Journal articles on the topic 'Least Pth'
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1
Gokhale, M. Y., and Daljeet Kaur Khanduja. "Analysis and synthesis of speech using least Pth norm filter design." International Journal of Speech Technology 11, no. 1 (March 2008): 51–61. http://dx.doi.org/10.1007/s10772-009-9035-7.
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Phillips, IJ, TR Kurzawinski, and JW Honour. "Potential pitfalls in intraoperative parathyroid hormone measurements during parathyroid surgery." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 42, no. 6 (November 1, 2005): 453–58. http://dx.doi.org/10.1258/000456305774538283.
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Background: The outcome of parathyroid surgery is often not clear for at least 24 h after the operation. A frozen section does not always distinguish between an adenoma and hyperplasia. Minimally invasive surgical techniques are being refined, so the need for perioperative assurance about the completeness of surgery has increased. The value of intraoperative parathyroid hormone (PTH) measurements in 26 surgical cases undergoing parathyroidectomy has been evaluated. Methods: Twenty-one patients were diagnosed as having primary hyperparathyroidism, including two patients with multiple endocrine neoplasia type I (MEN I). Five patients had tertiary hyperparathyroidism, including one patient with X-linked hypophosphataemia and four with renal hyperparathyroidism (RHPT). Blood samples were taken at the onset of surgery, at the time of tumour resection and at 5-min intervals following removal of the tumour. PTH was measured using a PTH Turbo assay on the DPC Immulite analyser. Results: Current practice suggests that the PTH concentration should fall to less than 50% of the pre-incision value or to less than 50% of the level at the time of tumour resection (time equals zero). PTH levels were therefore monitored at 5-min intervals following removal of the tumour. In most of the case studies PTH followed the suggested pattern, but not when further exploration was warranted to determine if another adenoma was present. In some cases the PTH levels fell by the appropriate margin to deem the procedure a success but at 10 min post-gland excision the PTH began to rise again. Further exploration was required to confirm the continued source of PTH. Conclusion: We recommend that intraoperative PTH measurements continue until at least 15 min post-gland removal in cases of suspected single-gland disease. A decline in PTH concentration to at least 50% of the pre-incision or time of gland resection levels should be observed. If the PTH remains elevated or rises again after an appropriate decrease in levels, then multigland disease or ectopic sources should be considered. Caution is recommended in interpreting intraoperative PTH measurements to ensure complete success of the surgical procedure.
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Chien-Cheng Tseng. "Design of IIR digital all-pass filters using least pth phase error criterion." IEEE Transactions on Circuits and Systems II: Analog and Digital Signal Processing 50, no. 9 (September 2003): 653–56. http://dx.doi.org/10.1109/tcsii.2003.816914.
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Murer, H., A. Werner, S. Reshkin, F. Wuarin, and J. Biber. "Cellular mechanisms in proximal tubular reabsorption of inorganic phosphate." American Journal of Physiology-Cell Physiology 260, no. 5 (May 1, 1991): C885—C899. http://dx.doi.org/10.1152/ajpcell.1991.260.5.c885.
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Filtered inorganic phosphate (Pi) is largely reabsorbed in the proximal tubule. Na-Pi cotransport, with a stoichiometry of at least 2:1, mediates uphill transport at the apical membrane; at the basolateral membrane different types of transport systems can be involved in efflux and uptake of Pi from the interstitium. Regulation of transcellular Pi flux involves alteration of the apical Na-Pi cotransport; at least three different cellular control/sensing systems seem to participate in this regulation and are exemplified by parathyroid hormone (PTH)-dependent inhibition, Pi deprivation-dependent increase, and insulin-like growth factor I (IGF-I)-dependent increase in Na-Pi cotransport. For PTH inhibition, recent evidence suggests a role of the phospholipase C/protein kinase C-dependent regulatory cascade in inhibition of Na-Pi cotransport, at least at low PTH concentrations. In addition, an endocytic mechanism seems to be involved in this PTH action. Little is known of the cellular mechanisms in Pi deprivation-dependent and/or IGF-I-dependent increases in Na-Pi cotransport; they are dependent on de novo protein synthesis. Recent experiments involving an expression in Xenopus laevis oocytes led to the identification of an approximately 50 kDa membrane protein that is a good candidate for being involved in brush-border membrane Na-Pi cotransport activity.
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Takano, T., M. Takigawa, E. Shirai, K. Nakagawa, M. Sakuda, and F. Suzuki. "The Effect of Parathyroid Hormone (1-34) on Cyclic AMP Level, Ornithine Decarboxylase Activity, and Glycosaminoglycan Synthesis of Chondrocytes from Mandibular Condylar Cartilage, Nasal Septal Cartilage, and Spheno-occipital Synchondrosis in Culture." Journal of Dental Research 66, no. 1 (January 1987): 84–87. http://dx.doi.org/10.1177/00220345870660011801.
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Previously, we reported methods for isolating chondrocytes from the craniofacial complex and their culture in vitro. The response of these chondrocyte cultures to bovine parathyroid hormone (1—34) (PTH) has now been investigated. PTH stimulated glycosaminoglycan (GAG) synthesis, a characteristic of the cartilage phenotype in cultured chondrocytes isolated from mandibular condylar cartilage (MCC), nasal septal cartilage (NSC), and spheno-occipital synchondrosis (SOS). These stimulations of GAG synthesis by PTH were dose-dependent. PTH also increased accumulation of cyclic AMP (cAMP) and the activity of ornithine decarboxylase (ODC), a rate-limiting enzyme in polyamine biosynthesis. However, PTH did not stimulate DNA synthesis. The increases in the cAMP level, ODC activity, and GAG synthesis after addition of PTH (10-7 mol/L) were greatest in MCCchondrocytes and least in NSC-chondrocytes. The difference in the responses to PTH of these three types of chondrocytes may reflect differences of the characteristics of these cells in vivo.
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Ingle, A. R., J. E. Bailey, H. L. Matthews, and J. S. Harrop. "Performance and Clinical Utility of a Commercially Available ‘C-terminal’ PTH Assay." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 23, no. 4 (July 1986): 434–39. http://dx.doi.org/10.1177/000456328602300409.
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The performance and clinical utility of a ‘C-terminal’ parathyroid hormone (PTH) radioimmunoassay (Dac-Cel, Wellcome Diagnostics) is described. Parathyroid hormone, as measured by the Dac-Cel method, is stable in whole blood samples for at least 24 h. 84% of patients with hypercalcaemia due to primary hyperparathyroidism have values above the upper limit seen in normocalcaemic subjects (0·5 μg/L), with detectable serum PTH demonstrable in the remaining 16%. In patients with hypocalcaemia due to hypoparathyroidism serum PTH was undetectable in 73% and ‘inappropriately’ low in the remainder. In 50% of patients with malignancy-associated hypercalcaemia serum PTH was undetectable, but was above 0·5 μg/L in 13%. Increased PTH concentrations were invariably found in patients with renal failure. The Dac-Cel method is a reliable and robust technique for measurement of PTH and in conjunction with determination of calcium facilitates the diagnosis of primary parathyroid disorders. Caution is required in the interpretation of PTH measurements in patients with renal failure; the significance of detectable PTH in some patients with malignancy-associated hypercalcaemia is not clear.
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Levy, Dan, Shahaf Edut, Renana Baraz-Goldstein, Vardit Rubovitch, Ruth Defrin, Dara Bree, Helaine Gariepy, Jun Zhao, and Chaim G. Pick. "Responses of dural mast cells in concussive and blast models of mild traumatic brain injury in mice: Potential implications for post-traumatic headache." Cephalalgia 36, no. 10 (July 20, 2016): 915–23. http://dx.doi.org/10.1177/0333102415617412.
