Biomedical subjects
T Tsumita
Publications and source records attributed to T Tsumita.
Deficiency of kallikrein-like enzyme activities in cerebral tissue of patients with Alzheimer's disease.
We examined the changes in the intracerebral activities, at the time of postmortem autopsy, in patients with Alzheimer's disease. When compared with the control group, the activity of kallikrein-like enzyme was significantly decreased, while prolyl endopeptidase activity increased, in the patients group. Aprotinin inhibited 50% of the activity of the former enzyme at 2 x 10(-7) M. Taken together with the results of a multivariate study, the above findings may indicate that intracerebral kallikrein deficiency plays an important role in the pathogenesis of Alzheimer's disease.
Increased gamma-aminobutyrate aminotransferase activity in brain of patients with Alzheimer's disease.
In order to search for more proximal factors in the pathogenesis of Alzheimer's disease, we studied the activities of various enzyme in the brains of patients, as well as control cases, by postmortem autopsy. In addition to the findings already known, such as the increase in prolyl endopeptidase (post-proline cleaving enzyme, PPCE) activity and the decrease in kallikrein activity, we found, anew, an increase in aminobutyrate aminotransferase (GABA-T) activity in the Alzheimer brain. This may be an important impetus for the reduction of gamma-aminobutyric acid (GABA) in the brain, one of the neurotransmitters. It has to be determined whether the former two abnormalities offer a background for such an abnormality of the neurotransmitter.
A defect of the myo-inositol maintenance mechanism in the lens of hereditary cataract mice.
The myo-inositol uptake system was studied in lenses of normal and hereditary cataract mouse. The normal mouse was able to accumulate myo-inositol continuously from medium and keep it in a high concentration. The specific myo-inositol uptake was dependent on temperature and it decreased in Ca(2+)-free medium. In contrast, specific uptake of myo-inositol reached a plateau after 15 min in the cataract mouse lens although initial incorporation was more rapid than that in normal mouse lens. This uptake system was not affected by temperature or Ca(2+) in the medium. The rate of myo-inositol efflux into the medium was more rapid in the cataract lens than that of the normal lens. It was shown that the low level of myo-inositol in the lens of hereditary cataract mouse was due to the defect of myo-inositol transport system and the enhanced efflux rate. These results suggest a dysfunction of the lens membrane.
Myo-inositol content of the lens in hereditary cataract mice.
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Systemic antitumor activity of Bacillus Calmette Guerin and purified protein derivatives against tumors in mice having tuberculin allergy.
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myo-Inositol binding and transport in brush border membranes of rat kidney.
Using hypotonically treated brush border membranes, binding and transport of myo-inositol were examined. By hypotonic treatment, both total and non-specific uptake decreased significantly, but specific uptake was not affected. myo-Inositol release from membranes preloaded by incubation for 2 min was very rapid and about 98% of preloaded myo-inositol was released in 5 min of incubation. However, myo-inositol release from membranes preloaded by incubation for 20 min was fairly slow and 50% of myo-inositol remained in the membranes even after 10 min of incubation. Uptake of myo-inositol decreased by the increase of osmolarity in the medium. However, effect of osmolarity on the uptake was less significant when myo-inositol concentration was lower. Under conditions in which mainly binding occurred, myo-inositol binding to the membranes was measured. Two binding systems were demonstrated and high affinity site could bind 22 pmol/mg protein at most and the apparent Km value was 8.3 muM. Both binding and transport processes were dependent on Na+ and enhanced by Na+-gradient.
Preparation of radioactive basic protein of bovine nervous tissue.
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Alpha-aminoadipic acid delta-semialdehyde in bovine and guinea pig myelin proteins.
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Enhancement of encephalitogenic activity by the formation of myelin basic protein-brain acidic protein complex.
Encephalitogenic protein fraction (BEC) was isolated from bovine brain tissue by extraction with salt-ethanol mixture at neutral pH, instead of employing dilute mineral acid. The fraction BEC was separated into two fractions. An acid-soluble protein was encephalitogenic and the major component was very alike to the basic protein of myelin (Al). The other was acid-insoluble acidic protein that was not encephalitogenic even at a dose of 100 mug. The acidic protein formed an insoluble complex with Al rotein which was purified by Eylar's method. Encephalitogenic activity of the complex was higher than Al protein in young guinea pigs when injected with complete Freund's adjuvant.However, this enhancement of encephalitogenic activity was not observed in aged guinea pigs. The complex showed higher blastogenic activity than Al protein alone with peripheral blood lymphocytes from guinea pigs immunized with Al protein and complete Freund's adjuvant. These results show that an adjuvant-like acidic protein is present in brain tissue and the complex with Al protein enhances the induction of experimental allergic encephalomyelitis (EAE).
Experimental allergic encephalomyelitis (EAE) in mice. I. Induction of EAE with mouse spinal cord homogenate and myelin basic protein.
The condition of experimental allergic encephalomyelitis (EAE) induction was investigated in several mice strains. SJL and C3H/He strains were found to be susceptible. A single immunization with mouse spinal cord, complete Freund's adjuvant (CFA) and pertussis vaccine produced clinical signs of EAE in SJL and C3H/He strains after 11 to 18 days. Isogenic spinal cord produced EAE in C3H/He strain. A single immunization with myelin basic protein from bovine spinal cord in CFA and pertussis vaccine produced EAE in SJL strain. EAE susceptibility of SJL strain correlated with the amount of mycobacteria used for sensitization. It was necessary to give pertussis vaccine intravenously in all cases.
[Glycolipids of Mycobacterium tuberculosis].
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