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  • Artikel  (56)
  • Parathyroid hormone  (56)
  • Springer  (56)
  • American Chemical Society (ACS)
  • 2020-2024
  • 1980-1984  (35)
  • 1975-1979  (21)
  • Physik  (56)
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  • Artikel  (56)
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  • Springer  (56)
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  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Calcified tissue international 33 (1981), S. 375-380 
    ISSN: 1432-0827
    Schlagwort(e): Parathyroid hormone ; Radioimmunoassay
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary Metabolism of parathyroid hormone (PTH) is known to involve cleavage in the 28-48 region. With the goal of establishing a radioimmunoassay specific for the intact PTH molecule, we have tested the hypothesis that assays specific for the 28-48 region might fail to recognize the hormone fragments arising in vivo. Antisera against native bovine PTH (bPTH) contain antibody species directed at the 28-48 region of bPTH, since (a) 5 of 6 such antisera showed inhibition of binding of125I-labeled bPTH-(1-84) by unlabeled synthetic bPTH-(28-48), and (b) 9 of 9 such antisera bound125I-labeled bPTH-(28-48). The latter radioligand yields assays specific for the 28-48 region; 5 of 5 such assays recognized intact bPTH-(1-84), but none recognized bPTH-(1-34), bPTH-(37-84), or both fragments together. Binding of125I-bPTH-(28-48) to anti-bPTH sera was not inhibited by intact human PTH (hPTH). Likewise, only 1 of 6 antisera against native hPTH would bind125I-bPTH-(28-48) or show inhibition of125I-bPTH-(1-84) binding by unlabeled bPTH-(28-48). This poor immunological cross-reactivity between the 28-48 regions of bPTH and hPTH implies a major conformational transition between the two hormones in the 40–47 region of the molecule where the primary structure differs at 5 of 8 positions. A 28-48 specific assay employing an antiserum raised against both bPTH and hPTH did recognize both bPTH-(1-84) and hPTH-(1-84), but not bPTH-(1-34), hPTH-(1-34), bPTH-(37-84), or hPTH-(44-68). Thus, 6 different 28-48 region-specific assays have been shown to recognize intact PTH but not hormone fragments resembling those thought to be formed in vivo.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Calcified tissue international 33 (1981), S. 409-416 
    ISSN: 1432-0827
    Schlagwort(e): Bone Cells ; Cyclic AMP ; Calcium ; Parathyroid hormone ; Prostaglandin
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary We have examined the influence of extracellular Ca2+ on cyclic AMP metabolism in an osteoblast-enriched population of bone cells isolated from the calvaria of rat fetuses. The cyclic AMP1 response to stimulators of cyclic AMP formation (PTH and PGE2), but not basal cyclic AMP levels, increased progressively as the extracellular Ca2+ concentration was raised from 0.2 to 4.0 mM. The response to changes in extracellular Ca2+ were rapid (within 3.5 min), and the level of responsivity that characterized each Ca2+ concentration persisted for at least 6 h when the Ca2+ concentration was kept constant. The effect of Ca2+ spanned the entire time course of PTH action, was not accompanied by altered excretion of cyclic AMP from the cells, and was evident at low as well as at high hormone concentrations. Ca2+ augmented the action of PTH in the presence as well as in the absence of cyclic AMP phosphodiesterase inhibitors, and failed to decrease cyclic AMP phosphodiesterase activity in the short term. Mn2+ and, to a smaller degree, Ba2+ substituted for Ca2+ in promoting the cyclic AMP response to PTH. Verapamil, an inhibitor of Ca2+ penetration, blunted the Ca2+-mediated increments in the cyclic AMP response, and the divalent cation ionophore A23187 enhanced these increments. These results indicate that Ca2+ and other cations are positive effectors of the stimulated cyclic AMP response in isolated bone cells. Accumulation into an as yet unknown cellular compartment may be required for the cation effect. The data are most consistent with enhancement of adenylate cyclase reactivity as the mode of cation action.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Calcified tissue international 24 (1977), S. 209-214 
    ISSN: 1432-0827
