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  • Articles  (20)
  • Parathyroid hormone  (20)
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  • Articles  (20)
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  • Springer  (20)
  • Blackwell Publishing Ltd
  • Elsevier
  • International Union of Crystallography
  • Taylor & Francis
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  • 1985-1989
  • 1980-1984  (20)
  • 1940-1944
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 36 (1984), S. 384-391 
    ISSN: 1432-0827
    Keywords: 1,25(OH)2D3 ; Vitamin D metabolities ; Parathyroid hormone ; PTH secretion regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The effect of vitamin D metabolites on parathyroid hormone secretion was studied using rat parathyroid gland cultured in basal medium Eagle containing 5% serum obtained from thyroparathyroidectomized rat, 1 mM magnesium, and calcium concentration varying from 0.75–2.25 mM, and radioimmunoassay for rat parathyroid hormone (rPTH). 1,25 dihydroxycholecalciferol (1,25(OH)2D3), 5×10−10−2.5×10−8M, consistently decreased rPTH secretion in dose-related manner; the effect reached steady state after 24 hin vitro addition of 1,25(OH)2D3 and was also observed at different medium calcium concentrations (0.75, 1.25, 1.75 mM). Comparison of dose-responses for inhibitory activity of some vitamin D metabolites on rPTH secretion showed: 1,25(OH)2D3=1,24,25(OH)3D3〉1α OHD3〉25 OHD3. Cholecalciferol (10−5M), 24,25-dihydroxycholecalciferol (10−8−10−6M) and 25,26-dihydroxycholecalciferol (5×10−9−5×10−7M) did not inhibit rPTH secretion. Analysis of structural activity relation of vitamin D metabolites studied indicated that 1α or pseudo-1α hydroxylated metabolites or analogs were active in inhibiting rPTH secretion, while, non-1α hydroxylated metabolites were without or were weakly inhibitory only at very high concentrations. This study provides further evidence for a direct role of 1,25(OH)2D3 on a negative feedback loop for regulation of parathyroid gland function.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 34 (1982), S. 270-272 
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Minipumps ; Bone resorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary To determine if osmotic minipumps can be used for the local delivery of parathyroid hormone (PTH), we examined the bone resorbing activity of PTH in minipumps, either removed and assayed in bone organ cultures or released over rat calvaria. Biological activity of PTH was maintained for up to 6 days when the hormone solution contained serum and the minipumps and tubing were siliconized and flushed with diluent prior to use. Addition of cysteine did not enhance activity.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 34 (1982), S. 470-473 
    ISSN: 1432-0827
    Keywords: Calcitonin ; Premature ; Osteopenia ; Hypocalcemia ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Twenty-eight premature infants of mean gestation 30.9±2.5 weeks and mean birth weight 1175±206 g had repeated serum calcitonin concentrations determined over the first 12 weeks of life. Serum calcitonin concentrations slowly fell but remained elevated even at 12 weeks of age [normal adult=71±48, 1 week (N=15)=327±167, 3 week (N=23)=270±129, 6 week (N=16)=249±154, 9 week (N=13)=214±108, 12 week (N=12)=174±11]. Throughout this period, serum total calcium was normal or low (8.4±.8–9.3±1.0). Serum phosphorus was normal or low (6.0±1.4–6.5±1.0), and serum magnesium was normal (1.7±0.24–1.8±0.34). The reason for the sustained elevation of serum calcitonin in these very small, sick, premature infants in unclear.
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  • 4
    ISSN: 1432-0827
    Keywords: Serum calcium ; Parathyroidectomized rat ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary This work was conducted to estimate the replacement dose of the synthetic bovine parathyroid hormone [PTH(1–34)] that is required for maintenance of serum calcium (Ca) in parathyroidectomized (PTX) rats. Male rats were PTX and used in this study only if serum Ca was reduced to at least 7 mg/dl. We found that a solution of 2% cysteine, 150 mM NaCl, and 1 mM HCl was superior to 20 mM acetic acid for maintenance of biological activity of PTH (1–34) in situ during the period of hormone infusion studied. The PTH dose—calcemic response relationship was investigated using PTH in doses of 0.6, 1, and 3 U/h. The infusion of 1 U PTH per hour raised Ca to the normal level, whereas rats infused with 0.6 U/h were hypocalcemic and 3 U/h resulted in marked hypercalcemia. To extend this observation we carried out an infusion of 1 U PTH per hour for 14 days. We found that this infusion rate of bovine PTH (1–34) provided a relatively stable level of serum calcium with modest fluctuation from normocalcemic to somewhat hypercalcemic levels for the entire 14-day period of PTH infusion. Serum calcitonin was also elevated during the infusion period and then returned to the initial level when PTH treatment was stopped. After the minipumps containing PTH were removed, the serum Ca dropped rapidly to 5 mg/dl, which was significantly lower than the control (vehicle-infused) or initial values of serum Ca (7 mg/dl). Infusion of PTH at 3 U/h for 4 days did not produce this rebound hypocalcemia after the pumps were removed. Serum Ca in those experiments returned to the initial level after hormone treatment was discontinued.