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Background Chronic post-traumatic headache (PTH) is one of the most common symptoms of mild traumatic brain injury (mTBI) but its underlying mechanisms remain unknown. Inflammatory degranulation of dural mast cells (MCs) is thought to promote headache, and may play a role in PTH. Whether mTBI is associated with persistent degranulation of dural MCs is yet to be determined. Methods Histochemistry was used to evaluate time course changes in dural MC density and degranulation level in concussive head trauma and blast mouse models of mTBI. The effects of sumatriptan and the MC stabilizer cromolyn sodium on concussion-evoked dural MC degranulation were also investigated. Results Concussive head injury evoked persistent MC degranulation for at least 30 days. Blast trauma gave rise to a delayed MC degranulation response commencing at seven days that also persisted for at least 30 days. Neither sumatriptan nor cromolyn treatment reduced concussion-evoked persistent MC degranulation. Conclusions mTBI evoked by closed head injury or blast exposure is associated with persistent dural MC degranulation. Such a response in mTBI patients may contribute to PTH. Amelioration of PTH by sumatriptan may not involve inhibition of dural MC degranulation. If persistent dural MC degranulation contributes to PTH, then cromolyn treatment may not be effective.
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Akatsu, Takuhiko, Naokazu Nagata, Nobuo Kugai, Yoshirou Yasutomo, Tokuyasu Kinoshita, Hiroshi Kosano, Osamu Takatani, Kunio Takishima, and Gunzi Mamiya. "On the activities of parathyroid hormone-like factor and transforming growth factors in extract of pancreatic cancer associated with humoral hypercalcemia of malignancy." Acta Endocrinologica 118, no. 2 (June 1988): 232–38. http://dx.doi.org/10.1530/acta.0.1180232.
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Abstract. Extract of exocrine pancreatic cancer associated with humoral hypercalcemia of malignancy was examined for biological activities of PTH-like factor and transforming growth factor (TGFA and TGFB), both of which are possible causes of hypercalcemia. The crude extract had both PTH-like and TGF activities. On Bio Gel P-60 column chromatography, PTH-like and TGFA activities were eluted at around 10 kD, whereas TGFB activity was eluted at around void fractions, 10 kD and 6 kD. Liver extract, used as a control material, exhibited only TGFB activity at around 6 kD. CM-cellulose column chromatography of 10 kD fractions resulted in a subtle distinction between PTH-like activity and TGF activities. Further fractionation of the peak with PTH-like activity on reverse-phase high performance liquid chromatography separated PTH-like activity distinctly from TGFB activity. TGFA activity was lost through the procedure. It was concluded that the exocrine pancreatic cancer associated with hypercalcemia produced not only PTH-like activity but also TGFA and TGFB activities. Several chromatographic analyses suggested that PTH-like activity and at least TGFB activity stem from distinct molecules and that the PTH-like factor has no significant TGFB activity intrinsically.
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Chobanian, M. C., and M. R. Hammerman. "Parathyroid hormone stimulates ammoniagenesis in canine renal proximal tubular segments." American Journal of Physiology-Renal Physiology 255, no. 5 (November 1, 1988): F847—F852. http://dx.doi.org/10.1152/ajprenal.1988.255.5.f847.
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To determine whether parathyroid hormone (PTH) affects ammoniagenesis in renal proximal tubule, we measured ammonia production in suspensions of canine renal proximal tubular segments incubated with 10 mM L-glutamine in the absence or presence of 10(-7) M PTH. Productions of ammonia were linear functions of time for 120 min and averaged 231 +/- 55 and 311 +/- 67 mumol ammonia/g protein in the absence and presence of PTH, respectively. When measured over the range of 10(-11)-10(-7) M PTH, half-maximal stimulation of ammonia production occurred between 10(-10) and 10(-9) M PTH. Maximal production of ammonia was observed at 10(-8) M PTH. Incubation of proximal tubular segments with PTH increased levels of adenosine 3',5'-cyclic monophosphate (cAMP) in vitro. Ammonia production was significantly enhanced by incubation of segments with the cAMP analogue, 8-bromoadenosine 3',5'-cyclic monophosphate. PTH also increased ammonia production in segments incubated with 1 mM L-glutamine. We conclude that PTH stimulates ammonia production in canine renal proximal tubular segments. This effect appears to be mediated, at least in part, through cAMP in vitro. Such stimulation could reflect a direct action of PTH on the proximal tubule to enhance ammoniagenesis in vivo.
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Bastepe, Murat, Serap Turan, and Qing He. "Heterotrimeric G proteins in the control of parathyroid hormone actions." Journal of Molecular Endocrinology 58, no. 4 (May 2017): R203—R224. http://dx.doi.org/10.1530/jme-16-0221.
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Parathyroid hormone (PTH) is a key regulator of skeletal physiology and calcium and phosphate homeostasis. It acts on bone and kidney to stimulate bone turnover, increase the circulating levels of 1,25 dihydroxyvitamin D and calcium and inhibit the reabsorption of phosphate from the glomerular filtrate. Dysregulated PTH actions contribute to or are the cause of several endocrine disorders. This calciotropic hormone exerts its actions via binding to the PTH/PTH-related peptide receptor (PTH1R), which couples to multiple heterotrimeric G proteins, including Gs and Gq/11. Genetic mutations affecting the activity or expression of the alpha-subunit of Gs, encoded by the GNAS complex locus, are responsible for several human diseases for which the clinical findings result, at least partly, from aberrant PTH signaling. Here, we review the bone and renal actions of PTH with respect to the different signaling pathways downstream of these G proteins, as well as the disorders caused by GNAS mutations.
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Matovcik, Lisa M., Steven S. Rhee, Jean F. Schaefer, and Barbara K. Kinder. "Reconstitution of Calcium-Regulated Parathyroid Hormone Secretion from Streptolysin-O-Permeabilized Parathyroid Cells by Guanosine 5′-O-(Thio)Triphosphate*." Endocrinology 138, no. 3 (March 1, 1997): 1170–79. http://dx.doi.org/10.1210/endo.138.3.4971.
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Abstract Intracellular Ca2+ levels determine the amount of PTH secretion from parathyroid cells. Dissociated calf parathyroid cells were permeabilized with streptolysin-O (SLO) to provide an in vitro model system to examine Ca2+-dependent regulation of hormone secretion. PTH release from these cells was energy dependent and increased by cytosolic cofactors. Guanosine 5′-O-(thio)triphosphate (GTPγS) increased PTH secretion from SLO-permeabilized cells in a dose-dependent manner from 0.1–100 μm. In the absence of GTPγS there was no relationship between the ambient Ca2+ concentration and the rate of PTH secretion. However, in the presence of GTPγS, intracellular Ca2+ inhibited PTH secretion with an EC50 of approximately 0.1 μm, corresponding to physiological intracellular Ca2+ levels. Thus, the addition of GTPγS to SLO-permeabilized parathyroid cells reconstituted the inverse relationship between extracellular Ca2+ and PTH secretion that is observed in vivo and in intact cells. The data indicate that this effect is mediated at least in part by heterotrimeric guanosine triphosphatases. In addition, calcium/calmodulin-dependent protein kinase II appears to mediate low Ca2+-dependent PTH secretion from these cells.
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Kidambi, Sunder. "Design of Noise Transfer Functions for Delta–Sigma Modulators Using the Least-pth Norm." IEEE Transactions on Circuits and Systems II: Express Briefs 66, no. 4 (April 2019): 707–11. http://dx.doi.org/10.1109/tcsii.2018.2880925.
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Rai, Amrita, and Amit Kumar Kohli. "Adaptive Polynomial Filtering using Generalized Variable Step-Size Least Mean pth Power (LMP) Algorithm." Circuits, Systems, and Signal Processing 33, no. 12 (June 10, 2014): 3931–47. http://dx.doi.org/10.1007/s00034-014-9833-2.
