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Biomedical subjects

D J Baylink

Publications and source records attributed to D J Baylink.

At least 343 records · Page 19Linked to original sources
PubMed1978

Resorption of bone implants. The effect of in vivo incorporation of a diphosphonate and fluoride on resorption.

Weanling isogenously related rats were divided into one control group, one group given a fluoride supplement of 100 parts/10(6) of F- in the drinking water, and a third group given 0.5 mg per kg body weight of phosphorus as dichloromethylene diphosphanic acid (Cl2MDP). The rats were labeled with 1 muCi per g body weight of 3H proline and 40 muCi of 45Ca. Four weeks after labeling, the animals were sacrificed and one scapula was implanted subcutaneously in the back of an isogenously related rat of the same age. The other scapula was stored in a freezer pending analysis. After another 4 weeks the implants were recovered and the radioactivity of each isotope was compared with that of the initially stored scapulae. A 30-40% loss of activity was found, reflecting a considerable loss of bone. However, this loss was significantly lower (P less than 0.01) when Cl2MDP was given to the donor animals, whereas fluoride treatment did not affect the resorption.

Animals↗
PubMed1978

Alveolar atrophy and decreased skeletal mass of the radius.

Using absorptiometry, the bone calcium mass (BCM) at two different sites of the radius was measured in 12 male patients referred for vestibuloplasty of the mandible. The most distal site contained both cortical and cancellous bone while the other site contained cortical bone only. The BCM values were compared with those for normal patients of the same age. The patients with mandibular atrophy all had less bone in the radius than their age-matched controls (p less than 0.01). This is indicative of a systemic factor or factors operating both in the mandible and in the radius. The examination prior to oral surgery should therefore include an evaluation for diseases causing general bone loss.

Absorption↗
PubMed1978

Specific binding of estrogen to nuclei from Japanese quail kidney cells.

The binding properties of estrogen to Japanese quail kidney cell nuclei were evaluated by 3H-17 beta-estradiol exchange. Kidney cell nuclei from estrogenized male, as well as laying female quail, had a single class of saturable (0.1-0.2 pmol/mg DNA), high affinity (Kd = 1-2 x 10-10M) nuclear binding sites for 17 beta-estradiol. High affinity estrogen binding sites were not found in kidney cell nuclei from untreated males. Various non-radioactive estrogens (17 beta-estradiol, estrone, estriol and diethylstilbestrol) competed effectively with 3H-17 beta-estradiol for the high affinity binding sites, whereas nonestrogens (testosterone and progesterone) did not complete. It is concluded that the 3H-estradiol binding characteristics of kidney cell nuclei provides strong evidence for a nuclear estrogen receptor in the avian kidney.

Animals↗
PubMed1978

Neuroendocrine modulation of calcitonin and parathyroid hormone in man.

Recent evidence suggests that of calcitonin (CT) and parathyroid hormone (PTH) is controlled by factors other than the ambient serum calcium concentration. We studied the effects of infusions of four neuroendocrine modulators upon CT and PTH levels: isoproterenol (beta-adrenergic agonist), methoxamine (alpha adrenergic agonist), prostaglandin E2, and somatostatin. Isoproterenol was a consistent secretagogue for both hormones. Maximal CT increments during isoproterenol infusion in normal subjects were 13 +/- 2 pg/ml (mean +/- SEM, n = 6, P less than 0.001; basal, 26 +/- 5). Maximal increments in PTH were 113 +/- 22 pg/ml (P less than 0.01, n = 6; basal, 430 +/- 11). Infusions of methoxamine increased CT by 13 +/- 5 pg/ml (n = 5, P less than 0.05; basal, 43 +/- 13), but had no effect on PTH. The means of the maximal CT increments during isoproterenol (21 +/- 8 pg/ml) and methoxamine infusion (28 +/- 11 pg/ml) were not statistically different from those achieved by acute elevations of serum calcium levels within the physiological range (41 +/- 23 pg/ml). Infusions of somatostatin and prostaglandin E2 had no or only transient effects on basal or stimulated CT or PTH levels. Our data suggest that adrenergic input modulates CT and PTH secretion in humans independently of changes in serum calcium.

