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Biomedical subjects

Y Kono

Publications and source records attributed to Y Kono.

At least 217 records · Page 12Linked to original sources
PubMed1981

Hemagglutination-inhibition tests with different strains of equine infectious anemia virus.

The serologic relationships between 6 strains of equine infectious anemia (EIA) viruses were investigated by hemagglutination-inhibition (HI) tests. Cross HI tests, using sera from horses in the early stage of infection, revealed that all strains were inhibited only by homologous strain antisera and that HI antibody was always detectable before virus-neutralizing antibody. In the later stages of infection, both homologous and heterologous HI antibodies were detected in a sera of most of the horses, and the order of appearance of heterologous HI antibodies was random in 2 horses inoculated with the same virus strain. The viruses sequentially isolated from 1 horse had serologically the same hemagglutinating antigenicity to their parent virus. These results indicate that hemagglutinating antigens of EIA virus were type specific, but different from the antigens detectable by neutralization. The possible role of EIA virus hemagglutinin and HI antibody in causing periodic anemia is discussed.

Animals↗
PubMed1981

Pathogenicity of Getah virus for mice.

The Sakai strain of Getah virus isolated from a feverish horse was examined for pathogenicity for mice. Its pathogenicity depended on the age of the host and the route of inoculation. Intracerebral inoculation caused death to mice less than 9 days old. It induced retarded growth, insufficient hair growth, paralysis, and sporadic death in mice 11 days old, but no symptoms in mice 13 days old. The virus multiplied rapidly and extensively in every tested organ, particularly in the muscular tissue, of the suckling mouse. It was also observed that the virus was transmitted horizontally among the litter-mates and vertically from the dam to her offspring via milk.

Alphavirus↗
PubMed1980

A Comparison of Purified Host Specific Toxin from Helminthosporium maydis, Race T, and Its Acetate Derivative on Oxidation by Mitochondria from Susceptible and Resistant Plants.

NADH or succinate oxidation and malate oxidation were differentially affected in mitochondria from both susceptible and resistant corn by a purified and chemically characterized preparation of host-specific toxin from Bipolaris (Helminthosporium) maydis, race T. NADH and succinate oxidation by susceptible T corn mitochondria were stimulated 50 to 200% with apparent uncoupling from the cytochrome chain at approximately 10(-9)m toxin (5 to 20 ng/ml). Significant inhibition of malate oxidation was observed at slightly higher toxin concentrations, but oxidation was still coupled to ADP utilization. Inhibition of malate oxidation also was observed in N corn (resistant) and soybean mitochondria at approximately 1,000-fold greater concentrations, but stimulation of NADH and succinate oxidation was not found at any toxin concentration tested.A fully acetylated toxin derivative at approximately 1 microgram per milliliter also caused stimulation of NADH or succinate oxidation in T corn mitochondria, but not those of N corn or soybean mitochondria at 100 micrograms per milliliter. Malate oxidation was inhibited to the same extent by toxin acetate with mitochondria from T corn, N corn, and soybean. The blocking of hydroxyl groups in race T toxin by acetyl functions eliminated selectivity toward malate oxidation only. The data suggest that inhibition of malate oxidation is either a separate or secondary effect of selective action of toxin on T corn mitochondria, perhaps by interference with transport in or out of the matrix. Sensitivity of T, but not N, corn mitochondria to purified toxin decays within minutes after pellets are suspended in aqueous osmotica, with no obvious change in mitochondrial integrity. The action of race T toxin seems to involve a labile process, such as ion gradient(s), or an unstable structural conformation of T corn mitochondria.

Journal Article↗
PubMed1980

Augmentation of delayed-type hypersensitivity by vesicular stomatitis virus infection in mice.

Effects of the infection with vesicular stomatitis virus (VSV) on delayed-type hypersensitivity (DTH) to heterologous erythrocytes were investigated in mice. Infection at the time of immunization resulted in production of high levels of DTH that were specific to the antigen used for immunization. The high level of DTH produced in VSV-infected mice could not be attributed to the nonspecific enhancement of the footpad swelling with the infection. Augmentation of DTH was observed in all strains of the mouse (CBA, BALB/c, C3H/He, and C57BL/6) used. The augmenting effect of VSV infection was not as apparent in adult thymectomized mice in which the level of VSV-replicating T cells was reduced. These results strongly suggest that DTH-mediating T cells are resistant to infection by VSV, and also that there are VSV-sensitive cells that may be engaged in the suppression of DTH. It seems improbable, however, that the cells sensitive to VSV infection represent the suppressor cells themselves, since the enhancing effect was not observed in mice in which the suppressor cells were induced by the administration of high doses of the antigen.

Animals↗
PubMed1980

Survey on antibody to Getah virus in horses in Japan.

A seroepidemiological survey was performed on antibody against Getah virus in horses in Japan by the complement fixation test. The positive rate was 35 and 53% in two areas where an outbreak of the infectious disease was reported, whereas it was in a range of 3.3 to 24.2% in other areas, except in certain prefectures of the Kyushu district where a high positive rate was observed. In the Hokkaido district, the northernmost part of Japan, no reactors were found in horses under 6 years old, unlike in any other district. It was also suggested that Getah virus infection might have already been prevalent among horses in Japan before the outbreak of the disease in 1978. It remained to be elucidated, however, that the antibody detected might have been produced by some virus which was antigenically related to Getah virus.

Animals↗
PubMed1980

An epidemic of Getah virus infection among racehorses: isolation of the virus.

During the autumn of 1978 a disease characterised by fever and occasionally by exanthema and/or oedema of the limbs was seen in approximately 13 per cent of horses in a training stable in the Kanto district of Japan. A virus was isolated by the intracerebral inoculation of one-day-old mice from blood and nasal swabs taken from naturally and experimentally infected horses. The virus was subsequently passaged in two monkey kidney cell lines in which it produced complete cytopathic changes. Infected horses developed neutralising, complement fixing and haemagglutinin inhibiting antibodies to the virus and the results of serological investigations indicated that approximately 56 per cent of horses in the training centre had been infected. The virus was subsequently identified as Getah virus, a member of the alphavirus subgroup of Togaviridae.

Alphavirus↗
PubMed1980

An epidemic of Getah virus infection among racehorses: properties of the virus.

A virus (Sakai) which had been recovered from an outbreak of disease in horses was found to be a small spherical enveloped RNA virus with a diameter of approximately 70 nm and a buoyant density of 1.22 g per ml. It grew well and produced a cytopathic effect in a variety of cell cultures; it was sensitive to organic solvents, heat and low pH. It agglutinated goose erythrocytes in a 0.35 M sodium chloride solution at an optimum pH of 6.2 and was antigenically identical or closely related to Getah virus, a member of the alphavirus subgroup of the Togaviridae.

Alphavirus↗