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Ritter, Cynthia S., Sangeeta Pande, Irina Krits, Eduardo Slatopolsky, and Alex J. Brown. "Destabilization of parathyroid hormone mRNA by extracellular Ca2+ and the calcimimetic R-568 in parathyroid cells: role of cytosolic Ca and requirement for gene transcription." Journal of Molecular Endocrinology 40, no. 1 (November 15, 2007): 13–21. http://dx.doi.org/10.1677/jme-07-0085.
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Extracellular Ca reduces parathyroid hormone (PTH) levels through several mechanisms, but many details of the intracellular steps involved have been difficult to elucidate because of the lack of a suitable parathyroid cell model. The present studies utilized our Ca-responsive bovine parathyroid organoid culture system (pseudoglands) to examine PTH mRNA in intact parathyroid cells. Increasing medium calcium from 0.4 to 3.0 mM reduced PTH mRNA to 20–30% of basal by 16 h. Reducing medium Ca from 3.0 to 0.4 mM restored PTH mRNA levels over a 24-h period. PTH mRNA was also reduced by the calcimimetic R-568, confirming the role of the calcium-sensing receptor. PTH decay rates were determined by placing pseudoglands in either 0.4 or 3.0 mM Ca for 2 h and then blocking gene transcription. PTH mRNA remained stable for at least 24 h in pseudoglands incubated in 0.4 mM Ca, but fell gradually by 62% in the presence of 3.0 mM Ca. Blocking transcription prior to the addition of high-Ca medium dramatically blunted the Ca-induced degradation of PTH mRNA, indicating that acceleration of PTH mRNA decay by Ca requires gene transcription. Pharmacologic investigation of the signaling pathways involved indicated that the Ca-induced reduction of PTH mRNA did not involve MAP kinase, phospholipase D, or cyclic AMP. However, increasing cytosolic Ca with thapsigargin or the Ca ionophore A23187 decreased PTH mRNA levels. In summary, Ca-mediated destabilization of PTH mRNA requires gene transcription and involves increases in cytosolic Ca.
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Dilena, Beverly A., and Graham H. White. "Assessing acute parathyroid responsiveness in hemodialysis patients by measuring intact parathyrin in pre- and post-dialysis serum." Clinical Chemistry 37, no. 7 (July 1, 1991): 1216–20. http://dx.doi.org/10.1093/clinchem/37.7.1216.
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Abstract We measured pre- and post-dialysis concentrations of ionized calcium (iCa) in whole blood, total calcium (tCa) in plasma, and intact parathyrin (PTH) in serum of 19 patients undergoing maintenance hemodialysis. Plasma tCa was inappropriately increased relative to iCa in 63% of the specimens; the iCa correlated with the PTH concentration in 12 of 19 pre-dialysis specimens, whereas tCa correlated with PTH in only five patients. During dialysis, 16 patients had analytically significant changes in iCa (i.e., exceeded the analytical imprecision of 0.04 mmol/L). Pre- and post-dialysis concentrations of PTH were normal in six patients, four of whom showed a detectable response to changes in iCa. Ten patients had increased PTH in at least one specimen; of these, eight had responsive parathyroid glands. Five of the 16 patients had an increased set point for calcium. The minimal PTH responses of two patients suggested refractory hyperparathyroidism. We conclude that routine estimation of iCa, rather than tCa, in dialysis patients markedly improves the identification of patients at risk for secondary hyperparathyroidism, and that measurement of intact PTH in pre- and post-dialysis serum offers a simple means of assessing parathyroid responsiveness in dialysis patients.
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Lanzano, Luca, Tim Lei, Kayo Okamura, Hector Giral, Yupanqui Caldas, Omid Masihzadeh, Enrico Gratton, Moshe Levi, and Judith Blaine. "Differential modulation of the molecular dynamics of the type IIa and IIc sodium phosphate cotransporters by parathyroid hormone." American Journal of Physiology-Cell Physiology 301, no. 4 (October 2011): C850—C861. http://dx.doi.org/10.1152/ajpcell.00412.2010.
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The kidney is a key regulator of phosphate homeostasis. There are two predominant renal sodium phosphate cotransporters, NaPi2a and NaPi2c. Both are regulated by parathyroid hormone (PTH), which decreases the abundance of the NaPi cotransporters in the apical membrane of renal proximal tubule cells. The time course of PTH-induced removal of the two cotransporters from the apical membrane, however, is markedly different for NaPi2a compared with NaPi2c. In animals and in cell culture, PTH treatment results in almost complete removal of NaPi2a from the brush border (BB) within 1 h whereas for NaPi2c this process in not complete until 4 to 8 h after PTH treatment. The reason for this is poorly understood. We have previously shown that the unconventional myosin motor myosin VI is required for PTH-induced removal of NaPi2a from the proximal tubule BB. Here we demonstrate that myosin VI is also necessary for PTH-induced removal of NaPi2c from the apical membrane. In addition, we show that, while at baseline the two cotransporters have similar diffusion coefficients within the membrane, after PTH addition the diffusion coefficient for NaPi2a initially exceeds that for NaPi2c. Thus NaPi2c appears to remain “tethered” in the apical membrane for longer periods of time after PTH treatment, accounting, at least in part, for the difference in response times to PTH of NaPi2a versus NaPi2c.
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Cosman, Felicia, Jeri Nieves, Lillian Woelfert, Susan Gordon, Victor Shen, and Robert Lindsay. "Parathyroid Responsivity in Postmenopausal Women with Osteoporosis During Treatment with Parathyroid Hormone1." Journal of Clinical Endocrinology & Metabolism 83, no. 3 (March 1, 1998): 788–90. http://dx.doi.org/10.1210/jcem.83.3.4639.
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Endocrine systems may be affected permanently by administration of supraphysiologic doses of hormone. This is a well known complication of glucocorticoid treatment where the pituitary/adrenal axis may never fully recover, especially when large doses of steroids are needed during significant physical stress. The goal of this investigation was to determine whether responsivity of the parathyroid gland was normal after use of (1–34)PTH daily as an investigational therapy for osteoporosis. Patients were all postmenopausal osteoporotic women treated with estrogen and enrolled in a 3-yr trial of (1–34)PTH by daily subcutaneous injection (400 IU/day) in addition to their estrogen therapy. A volunteer subgroup (n = 10) of this population was recruited for this investigation. All patients had an EDTA-provoked hypocalcemic challenge before beginning PTH treatment. The same patients had repeat EDTA-challenge tests at various times during the 3-yr PTH treatment trial. Three patients had 2 infusions while on PTH treatment (interim and at the end of 3 yr). Ionized calcium declined identically before and during PTH treatment in response to the EDTA stimulus. PTH(1–84) responses were identical before and during PTH therapy. Furthermore, there were no differences in 1,25(OH)2D elevation or in phosphorus reduction over the course of the EDTA infusion during daily PTH treatment. Osteocalcin levels were higher during PTH treatment, as expected, but responsivity to acute endogenous PTH elevations was the same after PTH treatment. We conclude that 1–34PTH therapy, at 400 IU/day for up to 3 yr, does not suppress parathyroid responsivity and should therefore (at least within this period of treatment) have no permanent adverse effect on the ability of the body to maintain calcium homeostasis. Additionally, there is no difference in target organ responsivity to acute endogenous elevations of PTH after exogenous PTH therapy.
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Francis, David O., Christopher Fonnesbeck, Nila Sathe, Melissa McPheeters, Shanthi Krishnaswami, and Sivakumar Chinnadurai. "Postoperative Bleeding and Associated Utilization following Tonsillectomy in Children: A Systematic Review and Meta-analysis." Otolaryngology–Head and Neck Surgery 156, no. 3 (January 17, 2017): 442–55. http://dx.doi.org/10.1177/0194599816683915.
