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Biomedical subjects

J A Fischer

Publications and source records attributed to J A Fischer.

At least 199 records · Page 11Linked to original sources
PubMed1976

[Sporadic adult hypophosphatemic vitamin D resistant osteomalacia (phosphate diabetes) and hyperparathyroidism].

Report on a patient with osteomalacia due to renal phosphate loss. At onset the patient was aged 43 years. No other tubular defects were detected except glycinuria. The patient was followed over a period of 12 years. 3 years after treatment with oral phosphate and vitamin D3 persistent hypercalcemia developed with highly elevated levels of parathyroid hormone. After removal of one enlarged parathyroid gland serum calcium normalized, but elevated parathyroid hormone levels still persist. The spontaneous occurrence of hypophosphatemic osteomalacia in an adult male and its connections with the development of hyperparathyroidism are discussed.

Adult↗
PubMed1975

Regulation of circulating parathyroid hormone levels: normal physiology and consequences in disorders of mineral metabolism.

A review of the chemistry, the biosynthesis, the regulation of the secretion and the metabolism of parathyroid hormone (PTH) provides a background to problems related to the determination of immunoreactive PTH levels in the blood of normal subjects and of patients suffering from disorders of mineral metabolism. Immunoreactive PTH measurements have to be interpreted in the light of the immunoheterogeneity encountered and the occurrence of several circulating PTH species with different molecular weights and immunological properties.

Calcitonin↗
PubMed1975

Pseudohypoparathyroidism. Disappearance of the resistance to parathyroid extract during treatment with vitamin D.

Serum immunoreactive parathyroid hormone (iPTH) levels were increased in a 15 year old girl with pseudohypoparathyroidism, hypocalcemia, hyperphosphatemia, and minimal phosphaturic and absent hypercalcemic responses to exogenous parathyroid extract (PTE). Following normalization of the serum calcium concentration with vitamin D, serum iPTH and phosphate concentrations returned to the normal range, and phosphaturia could be clearly stimulated and hypercalcemia induced by PTE. On the other hand, the urinary cyclic adenosine 3',5'-monophosphate (cyclic AMP) excretion could not be stimulated, suggesting that in this case, there appears to be no relationship between the urinary excretion of cyclic AMP and the phosphaturic effect of PTE. The minimal phosphaturic effect and the lack of hypercalcemic effects of PTE in untreated pseudohypoparathyroidism can be explained by the secondary hyperparathyroidism causing elevated iPTH levels rather than by a defect at the level of the receptor sites. A requirement of pharmacologic amounts of vitamin D per se, however, for the responsiveness of patients with pseudohypoparathyroidism to PTE cannot be ruled out.

Adolescent↗
PubMed1975

Synthetic human calcitonin: analysis of antibodies obtained from various animal species and determination of immunoreactive hormone in human sera.

Antibodies to synthetic human calcitonin (hCT) were developed in rabbits, goats and mice. The free peptide (32 amino-acid residues, Mwt. 3418) was administered together with adjuvant, and the effect of various immunization procedures, as well as of different dose-levels, was evaluated comparatively. Synthetic hCT was found to be a good immunogen for the three animal species examined. The relative importance of various structural parts of the hCT molecule with regard to immunological specificity was determined by reference to the inhibition of the specific binding of 125I-hCT to antibodies by peptide fragments of hCT. All the antisera studied were directed to structural and/or conformational properties of the 11-28 or 11-32 amino acid sequence of hCT. Six different antisera from rabbits and goats were selected for radioimmunological assay of hCT on the basis of their inhibitory dose50-values and immunological specificity. To improve the sensitivity of the radioimmunoassay (RIA), we studied the preparation of radioiodinated hCT and assessed various parameters determining the sensitivity of the assay. Despite all the efforts, CT in human plasma from healthy subjects could not be determined with certainty. The difficulties encountered in the determination of normal levels of circulating CT are discussed in terms of the sensitivity of RIA and non-specific interference of serum factors with RIA.

Animals↗
PubMed1974

Human parathyroid hormone. Immunological characterization of antibodies against a glandular extract and the synthetic amino-terminal fragments 1-12 and 1-34 and their use in the determination of immunoreactive hormone in human sera.

Antibodies to a urea-trichloroacetic acid extract [hPTH-(TCA)] of human parathyroid tumors and to the synthetic NH(2)-terminal fragments of human parathyroid hormone hPTH-(1-12) and -(1-34) were developed in goats to characterize immunochemically various PTH preparations and to estimate immunoreactive PTH (iPTH) in human sera. They were quantitated on the basis of their capacity to bind [(131)I]-hPTH-(1-12), [(131)I]hPTH-(1-34) or [(131)I]bovine PTH (bPTH-(1-84)). The quality of the antibodies was assessed by reference to inhibition of their interaction with labeled peptides by synthetic hPTH comprising 34 NH(2)-terminal amino acid residues or fragments thereof [hPTH-(1-12), -(13-34), -(18-34), -(25-34), -(18-24)] or by the Sephadex G-100-purified full-length peptide hPTH-(1-84) [hPTH-(1-84)G-100]. The synthetic peptides used in this work correspond in their structure to the NH(2)-terminal amino acid sequence 1-34, as elucidated by Brewer and collaborators (1972. Proc. Natl. Acad. Sci. U. S. A.69: 3583-3588). Inhibition studies were also carried out with bPTH-(1-34) and bPTH-(1-84). Anti-hPTH-(TCA) exhibited specificities directed to determinants in the COOH-terminal and NH(2)-terminal part of hPTH-(1-84) and exhibited cross-reactivity with bPTH-(1-84). Anti-hPTH-(1-34), on the other hand, showed immunological specificities mainly directed to antigenic determinants located in the COOH-terminal half of hPTH-(1-34). In addition, some reactivity with the NH(2)-terminal hPTH-(1-12) and with the extractive full-length peptides of human and bovine origin was observed. Antibodies to hPTH-(1-12) cross-reacted with hPTH-(1-34) and -(1-84)G-100.IPTH WAS RADIOIMMUNOLOGICALLY DETERMINED IN HUMAN SERA BY THE FOLLOWING SYSTEMS: (a) [(131)I]bPTH-(1-84), anti-hPTH-(TCA) and hPTH-(1-84)G-100 as standard; (b) [(131)I]hPTH-(1-34), anti-hPTH-(1-34) and hPTH-(1-34) as standard. With system (a), COOH-terminal fragments of hPTH-(1-84) having a molecular weight of approximately 7,000 were detected, and there was an almost total discrimination of serum iPTH levels in normal and in hyperparathyroid subjects. With system (b), on the other hand, several molecular species of iPTH were detected, including a component larger than hPTH-(1-84) and others similar to hPTH-(1-84) and to a fragment co-eluting with the NH(2)-terminal fragment hPTH-(1-34). When serum iPTH was assayed in system (b), there was a large overlap of iPTH levels in control subjects and in patients with primary hyperparathyroidism.

Animals↗