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Biomedical subjects

A Uezu

Publications and source records attributed to A Uezu.

12 recordsLinked to original sources
PubMed1988

[Parathyroid hormone and bone mineral content in male and female patients receiving hemodialysis].

Relative bone mineral content in the lumbar spine was measured by phantom B-MAs with the apparatus of computerized tomography in order to study the relationships between bone mineral content with age and parathyroid hormone in sera of randomized out- and in-patients and the hemodialysis patients. There exists a significant difference between male and female in the loss of bone mineral content of three groups.

Adult↗
PubMed1980

Vitamin D and parathyroid hormone degradation by the kidney.

Parathyroid function is controlled by the regulation of hormone secretion as well as degradation, through the action of calcium and vitamin D derivatives. In order to clarify the relationship between vitamin D metabolism and parathyroid degradation system, parathyroid hormone (PTH)-degrading activities of the kidney were measured in vitamin D repleted and depleted rats given various derivatives of vitamin D. Kidney calcium content rose markedly in animals given 10 microgram/kg 1 alpha(OH) vitamin D3 and 1,000 microgram/kg dihydrotachysterol and PTH-degrading activity rose only in these animals, indicating a parallelism between kidney calcium content and PTH-degrading activity of the kidney tissue. These vitamin D derivatives also increased the PTH-degrading activity of kidney tissue when they were added in vitro.

Animals↗
PubMed1978

[Degradation of the parathyroid hormone in the kidney and liver (author's transl)].

The cleavage of the parathyroid hormone has been reported to take place in various peripheral tissues, especially in the kidney and liver. In order to claify the mechanism of such a degradation, bovine PTH (bPTH 1--84) and its synthetic N-terminal peptide (bPTH 1--34) labelled with 125I by the chroramine-T method (125I-bPTH 1--84) and (125I-bPTH 1--34) or labelled with horseradish peroxidase Pox-125I-bPTH 1--84 and Pox 125I-bPTH 1 34) were used to study the disappearance from the blood stream and degradation and retension in the kidney and liver after intravenous injections in male Wiastar rats, weighing approximately 200g. Degradation of PTH was also studied in vitro, using isolated cells and a homogenate of the kidney and liver. PTH labeled with 125I and Pox was more readily degraded by the kidney than PTH labelled with 125I alone, but the opposite was found in the degradation by the liver. Isolated intact kidney cells degraded PTH less efficiently than the homogenate, but the isolated intact liver cells degraded PTH more efficiently than the homogenate, indicating the prominence of an intracellular mechanism of degradation in the kidney and an extracellular mechanism in the liver.

Animals↗
PubMed1977

Control of parathyroid hormone hydrolysis by the kidney.

In order to assess the role of the kidney in controlling the degradation, fate, half-life, and consequently the functional level of the parathyroid hormone in vivo, highly purified bovine parathyroid hormone (bPTH 1-84) and synthetic N-terminal peptide of the bovine parathyroid hormone (bPTH 1-34) were iodinated and their hydrolysis by the kidney and liver tissue of rats were measured under various levels of parathyroid function and calcium metabolism. While the hydrolysis of bPTH 1-84 did not change significantly in response to acute change of serum parathyroid hormone in response to injections of EDTA, phosphate, and calcium or after parathyroidectomy, less bPTH 1-34 was hydrolyzed 60 min after injection of EDTA or phosphate along with the rise of serum PTH than in the controls. No significant change was found in the hydrolysis of bPTH 1-34 after calcium infusion or parathyroidectomy with a consequent fall of serum parathyroid hormone. Increase of calcium ions in the incubation medium in vitro resulted in a more pronounced increase of bPTH 1-34 hydrolysis than that of bPTH 1-84. Hydrolysis of the N-terminal portion of parathyroid hormone probably plays a more important role in the acute control of the functional level of the parathyroid hormone than the hydrolysis of the whole molecule.

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↗