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Objective To assess posttonsillectomy hemorrhage (PTH), associated nonoperative readmissions/revisits, and reoperations in children. Data Sources MEDLINE, EMBASE, and the Cochrane Library. Review Methods Two investigators independently screened studies against predetermined criteria and extracted key data. Investigators independently assessed study risk of bias and the strength of the evidence of the body of literature. We calculated unadjusted pooled estimates of PTH frequency and conducted a Bayesian meta-analysis to estimate frequency of primary and secondary PTH and PTH-associated reoperation and revisits/readmissions by partial and total tonsillectomy and surgical approach. Results In meta-analysis, the frequency of primary and secondary PTH associated with total and partial tonsillectomy was <4% for any technique and with overlapping confidence bounds. Pooled frequencies of PTH were also <5% overall (4.2% for total tonsillectomy, 1.5% for partial tonsillectomy) in comparative studies. Fewer PTH episodes occurred with tonsillectomy for obstructive sleep-disordered breathing than for throat infection. In meta-analysis, frequency of PTH-associated nonoperative revisits/readmission or reoperation ranged from 0.2% to 5.7% for total tonsillectomy and from 0.1% to 3.7% for partial tonsillectomy. At least 4 deaths were reported in case series including 1,778,342 children. Conclusions PTH occurred in roughly 4% of tonsillectomies in studies included in this review. Although studies typically did not report bleeding severity or amount, relatively few episodes of PTH necessitated reoperation for hemostasis. Nonetheless, tonsillectomy is not without risk of harm. Frequency of PTH across techniques was similar; thus, we cannot conclude that a given technique is superior.
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Korn, Agnes. "Parthian ž." Bulletin of the School of Oriental and African Studies 73, no. 3 (October 2010): 415–36. http://dx.doi.org/10.1017/s0041977x1000039x.
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AbstractThis article argues that the opposition between Old Iranian *č and *ǰ was preserved in Manichaean Parthian not only word-initially, but also in postvocalic position, at least at the time of the introduction of the Manichaean script. The approach is phonological, and attempts to show that Pth. /č/ (< OIr. *č), written <c> and <z̈>, and Pth. /ž/ (< OIr. *ǰ and *ž), written <j>, are consistently distinguished in the Manichaean script. Pth. /č/ may have developed a postvocalic allophone [ǰ] (not affecting the phonematic opposition), which might have been a motivation for the use of the letter <z̈>. Transcriptions into Sogdian script and the cantillations suggest a coalescence of the Pth. phonemes, but it is not clear whether this is a later development of the Pth. language itself or a peculiarity of the liturgical pronunciation of Parthian as practised by Manichaeans in Central Asia.1
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Sasaki, S., and F. Marumo. "Mechanisms of inhibition of proximal acidification by PTH." American Journal of Physiology-Renal Physiology 260, no. 6 (June 1, 1991): F833—F838. http://dx.doi.org/10.1152/ajprenal.1991.260.6.f833.
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The parathyroid hormone (PTH) effects on luminal Na-H exchange and basolateral Na-HCO3 cotransport were examined in isolated perfused rabbit proximal convoluted tubules. Lumen pH (pHi) and cell pH (pHi) were measured by a fluorescent technique using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The time course of the PTH effect on proximal acidification was first determined by continuous monitoring of pHi in a stop-flow condition. PTH 10(-8) M added to the bath promptly inhibited the acid pHl generation. Adenosine 3',5'-cyclic monophosphate (cAMP) (10(-4) M) added to the bath mimicked the PTH effect. Luminal Na-H exchange was assayed by monitoring changes in pHi (dpHi/dt) in response to luminal Na+ removal in HCO3- free condition. The addition of PTH or cAMP for 5 min decreased dpHi/dt by 30 and 37%, respectively. Basolateral Na-HCO3 cotransport was assayed by measuring dpHi/dt caused by bath Na+ removal. The addition of PTH or cAMP for 5 min did not change the dpHi/dt. PTH also did not alter the dpHi/dt induced by reducing the bath HCO3- from 25 to 5 mM. The addition of PTH or cAMP to the bath slightly reduced pHi by 0.05. These results suggest that 1) PTH inhibits proximal acidification very rapidly and the effect reached a maximum within 10 min, 2) PTH rapidly inhibits luminal Na-H exchange but not basolateral Na-HCO3 cotransport in a short period, and 3) this effect is at least partly mediated by cAMP-dependent mechanisms.
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Celic, S., Y. Katayama, PJ Chilco, TJ Martin, and DM Findlay. "Type I collagen influence on gene expression in UMR106-06 osteoblast-like cells is inhibited by genistein." Journal of Endocrinology 158, no. 3 (September 1, 1998): 377–88. http://dx.doi.org/10.1677/joe.0.1580377.
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We have previously shown that an exogenous type I collagen matrix can regulate expression of mRNA for parathyroid hormone (PTH)-related protein (PTHrP) and its receptor, the PTH/PTHrP receptor, in the UMR106-06 osteogenic sarcoma cell line, which is considered to be representative of a relatively mature osteoblast phenotype. Consistent with those data, we show here that growth of UMR106-06 cells on type I collagen increased PTH/PTHrP receptor-binding capacity. Analysis of the binding data showed that the number of PTH/PTHrP receptors expressed by cells cultured on collagen was at least 2-fold greater than that of cells cultured on plastic. Expression of mRNA encoding alkaline phosphatase (ALP) and osteopontin (OP) was also upregulated in cells cultured on collagen, suggesting that interaction with collagen promotes the osteoblast phenotype in this cell line. Retinoic acid (RA), which has also been shown to promote osteoblastic differentiation, synergized with type I collagen to cause super-induction of OP mRNA. In contrast, RA abolished the collagen-induced increase in ALP mRNA and PTH/PTHrP receptor mRNA. The collagen-mediated increase in the expression of OP and PTH/PTHrP receptor mRNA, but not that of ALP, was perturbed by prior covalent modification of the collagen by non-enzymatic glycation. The collagen effects did not occur via interaction with RGD amino acid domains in type I collagen, but evidence was obtained for involvement of the DGEA amino acid cell-binding domain. The mechanism by which plating of UMR106-06 cells on a type I collagen substrate affects PTH/PTHrP receptor mRNA levels was investigated. Inhibition of cytoskeletal organization using cytochalasin D, and inhibitors of protein phosphatases, protein kinase C, phospholipase C and cyclooxygenase, did not abrogate the collagen-mediated effects. In contrast, treatment of cells with the protein tyrosine kinase inhibitor genistein, but not herbimycin A, dose-dependently abolished the collagen effects on the expression of PTH/PTHrP receptor, ALP and OP mRNA. These results show that a type I collagen substrate influences the expression of osteoblast-associated genes in a cell model of mature osteoblasts and suggests that this involves, at least in part, changes in intracellular tyrosine phosphorylation.
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Miedlich, Susanne U., and Abdul B. Abou-Samra. "Eliminating phosphorylation sites of the parathyroid hormone receptor type 1 differentially affects stimulation of phospholipase C and receptor internalization." American Journal of Physiology-Endocrinology and Metabolism 295, no. 3 (September 2008): E665—E671. http://dx.doi.org/10.1152/ajpendo.00036.2008.
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The parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor (PTH1R) belongs to family B of seven-transmembrane-spanning receptors and is activated by PTH and PTHrP. Upon PTH stimulation, the rat PTH1R becomes phosphorylated at seven serine residues. Elimination of all PTH1R phosphorylation sites results in prolonged cAMP accumulation and impaired internalization in stably transfected LLC-PK1 cells. The present study explores the role of individual PTH1R phosphorylation sites in PTH1R signaling through phospholipase C, agonist-dependent receptor internalization, and regulation by G protein-coupled receptor kinases. By means of transiently transfected COS-7 cells, we demonstrate that the phosphorylation-deficient (pd) PTH1R confers dramatically enhanced coupling to Gq/11 proteins upon PTH stimulation predominantly caused by elimination of Ser491/492/493, Ser501, or Ser504. Reportedly, impaired internalization of the pd PTH1R, however, is not dependent on a specific phosphorylation site. In addition, we show that G protein-coupled receptor kinase 2 interferes with pd PTH1R signaling to Gq/11 proteins at least partially by direct binding to Gq/11 proteins.
