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Biomedical subjects

J A Fischer

Publications and source records attributed to J A Fischer.

At least 181 records · Page 10Linked to original sources
PubMed1979

Distribution of circulating immunoreactive components of parathyroid hormone in normal subjects and in patients with primary and secondary hyperparathyroidism: the role of the kidney and of the serum calcium concentration.

1. The distribution of intact parathyroid hormone-(1-84) [PTH-(1-84)] and of its COOH-terminal fragments was determined in human serum by column chromatography. In addition to PTH-(1-84) (peak I), COOH-terminal fragments having molecular weights of approximately 4000-7000 (peak II) and immunoreactive components co-eluting with human PTH-(1-12) (peak III) were observed. 2. Mean concentrations of intact PTH-(-84) and of its COOH-terminal fragments were significantly raised in chronic renal failure as compared with those of normal subjects. Mean amounts of peak II were higher in patients with chronic renal insufficiency than in nutritional vitamin D deficiency, in pseudohypoparathyroidism and in primary hyperparathyroidism, despite comparable amounts of PTH-(1-84). 3. In chronic renal failure as well as in a group of patients with vitamin D deficiency, pseudohypoparathyroidism and primary hyperparathyroidism and in controls, significant linear relations were found between the serum concentrations of calcium and log (peak II/peak I). Our findings suggest that the conversion of intact PTH-(1-84) into COOH-terminal fragments by the parathyroid glands (resulting in a raised secretion of fragments) and/or in peripheral organs may be directly related to the serum concentration of calcium. However, the degradation of the fragments may also be suppressed in a calcium-dependent manner.

Calcium↗
PubMed1979

Plasma catecholamine and parathyroid hormone responses in cattle during treadmill exercise at simulated high altitude.

When steers were exposed to treadmill exercise at a simulated altitude of 3500 m, plasma concentrations of epinephrine and norepinephrine as well as of parathyroid hormone increased within minutes. Heart rate, erythrocyte number and plasma lactic acid level rose at the same time, whereas plasma free fatty acids showed a later increase. It is concluded, that the elevated parathyroid hormone levels were probably caused by sympathetic stimulation.

Altitude↗
PubMed1979

Plasma kinetics and urinary excretion of exogenous human and salmon calcitonin in man.

The metabolism and the urinary excretion of synthetic human and salmon calcitonin-(1--32) [hCT-(1--32), sCT-(1--32)] administered by constant infusions for 240 min were investigated in eight normal subjects. On gel filtration of plasma obtained during the infusions mainly intact hCT-(1--32) and sCT-(1--32) were recognized with homologous radioimmunoassay systems. During constant infusions to equilibrium of 0.04 mg hCT-(1--32) and sCT-(1--32), the metabolic clearance rates (MCR) amounted to 8.4 +/- 1.1 and 3.1 +/- 0.1 ml/kg per min, respectively (P less than 0.01). When hCT-(1--32) was infused at rates of 1 and 4 mg/240 min, the MCR were lower than with 0.04 mg hCT-(1--32), but still higher than with 0.04 mg sCT-(1--32). The half-lives of disappearance of hCT-(1--32) were faster compared to sCT-(1--32), but the difference was not statistically significant. The urinary clearance of hCT-(1--32) determined during the 1 and 4 mg/240 min infusions of hCT-(1--32), as well as of sCT-(1--32) determined during the 0.04-mg infusions of sCT-(1--32) was about 0.1% of the MCR. The half-lives of disappearance of hCT- and sCT-(1--32) incubated in vitro in plasma and urine ranged from 17 to more than 72 h, and the degradation did not affect our calculations of the metabolic breakdown of exogenous CT in vivo.

Adult↗
PubMed1979

Formation of antibodies to synthetic human calcitonin during treatment of Paget's disease.

Low-titre antibodies to synthetic human calcitonin (hCT) were detected in a 69-year-old woman suffering from Paget's disease who was treated for 16 months with hCT and the diphosphonate EHDP. Levels of antibody were highest between 10 and 18 months after commencement of therapy, slowly decreased after completion of treatment and were later no longer measurable. There was no immunological response to a single re-injection of hCT 14 months after discontinuation of therapy. Formation of antibodies to hCT in man is a very rare event, this being the first recorded case of an immune response to synthetic human calcitonin, whereas synthetic salmon calcitonin induces an immune response in a high percentage (up to 78%) of the patients treated with this hormone.