Adult↗
PubMed1977

Selective deficiency of 1,25-dihydroxycholecalciferol. A cause of isolated skeletal resistance to parathyroid hormone.

To investigate the role of vitamin D metabolites in the pathogenesis of pseudohypoparathyroidism, we studied an elderly man with a unique variant of the disease, which was characterized by hypocalcemia, elevated serum parathyroid hormone (513 +/- 13 pg per milliliter, mean +/- S.E.M., normal, less than 450) but normal renal responses (phosphate and cyclic AMP) to exogenous parathyroid extract. Treatment with parathyroid extract did not produce a calcemic effect, suggesting an isolated skeletal hyporesponsiveness to parathyroid hormone. Although 25-hydroxyvitamin D levels were not reduced, levels of 1,25-dihydroxycholecalciferol were extremely low (0.52 ng per deciliter; normal 3.3 +/- 0.06, S.D.). Treatment with 1,25-dihydroxycholecalciferol (1 microgram by mouth per day for four days) increased circulating levels to normal (4.60 ng per deciliter) and restored to normal the calcemic response to parathyroid (change in calcium 3.0 mg per deciliter). These data suggest that 1,25-dihydroxycholecalciferol deficiency may explain the skeletal resistance, but not the renal resistance, often present in classic pseudohypoparathyroidism.

Aged↗
PubMed1977

Effect of methandrostenolone on postmenopausal bone wasting as assessed by changes in total bone mineral mass.

To assess the efficacy of methandrostenolone in the treatment of osteoporosis a 26-mo double-blind study was performed with 13 treated and 13 control (placebo) postmenopausal osteoporotic females. Drug effect was assessed primarily by determinations of total body calcium (TBC) by neutron activation analysis, essentially a measurement of total bone mineral mass. Results in the 16 patients completing the study (10 treated and 6 placebo), as well as in all 26 patients participating in the study, showed significant (p less than 0.01) differences in the change in TBC between treated and control groups. In patients dropping out, TBC changes through the time of dropout were similar to those in patients completing the study. In those patients completing the study, TBC increased 2% in the treated group and decreased 3% in the placebo group. An approximate sixfold difference in extraskeletal calcium balance would be required to explain the magnitude of the observed intergroup TBC difference. The drug effect appeared to persist throughout the 26-mo observation period. Thus these data strongly suggest that long-term use of methandrostenolone in postmenopausal osteoporosis prevented bone loss; the possibility that it increased bone mass above initial values is less certain.

Aged↗
PubMed1977

Hypercalcemia induced by prostaglandin E2 in thyroparathyroidectomized but not intact rats.

Prostaglandin E2 was infused into thoracic aorta of thyroparathyroidectomized (TPTX) and intact rats. Circulating calcium increased significantly in the TPTX group by 30 minutes and reached an increment of 1.5 +/- 0.21 mg/dl (x +/- SE, p less than .001) by 90 minutes. No calcium increments were observed in the intact rats. It is postulated that prior failures to demonstrate hypercalcemia during PGE2 infusion may have been due to calcitonin counterregulation.

Animals↗
PubMed1977

Pore size measurements and some age-related changes in human alveolar bone and rat femur.

Bone pore volume of pores ranging from 0.1 to 77 mum in diameter was unchanged in alveolar bone from patients with periodontal disease compared with control subjects, a finding that is inconsistent with the involvement of systemic factors in alveolar bone loss in this disease. Bone density was decreased in alveolar bone from patients with periodontal disease. Bone density of normal alveolar bone increased with age. A similar finding was obtained in rat diaphyseal bone, suggesting that this is a general phenomenon in aging bone. This could be significant inasmuch as high density bone would be expected to be more brittle. In contrast to these findings in normal alveolar bone, bone density decreased rather than increased in the 50- to 59-year-old age group in patients with periodontal disease. The cause of decreased bone density remains to be established.