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  • 5
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Adenylate cyclase ; 3′5′ cyclic adenosine monophosphate ; Forskolin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Forskolin, a diterpene which directly stimulates adenylate cyclase, markedly stimulated cAMP production in intact rat parathyroid glands and dispersed cells from hyperplastic and adenomatous human parathyroid tissues. Stimulation of cAMP production in human parathyroid adenomas occurred as early as 2 min and continued for at least 2 h; furthermore, a dose-response relationship was observed, with a maximal 80-fold cAMP response occurring at 100 µM forskolin. When PTH secretion by rat or human parathyroid tissues was studied at low (0.5 mM) and high (2.5 mM) extracellular Ca2+ in either the presence or absence of forskolin, no significant stimulation by forskolin was observed at 15 min, 1 h, and 2 h. When 10 human parathyroid specimens were studied with varying concentrations of forskolin at 1 mM Ca2+, 6 failed to show stimulation of PTH secretion and 4 showed modest but detectable increases in PTH that did not appear dose-related. We conclude that (1) at low and high Ca2+ levels, marked stimulation of cAMP production by forskolin can occur without a corresponding increase in PTH secretion; (2) inhibition of PTH secretion by high extracellular Ca2+ levels continues unchanged despite stimulation of cAMP production by forskolin; and (3) at intermediate Ca2+ levels (1.0 mM), PTH secretion is affected either minimally or not at all by forskolin in human hyperparathyroid tissue preparations. The marked stimulation of parathyroid adenylate cyclase by forskolin without concomitant increases in PTH secretion in the majority of tissues suggests that the level of cAMP production is not a primary or sufficient determinant of hormone secretion.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 36 (1984), S. 189-193 
    ISSN: 1432-0827
    Keywords: Protamine ; Hypocalcemia ; Parathyroid hormone ; Bone resorption ; Bone turnover
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Protamine is shown to be a powerful disrupter of calcium homeostasis, acutely inducing a severe hypocalcemia in both rabbits and rats. The magnitude of its effect correlates with bone turnover. Protamine does not significantly alter the renal excretion of calcium, and is effective whether or not there is calcium present in the gut. Protamine causes a significant fall in the specific activity of45Ca in the blood in animals whose bone has been prelabeled with45Ca. These data suggest that protamine induces hypocalcemia by blocking calcium efflux from bone. Further work seems indicated to define the biochemical mechanism of this action.
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 36 (1984), S. 279-284 
    ISSN: 1432-0827
    Keywords: Bone cells ; Parathyroid hormone ; PGE2 ; Adriamycin ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We have examined the effect of adriamycin, an anthracycline antibiotic which modifies plasma membrane functions, on the cyclic AMP response to PTH and PGE2 in isolated osteoblastlike cells. Adriamycin blunted the increment in bone cell cyclic AMP caused by exposure to PTH. This effect appeared rapidly (within 3 min after bone cells were exposed to adriamycin) and disappeared soon after exposure of adriamycin-treated cells to adriamycin-free incubation medium. Inhibition was evident over the entire time course of PTH action, at low as well as high PTH concentrations, and was one-half maximal at 31 µM adriamycin. It could not be attributed to alterations in cyclic AMP exodus, degradation or interference with the cyclic AMP assay, nor to impaired cell viability. Adriamycin also reduced the stimulatory effect of PTH on adenylate cyclase activity in a crude plasma membrane preparation. By contrast, adriamycin failed to modify the effects of PGE2 on cyclic AMP generation in intact bone cells, and on adenylate cyclase activity in broken cells. Moreover, concentrations of adriamycin that blunted the effect of PTH on adenylate cyclase activity did not inhibit the stimulatory effects of sodium fluoride or of GppNHp. These results suggest that adriamycin selectively alters the interaction between PTH and its receptor or impairs the transmission of information from hormone-receptor complex to adenylate cyclase (or both), perhaps by binding to specific lipid domains in the plasma membrane. Structural analogues of adriamycin, which vary in their lipophilic properties, also varied in their capacity to perturb the cyclic AMP response. One such analogue in fact inhibited the response to PGE2, and several appeared to augment the PGE2 effect. These substances may well be useful in probing the membrane properties required for selectivity in hormone action.