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Kempson, S. A., C. Helmle, M. I. Abraham, and H. Murer. "Parathyroid hormone action on phosphate transport is inhibited by high osmolality." American Journal of Physiology-Renal Physiology 258, no. 5 (May 1, 1990): F1336—F1344. http://dx.doi.org/10.1152/ajprenal.1990.258.5.f1336.
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Parathyroid hormone (PTH) produces rapid inhibition of Na(+)-phosphate cotransport, characterized by a decreased maximal rate of transport, and the inhibition is independent of de novo protein synthesis. The present study determined whether the action of PTH on Na(+)-phosphate cotransport is mediated, at least in part, by rapid endocytic internalization of Na(+)-phosphate cotransporters present in the plasma membrane. Horseradish peroxidase, a fluid-phase marker, was used to demonstrate the presence of endocytosis in opossum kidney (OK) epithelial cells in monolayer culture. An increase in medium osmolality to 500 mosmol/kgH2O, by addition of sucrose, produced 80% inhibition of endocytosis within 1 h. The inhibition was reversed on returning the cells to normal medium. Incubation of OK cell monolayers with PTH (10(-8) M) for 3 h at normal osmolality (281 mosmol/kgH2O) inhibited Na(+)-phosphate cotransport (4 min uptakes) by 56-67%. In hyperosmolar medium (513 mosmol/kgH2O), when endocytosis was inhibited, PTH inhibited Na(+)-phosphate cotransport by only 25-39%, a change that was significantly different from the inhibition in normal medium. Hyperosomolality had no effect on PTH inhibition of Na(+)-H+ exchange or on PTH stimulation of intracellular adenosine 3',5'-cyclic monophosphate. We conclude that the full inhibitory action of PTH on Na(+)-phosphate cotransport may require an intact endocytic mechanism.
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Gopalakrishnan, Rajaram, Hongjiao Ouyang, Martha J. Somerman, Laurie K. McCauley, and Renny T. Franceschi. "Matrix γ-Carboxyglutamic Acid Protein Is a Key Regulator of PTH-Mediated Inhibition of Mineralization in MC3T3-E1 Osteoblast-Like Cells." Endocrinology 142, no. 10 (October 1, 2001): 4379–88. http://dx.doi.org/10.1210/endo.142.10.8413.
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Abstract As part of its overall function as a major regulator of calcium homeostasis, PTH stimulates bone resorption and inhibits osteoblast-mediated biomineralization. To determine the basis for the inhibitory actions of this hormone, we compared the time course of PTH-dependent inhibition of mineralization in MC3T3-E1 osteoblast-like cells with changes in mRNA levels for several extracellular matrix proteins previously associated either with induction or inhibition of mineralization. Mineralizing activity was rapidly lost in PTH-treated cells (∼30% inhibition after 3 h, 50% inhibition at 6 h). Of the proteins examined, changes in matrix γ-carboxyglutamic acid protein were best correlated with PTH-dependent inhibition of mineralization. Matrix γ-carboxyglutamic acid protein mRNA was rapidly induced 3 h after PTH treatment, with a 6- to 8-fold induction seen after 6 h. Local in vivo injection of PTH over the calvaria of mice also induced a 2-fold increase in matrix γ-carboxyglutamic acid protein mRNA. Warfarin, an inhibitor of matrix γ-carboxyglutamic acid protein γ-carboxylation, reversed the effects of PTH on mineralization in MC3T3-E1 cells, whereas vitamin K enhanced PTH activity, as would be expected if a γ-carboxyglutamic acid-containing protein were required for PTH activity. Levels of the other mRNAs examined were not well correlated with the observed changes in mineralization. Osteopontin, an in vitro inhibitor of mineralization, was induced approximately 4-fold 12 h after PTH addition. Bone sialoprotein mRNA, which encodes an extracellular matrix component most frequently associated with mineral induction, was inhibited by 50% after 12 h of PTH treatment. Osteocalcin mRNA, encoding the other known γ-carboxyglutamic acid protein in bone, was also inhibited by PTH, but, again, with a significantly slower time course than was seen for mineral inhibition. Taken together, these results show that the rapid inhibition of osteoblast mineralization induced by in vitro PTH treatment is at least in part explained by induction of matrix γ-carboxyglutamic acid protein.
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Matsumoto, T., K. Morita, Y. Kawanobe, and E. Ogata. "Effect of parathyroid hormone on phospholipid metabolism in osteoblast-like rat osteogenic sarcoma cells." Biochemical Journal 236, no. 2 (June 1, 1986): 605–8. http://dx.doi.org/10.1042/bj2360605.
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Previous results have shown that 1,25-dihydroxycholecalciferol [1,25(OH)2D3] enhances the synthesis of phosphatidylserine (PS) and suppresses the synthesis of phosphatidylethanolamine (PE) in osteoblast-like rat osteogenic sarcoma UMR 106 cells [Matsumoto, Kawanobe, Morita & Ogata (1985) J. Biol. Chem. 260, 13704-13709]. In the present study, the effect of parathyroid hormone (PTH) on phospholipid metabolism is examined by using these cells. Treatment of UMR 106 cells with human PTH-(1-34)-peptide suppresses the synthesis of phosphatidylethanolamine in a dose- and time-dependent manner without affecting the synthesis of PS. The maximal effect on PE synthesis is obtained with 2.4 nM-human PTH-(1-34)-peptide when the cells are treated for 48 h or longer. In addition, when human PTH-(1-34)-peptide is added together with the maximal dose of 1,25(OH)2D3, there is a further decline in PE synthesis, whereas the stimulation of PS synthesis by 1,25(OH)2D3 is not altered. Because methylation of PE is suggested to affect hormone receptor-adenylate cyclase coupling, the observed change in PE metabolism by PTH and 1,25(OH)2D3 may be, at least in part, involved in the development of desensitization phenomenon to PTH in these cells.
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Hall, A. K., and I. R. Dickson. "The effects of parathyroid hormone on osteoblast-like cells from embryonic chick calvaria." Acta Endocrinologica 108, no. 2 (February 1985): 217–23. http://dx.doi.org/10.1530/acta.0.1080217.
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Abstract. A bone cell fraction was isolated from 16 day old embryonic chick calvaria using a sequential enzymatic digestion procedure. The fraction contained cells, of an osteoblast-like character, which responded to parathyroid hormone (PTH) and prostaglandin E2, but not to calcitonin, in terms of increased production of cyclic AMP. Primary cultures of cells maintained their responsiveness to PTH for at least 2 weeks after reaching confluence. Production of alkaline phosphatase by the bone cells was inhibited when 1,25(OH)2 vitamin D3 was added to cultures at concentrations of 10−8 m or greater. When cells were cultured in the presence of PTH a biphasic effect was observed; alkaline phosphatase levels were stimulated at low concentrations of this hormone but were decreased at higher concentrations. The latter finding appears consistent with observations that PTH can in vivo exert either anabolic or catabolic effects on bone, depending upon the circulating level of hormone present.
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Papavramidis, Theodossis S., Olympia E. Anastasiou, Ioannis Pliakos, Nick Michalopoulos, Mike Polyzonis, Konstantina Triantafyllopoulou, Georgia Kokaraki, and Spiros Papavramidis. "Patterns in the Parathyroid Response to Sodium Bicarbonate Infusion Test in Healthy Volunteers." BioMed Research International 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/704394.