Adolescent↗
PubMed1977

Stimulation of bone formation and bone resorption by fluoride in thyroparathyroidectomized rats.

In sham-operated and TPTX animals, F treatment did not affect final body weight, or serum Ca and P. In sham-treated rats, serum iPTH was not affected by F treatment. At the periosteum, F increased bone formation rate and bone and matrix apposition rates. At the endosteum, F treatment decreased forming surface, bone formation rate, bone and matrix apposition rates, and osteoid maturation rate; and increased endosteal resorbing surface and medullary area. The above-described F effects on bone were observed in TPTX as well as sham-treated animals. The effect of F treatment to stimulate periosteal matrix apposition was enchanced by TPTX. These results indicate that bone changes seen in animals treated with large amounts of F are not due to increased parathyroid activity.

Animals↗
PubMed1977

Influence of dietary vitamin D3 on the circulating concentration of its active metabolites in the chick and rat.

Plasma concentrations of 25-hydroxyvitamin D3 (25-OHD3) and 1 alpha,25-dihydroxyvitamin D3 (1 alpha, 25-(OH)2D3) in growing chicks and weanling rats were measured by a new radioreceptor assay to determine the effects of varying dietary levels of vitamin D3. The plasma concentration of 25-OHD3 fell from 14.1 ng/ml in 1-day-old chicks to undetectable levels after 3 weeks on a rachitogenic diet. Circulating 1 alpha,25-(OH)2D3 hormone also decreased from 8.9 ng/100 ml to undetectable levels at 3 weeks in these chicks. Chicks receiving an optimal supplement of vitamin D3 (1.4 IU/g diet) for three to four weeks had plasma 25-OHD3 and 1 alpha,25-(OH)2D3 levels of 21-35 ng/ml and 5.1-7.5 ng/100 ml, respectively. Nutritional supplementation with a 50-fold excess of vitamin D3 (70 IU/g diet) elicited a substantial increase in plasma 25-OHD3 to 87-130 ng/ml, while plasma 1 alpha,25-(OH)2D3 was not increased. Increasing dietary calcium from 1.4 to 2.8% did not alter the circulating level of vitamin D3 metabolites in chicks fed 1.4 IU of vitamin D3/g diet. Direct measurement of the renal 25-OHD3-1 alpha-hydroxylase in vitro, showed that lowering dietary calcium or exclusion of vitamin D3 stimulated the biosynthesis of 1 alpha,25-(OH)2D3, but raising calcium did not alter the enzyme activity. It is concluded that the circulating concentration of the 1 alpha,25-(OH)2D3 hormone in the chick is unaffected by abnormally high intakes of vitamin D3 or calcium, but the renal production of the hormone increases during vitamin D3 or calcium deprivation. Additional studies in rats fed a diet supplemented with either 2 or 1000 IU of vitamin D3/g verify that the circulating concentration of 25-OHD3 is markedly increased when the dietary intake of vitamin D3 is elevated. Moreover, 1 alpha,25(OH)2D3 is not increased under these conditions, but actually falls significantly when the dietary level of vitamin D3 is raised from 2 to 1000 IU/g. These studies in both the chick and rat indicate that dietary vitamin D3 excess enhances circulating 25-OHD3, probably because the vitamin D3-25-hydroxylase enzyme is not strigently controlled. The fact that the circulating 1 alpha,25-(OH)2D3 is not concomitantly increased may reflect either decreased synthesis or increased utilization of the 1 alpha,25-(OH)2D3 sterol.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1977

Use of 1,25(OH)2-vitamin D3 to separate 'types' on renal osteodystrophy.