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  • 8
    ISSN: 1432-0827
    Keywords: Calcium ; Vitamin D deficiency ; 1,25(OH)2D3 ; Parathyroidectomy ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Studies presented here were designed to investigate further the basis for an impaired cAMP response to parathyroid hormone (PTH) in osteoblastlike calvarial bone cells isolated from vitamin D-deficient rat pups. The goal was to perturb Ca, PTH, and vitamin Din vivo in order to see which factors might be responsible for the impairedin vitro bone cell cAMP response. Pups either were parathyroidectomized (PTX) 3–5 days, implanted with osmotic minipumps delivering high doses of PTH, given repeated, high doses of 1,25(OH)2D3, or were D-deficient (-D, i.e., born and suckled by D-deficient mothers). Osteoblastlike bone cells, isolated by sequential enzyme digestion and centrifugation, were exposed to PTH for 5 min in the presence of a phosphodiesterase inhibitor. In bone cells isolated from -D rat pups, both basal and PTH-induced cAMP accumulation were significantly lower than in +D bone cells. Earlier, we had shown that two daily injections of -D pups with 50 ng 1,25(OH)2D3 restores this reduced bone cAMP response of -D pups toward normal. In the present study, neither basal nor PTH-induced bone cell cAMP accumulation was affected by subjecting D-replete pups to PTX, PTH infusion, or repeated high doses of 1,25(OH)2D3 despite the fact that each treatment markedly changed serum Ca or serum immunoreactive PTH. The results indicate that the impaired bone cell cAMP response seen in -D pups is not a direct result of chronic hypocalcemia and that the “heterologous desensitization” seenin vitro with added 1,25(OH)2D3 could not be duplicated byin vivo treatment of +D pups with supraphysiologic doses of 1,25(OH)2D3. Finally the lack of alteration in the bone cell cAMP response to PTHin vitro after chronic PTH infusionin vivo fails to support the notion that the impaired response in -D bone cells can be explained entirely by “homologous desensitization” induced by high circulating levels of PTH in the hypocalcemic, -D rat pup.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 34 (1982), S. 9-12 
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Pregnancy ; Nephrogenous cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Parathyroid hormone (PTH) metabolism in pregnancy has not been clearly defined. Studies have reported either increased or unchanged values of immunoreactive PTH (iPTH). However, iPTH levels do not necessarily correlate with hormonal bioactivity due to the presence of immunoreactive but nonbioactive PTH fragments. In this study we evaluated PTH metabolism in the third trimester of pregnancy by determining iPTH blood levels as well as the biological effects of PTH, assessed by tubular maximum phosphate reabsorption (TmP) and nephrogenous cAMP (ncAMP) excretion, in 10 young, healthy pregnant patients (mean gestational age 35 weeks) and 10 young, healthy age-matched female controls. Pregnancy was associated with a significant increase in creatinine clearance (146±13 vs 106±9 ml/min,P〈0.01), and a significant decrease in total fasting serum calcium (8.4±0.1 vs 9.0±0.1 mg/dl,P〈0.001) and serum albumin (3.6±0.1 vs 4.2±0.1 g/dl,P〈0.001). There was no significant difference in iPTH (3.7±0.4 vs 4.3±0.5 µlEq/ml), serum phosphorus (3.6±0.1 vs 3.8±0.2 mg/dl), TmP (3.61±0.13 vs 3.75±0.25 mg/100 ml GFR), or ncAMP (1.68±0.20 vs 1.88±0.23 nmoles/100 ml GFR) between the two groups. Pregnancy was attended by a significant increase in fasting urinary calcium to creatinine ratio (0.14±0.03 vs 0.06±0.01,P〈0.05), an index of bone resorption. The data suggest that the biological effects of PTH are unchanged in pregnancy, and that reported increments in 1,25(OH)2 vitamin D in pregnancy are not regulated by changes in either PTH, calcium, or phosphate.
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  • 10
    ISSN: 1432-0827
    Keywords: Calcium ionophore A23187 ; Parathyroid hormone ; 45Ca release ; DNA concentration ; Nucleic acid synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary It has recently been demonstrated that calcium ionophore A23187 mimics certain of the effects of parathyroid hormone (PTH) on bone in vitro, including stimulation of45Ca release and cAMP formation. To further examine the relative effects of these two agents on bone cell metabolism, we compared the effects of synthetic PTH 1–34 (50 ng/ml) and calcium ionophore A23187 (0.5µg/ml) on45Ca release, DNA concentration, and nucleic acid synthesis in fetal rat forelimb rudiments cultured for periods up to 120 h. Both agents stimulated45Ca release; however, the effects of PTH were apparent after a shorter period of exposure. Bone DNA concentration (expressed asµg DNA/mg bone) was not affected by PTH but was significantly increased relative to control values by exposure to A23187 for 8–120 h of incubation. PTH increased the incorporation of3H-thymidine into DNA at 30 and 48 h, and increased the incorporation of14C-uridine into RNA at 48 h, time points which corresponded to a period of accelerated PTH stimulation of45Ca release. In contrast,3H-thymidine and14C-uridine incorporation were both uniformly suppressed by A23187 at all time points examined. Thus the increased DNA concentration observed in A23187-treated rudiments appeared to be the result of a decreased rate of bone maturation and mineralization. The markedly different patterns of nucleic acid synthesis in response to PTH and A23187 suggest that these agents differ significantly in their mechanisms of action on bone cell metabolism.
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