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Background. The sodium bicarbonate infusion test evaluates the function of the parathyroid glands. The present study aims to evaluate the range of parathyroid response in healthy individuals and the potential influence of various factors.Methods. Fifty healthy volunteers were subjected to the test. Levels of vitamin D, calcium, albumin, and PTH were measured before infusion. PTH was measured at 3, 5, 10, 30, and 60 minutes after infusion.Results. A curve describing the response of parathyroids to the test was drawn. Twenty percent of the subjects had blunted PTH response. No significant difference was observed between normal and blunted responders concerning age, BMI, baseline PTH, or calcium levels. Nonetheless, there was a significant difference in vitamin D levels (P=0.024).Interpretation. The test is easy to perform and may be used for everyday screening. It has to be clarified whether our observations are, at least partly, produced due to the presence of individuals with a constitutively blunted response or if low levels of vitamin D decrease the ability of the parathyroids to respond. Whichever the case, PTH response of normal individuals to sodium bicarbonate infusion test is more varied than previously thought and vitamin D levels influence it.
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Wallfelt, C., E. Gylfe, R. Larsson, S. Ljunghall, J. Rastad, and G. Åkerström. "Relationship between external and cytoplasmic calcium concentrations, parathyroid hormone release and weight of parathyroid glands in human hyperparathyroidism." Journal of Endocrinology 116, no. 3 (March 1988): 457–64. http://dx.doi.org/10.1677/joe.0.1160457.
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ABSTRACT Parathyroid hormone (PTH) release and cytoplasmic calcium concentrations were investigated at ambient calcium concentrations of 0·5–3·0 mmol/l in dispersed parathyroid cells from 44 hypercalcaemic patients with primary or uraemic hyperparathyroidism (HPT). In comparison with parathyroid cells from adult cattle, release of PTH by human preparations was reduced and values of the ambient calcium concentration causing half-maximal inhibition of PTH release (median effective dose, ED50) were significantly increased. Half-maximal inhibition of PTH release was obtained with concentrations of cytoplasmic calcium almost identical to the concentrations of ionized calcium in the plasma of the individual patients. Cytoplasmic concentrations of calcium in the parathyroid cells were inversely related to release of PTH. Concentrations of cytoplasmic calcium were significantly lower in human than in bovine cells and the ED50 for ambient calcium increase on cytoplasmic calcium was raised to the same extent as the ED50 for ambient calcium inhibition of PTH release in human compared with bovine cells. The magnitude of the increased ED50 for ambient calcium inhibition of PTH release and increase of cytoplasmic calcium concentration was similar in adenomas and sporadic as well as hereditary primary hyperplasias, but the secretion was the least aberrant in uraemic hyperplasias, although they had by far the largest glandular mass. Serum concentrations of total calcium before surgery correlated with the ED50 for ambient calcium effects of PTH release and cytoplasmic calcium, but not with glandular weight. These findings demonstrate a universally abnormal regulation of cytoplasmic calcium in HPT and its importance for PTH release, and that disturbance of cytoplasmic calcium rather than the increased glandular mass contributes to the hypercalcaemia in adenomatous and hyperplastic HPT. J. Endocr. (1988) 116, 457–464
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Kuriwaka-Kido, Rika, Shinsuke Kido, Yuka Miyatani, Yuji Ito, Takeshi Kondo, Takashi Omatsu, Bingzi Dong, Itsuro Endo, Ken-ichi Miyamoto, and Toshio Matsumoto. "Parathyroid Hormone (1-34) Counteracts the Suppression of Interleukin-11 Expression by Glucocorticoid in Murine Osteoblasts: A Possible Mechanism for Stimulating Osteoblast Differentiation Against Glucocorticoid Excess." Endocrinology 154, no. 3 (March 1, 2013): 1156–67. http://dx.doi.org/10.1210/en.2013-1915.
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Abstract Glucocorticoid (GC) excess causes a rapid loss of bone with a reduction in bone formation. Intermittent PTH (1-34) administration stimulates bone formation and counteracts the inhibition of bone formation by GC excess. We have previously demonstrated that mechanical strain enhances interleukin (IL)-11 gene transcription by a rapid induction of ΔFosB expression and protein kinase C (PKC)-δ-mediated phosphorylation of phosphorylated mothers against decapentaplegic (Smad)-1. Because IL-11 suppresses the expression of dickkopf-1 and -2 and stimulates Wnt signaling, IL-11 appears to mediate at least a part of the effect of mechanical strain on osteoblast differentiation and bone formation. The present study was undertaken to examine the effect of PTH(1-34) and GCs on IL-11 expression in murine primary osteoblasts (mPOBs). PTH(1-34) treatment of mPOBs enhanced IL-11 expression in a time- and dose-dependent manner. PTH(1-34) also stimulated ΔFosB expression and Smad1 phosphorylation, which cooperatively stimulated IL-11 gene transcription. PTH(1-34)-induced Smad1 phosphorylation was mediated via PKCδ and was abrogated in mPOBs from PKCδ knockout mice. Dexamethasone suppressed IL-11 gene transcription enhanced by PTH(1-34) without affecting ΔFosB expression or Smad1 phosphorylation, and dexamethasone-GC receptor complex was bound to JunD, which forms heterodimers with ΔFosB. High doses of PTH(1-34) counteracted the effect of dexamethasone on apoptosis of mPOBs, which was blunted by neutralizing anti-IL-11 antibody or IL-11 small interfering RNA. These results demonstrate that PTH(1-34) and GCs interact to regulate IL-11 expression in parallel with osteoblast differentiation and apoptosis and suggest that PTH(1-34) and dexamethasone may regulate osteoblast differentiation and apoptosis via their effect on IL-11 expression.
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Mitchell, J., and A. Bansal. "Dexamethasone increases G alpha q-11 expression and hormone-stimulated phospholipase C activity in UMR-106-01 cells." American Journal of Physiology-Endocrinology and Metabolism 273, no. 3 (September 1997): E528. http://dx.doi.org/10.1152/ajpendo.1997.273.3.e528.
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Glucocorticoids regulate responsiveness of many cells to hormones that bind to G protein-coupled receptors. We examined the effect of glucocorticoids on parathyroid hormone (PTH) activation of two G protein-activated signal transduction pathways, phospholipase C (PLC) and adenylyl cyclase, in osteosarcoma UMR-106-01 cells. Dexamethasone (100 nM) increased PTH-stimulated and NaF-stimulated PLC activity by > 100% over 4 days (223 +/- 8 and 293 +/- 8.2% of control after 4 days for PTH and NaF-stimulated activity, respectively). The increase in PTH-stimulated adenylyl cyclase response in the same cells was more modest (162 +/- 5.4 and 171 +/- 6.8% of control after 4 days for PTH and NaF-stimulated activity, respectively). PTH activation of PLC was blocked by antiserums to G alpha q-11 and activation of adenylyl cyclase by G alpha s antiserums. Quantification of these G protein subunits in control and dexamethasone-treated cells showed a 78% increase in G alpha q-11 (from 18.1 +/- 1.2 to 32.2 +/- 1.5 pmol/mg), whereas G alpha s was increased only 34% (from 6.2 +/- 0.5 to 8.2 +/- 0.3 pmol/mg) and G beta-subunits were increased 40% (from 54 +/- 2.3 to 75.2 +/- 3.8 pmol/mg). These results suggest that glucocorticoids are more potent regulators of PLC activity than adenylyl cyclase activity in UMR cells, and this is mediated, at least in part, by differential increases in G alpha q-11 proteins.
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Sotunde, Olusola Funmilayo, Herculina Salome Kruger, Hattie H. Wright, Lize Havemann-Nel, Carina M. C. Mels, Chrisna Ravyse, and Marlien Pieters. "Association of 25-hydroxyvitamin D and parathyroid hormone with the metabolic syndrome in black South African women." Applied Physiology, Nutrition, and Metabolism 42, no. 4 (April 2017): 413–19. http://dx.doi.org/10.1139/apnm-2016-0257.
