Search PubMed⌕ Search

Biomedical subjects

T Tsuda

Publications and source records attributed to T Tsuda.

At least 721 records · Page 40Linked to original sources
PubMed1977

A new factor from enteric bacteria of rats amplifying induction of liver enzyme by glucocorticoid. 1. Purification, properties and biological action.

1. A factor, which amplifies the inductions of several liver enzymes by glucocorticoid, was partially purified from Proteus mirabilis from rat intestine. The factor (amplifier) was completely inactivated by alpha-glucosidase, but not by other glycoside hydrolases, proteases, nucleases or phosphatases tested; it was also hydrolysed by HCl with liberation of reducing sugars. Thus the oligosaccharide in this factor seems to be essential for the amplification. 2. In adrenalectomized rats the amplifier increased the inductions of several liver enzymes, such as tyrosine aminotransferase and leucine aminotransferase, by glucocorticoid. But it did not amplify the induction of tyrosine aminotransferase by glucagon or insulin or the activities of enzymes that are not induced by glucocorticoid. The amplifier by itself did not have any glucocorticoid-like action in adrenalectomized rat. These results show that the amplifier specifically increases the inductions of liver enzymes by glucocorticoid. 3. Since similar amplification was also observed in isolated perfused liver and cultured hepatoma cells in vitro, the amplifier seems to act directly on the target organ or cells.

Animals↗
PubMed1977

Effect of 1alphaOH-vitamin D3 in a case of pseudohypoparathyroidism.

A 37-year-old woman with typical features of pseudohypoparathyroidism (chronic tetany, paresthesia, persistent hypocalcemia, round face, short stature, short metacarpals and metatarsals, cucutaneous calcification and lack of response to exogenous and endogenous parathyroid hormone as regards urinary phosphate and cyclic AMP excretion) was treated with oral administration of 2 microgram/day of 1alphaOH-vitamin D3. Serum calcium started to rise within 3 days returning to the normal level with disappearance of symptoms referrable to hypocalcemia. Such a favorable effect of a small dose of 1alphaOH-vitamin D3 in a patient with typical hypoparathyroidism suggests an important role of disturbance of 1alpha-hydroxylation of vitamin D3 by the kidney in the pathogenesis of calcium and phosphorus abnormality in this disease. Forty-four cases of pseudohypoparathyroidism in the Japanese literature were briefly reviewed.

Administration, Oral↗
PubMed1976

Aging and parathyroid hormone secretion.

Influence of age on parathyroid hormone secretion and release was studied in vitro using rat parathyroid glands in culture and in vivo by EDTA injection. Parathyroid hormone was measured by radioimmunoassay using guinea pig antibody for bovine parathyroid hormone and 125I-labeled synthetic N-terminal peptide of bovine parathyroid hormone. Significantly less PTH was released from parathyroid glands of 18-mo-old rats than from those of 1 mo of age at various calcium concentrations of the medium in vitro. Secretion of parathyroid hormone in response to EDTA-induced hypocalcemia in vivo was also less in older rats than in younger ones, giving lower deltaPTH/deltaCa values in the older animal. Secretion of parathyroid hormone therefore appears to decrease along with aging in rats.

Aging↗
PubMed1976

Mononuclear cell turnover in chronic inflammation: studies on tritiated thymidine-labeled cells in blood, tuberculin traps, and dermal BCG lesions of rabbits.

Rabbits were injected intradermally in multiple sites with BCG. Four days after the BCG injection, they were injected intravenously with a single pulse of tritiated thymidine (3H-TdR) at various times thereafter, the BCG lesions were biopsied and evaluated for 3H-TdR-labeled mononuclear cells (MN). Periodically, Old Tuberculin (OT) was injected intradermally, creating MN traps which were biopsied and evaluated 1 day after their onset. 3H-TdR-labeled cells were also evaluated in samples of blood. During the first 8 days after the 3H-TdR pulse, the labeled MNs represent short-lived cells, i.e., recently dividing monocytes and lymphocytes. During this time, the percentage of labeled MNs in the blood, in the traps, and in the BCG lesions rose and fell together. This result suggests that the majority of the MNs in the BCG lesions had a turnover rate of about a week. By 12 days and afterward, the percentage of MNs labeled by 3H-TdR in the blood was higher than that in the BCG lesions which was in turn higher than that in the traps. At this time the circulating MN population probably contained labeled long-lived lymphocytes that did not enter inflammatory sites (the traps) as readily as the short-lived lymphocytes. The labeled MNs remaining in the BCG lesions probably did not divide and dilute out their 3H-TdR label as readily as those that were trapped from the bone marrow via the blood. The percentage of MNs labeled with 3H-TdR in the traps had decreased to about one-fifteenth of its peak value by 12 days, suggesting that the bone marrow's supply of labeled MNs was depleted at this time, except for the few cells labeled as a result of 3H-TdR reutilization.

Animals↗
PubMed1975

Capillary density in developing and healing tuberculous lesions produced by BCG in rabbits. A quantitative study.

Dermal tuberculous lesions were produced in rabbits by the intradermal injection of BCG. At various times after infection, anesthetized animals were perfused with a gelatin-colloidal carbon medium via the abdominal aorta. The capillary density of the nonnecrotic granulation tissue in the lesions was determined quantitatively by counting the capillaries under an ocular grid of a microscope. The capillary density in normal skin near the lesions was 3.8 plus or minus 0.5 in millimetersof capillary lengths per square millimeter in 250-mu tissue sections. The capillary density of the nonnecrotic tissue in BCGlesions averaged 6.1 plus or minus 0.6 mm/sq mm, an increase of 60%. The capillary density remained more or less constant as the BCG lesions grew and then regressed. The development of delayed hypersensitivity seemed to increase the capillary density, but this increase may have been a response to an extension of the necrosis at the time delayed hypersensitivity developed. Capillary densities in tuberculin reactions resembled those in BCG lesions. In the early stages, the increaseed capillary network of dermal BCG lesions was derived mainly from the subpapillary vascular plexus of the deep dermis supplied branches that surrounded the lower half of the caseous necrotic center and anastomosed with capillaries from the subpapillary plexus supplying the upper half. When the necrotic center extended, nearby capillaries thrombosed and in turn became necrotic. Peripherally, new capillaries formed and anastomosed with existing capillaries. From these vessels, mononuclear phagocytes emigrated, destroyed the tubercle bacilli, and enabled the lesion to heal. In the BCG lesions at all stages of development and healing, the capillary network in the nonnecrotic areas seemed adequate to supply and nourish the defense cells controlling the infection.

Animals↗