PubMed Health⌕ Search

Biomedical subjects

R V Talmage

Publications and source records attributed to R V Talmage.

84 records · Page 5Linked to original sources
PubMedDate not supplied

Calcium homeostasis: solving the solubility problem.

This report summarizes the evidence that the control of the concentration of free calcium ions in body fluids is centered at mineralized bone surfaces. This process involves an increase in the solubility of bone mineral produced by the non-collagenous proteins existing in the bone extracellular fluid (ECF) and on the adjacent surfaces of bone. The result is a basic equilibrium level produced in the absence of parathyroid hormone (PTH), which is well above the solubility of bone mineral. The effect of PTH is to increase the solubility of bone mineral still further, but the mechanism by which the hormone acts is unknown. The lining cells of the bone contain receptors for PTH and can be observed to respond to this hormone, but the relationship between this response and the increased solubility of bone remains to be discovered. Further research in this field is strongly urged.

Animals↗
PubMedDate not supplied

Electron microscopic study of the effects of calcitonin on bone cells and their extracellular milieu.

This is a scanning and transmission electron microscopic study of the changes produced by small doses of calcitonin (0.15 mU/g body weight) in the lining cells and their microenvironment at the endosteal surfaces of the tibia of neonate rats. The techniques used included "freeze substitution" preparation, staining with lead acetate, and with lanthanum added to the fixative. Rats were sacrificed 5, 15, and 30 minutes after subcutaneous injection of salmon calcitonin. The following observations were made; within 5 minutes following calcitonin injection, the response of the endosteal lining cells included increased numbers of microvilli and surface blebs. Cell contraction was apparent, including an irregular appearance of the plasma membrane and enlarged intercellular channel size, though cell-to-cell contact still occurred. By 15 minutes, following hormone injection, the cells were returning to normal morphology and were in close contact with each other. Calcitonin caused a marked accumulation of lanthanum around osteocytes and in bone fluid adjacent to lining cells. The lanthanum was found in large aggregates and appeared to "clump." Following "freeze substiuttion" preparation, the edge of the osteoid was bordered by what appeared to be mineral aggregates. We conclude that bone lining cells and osteocytes respond rapidly to low doses of calcitonin, thereby suggesting that they play a role in the physiological action of the hormone. This function includes a modification of the fluid microenvironment of these cells, possibly providing a site for temporary storage of calcium.

Animals↗
PubMedDate not supplied

A laboratory model demonstrating osteocyte-osteoblast control of plasma calcium concentrations. Table model for plasma calcium control.

This report describes a laboratory model designed to illustrate a newer concept for the control of plasma calcium concentrations. This postulate suggests that plasma calcium levels are the result of a balance or imbalance in opposing calcium ion fluxes between plasma and bone fluid compartments existing around osteocyte-lining cells (osteoblasts) units in bone. The metabolic control of these fluxes is postulated to reside within the lining cells on the surface of bone. These cells serve as a cellular interface between the two fluid compartments. The model described in this report illustrates these principles by using the height of columns of water in cylinders to represent calcium ion concentrations. A water pump, representing the calcium transcellular transport system in the lining cells, maintains a higher level of water in the cylinder representing plasma than in that representing bone fluid. This is accomplished by continuous pumping of water from the bone fluid cylinder to the plasma cylinder. Water is returned to the bone fluid cylinder as long as a differential in the height of water in the two cylinders exists. A constant height of water in the plasma cylinder is maintained when the two fluxes are in equilibrium. A constant height of water in the cylinder representing bone fluid is maintained by the level of water in a much larger cylinder representing calcium equilibrium between the solid and liquid phases of bone. The primary hormone controlling the rate of calcium transfer from bone fluid to blood, or in the model regulating the speed of water pump, is parathyroid hormone.

Adult↗
PubMedDate not supplied

The presence of lining cells on surfaces of human trabecular bone.

Sixteen human trabecular bone biopsies were obtained from sites located in the ilium and in the area of the greater trochanter of the femur. Patients ranged from 19 to 85 years old and included men and women. All bone surfaces observed contained osteoid. Flat, branched fibroblastic-like cells were observed lining bone surfaces in all biopsy specimens. The presence of these cells was not dependent on age, sex, race, or disease state of the patient. Based on this study, we believe that the majority of human trabecular bone surfaces are covered with these thin lining cells.

Adult↗
PubMedDate not supplied

Calcitonin and the bone fluid compartment: effect of calcitonin and/or parathyroid hormone on plasma radiocalcium changes.

Changes in plasma calcium and 45Ca concentrations were followed after injection of calcitonin or a combination of calcitonin (CT) and parathyroid hormone (PTH) into thyroparathyroidectomized rats maintained on thyroxine. Comparison was made between rats injected with the hormone(s) after a recent feeding and after an overnight fast. Also cor (18 hr 45Ca) before, and more than 6 days (greater than 6 day 45Ca) prior to hormone administration. The following results were obtained: The action of CT predominated over that of PTH for the first few hours after injection. However, the effects of PTH were eventually manifested even when additional CT was administered. In the "greater than 6 day" 45Ca groups, PTH normally produced an increase in plasma 45Ca specific activity. However, in fasted rats, plasms 45Ca fell with total calcium with no change in specific activity following CT injection. In fed rats CT injection was followed by a decrease in plasma 45Ca specific activity. When both hormones were administered plasma 45Ca specific activity changes mimicked those produced by CT alone even after PTH plasma effects were manifested. In the "18 hr" 45Ca groups, CT produced first a drop in plasma 45Ca, followed by a reduction in the rate of its removal from plasma. It is concluded that the data can best be explained by the postulate that plasma calcium concentrations are maintained by the control of fluxes between bone fluid in the osteocyte-lining cell bone unit and the extracellular fluid. PTH increases the efflux from this bone fluid compartment while CT restricuts the source of calcium and, therefore, the efflux. Plasma 45Ca changes are due to a combination of changes in flux rates and mixing processes between the extracellular fluid compartment and the bone fluid compartment.

Animals↗