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The relationship between 25 hydroxyvitamin D (25(OH)D), parathyroid hormone (PTH) and metabolic traits appear to differ among ethnicities and may be influenced by obesity. The aim of the study was to examine the association of serum 25(OH)D or PTH with metabolic syndrome (MetS) while controlling for adiposity in black women. Using a cross-sectional study design, 209 urban black women aged ≥ 43 years from the North West Province, South Africa, were included. Multiple regression models were used to explore the relationship between 25(OH)D or PTH and body composition. To explore the association between 25(OH)D or PTH and MetS, a separate variable was created including at least 3 of the MetS criteria, but excluding elevated waist circumference as a diagnostic criterion in a logistic regression model. The majority of the women (69.9%) were overweight or obese and 65.5% of the women had excessive adiposity using the age-specific cut-off points for body fat percentage. All body composition variables were positively associated with PTH, whereas body mass index and waist circumference, but not body fat percentage, had negative associations with 25(OH)D also after adjusting for confounders. Before and after adjusting for age, body fat, habitual physical activity, tobacco use, season of data collection, and estimated glomerular filtration rate, neither 25(OH)D nor PTH showed significant associations with MetS. Although PTH was positively associated and 25(OH)D was negatively associated with adiposity in black women, there was no association between either 25(OH)D or PTH and MetS in this study population, nor did adiposity influence these relationships.
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GUPTA, AJAY, LEE R. KALLENBACH, GERARD ZASUWA, and GEORGE W. DIVINE. "Race Is a Major Determinant of Secondary Hyperparathyroidism in Uremic Patients." Journal of the American Society of Nephrology 11, no. 2 (February 2000): 330–34. http://dx.doi.org/10.1681/asn.v112330.
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In the general population, blacks have higher parathyroid gland mass and circulating parathyroid hormone (PTH) levels than whites. This may predispose black patients to more severe parathyroid disease when renal failure develops. Therefore, racial differences in the severity of uremic hyperparathyroidism were examined in a population of patients with endstage renal disease (ESRD). Among ESRD patients receiving hemodialysis or peritoneal dialysis, two or more values of intact PTH (immunoradiometric assay, pg/ml) obtained at least 90 d apart were available in 1270 prevalent cases (61.1% blacks, 51% males, and 31.1% diabetic), including 466 incident cases with onset of ESRD after 1993. Maximum PTH levels were analyzed as a function of race, gender, age, diabetic status, and levels of serum calcium, phosphorus, alkaline phosphatase, and aluminum. Using a stepwise multiple regression model, the determinants of maximum PTH in the order of their importance were black race, serum phosphorus, absence of diabetes, younger age, serum calcium, and female gender. The maximum PTH levels averaged 641.7 in blacks and 346.0 in whites after adjusting for age, gender, diabetic status, serum calcium, and phosphorus (P < 0.0001). In blacks compared with whites, the odds ratio (95% confidence interval) for adynamic bone disease (maximum PTH < 150 pg/ml) was 0.26 (0.17 to 0.41), whereas the odds ratio for hyperparathyroid bone disease (mean PTH > 500 pg/ml) was 4.4 (2.10 to 9.25). Race is a major independent determinant of uremic secondary hyperparathyroidism. Among ESRD patients, blacks may be at an increased risk for hyperparathyroid bone disease and whites for adynamic bone disease.
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Kantham, Lakshmi, Steven J. Quinn, Ogo I. Egbuna, Khanjan Baxi, Robert Butters, Jian L. Pang, Martin R. Pollak, David Goltzman, and Edward M. Brown. "The calcium-sensing receptor (CaSR) defends against hypercalcemia independently of its regulation of parathyroid hormone secretion." American Journal of Physiology-Endocrinology and Metabolism 297, no. 4 (October 2009): E915—E923. http://dx.doi.org/10.1152/ajpendo.00315.2009.
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The calcium-sensing receptor (CaSR) controls parathyroid hormone (PTH) secretion, which, in turn, via direct and indirect actions on kidney, bone, and intestine, maintains a normal extracellular ionized calcium concentration (Ca2+o). There is less understanding of the CaSR's homeostatic importance outside of the parathyroid gland. We have employed single and double knockout mouse models, namely mice lacking PTH alone (CaSR+/+ PTH−/−, referred to as C+P−), lacking both CaSR and PTH (CaSR−/− PTH−/−, C−P−) or wild-type (CaSR+/+ PTH+/+, C+P+) mice to study CaSR-specific functions without confounding CaSR-mediated changes in PTH. The mice received three hypercalcemic challenges: an oral Ca2+ load, injection or constant infusion of PTH via osmotic pump, or a phosphate-deficient diet. C−P− mice show increased susceptibility to developing hypercalcemia with all three challenges compared with the other two genotypes, whereas C+P− mice defend against hypercalcemia similarly to C+P+ mice. Reduced renal Ca2+ clearance contributes to the intolerance of the C−P− mice to Ca2+ loads, as they excrete less Ca2+ at any given Ca2+o than the other two genotypes, confirming the CaSR's direct role in regulating renal Ca2+ handling. In addition, C+P+ and C+P−, but not C−P−, mice showed increases in serum calcitonin (CT) levels during hypercalcemia. The level of 1,25(OH)2D3 in C−P− mice, in contrast, was similar to those in C+P− and C+P+ mice during an oral Ca2+ load, indicating that increased 1,25(OH)2D3 production cannot account for the oral Ca2+-induced hypercalcemia in the C−P− mice. Thus, CaSR-stimulated PTH release serves as a “floor” to defend against hypocalcemia. In contrast, high-Ca2+o-induced inhibition of PTH is not required for a robust defense against hypercalcemia, at least in mice, whereas high-Ca2+o-stimulated, CaSR-mediated CT secretion and renal Ca2+ excretion, and perhaps other factors, serve as a “ceiling” to limit hypercalcemia resulting from various types of hypercalcemic challenges.
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Minagawa, Masanori, Toshiyuki Yasuda, Yasuyuki Kobayashi, and Hiroo Niimi. "Transient pseudohypoparathyroidism of the neonate." European Journal of Endocrinology 133, no. 2 (August 1995): 151–55. http://dx.doi.org/10.1530/eje.0.1330151.
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Minagawa M, Yasuda T, Kobayashi Y, Niimi H. Transient pseudohypoparathyroidism of the neonate. Eur J Endocrinol 1995:133:151–5. ISSN 0804–4643 We report three neonates with transient hypoparathyroidism with elevated parathyroid hormone (PTH) levels to clarify further the pathogenesis of late neonatal hypocalcemia and calcium homeostasis. Clinical signs were seizures starting at the age of 10 and 11 days. The biochemical features were characterized by transient hypocalcemia and hyperphosphatemia due to a high transport maximum of the phosphate/glomerular filtration rate, despite high PTH levels. All had normal magnesium and calcidiol levels (at least 5 μg/l) for their age, and this precludes hypoparathyroidism due to low magnesium levels and hyperparathyroidism due to overt vitamin D deficiency. To diagnose pseudohypoparathyroidism type I, intravenous human PTH (1–34) infusions were performed; however, they showed brisk responses of plasma and/or urine cyclic AMP in response to the PTH infusion, but the phosphaturic response to the PTH was sluggish compared to the controls. All three showed an increase in serum alkaline phosphatase activity, suggesting PTH stimulation of osteoblasts. They were treated initially with calcium lactate or (1α)-hydroxycalciol/calcitriol. Their hypoparathyroid condition, however, was transient: they maintained normal serum calcium and PTH levels without medication before the age of 6 months. The etiology, possibly intracellular signal transduction distal to cyclic AMP and/or distinct from adenylate cyclase in the kidney, is developmental and the condition was resolved completely within 6 months of age. We have termed this condition "transient pseudohypoparathyroidism of the neonate". M Minagawa, Department of Pediatrics, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260, Japan
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Lenzini, Livia, Selene Prisco, Paul Emmanuel Vanderriele, Silvia Lerco, Francesca Torresan, Giuseppe Maiolino, Teresa Maria Seccia, Maurizio Iacobone, and Gian Paolo Rossi. "PTH Modulation by Aldosterone and Angiotensin II is Blunted in Hyperaldosteronism and Rescued by Adrenalectomy." Journal of Clinical Endocrinology & Metabolism 104, no. 9 (March 13, 2019): 3726–34. http://dx.doi.org/10.1210/jc.2019-00143.
