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Biomedical subjects

Y Sakagami

Publications and source records attributed to Y Sakagami.

At least 181 records · Page 10Linked to original sources
PubMed1980

Effects of retinoids on induction of differentiation of cultured mouse myeloid leukemia cells.

Retinoic acid, retinol, retinyl acetate, and retinal induced activities of lysosomal enzymes, such as lysozyme, acid protease, and acid phosphatase, in mouse myeloid leukemia cells (M1), while the pyridyl analog of retinoic acid had no effect. Retinoic acid was the most potent inducer of lysosomal enzyme activities. The induction of lysozyme activity by retinoic acid was inhibited by treatment with puromycin. The retinoids did not induce phagocytic and locomotive activities or morphological changes in M1 cells, and they inhibited the induction of these differentiation-associated properties by various inducers without inhibiting cell growth. Retinoic acid was the most potent inhibitor of induction of these differentiation-associated properties. The inhibitory effect of retinoic acid was found to be reversible. These results suggest that distinct mechanisms exist for control of induction of lysosomal enzyme activities and of other differentiation-associated properties of M1 cells, such as phagocytosis, morphological changes, and migration.

Animals↗
PubMed1979

Acceleration of mammary cancer development by grafting of fetal mammary mesenchymes in C3H mice.

Transplantation of fetal mammary gland mesenchyme into mammary glands of 2-month-old syngeneic virgin mice resulted in focal re-enactment of events that normally occur probably during fetal and early postnatal development of the mammary gland. Portions of the recipient's mammary duct system in contact with the fetal mammary mesenchyme underwent branching and proliferation in a pattern resembling that of rudimentary mammary gland development. This process occurred in C3H mice regardless of whether or not the milk-transmitted mammary tumor virus (MTV-S) was present. In mice carrying MTV-S, mammary cancers of Types A and B appeared earlier and more frequently in the mammary glands that had received transplants of fetal mammary mesenchyme, compared with those in the glands that received no fetal mesenchyme. Some of the smaller cancers were shown to develop directly from portions of the mammary gland interacting with fetal mammary mesenchyme, without preformation of typical hyperplastic alveolar nodules. In C3H mice not carrying MTV-S, cancers did not appear in the similarly treated mammary glands. These facts suggest that non-hormonal and probably nonviral factors that stimulate focal proliferation in the mammary duct system resulting from transplantation of fetal mesenchymes eventually accelerate local development of mammary cancers.

Animals↗
PubMed1978

Insulin secretion after oral calcium load.

Oral glucose tolerance test with 50 g glucose was carried out with and without simultaneous oral administration of 3 g calcium lactate. Blood sugar and serum immunoreactive insulin (IRI) were measured before and 30, 60, 90 and 120 min after glucose load in 11 diabetics and 11 non-diabetics. Similar oral glucose tolerance test was performed with and without intravenous administration of 10 ml 8.5% calcium gluconate in 6 diabetics and 6 non-diabetics. Maximum serum level after glucose load (Max IRI), maximum rise of serum IRI following glucose load (Max delta IRI), maximum delta IRI/delta BS following oralglu cose load (Max delta IRI/delta BS), the area surrounded by the delta IRI curve and the abscissa (sigma delta IRI) and the area surrounded by the delta IRI/delta BS curve and the abscissa (sigma delta IRI/delta BS) significantly increased in diabetics but not in non-diabetics after oral calcium load, whereas intravenous calcium load failed to influence any of these values. Oral calcium load thus appears to augment glucose-induced insulin secretion only in diabetics, suggesting some abnormality in the mechanism of insulin secretion with reference to calcium in diabetes mellitus.

Administration, Oral↗
PubMed1977

Calcium metabolism in aging inhabitants of mountain versus seacoast communities in the Kii Peninsula.

A survey was conducted on age-related changes in various measures of calcium metabolism in 609 men and women over the age of 30 (more than half were over the age of 60) in two communities of the Kii Peninsula at the central southern tip of the Japanese mainland. One community was on Oshima Island, with adequate nutritional intake; the other community was in the mountainous Shichikawa district, with a low intake of calcium and protein. The subjects of the Shichikawa study showed shorter stature, higher prevalence of lumbago, thinner clavicular cortex, lower serum levels of phosphorus, total protein and cholesterol, and a higher level of alkaline phosphatase than did the subjects of the Oshima study. There was no difference in the serum calcium levels.

Adult↗
PubMed1977

Elevation of serum 25-hydroxycalciferol levels in androgen-treated and ultraviolet-irradiated rats.

Administration of 4-8 mg testosterone propionate significantly raised 25-hydroxycalciferol levels in the ultraviolet irradiated rats compared to the ultraviolet irradiated controls, but failed to influence serum 25-hydroxycalciferol levels in the non-irradiated animals. Estradiol benzoate and progesterone did not influence serum 25-hydroxycalciferol levels regardless of the ultraviolet irradiation. These findings implicate that testosterone enhances vitamin D biosynthesis induced by ultraviolet irradiation in rats, in accordance with the clinical observation that males often show higher levels of serum 25-hydroxycalciferol than females.

Animals↗