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Biomedical subjects

D J Baylink

Publications and source records attributed to D J Baylink.

At least 325 records · Page 18Linked to original sources
PubMed1981

Improved method for quantitative determination in serum of alkaline phosphatase of skeletal origin.

In this quantitative method for detection of skeletal alkaline phosphatase (EC 3.1.3.1) activity in human serum, intestinal and placental alkaline phosphatase activities are recognized by their susceptibility to inhibition by L-phenylalanine, and skeletal and hepatic alkaline phosphatases are distinguished by their different sensitivities to inactivation by heat. Alkaline phosphatase isoenzymes prepared from organ sources may behave differently from the corresponding isoenzymes in serum. Our procedure allows us to include organ-derived internal standards of skeletal, intestinal, and biliary alkaline phosphatase to minimize between-assay variation. In preliminary applications, we have found that (a) total serum alkaline phosphatase activity is extremely variable in post-menopausal osteoporotic subjects and is not a reliable index of skeletal alkaline phosphatase activity; (b) seven osteoporotic patients responding to therapy with sodium fluoride with increased bone formation showed increased skeletal alkaline phosphatase activity in their serum as compared with age-matched controls (p less than 0.005); and (c) 10 post-menopausal osteoporotic patients responding to therapy with stanozolol with increased total body calcium showed an increase in circulating skeletal alkaline phosphatase activity (p less than 0.001).

Alkaline Phosphatase↗
PubMed1980

Basal plasma immunoreactive calcitonin in postmenopausal osteoporosis.

Calcitonin (CT) deficiency has been suggested as an etiologic factor in postmenopausal osteoporosis (PM-OP). Basal immunoreactive calcitonin (iCT) was measured with a sensitive radioimmunoassay (RIA) in 62 PM-OP women with compression fractures (CF) and in 28 normal age-matched women. Mean iCT values in the two groups were not significantly different (43.5 and 45.1 pg/ml, p greater than 0.10). In the 62 PM-OP females, no significant correlation was noted between basal plasma iCT levels and (1) age; (2) severity of disease as assessed by number of CF; (3) serum calcium, phosphorus, alkaline phosphatase, and immunoreactive parathyroid hormone; and (4) total bone mass as assessed by neutron activation analysis determinations of total body calcium (TBC). In 20 PM-OP patients treated for 24 mo with 100 Medical Research Council (MRC) units daily of synthetic salmon CT, no correlation was observed between basal plasma iCT and response of bone mass (TBC) to therapy. These data suggest that basal CT is not decreased in women with PM-OP, and that the level of circulating CT does not influence therapeutic changes in bone mass during CT therapy. CT is probably not a major etiologic or pathogenetic factor in PM-OP.

Aged↗
PubMed1980

In vitro synthesis of 1 alpha,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol by isolated calvarial cells.

The question of whether the skeleton metabolizes 25-hydroxycholecalciferol [25(OH)D3] to more-polar products was studied. Calvarial cells were dispersed from 16-day old chicken embryos by using collagenase and then grown in culture in serum-free medium. Confluent cell cultures were incubated with 7 nM 25(OH)[3H]D3 for 2 hr, and the vitamin D metabolites were then extracted. At least four polar metabolites were produced. Based on separation by Sephadex LH-20 chromatography followed by high-pressure liquid chromatography, two of these metabolites were identified as 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and 24,25-dihydroxycholecalciferol [24,25(OH)2D3]. These metabolites were also produced by cultured kidney cells but not by liver, heart muscle, or skin cells isolated from the same embryos. The specific activities of the calvarial 1- and 24-hydroxylases were similar in magnitude to those in isolated kidney cells. The specific activity of the calvarial 25(OH)D3:1-hydroxylase was inhibited by an 8-hr preincubation with 1,25(OH)2D3, whereas the 24-hydroxylase was enhanced. It is concluded that (i) vitamin D metabolism by isolated cells is organ-specific, (ii) calvarial cells produce active metabolites of vitamin D in significant amounts, (iii) vitamin D metabolism by calvarial cells is regulated by 1,25(OH)2D3, and (iv) locally produced, active metabolites could act locally, thereby adding a new dimension to the regulation of mineral metabolism by vitamin D metabolites.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1980

In vitro metabolism of 25-hydroxyvitamin D3 by isolated rat kidney cells.

Cells were dispersed from rat kidney after enzymatic digestion of the extracellular matrix. When the cells were suspended in a serum-free medium and incubated with (3)H-labeled 25-hydroxyvitamin D(3) (25-OH-D(3)) several polar metabolites, including 1,25-(OH)(2)[(3)H]D(3) and 24,25-(OH)(2)[(3)H]D(3) were produced. The specific activities of the 25-OH-D(3):1- and 24-hydroxylases in isolated rat kidney cells were 10-100 times greater than in avian kidney homogenates. The rates of production of 1,25-(OH)(2)D(3) and 24,25-(OH)(2)D(3) were linear over a wide range in cell densities (0.65-5.0 x 10(6) cells per ml) and substrate concentrations (3.5-70 nM). The rate of production of 24,25-(OH)(2)[(3)H]D(3) from 25-OH-[(3)H]D(3) by cells isolated from rats fed control diet was linear with time for up to 30 min, while the synthesis of 1,25-(OH)(2)[(3)H]D(3) was linear for over 90 min. The specific activity of the 25-OH-D(3):1-hydroxylase was increased in kidney cells from vitamin D-deficient rats (11.5 fmol/min per 10(6) cells) as well as calcium-deficient rats (8.1 fmol/min per 10(6) cells) when compared to cells from rats fed the control diet (2.0 fmol/min per 10(6) cells). Also, the specific activity of the 25-OH-D(3):24-hydroxylase was reduced in cells from the vitamin D-deficient rats (<0.2 fmol/min per 10(6) cells) and calcium-deficient rats (5.1 fmol/min per 10(6) cells) compared to the controls (15.2 fmol/min per 10(6) cells). On the basis of these results, as well as previous in vivo studies, we conclude that the metabolism of 25-OH-D(3) by freshly isolated rat kidney cells reflects the in vivo activities of the renal vitamin D-metabolizing enzymes and may prove useful as an assay.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1979

Bone mineralization and metabolism of 3H-25-hydroxyvitamin D3 in thyroparathyroidectomized rats treated with parathyroid extract.