    Schlagwort(e): Parathyroid hormone ; Plasma calcium ; Radiocalcium ; Bone
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary The net rate of loss of45Ca from plasma was monitored in normal, thyroparathyroidectomized (TPTX), and nephrectomized rats. Also studied was the effect of a 24 h intravenous infusion of PTH in TPTX rats. The45Ca was injected after an overnight fast and 1 to 4 h prior to the time the first blood sample was obtained. In normal rats, the net rate of loss of45Ca from plasma was slower than in TPTX rats for at least 12 h after radionuclide injection. Nephrectomy did not affect this difference between control and TPTX rats until 8 h after45Ca injection or about 18 h after nephrectomy. At this time a reversal occurred and the net rate of plasma45Ca loss in nephrectomized rats with parathyroids became faster than in TPTX nephrectomized rats. When PTH was infused at a constant rate (3 mU/g body weight/h) plasma calcium concentrations rose gradually for approximately 12 h after which a constant plasma calcium level was maintained with continued PTH infusion. During the period when plasma calcium concentrations were rising, the net rate of loss of45Ca from plasma was slower than in TPTX controls infused only with saline. However, when plasma levels stabilized, plasma45Ca disappearance rates changed such that the rate loss of45Ca from plasma became faster in PTH-infused than in TPTX controls. It is concluded that PTH increases calcium efflux from the same compartment in bone which receives calcium from plasma, thereby returning some recently deposited45Ca to plasma. In the non-equilibrated state, this returns additional45Ca to plasma causing anet decrease in the rate of loss of45Ca from plasma. However, in the equilibrated condition, when both calcium efflux from bone and influx into bone are in balance but at higher flux rates, PTH stimulates the diffusion of45Ca into other bone compartments.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Digitale Medien
    Digitale Medien
    Springer
    Calcified tissue international 28 (1979), S. 79-81 
    ISSN: 1432-0827
    Schlagwort(e): Parathyroid hormone ; Fragments ; Infusion ; Dog
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary Radioiodinated parathyroid hormone [125I-PTH(1-84)] was infused into intact dogs. At various times venous samples were chromatographed to determine the levels of intact hormone (1-84) and large fragments in the circulation. Both bioactive (electrolytically iodinated) and inactive (chloramine-T-labeled) preparations were used. In both instances, plateau concentrations of intact hormone and of large metabolite(s) were quickly reached. After cessation of infusion the levels of intact hormone and metabolite(s) quickly declined. Clearly, in the dog, the peripheral formation and disappearance of large fragments of exogenous PTH occur at rates comparable to the clearance of the intact hormone itself.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Digitale Medien
    Digitale Medien
    Springer
    Calcified tissue international 28 (1979), S. 113-119 
    ISSN: 1432-0827
    Schlagwort(e): Parathyroid hormone ; Calcitonin ; Plasma phosphate ; Bone phosphate ; Plasma32P specific activity
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary The influence of calcitonin (CT) on parathyroid hormone-induced changes in plasma phosphate, urine phosphate, plasma32P and32P specific activity (32P-S.A.) was studied using thyroparathyroidectomized rats. Radiophosphorus was injected at either 10 h (32P-10 h) or 8 days (32P-8 d) before commencing hormonal treatment. In order to produce consistent plasma32P-S.A. changes in rats treated with parathyroid hormone (PTH) alone, we maintained all animals for 48 h prior to hormone injection on a closely regulated carbohydrate intake (both quantity of food and time of feeding). Rats were then fasted 10 h prior to injection of PTH (0.01 U/g body weight/h), or CT (0.1 mU/g body weight/h), or both hormones injected simultaneously. Under these conditions, PTH produced a rise (relative to controls) in plasma32P-S.A. (-8 d) during an 8-h experimental period, while plasma32P-S.A. (-10 h) fell. Calcitonin treatment alone did not affect plasma32P-S.A., regardless of when32P was administered. When both hormones were injected concurrently, CT augmented the PTH-induced hypophosphatemia and magnified the fall in plasma32P levels, but the addition of CT did not affect PTH-induced changes in either renal calcium or phosphate excretion. However, the PTH-induced changes in plasma32P-S.A. were abolished. These data could not be explained by the opposing effects of the two hormones on rates of bone resorption. We interpret the results as adding support to the postulate that calcitonin moves phosphate into and prevents its loss from bone and bone fluid.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    ISSN: 1432-0827