Aged↗
PubMed1979

[Differential diagnosis of osteoporosis (author's transl)].

This is a review of the diagnostic procedures used in patients with osteoporosis. The differential diagnosis of various forms with recognized etiology is used as a background for the study of postmenopausal osteoporosis with largely unknown pathogenesis.

Age Factors↗
PubMed1978

Effects of calcium intake and renal function on plasma immunoreactive parathyroid hormone levels in rats.

Parathyroid hormone (PTH) was estimated with a radioimmunoassay system which recognised presumably intact rat PTH as the major circulating species. A low calcium diet was found to increase PTH levels in shamoperated and in 5/6-nephrectomized rats. In rats with normal renal function, a low calcium intake resulted in a significant mean increase of PTH levels, while changes in plasma calcium, magnesium, phosphate and protein concentrations were not detectable; at the same time the ability of the duodenum to transport calcium in vitro was accelerated. In 5/6-nephrectomized rats, on the other hand, PTH levels were dramatically increased in hypocalcemic animals kept on a calcium deficient diet, while intestinal calcium transport was impaired. These data support the concept that hypocalcemia is the most important stimulus for increased PTH release. Since increased PTH levels can be seen in situations where increased 1,25-dihydroxy-cholecalciferol synthesis is known to occur, it appears that this metabolite cannot inhibit a rise in plasma PTH levels.

Animals↗
PubMed1978

Calcitonin and calcium ionophores: cyclic AMP responses in cells of a human lymphoid line.

Receptors for calcitonin, as assayed by the specific binding of 125I-labeled salmon calcitonin and stimulation of cyclic AMP formation, were found in 8866 cells derived from a human lymphoid line. The affinity of calcitonin from different species and of various analogues of human calcitonin for the binding sites and their ability to stimulate cyclic AMP formation were closely related to their hypocalcemic activity and presumably reflected biological properties of the hormones. Besides calcitonin, prostaglandin E1 and beta-adrenergic catecholamines stimulated cyclic AMP formation in these cells. The calcium ionophores, A23187 and Br-X-573A, did not influence the specific binding of 125I-labeled salmon calcitonin. A23187, however, suppressed basal and calcitonin-stimulated formation of cyclic AMP in the presence of at least 0.6 mM calcium in the incubation medium. Br-X-537A did not require extracellular calcium to suppress basal and calcitonin-stimulated formation of cyclic AMP, suggesting that the release of calcium from internal stores may regulate adenylyate cyclase activity in 8866 cells.

Calcimycin↗
PubMed1978

Parathyroid hormone responses to catecholamines and to changes of extracellular calcium in cows.

Modifications of the plasma level of immunoreactive parathyroid hormone (PTH) in cattle were induced by changes of the plasma concentrations of epinephrine, isoproterenol, or calcium. During abrupt hypocalcemia, PTH, obtained by infusions with ethylene glycol-bis (beta-aminoethylether) N, N'-tetraacetate (EGTA), increased during the first 4-8 min. After a transient decline, the hormone levels rose again and remained elevated. Infusions of calcium suppressed the hypocalcemia-induced augmentation of PTH levels within a few minutes. Prolonged epinephrine (and isoproterenol) infusions also rapidly increased PTH levels, however, in this case, they returned to basal concentrations after 50-60 min. Additional epinephrine infusions could not further raise PTH values. Moreover, three short-lasting infusions of epinephrine (7 min each), given at 30-min intervals, increased PTH levels to the same extent, whereas additional infusions were much less effective. The PTH response to epinephrine was completely restored, when the interval after a prolonged epinephrine infusion had been prolonged to > 100 min. During moderate hypocalcemia, occurring at the end of EGTA infusions and lasting for 90 min, the PTH response to a short-lasting epinephrine infusion (7 min) was more pronounced than in normocalcemic animals. During severe hypocalcemia, in which superimposed short-lasting infusions of EGTA (7 min) led to an additional abrupt fall of plasma calcium concentrations but not to a corresponding additional rise of the PTH levels, epinephrine rapidly and further increased PTH concentrations. On the other hand, at the end of prolonged infusions of epinephrine, when additional infusions of epinephrine were ineffective in raising PTH levels, EGTA-induced hypocalcemia consistently increased PTH concentrations. The EGTA-induced augmentation of PTH levels was enhanced by epinephrine and isoproterenol but not by propranolol. The present findings indicate, that variations of the extracellular calcium concentrations and beta-adrenergic agonists modify PTH levels by two different and independent mechanisms. On the other hand, it appears that the magnitude of change of the PTH levels to either stimulus is partially modulated by exposure to the other.