Thyroparathyroidectomized rats fed a diet containing 1.2% calcium, 0.55% phosphorus maintain normal serum levels of these ions. Treatment of such rats with parathyroid extract (PTE; 20 U/100 g twice daily; 10 days) has no statistically significant effect on rates of bone formation, matrix apposition, or osteoid maturation. Significant decreases in osteoid width and mineralizing front width, as well as a 60% increase in the rate of initial mineralization were observed in the PTE-treated group. Conversion of 3H-25-hydroxyvitamin D3 to 3H-1,25-dihydroxyvitamin D3 was 4-fold higher in the PTE-treated group than in the untreated animals. Increased formation of 1,25-dihydroxyvitamin D3 in response to treatment with PTE may play a major role in correcting the mineralizing defect resulting from thyroparathyroidectomy.

Animals↗
PubMed1979

Calcium and phosphorus deficiency in rats: effects on PTH and 1,25-dihydroxyvitamin D3.

Weanling male Holtzman rats were fed calcium.deficient, phosphorus-deficient, or control diets for 8 wk. Parathyroid hormone (PTH) was measured by radioimmunoassay, and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) by a competitive binding assay. Rats fed the calcium-deficient diet (0.01% calcium, 0.6% phosphorus) became mildly hypocalcemic after 6 days. Serum calcium levels reached 5.5 +/- 0.4 mg/dl (mean +/- SD) in 5 wk (control 10.3 +/- 0.4 mg/dl). PTH increased from 285 +/- 112 to 3658 +/- 428 pg/ml within 6 wk. Maximum serum levels of 1,25(OH)2D3 (111.8 +/- 17.3 vs. control 11.4 +/- 3.8 ng/dl) were reached at 3 wk and thereafter declined to 44.6 +/- 14.0 ng/dl. In rats fed the phosphorus-deficient diet (0.6% calcium, 0.04% phosphorus), serum phosphorus fell within 24 h from 9.1 +/- 0.6 to 3.2 +/- 0.1 mg/dl, recovered to 5.6 +/- 0.4 mg/dl for 2-3 days, and then declined again. Serum calcium reached a maximum of 14.4 +/- 0.4 mg/dl at day 2 (control 10.8 +/- 0.5 mg/dl) and then slowly declined. PTH decreased within 24 h from 243 +/- 59 to 36 +/- 0 pg/ml in phosphorus-depleted rats. Serum levels of 1,25(OH)2D3 increased within 24 h and remained elevated after 6 wk of phosphorus deprivation (61.2 +/- 11.7 ng/dl vs. control 18.3 +/- 0.4 ng/dl).

Animals↗
PubMed1979

Parathyroid hormone release is not associated with acute sympathetic arousal in goats.

Physiological activation of the sympathetic adrenomedullary (SAM) axis following both thermal and non thermal stress was assessed by changes in serum norepinephrine, glucose and/or protein as well as indices of peripheral blood flow. The occurrence of elevated serum parathyroid hormone (PTH) did not reliably reflect SAM activation as might be predicted from pharmacological studies that document a beta adrenergic receptor mechanism in the parathyroid gland that mediates catecholamine stimulated release of PTH into the circulation. The beta agonist isoproterenol at 1 microgram/min for 60 min did produce a transient increase in serum PTH at 20 min. Overall, the data raise doubts about the physiological significance of the adrenergic receptor in the parathyroid gland. Significant increases in serum PTH of 67% and 109% above basal respectively were seen following ruminal loading with cold and thermoneutral water. Associated with the PTH change were increased serum phosphorus and elevated or constant serum protein and serum total calcium.

Animals↗
PubMed1978

Inhibition of bone formation during space flight.

Parameters of bone formation and resorption were measured in rats orbited for 19.5 days aboard the Soviet Cosmos 782 biological satellite. The most striking effects were on bone formation. During flight, rats formed significantly less periosteal bone than did control rats on the ground. An arrest line at both the periosteum and the endosteum of flight animals suggest that a complete cessation of bone growth occurred. During a 26-day postflight period, the defect in bone formation was corrected. No significant changes in bone resorption were observed.

Aerospace Medicine↗
PubMed1978

The effects of phosphate depletion on bone.

Phosphate depletion causes significant changes in the composition of the cell population in bone and the metabolic activities of these cells. The data presented indicate that a vitamin D metabolite has a significant role in producing the increase in osteoclast number associated with phosphate depletion. The increased resorptive activity and number of osteoclasts leads to a marked increase in the rate of bone resorption resulting in the liberation of calcium phosphate, while the decrease in the rates of the processes involved in bone formation (matrix production, osteoid maturation, and mineralization) reduces the amount of phosphate which is removed from the circulation. Thus, all of the effects of phosphate depletion on bone are consistent with the interpretation that bone acts as a reservoir of phosphate and is used to maintain soft tissue and serum phosphate levels at the expense of bone.

Animals↗