    Schlagwort(e): Parathyroid hormone ; Osteoclasts ; Electron microscopy ; Morphometry ; Metaphysis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary The effects of parathyroid hormone (PTH) on the size of the osteoclasts, nuclei, ruffled borders, and clear zones in long bones of thyroparathyroidectomized (TPTX) rats were quantitated as a function of time. These data were compared with the number of osteoclasts in the bone and with plasma calcium levels. A significant increase in the average size of the ruffled borders was demonstrated 30 min after injection of 50 U of purified bovine PTH, and of the clear zones 30–90 min after PTH. This was followed at 90 min by an increase in the average size of the cells. The sizes of ruffled borders and clear zones dropped sharply to control levels after 6 h, whereas the size of the cells remained elevated up to 12 h and returned to control values at 24 h. Plasma calcium levels were increased, but not significantly, between 30 min and 6 h. An increase in the number of osteoclasts was significant after 12 h. Removal of the parathyroid glands did not diminish the normal activity of osteoclasts. In animals with intact glands injection of 50 U of PTH did not cause a significant change in cell size or resorbing apparatus. It is concluded that PTH acts to rapidly stimulate the bone resorptive activity of osteoclasts and to cause a delayed increase in their number.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
    ISSN: 1432-0827
    Schlagwort(e): Calcium homeostasis ; Radiocalcium ; Parathyroid hormone ; Bone cells ; Hyperparathyroidism
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary Early effects of parathyroid hormone (PTH) deficiency were studied in 12 patients with primary hyperparathyroidism due to single parathyroid adenoma by following the precise time course of changes in plasma calcium (Ca) and immunoreactive parathyroid hormone (iPTH) after parathyroid surgery and by prelabeling 2 patients with radiocalcium (Ca*). Surgical removal of the adenoma was immediately followed by a sudden increase in plasma Ca which preceded the usual fall. The increase in plasma Ca commenced simultaneously with the fall in iPTH and was accompanied by a parallel increase in specific activity (sp. act.) of plasma Ca*. Specific activity continued to rise for 2 h in both prelabeled patients, whereas blood calcium was already falling thereafter reaching a markedly low removal rate constant as long as plasma Ca decreased. When plasma Ca began to rise, sp. act. resumed a descending course. Our findings indicate that the initial hypercalemia depends on PTH withdrawal and results from a rapid flux into general extracellular fluid (ECF) of calcium coming from a compartment with higher sp. act., contained within the miscible pool, immediately followed by a reduction in calcium transfer from bone. These results suggest that acute PTH deficiency determines an outflow of calcium from bone cells and support the theory that PTH initiates its action by modifying their intracellular calcium content.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
    ISSN: 1432-0827
    Schlagwort(e): cyclic AMP ; Parathyroid hormone ; Prostaglandin E2 ; Down regulation ; Bone cells
