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Biomedical subjects

Y Higuchi

Publications and source records attributed to Y Higuchi.

At least 289 records · Page 16Linked to original sources
PubMed1983

Studies on delayed-type hypersensitivity (DTH) reactions in the pleural cavity in mice: prolonged DTH reaction and its interruption by cyclophosphamide treatment.

DTH reactions to sheep erythrocytes (SRBC) and purified protein derivative (PPD) antigens were produced in the pleural cavity in mice. The profiles of the DTH reactions with respect to time course and cellular exudate reactions differed greatly according to the strains of mice. In particular, HY mice that were established in our laboratory displayed prolonged DTH reactions, characterized by macrophage followed by lymphocyte reactions. HY X C3H F1 mice showed a similar tendency. On the other hand, strains such as C3H, BALB/c, DBA/2 and B6 mice showed short-lived and macrophage-predominant DTH reactions. BALB/c nu/nu mice showed no DTH reactions. Characteristic features of the prolonged DTH reactions in HY mice were transferred with sensitized T cells. However, DTH reactions in HY mice treated with cyclophosphamide (CY) terminated in a short period, and mainly consisted of macrophages and polymorphs, although they were greatly enhanced. Such profiles of the reactions could also be transferred with sensitized T cells from CY-treated and SRBC-sensitized mice. Spleen cells taken from CY-treated and SRBC-sensitized HY mice, when injected intravenously into SRBC-sensitized HY mice just prior to challenge, could not interrupt prolonged DTH reactions. These results thus indicated various phenotypes of the DTH reactions in terms of time course and exudate cellular component involved might be carried by the specific effector T cells in each phenotype of the DTH reactions and could be induced using strains of mice and CY.

Animals↗
PubMed1982

The relationship between senile plaques and cerebral blood vessels in Alzheimer's disease and senile dementia. Morphological mechanism of senile plaque production.

Several kinds of senile plaque found in 6 brains (4 from patients with Alzheimer's disease and 2 from patients with senile dementia) were examined in serial sections by light electron microscopy. The results obtained were as follows. All the senile plaques contained at least some amyloid fibrils, and these seemed to be produced at the basement membranes of capillary endothelial cells and projected into the surrounding parenchyma. Even when the senile plaques themselves appeared to lack amyloid fibrils by light microscopy, at least one degenerable capillary containing amyloid fibrils was demonstrable when serial sections were examined ultrastructurally. The findings described above suggest that the amyloid fibrils which form the cores of the several kinds of senile plaque, seem to be produced at the basement membrane of the endothelial cell. It is speculated that the capillary degeneration with the formation of amyloid fibrils may be primary change in the genesis of senile plaques.

Aged↗
PubMed1982

Changes of lipid peroxides and alpha-tocopherol in rats with experimentally induced myocardial necrosis.

Myocardial necrosis was produced in rats by injection of isoproterenol (80 mg per kg body weight). Lipid peroxides were measured by the thiobarbituric acid reaction. alpha-Tocopherol was assayed by fluorometric analysis. Immediately after isoproterenol injections, serum lipid peroxides increased and serum alpha-tocopherol decreased, then gradually returned to the pre-injection levels. Lipid peroxides increased more rapidly in the heart and liver than in serum. Alpha-Tocopherol decreased in the heart and liver, then gradually returned to the pre-injection levels. These results indicate that increase in serum lipid peroxides reflects production of peroxides in myocardial tissue and in liver. The decrease in alpha-tocopherol may be due to consumption as anti-oxidants in the vascular system and organs.

Animals↗
PubMed1982

Lipid peroxides and alpha-tocopherol in rat streptozotocin-induced diabetes mellitus.