Patients with severe symptomatic renal osteodystrophy were treated with either 1,25(OH)2D3 or 1 alpha(OH)D3. In 39 instances, there was either reversal of symptoms and/or a marked fall in plasma alkaline phosphatase. Bone biopsies showed improvement of either osteomalacia or osteitis fibrosa, and serum iPTH often fell. In thirteen patients, no improvement occurred. In seven patients, bone biopsy disclosed osteomalacia, and serum iPTH was normal or only slightly elevated. Thus, there was a defect in mineralisation. apparently unrelated to the lack of 1,25(OH)2D3 and in the absence of evidence of phosphate depletion. The other 'treatment failure' group showed osteitis fibrosa on biopsy and iPTH levels were markedly elevated. They are presumed to have marked secondary hyperparathyroidism. These 'treatment failure' groups had higher pre-treatment levels of serum Ca and Mg than in those showing a favourable response; also, hypercalcaemia developed rapidly during 1,25(OH)2D3 treatment. Thus, 1,25(OH)2D3 is efficacious in treating symptomatic osteodystrophy in many uraemic patients, and in other patients, it may help identify bone disease of other, as yet unknown, pathogenesis.

Adolescent↗
PubMed1977

Effect of beta-aminopropionitrile on bone mechanical properties.

In vivo beta-aminopropionitrile treatment caused significant changes in the mechanical properties of rat femora. In femora treated with beta-aminopropinitrile as compared with controls, there was a 44 per cent decrease in bone stiffness and a 47 per cent increase in bone deformation to failure. Bone ash was decreased 5 per cent in the treated group. It is likely that the decrease in bone ash was secondary to impaired intermolecular bone-collagen cross-linking, which is a well established consequence of treatment with beta-aminopropionitrile. Thus, beta-aminopropionitrile influences bone mechanical properties directly by impairing collagen cross-linking and indirectly by altering bone-matrix mineralization.

Aminopropionitrile↗
PubMed1976

The assay of 1alpha,25-dihydroxyvitamin D3: physiologic and pathologic modulation of circulating hormone levels.

A sensitive radioreceptor assay for 1alpha,25-dihydroxyvitamin D3 (1alpha,25-(OH)2D3) is utilized to quantitate the circulating concentration of this sterol in experimental animals and humans. When weanling rats are grown for 2 weeks on low calcium or low phosphate diets, limited availability of either ion elicits a five-fold increase in the plasma level of 1alpha,25-(OH)2D3. The enhancement of 1alpha,25-(OH)2D3 in calcium deficiency is dependent upon the presence of the parathyroid and/or thyroid glands, which is consistent with parathyroid hormone (PTH) mediation of this effect. In contrast, the response to phosphate deficiency is independent of these glands and may result from a direct action of low phosphate on the renal synthesis of 1alpha,25-(OH)2D3. Studies in humans indicate that the normal level of 1alpha,25-(OH)2D is 2.1--4.5 ng/100 ml plasma. Patients with chronic renal failure have markedly lower circulating 1alpha,25-(OH)2D and this kidney hormone is undetectable in anephric subjects, but returns to normal within 1 day after successful renal transplantation. Hypoparathyroidism and pseudohypoparathyroidism are associated with reduced plasma 1alpha,25-(OH)2D while patients with primary hyperparathyroidism have significantly elevated sterol hormone levels. Thus, from measurements in rats and humans, it appears that circulating 1alpha,25-(OH)2D3 is regulated by PTH and/or phosphate and that abnormal plasma 1alpha,25-(OH)2D3 is a part of the pathophysiology of renal osteodystrophy and parathyroid disorders.

Animals↗
PubMed1976

Radioligand receptor assay for 25-hydroxyvitamin D2/D3 and 1 alpha, 25-dihydroxyvitamin D2/D3.