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary Cells dispersed from human giant cell tumors of bone and grown in monolayer culture increase intracellular cyclic AMP (cAMP) when incubated with parathyroid hormone (PTH) or prostaglandin E2 (PGE2). When cells are continuously exposed to PTH, cAMP levels increase acutely but then decrease rapidly to pretreatment values despite continued presence of hormone or addition of new hormone. Preincubation of cells with PTH for periods as short as 10 min results in a decrease in the capacity of cells to increase cAMP content when re-exposed to maximal stimulatory concentrations of PTH. The decrease in the magnitude of the PTH-induced cAMP response observed in cells pretreated with this hormone is dependent on the concentration of PTH present during the pre-incubation. The loss of cAMP response in cells pre-treated with either PGE2 or PTH is hormone specific in that cells made refractory by pretreatment with one hormone still increase cAMP content when exposed to the other. Although the cells are not releasing measurable amounts of prostaglandins into the medium, pretreatment with indomethacin results in an increase in the magnitude of the cAMP response to PGE2. The PTH-induced cAMP response is not affected by indomethacin pre-treatment. The loss of PTH responsiveness produced by hormone preincubation is consistent with the phenomenon of “down-regulation” observed with ligand-receptor interactions in a variety of tissues.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
    ISSN: 1432-0827
    Schlagwort(e): Parathyroid hormone ; Bone resorption ; Collagen synthesis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary An analog of bovine PTH [nle-8, nle-18, tyr-34 bPTH-(1-34) amide, (PTH-Ana)] which is a potent stimulator of renal adenylate cyclase has been compared with the native hormone bPTH-(1-84) and the biologically active amino terminal portion, bPTH-(1-34), for its effects on bone resorption and bone collagen synthesis in organ culture. All three compounds stimulated the release of previously incorporated45Ca from cultured fetal rat long bone shafts with similar dose-response curves at 10−9 to 3 × 10−8 M. All three compounds inhibited bone collagen synthesis as measured by incorporation of proline into collagenase digestible protein, whereas incorporation into noncollagen protein was not inhibited. The effects were dose related and decreases in percent collagen synthesis were significant at 10−9 M. Thus PTH-Ana appears to have the same effects on bone resorption and collagen synthesis as bPTH-(1-84) and (1-34) and is likely to be a valid probe for investigating PTH receptors in bone as well as in kidney.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
    Digitale Medien
    Digitale Medien
    Springer
    Calcified tissue international 30 (1980), S. 209-216 
    ISSN: 1432-0827
    Schlagwort(e): Calvarium ; cAMP ; Vitamin D3 metabolites ; Calcium ; Parathyroid hormone
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin , Physik
    Notizen: Summary Results from in vitro works suggest that 1,25- and 24,25-dihydroxyvitamin D3 (1,25-(OH)2D3 and 24,25-(OH)2D3) act on bone via different mechanisms. The present investigation was performed to study the effect of these two metabolites and of their precursor 25-hyxdroxyvitamin D3 (25-(OH)D3) on bone cAMP content in vitro. Rats' paired half calvaria were incubated under sterile conditions with one vitamin D3 derivative (10−13 to 10−9 M) or with ethanol (0.005 ml for 15 min to 24 h in 1 ml medium containing 0, 0.2, 1, 2, or 3 mM calcium. In some experiments: (a) cycloheximide (10−5M) was added simultaneously with the vitamin D3 metabolites; (b) 1–84 bPTH (5 × 10−8 M) was added for 5 or 15 min at the end of the 24 h incubation. Calvaria were immersed in 1 ml TCA 5% 4°C and homogenized. The cAMP was extracted with diethylether and measured by a competitive protein binding assay. Results bring further evidence for a particular effect of low doses of 24,25-(OH)2D3 (10−9 to 10−12M) and of 25-(OH)D3 (10−9 to 10−11M) on bone, different from that of 1,25-(OH)2D3: cAMP content was higher in 24,25-(OH)2D3- or 25-(OH)D3-treated and lower in 1,25-(OH)2D3-treated calvaria than in ethanol-treated ones with 1 mM calcium. The 1,25-(OH)2D3 effect persisted in calcium-free medium whereas 25-(OH)D3 and 24,25-(OH)2D3 effects could not be observed with 0 mM nor with 3 mM calcium. The required duration of the preincubation (over 1 h) as well as the inhibitory action of cycloheximide may suggest an involvement of protein synthesis in the vitamin D3 metabolites effects. Neither 1,25-(OH)2D3 nor 24,25-(OH)2D3 affected the PTH-induced increase in bone cAMP content.
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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