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Biomedical subjects

K Yoshimura

Publications and source records attributed to K Yoshimura.

At least 577 records · Page 32Linked to original sources
PubMed1976

Animal experiments on thiamine avitaminosis and cerebral function.

Before industrial production of thiamine becam possible, among many beriberi patients some showed symptoms of encephalopathy, the cerebral form of the disease. In this animal experiment, thiamine-deficient rats showed failure or blocking of the operant behavior in the maze box, pole climbing box and shuttle box, indicating orientation disturbance and defective memory. This Wernicke's syndrome-like sign dramatically disappeared by treatment with thiamine. Potentiated narcosis with thiopental or alcohol induced in thiamine-deficient rats and mice was readily reversible by thiamine administration. These phenomena are associated with thiamine content of the brain and are found long before histopathological changes in the brain of deficient animals. It is easily surmised that thiamine deficiency in the brain may block the brain metabolism and subsequently cause changes in any chemical substances in the brain, refracting on biophysical phenomenon, such as EEG. However, in the present study, generally speaking, no meaningful results concerning these points were obtained.

Animals↗
PubMed1976

Angiostrongylus cantonensis: lymphoid cell responsiveness and antibody production in rats.

Angiostrongylus cantonensis-infected rats were examined for the presence of antigen sensitive lymphocytes, as assessed by the in vitro uptake of tritiated thymidine by cells of various lymphoid organs (cervical, mediastinal and mesenteric lymph nodes, spleen and periphereal blood), following stimulation by adult worm antigen. The lymphoid cell response of rats to A. cantonensis appeared to be local in nature in that significant responses were noted only in the cervical lymph node cells during the first 4 weeks of infection. The responses of spleen cells to phytohemagglutinin gradually declined as the infection progressed and this reduced responsiveness was statistically significant during the period of 5 to 10 weeks of infection. Homocytotropic antibody, demonstrated by 72-hour homologous passive cutaneous anaphylaxis, was detected throughout 2 to 17 weeks postinfection with a peak response at the 5th week of infection. The antibody was heat labile and sensitive to reduction by 2-mercaptoethanol and alkylation. Hemagglutinating antibody was first observed 5 weeks after infection and high titers occurred throughout 6 to 17 weeks postinfection.

Animals↗