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Biomedical subjects

M Tsuchida

Publications and source records attributed to M Tsuchida.

At least 163 records · Page 9Linked to original sources
PubMed1987

Trends in death and consultation rates of ischemic heart disease in Japan and the risk factors in a rural community.

In Japan, the age-adjusted death rate from ischemic heart disease has decreased for both male and female since 1970, although the rate appears to be slightly affected by mortality from senility without mention of psychosis, "cardiac insufficiency", and sudden death in elderly persons. On the other hand, consultation rate has shown an increase, suggesting an increase in the number of recovered patients and a lengthening in the duration of ischemic heart disease from onset to termination by CCU treatment. A 7.5-year prospective study of ischemic heart disease (myocardial infarction + angina pectoris on effort + sudden death) among residents 40 years and older was conducted at a rural community, Akadani-Ijimino district in Niigata Prefecture. Statistically significant risk factors appeared to be age, hypertension, ECG abnormalities and fuduscopic changes. Even in 1977-1984 when Japanese dietary habits were westernized, neither hyperlipidemia nor obesity was related to the development of ischemic heart disease in this agricultural district. Statistically significant risk ratios were not observed for any nutrient or food, although the ratio for animal fat, calcium, salted vegetables and caloric percent of animal protein was more than one respectively.

Adult↗
PubMed1985

Fluorescent substances in mouse and human sera as a parameter of in vivo lipid peroxidation.

Water-soluble fluorescent substances like lipofuscin were found in the protein fraction of mouse and human sera and had fluorescence characteristics with excitation and emission maxima at 335-340 and 435-440 nm for mice, and at 355-360 and 430-435 nm for human, respectively. When oxidized [U-14 C]linoleic acid was given intraperitoneally to mice, or added to the serum in vitro, both the fluorescence intensity and radioactivity of serum protein increased dose-dependently in the two tests. Also, the fluorescent substances responded well to acceleration of in vivo lipid peroxidation caused by carbon tetrachloride. These results indicate that the substances were some binding compounds between the degraded lipids and serum proteins, and that they could be taken as a parameter of in vivo lipid peroxidation. The distribution of the pigments in the serum proteins, albumin and globulins, was shown to depend upon the number of free amino groups in each protein which appear to be binding sites of degraded lipids. Spectral characteristics and some chemical properties of the substances suggest that they might not be conjugated Schiff bases formed from protein and malondialdehyde but might be due to some other stable compounds. Significantly high levels of the substances were observed in sera of patients with diabetes and hypertension.

Adult↗
PubMed1985

Tay-Sachs disease associated with precocious puberty.

A girl with Tay-Sachs disease developed enlargement of the mammary glands at the age of 4 years and menstruation at the age of 6 years. It was demonstrated that the precocious puberty in this patient was due to the hypersecretion of gonadotropins.

Child↗
PubMed1985

[Studies on hyperthermia and radiation treatment of uterine cancer using multicellular tumor spheroid].

Anticancer effects of hyperthermia and radiation on uterine cancer cells were studied using multicellular tumor spheroids and monolayer cultured cells. Cell lines used were SKG-3a(uterine cervical epidermoid carcinoma), HeLa-S3 (uterine cervical adenocarcinoma) and HEC-59 (uterine corpus adenocarcinoma). All cell lines grown in monolayer culture have similar growth rates, but as spheroids, their growth rate are HeLa-S3 greater than HEC-59 greater than SKG-3a cells. The radiosensitivity of all cell lines in monolayer are as follows according to dose-survival relationships. :HEC-59 greater than HeLa-S3 greater than SKG-3a cells. Survival assay to hyperthermia on SKG-3a and HEC-59 cells resulted in no response from 37 degrees to 41 degrees C and in cytotoxicity over 42 degrees C. There is no difference in sensitivity to hyperthermia between the two types of cells. The responses of three cell lines grown as spheroids in hyperthermia and radiation demonstrated that the combination therapy is not effective on the SKG-3a cell, but induced a 1.3-fold effectiveness ratio in HEC-59 and 1.6-fold in HeLa-S3 cells, i.e. more cytotoxicity than with radiation alone. These results suggests that hyperthermia and radiation employed together may be more effective on radioresistant adenocarcinoma cells than on radiosensitive epidermoid carcinoma cells.

Adenocarcinoma↗
PubMed1984

Elevation of thiobarbituric acid values in the rat liver intoxicated by T-2 toxin.

In the present study we first demonstrated that T-2 toxin markedly stimulated lipid peroxidation specifically in the liver of rats. The amount of lipid peroxides in the liver, estimated by the thiobarbituric acid (TBA) method, increased dose dependently, being proportional to the extent of its acute toxicity measured by various parameters in rats fed a commercial diet. Further, to elucidate the mechanism of lipid peroxidation and its role in hepatic injury caused by T-2 toxin, time-course studies on the correlation between lipid peroxide content and some biological and histopathological data were undertaken in rats given 4 mg of the toxin/kg perorally. The TBA reactive substances in the liver began to increase after 6 hr. However, much earlier than this there were some other alterations, which included decreases in the amount of cytochrome P-450 in the liver, of GPT (thereafter an increase) and phospholipids in the plasma, and of basophilic masses in the hepatocytes (arrayed as a rough endoplasmic reticulum in the electron micrograph). The vitamin E-deficient study showed that vitamin E markedly inhibited the stimulative effect of T-2 toxin on lipid peroxidation, but not diminish any other measured parameters of the injury. The toxin-induced stimulation of lipid peroxidation does not appear to be caused by activation of microsomal NADPH-cytochrome c reductase nor by a decrease in the level of cytosolic glutathione peroxidase. These results suggest that T-2 toxin might induce some alteration of the membrane structure and consequently might stimulate lipid peroxidation in situ.

Animals↗