Measurement of lipid peroxides and alpha-tocopherol was undertaken in rats with streptozotocin-induced diabetes. In sera and livers in diabetic rats, the lipid peroxides increased but alpha-tocopherol decreased. To study the effect of vitamin E deficiency in the diabetic state, diabetes was induced in rats maintained on a vitamin E deficient diet. Serum lipid peroxides increased greatly but alpha-tocopherol decreased. Lipid peroxides and alpha-tocopherol increased in the liver of vitamin E deficient states. In the liver, vitamin E deficient diabetic rats had lower lipid peroxides levels but higher alpha-tocopherol levels than vitamin E deficient non-diabetic rats. On the basis of the present experiments, it was considered that the decrease of alpha-tocopherol might be due to consumption as an antioxidant as lipid peroxides increased in sera and livers. The decrease of lipid peroxides in the liver was thought to play an important part of the increase in serum lipid peroxides.

Adult↗
PubMed1982

Biochemical and electron microscopic observations of cytotoxic effect of a fraction from hemolytic streptococcus on Ehrlich ascites carcinoma cells.

A protein fraction (60-F), obtained from cell-free extract of living hemolytic streptococcus, Su-strain, by 50-60% saturation with ammonium sulfate, inhibited the de novo synthesis of nucleic acids and proteins in Ehrlich ascites carcinoma (EAC) cells. 60-F released RNA but not DNA from EAC cells. This cytotoxic or cytolytic effect of 60-F was substantiated morphologically by scanning and transmission electron microscopic (SEM and TEM) observations, showing that 60-F induced cellular changes such as a loss of microvilli, bleb formation, cell deformity and partial gap of cell membrane in EAC cells. In addition, it was found that 60-F was more stable in RPMI-1640 medium supplemented with fetal calf serum than in other various media examined and was sensitive to temperature, pH changes and trypsin digestion.

Amino Acids↗
PubMed1982

[Mitral annular calcifications in patients with hypertrophic obstructive cardiomyopathy: an echocardiographic study].

From the echocardiographic files of 1,231 patients, eight revealed mitral annular calcification (MAC), in whom four had hypertrophic obstructive cardiomyopathy (HOCM). In the remaining four patients without HOCM, whose ages ranged from 69 to 80 years with a mean of 73 years, an additional calcification was observed in the either aorta or aortic valve. Therefore, MAC was thought to be a part of the aging process. Of the four patients with HOCM two were females (71 and 78 years, respectively) and two were males (50 and 51 years, respectively). The latter two younger male patients had MAC without another calcific lesion, and the cause of MAC was suspected as the pressure and/or mechanical strain on the mitral orifice due to excessive movements of either the chordae tendineae or papillary muscle.

Aged↗
PubMed1982

Enhancement of sheep erythrocyte (SRBC)-induced pleurisy in non-sensitized mice by cyclophosphamide: demonstration of natural cell-mediated immune reactivity to SRBC.

Intrapleural injection of 2 x 10(8) sheep erythrocytes (SRBC) into normal C57BL/6N (B6) mice produced a low but significant exudate leucocyte reaction, which was delayed in onset and mononuclear cell dominant. However, administration of 20-200 mg/kg cyclophosphamide (CY) in mice induced a dose-dependent enhancement of this reaction. In contrast, erythrocytes of syngeneic and allogeneic mice, rats, guinea-pigs rabbits and humans showed no or slight enhancement in CY-treated B6 mice. Maximal enhancement was observed on day 6 after CY treatment, but the reactions fell on day 7 and gradually decreased thereafter. B6 mice from specific pathogenfree colonies also showed strong reactions on day 6 after CY treatment. B6 mice demonstrated the highest reactions and C3H/He (C3H) mice were intermediate, while BALB/c mice showed very low responses. F1 hybrid (BALB/c x B6) mice showed an intermediate response as compared with the parent strains. The enhanced reactions reached their peak at 24 hr after SRBC injection and mainly consisted of macrophages and polymorphs. The enhancement could be successfully transferred to naive syngeneic mice by viable spleen cells from CY-treated mice but not by sera. The mediator cells could not bind to plastic petri dishes or a nylon-wool column, and were sensitive to anti-Thy-1.2 + C treatment . These results thus indicated that the enhancement was induced by the cell-mediated immune (CMI) mechanisms. The appearance of natural CMI reactivity to SRBC, and its role in relation to immunological reactions is discussed.

Animals↗