Animals↗
PubMed1978

Pseudohypoparathyroidism and idiopathic hypoparathyroidism: relationship between serum calcium and parathyroid hormone levels and urinary cyclic adenosine-3',5'-monophosphate response to parathyroid extract.

Forty patients with hypocalcemia and/or Albright's hereditary osteodystrophy were studied. Based on the estimation of serum calcium and parathyroid hormone (PTH) levels as well as the urinary cAMP response to infusions with parathyroid extract, it was possible to classify all of the patients studied as cases with idiopathic hypoparathyroidism (n = 6, low PTH, normal cAMP response), pseudohypoparathyroidism (PHP) type I (n = 18, high PTH, low cAMP response) and type II (n = 2, high PTH, normal cAMP response), as well as pseudopseudohypoparathyroidism (n = 14, normal PTH, normal cAMP response). In three cases studied at the age of 12, 17, and 23 yr, the signs of Albright's hereditary osteodystrophy were not observed. PTH levels were unusually high for a given serum calcium concentration in some patients with PHP, the increased PTH levels were, however, normalized during iv calcium infusions. In two young children with PHP, a gradual increase of serum PTH levels occurred despite persistent normocalcemia over a period of 3 yr. This suggests that factors other than hypocalcemia or frequent small unobservable falls of the serum calcium concentration, such as a deficient formation of 1,25-dihydroxyvitamin D3, secretion of an abnormal PTH, or an abnormal metabolism of the hormone, may contribute to the secondary hyperparathyroidism in PHP.

Adolescent↗
PubMed1978

Effects of alpha-adrenergic stimulation and blockade of plasma parathyroid hormone concentrations in cows.

Experiments were designed to investigate responses of immunoreactive parathyroid hormone (PTH) during alpha-adrenergic stimulation and blockade in cows. Alpha-adrenergic agonists (methoxamine, phenylephrine and noradrenaline, the beta-adrenergic action of which was blocked by propranolol) did not change PTH and free fatty acid levels, whereas they characteristically increased the blood pressure and decreased the heart rate. In contrast, alpha-adrenergic blockade by phentolamine progressively increased PTH levels. The elevated PTH concentrations, associated with increased plasma noradrenaline and free fatty acid levels, rising heart rate and decreasing blood pressure, indicated that all these changes can be related to a beta-adrenergic stimulatory mechanism. Beta-adrenergic stimulation was presumably responsible for the initial elevation of PTH concentrations, whereas, during the later phase of the phentolamine infusions, a concomitant hypocalcaemia probably also produced a stimulatory effect.

Adrenergic alpha-Agonists↗
PubMed1977

Plasma kinetics of exogenous bovine parathyroid hormone in calves.

The metabolism of purified bovine parathyroid hormone-(1-84) [bPTH-(1-84)] administered i.v. by constant infusions or rapid injections was investigated in 11 normocalcemic calves. Plasma kinetics of bPTH-(1-84) were derived with a radioimmunoassay system which recognised the intact hormone but no fragments. The metabolic clearance rates ranged from 9.1-22.9 ml/min/kg. The disappearance of the intact hormone and the reversible appearance of its NH2- and COOH-terminal fragments was investigated with additional and specific radioimmunoassay systems. At 2 min after the i.v. injection of bPTH-(1-84) a NH2-terminal fragment (M approximately 3500) was recognised and at 4 and 20 min COOH-terminal fragments (M approximately 7000 and 3500, respectively) were detected. The survival time in the circulation of the intact hormone and of its fragments was comparable. In conclusion, bovine bPTH-(1-84) and its NH2- and COOH-terminal fragments are metabolised in normocalcemic calves within minutes.

Animals↗