-1 and the remainder had the Stern-Volmer constant of 0.89 M-1. From these and the above data, it was concluded that one of the two ATP-binding sites of heavy meromyosin binds e-AMPPNP much more tightly than the other site does, and that the fluorescent group of e-AMPPNP bound to the former site is strongly isolated from the solvent as compared with that of e-AMPPNP bound to the latter site.

Adenosine Triphosphate↗
PubMed1984

Geniculocortical projection to layer I of area 17 in kittens: orthograde and retrograde HRP studies.

Using the orthograde and retrograde HRP methods, the distribution of geniculocortical (G-C) afferent terminals in area 17 was examined in kittens and an adult cat. Following HRP injection in the entire dorsal lateral geniculate nucleus (LGNd), afferent terminals were labeled in layer I and deeper layers. The terminals in layer I in young kittens (less than 2 weeks old) were densely distributed throughout layer I, whereas in old kittens (over 1 month old) they were sparsely distributed in the outer half of layer I. When the HRP injection site was confined to the A laminae (lamina A and lamina A1), a few HRP-labeled terminals in layer I were seen in young kittens but not in older kittens or an adult cat. Following HRP injection in layer I of area 17 in young kittens, relatively large neurons were labeled retrogradely. The labeled neurons were located chiefly in the C complex and partly in the A laminae. The present experiments revealed that the G-C afferents to layer I of area 17 in young kittens originate from relatively large neurons which are located chiefly in the C complex and partly in the A laminae and that these afferents give dense terminals covering the entire layer I. These findings contrast with those obtained in adult cats, in which the G-C afferents to layer I originate exclusively from small neurons in the C complex and give sparse terminals to the outer half of layer I.

Animals↗
PubMed1984

Causal agents of yusho.

Through the analysis of polychlorinated biphenyls (PCBs), polychlorinated quaterphenyls (PCQs), and polychlorinated dibenzofurans (PCDFs) retained in the blood of Japanese and Taiwanese patients who had been poisoned by ingesting contaminated cooking oils, in the blood of workers occupationally exposed to PCBs, and in the blood of unexposed individuals, it was strongly suggested that PCDFs might be the responsible compounds for the development of yusho disease. To confirm this, animal experiments were done. The dermal signs resembling those of yusho were observed among the cynomolgus monkeys that received a PCDF mixture consisting of PCDF components similar to those in the yusho oils. In addition, significant thymic atrophy and decreased body weight gain were noted in the rats fed PCDFs. However, the administration of PCBs or PCQs alone failed to cause such signs in the monkeys or rats. As a result, it became clear that PCDFs were the main causative agents in the pathogenesis of yusho disease.

Adipose Tissue↗
PubMed1984

Causal agents of yusho.

Through the analysis of polychlorinated biphenyls (PCBs), polychlorinated quaterphenyls ( PCQs ), and polychlorinated dibenzofurans ( PCDFs ) retained in the blood of Japanese and Taiwanese patients who had been poisoned by ingesting contaminated cooking oils, in the blood of workers occupationally exposed to PCBs, and in the blood of unexposed individuals, it was strongly suggested that PCDFs might be the responsible compounds for the development of yusho disease. To confirm this, animal experiments were done. The dermal signs resembling those of yusho were observed among the cynomolgus monkeys that received a PCDF mixture consisting of PCDF components similar to those in the yusho oils. In addition, significant thymic atrophy and decreased body weight gain were noted in the rats fed PCDFs . However, the administration of PCBs of PCQs alone failed to cause such signs in the monkeys or rats. As a result, it became clear that PCDFs were the main causative agents in the pathogenesis of yusho disease.

Animals↗