A competitive protein binding assay for measurement of the plasma concentration of 1 alpha, 25-dihydroxyvitamin D3 [1alpha, 25-(OH)2D3] has been extended to include the immediate precursor of this hormone, 25-hydroxyvitamin D3 (25-OHD3). In addition, the assay system is capable of measuring the two metabolic products of ergocalciferol, namely. 25-hydroxyvitamin D2 (25-OHD2) and 1alpha, 25-dihydroxyvitamin D2 [1alpha, 25-(OH)2D2]. The target tissue assay system consists of a high affinity cytosol receptor protein that binds the vitamin D metabolites and a limited number of acceptor sites on the nuclear chromatin. By utilizing a series of chromatographic purification steps, a single plasma sample can be assayed for any of the four vitamin D metabolites either individually or combined. Therefore, the assay procedure allows for both the quantitative and qualitative assessment of the total active vitamin D level in a given plasma sample. To show that the binding assay was capable of measuring 1alpha, 25-(OH)2D2 as well as 1alpha, 25 (OH)2D3, two groups of rats were raised. One group, supplemented with vitamin D3, produced assayable material that represented 1alpha, 25-(OH)2D3. The other group, fed only vitamin D2 in the diet, yielded plasma containing only 1alpha, 25-(OH)2D2 as the hormonal form of the vitamin. The circulating concentrations of the two active sterols were nearly identical (15 ng/100 ml) in both groups, indicating that the competitive binding assay can be used to measure both hormonal forms in plasma. In a separate experiment, 1alpha, 25-(OH)2D2 was generated in an in vitro kidney homogenate system using 25-OHD2 as substrate. Comparison of this sterol with 1alpha, 25-(OH)2D3 in the assay system showed very similar binding curves; the D2 form was slightly less efficient (77%). Comparison of the respective 25-hydroxy forms (25-OHD2 vs. 25-OHD3) at concentrations 500-fold that of 1alpha, 25-(OH)2D3, again suggested that the binding of the D2 metabolite was slightly less efficient (71%). Finally, the assay was employed to measure the total active vitamin D metabolite pools in the plasma of normal subjects and patients with varying degrees of hypervitaminosis D. The normal plasma levels of 25-OHD and 1alpha, 25-(OH)2D measured in Tucson adults were 25-40 ng/ml and 2.1-4.5 ng/100 ml, respectively. Both sterols were predominately (greater than 90%) in the form of vitamin D3 metabolites in this environment. Typical cases of hypervitaminosis D exhibited approximately a 15-fold increase in the plasma 25-OHD concentration, and a dramatic changeover to virtually all metabolites existing in the form of D2 vitamins. In contrast, the circulating concentration of 1alpha, 25-(OH)2D was not substantially enhanced in vitamin D-intoxicated patients. We therefore conclude that hypervitaminosis D is not a result of abnormal plasma levels of 1alpha, 25-(OH)2D but may be cuased by an excessive circulating concentration of 25-OHD.

Animals↗
PubMed1976

Plasma prostaglandin E in patients with cancer with and without hypercalcemia.

Circulating levels of immunoreactive (i) PGE, calcium and parathyroid hormone (iPTH) were examined in 21 patients with neoplasia and 3 patients with primary hyperparathyroidism. Plasma iPGE was elevated in 4 of 11 hypercalcemic cancer patients; all extracts of liver metastases obtained from 3 of these 4 patients had elevated iPGE levels (metastases = 19.43 +/- 3.43, n = 11; normal liver = 2.04 +/- 0.23; ng/g tissue, x +/- SE, P less than .001). In contrast, only one of 10 normocalcemic cancer patients and none of 3 hyperparathyroid patients had elevated plasma iPGE. There were no apparent relationships between the presence of metastases and either hypercalcemia or elevations of plasma iPGE. Serum iPTH levels were undetectable or below the mean of the normal range in 19 of 21 cancer patients; only the three hyperparathyroid patients had elevated levels. Seven hypercalcemic patients were treated with indomethacin; plasma iPGE decreased in 6 (-34 +/- 10% decrement, n = 6, P less than .01). Decreases in serum calcium occurred only in those patients (2 of 6) who had abnormally elevated plasma iPGE prior to the therapy. It is concluded that plasma iPGE elevations are found in some cancer patients, especially those with hypercalcemia, and that this marker may identify those patients who will respond to indomethacin treatment.

Bone Neoplasms↗