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Biomedical subjects

Y Kono

Publications and source records attributed to Y Kono.

At least 235 records · Page 13Linked to original sources
PubMed1977

HLA system in Japnaese patients with diabetes mellitus.

Seventy-eight Japanese diabetics were HLA-typed, with special reference to age at onset, insulin dependency, and family history. HLA-A9, B5, and BW40 were increased, but A1, A3, and B8, which are found frequently among Caucasians, were almost absent among Japanese healthy controls as well as diabetics. J-1, a Japanese specific subclass of BW22, was significantly increased in juvenile-onset diabetics as compared with controls or diabetics with late onset. J-1 was also increased in the diabetics with insulin dependency and/or positive family history. But the association of J-1 with juvenile-onset diabetes mellitus was found to be the strongest. A tendency to a decrease in B5 was also observed in Japanese diabetics with juvenile onset, but this did not reach statistical significance as far as corrected P was concerned. These results showed that genetic markers for diabetes mellitus, especially that with juvenile onset, were different among Japanese from those found among Caucasians. There is ample evidence to indicate a race specificity in HLA phenotypes in diabetics as well as in controls. These findings also strongly suggest that juvenile-onset diabetes mellitus is a disease entity in itself and different from late-onset diabetes mellitus in origin and pathogenesis.

Adult↗
PubMed1976

Hemagglutination by equine infectious anemia virus.

Equine infectious anemia (EIA) virus which was propagated on an equine dermal cell line agglutinated guinea pig erythrocytes. Viral fluids containing about 10(7.5) mean tissue culture infective doses/ml showed hemagglutinating (HA) titers ranging from 16 to 32 units/0.05 ml. Results of cesium chloride equilibrium density gradient centrifugation revealed that the hemagglutinin was inseparable from the virus particles. The hemagglutination reaction persisted over a wide range of temperature and pH, and the absence of divalent cations did not decrease its activity. The HA activity was stable at 4 degrees C but not at 56 degreesC. The activity was destroyed by virus-disrupting lipid solvents and moderately sensitive to a proteolytic enzyme. Neuraminidase enhanced HA activity slightly. Phospholipase C had no effect on HA titer, although it completely inactivated infectivity. It was relatively stable to ultraviolet irradiation. Thus, the hemagglutinin appears to be closely associated with virus particles, and its activity is dependent on the presence of its lipids and proteins. Hemagglutination was inhibited by sera from horses infected with EIA virus. Hemagglutinin receptors on the erythrocytes were inactivated by a proteolytic enzyme and formaldehyde but were not influenced by neuraminidase, sodium deoxycholate, or KIO4.

Animals↗
PubMed1976

Recrudescence of equine infectious anemia by treatment with immunosuppressive drugs.

Horses which had passed a few months to a few years asymptomatically after the last recurrence of equine infectious anemia (EIA) showed a typical febrile response after treatment with the immunosuppressive agent, dexamethasone (DM) or cyclophosphamide (CY). In horses showing a febrile response, EIA virus which had not been neutralized by neutralizing antibody previously produced was propagated. In DM-treated horses it disappeared from the blood soon after pyretolysis and antibody against the virus was produced promptly. In contrast, detectable viremia persisted in CY-treated horses for 10 to 84 days after pyretolysis. Antibody against the virus was barely produced for 42 to 126 days after treatment. After drug treatment, there was no decrease in neutralizing antibody previously produced. Then, it was inferred that this febrile response was due to propagation of an immunologically variant virus which might have been produced as a result of decline in cell-mediated immunity. The role of cellular mechanisms in the development of immunity to EIA was also discussed.

Animals↗