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Abstract Context Accumulating evidence suggests a link between adrenocortical zona glomerulosa and parathyroid gland through mechanisms that remain unexplored. Objectives To test the hypothesis that in vivo angiotensin II blockade affects PTH secretion in patients with hypertension and that aldosterone and angiotensim II directly stimulate PTH secretion ex vivo. Design and Setting We investigated the changes of serum PTH levels induced by oral captopril (50 mg) administration in patients with primary essential hypertension (EH) and with primary aldosteronism (PA) caused by bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenoma (APA), the latter before and after adrenalectomy. We also exposed primary cultures of human parathyroid cells from patients with primary hyperparathyroidism to angiotensin II (10−7 M) and/or aldosterone (10−7 M). Results Captopril lowered PTH levels (in nanograms per liter) both in patients with EH (n = 63; 25.9 ± 8.3 baseline vs 24.4 ± 8.0 postcaptopril, P < 0.0001) and in patients with APA after adrenalectomy (n = 27; 26.3 ± 11.6 vs 24.0 ± 9.7 P = 0.021). However, it was ineffective in patients with full-blown PA caused by APA and BAH. In primary culture of human parathyroid cells, both aldosterone (P < 0.001) and angiotensin II (P = 0.002) markedly increased PTH secretion from baseline, by acting through mineralocorticoid receptor and angiotensin type 1 receptor, as these effects were abolished by canrenone and irbesartan, respectively. Conclusion These results collectively suggest an implication of the renin-angiotensin-aldosterone system in PTH regulation in humans, at least in PTH-secreting cells obtained from parathyroid tumors. Moreover, they further support the concept that mild hyperparathyroidism is a feature of human PA that is correctable with adrenalectomy.
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Nelson, Marc, Olivia Dan, and Marshall Strome. "Direct Revascularization is Superior for Rat Parathyroid Allotransplantation with Fk506." Annals of Otology, Rhinology & Laryngology 114, no. 3 (March 2005): 207–13. http://dx.doi.org/10.1177/000348940511400307.
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Parathyroid gland allotransplantation has been a challenging goal for decades. Our objective was to optimize a parathyroid allotransplantation model for analysis of short-term or low-dose immunosuppressive regimens. Rats that had undergone parathyroidectomy received parathyroid allografts either by direct microvascular anastomoses as part of a composite laryngotracheal graft or by direct implantation into hind limb muscle. All rats were maintained on daily low-dose FK506 (tacrolimus). Intact serum parathyroid hormone (PTH) levels for both groups were recorded over a period of at least 45 days and compared with a repeated-measures mixed model. We found that microvascular anastomosis was superior to implantation for parathyroid gland survival, as all revascularized grafts immediately produced normal levels of PTH, whereas implanted grafts had a significantly slower recovery of function (p < .001). Four of the 11 implanted grafts (36%) never produced detectable PTH levels. Using this model, we are developing innovative strategies that will lead to successful parathyroid allotransplantation without the need for chronic immunosuppression.
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Oliveira, Thiago Costa de, Ivo Alves de Campos Neto, Manuel Hermínio de Aguiar-Oliveira, and Francisco de Assis Pereira. "Evaluation of parathyroid function and mineral metabolism in psychiatric patients using lithium salts." Arquivos Brasileiros de Endocrinologia & Metabologia 58, no. 6 (August 2014): 619–24. http://dx.doi.org/10.1590/0004-2730000002983.
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Objective: To evaluate parathyroid function and mineral metabolism in psychiatric patients users of lithium salts. Materials and methods: We measured the serum levels of calcium, ionized calcium, inorganic phosphorus, alkaline phosphatase, albumin, parathyroid hormone (PTH), urea, creatinine, 25-hydroxy-vitamin D and lithium of 35 patients diagnosed with bipolar disorder in use of lithium carbonate (LC) for at least one year (Lithium Group – LG) and 35 healthy subjects (Control Group – CG). Results: The LG and CG were matched by sex and age. There was only statistic difference in relation to the levels of PTH and ionized calcium, with p < 0.004 and p < 0.03, respectively. Secondary form of hyperparathyroidism (HPT) was found in eight (22.8%) LG patients and in none of the CG. There was no correlation between lithemia, usage time and dosage of LC. Conclusion: Our data demonstrate that lithium may create an imbalance in the parathyroid axis, characterized by elevated levels of PTH.
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Weber, Jonathan M., Benjamin J. Frisch, Rebecca L. Porter, Olga Bromberg, Adam J. Olm-shipman, Hani Awad, and Laura M. Calvi. "In Vivo Parathyroid Hormone Treatment Expands All Multipotent Primitive Hematopoietic Cell Subsets." Blood 114, no. 22 (November 20, 2009): 1449. http://dx.doi.org/10.1182/blood.v114.22.1449.1449.
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Abstract Abstract 1449 Poster Board I-472 Osteoblastic cells have been identified as a component of the hematopoietic stem cell (HSC) niche. This identification provides a novel strategy for in vivo expansion of HSCs by stimulating their regulatory microenvironment. This therapeutic approach could potentially expand the clinical use of HSCs in conditions where their number limits use. Activation of osteoblastic cells by Parathyroid Hormone (PTH) increases bone, osteoblastic and osteoclastic cell number and expands the HSC pool. Since HSCs do not express the PTH receptor, and genetic activation of PTH receptors in osteoblastic cells is sufficient to expand HSCs, the HSC increase must be initiated by PTH-dependent activation of osteoblastic cells. The HSC-enriched lineage-, sca-1+, and c-kit+ (LSK) compartment is heterogeneous and contains at least three subpopulations of cells with multilineage potential, but with progressively decreased quiescence and more limited self-renewal. In the initial evaluation of PTH effects on the HSC niche, the effects of osteoblastic activation on HSC subsets were not characterized in detail. The effect of PTH and osteoblastic activation on individual HSC subsets could suggest additional therapeutic uses if PTH increases not only Long Term-HSC (LT-HSC) but also the more proliferative Short-Term HSCs/ Multi Potent Progenitors (ST-HSCs/MPPs). In this study, our goal was to identify changes in the proportion of LT-HSC vs ST-HSC and MPPs after PTH treatment by utilizing flow cytometric analysis and competitive repopulation assays (primary, secondary and tertiary reconstitution). We developed an accelerated PTH treatment regimen in mice (40μg/kg body weight ip three times daily for 10 days), which minimizes the effects of normal aging on bone and hematopoiesis. We first analyzed the effect of this PTH regimen on bone. PTH-treated mice had increased trabecular bone volume (% BV/TV VEH 25±2 vs PTH 43±4 p<0.001) compared to their vehicle-treated controls when analyzed by micro-CT. Histologic analysis demonstrated a dramatic increase in trabecular bone as well as osteoblastic cells lining the trabecular surfaces and TRAP+ osteoclasts in the PTH-treated animals. PTH-treated mice also had increased primitive hematopoietic cells defined through flow cytometry as LSK (VEH 0.19±0.02 vs PTH 0.27±0.01 p<0.005). LSKs were further subdivided to phenotypically identify HSC subsets using the SLAM receptors. Surprisingly the frequency of subpopulations was increased in PTH treatment increased not only LT-HSCs (VEH 0.025±0.002 vs PTH 0.040±0.002 p<0.0001), but also the less quiescent ST-HSCs/MPPs (VEH 0.041±0.001 vs PTH 0.065±0.004 p<0.0001). HSC subsets can also be identified within the LSK pool based on expression of Flt3 and Thy1.1. This phenotypic analysis of bone marrow cells from mice treated with the intensive PTH regimen demonstrated a significant increase in all LSK subsets including MPPs (VEH 0.043±0.003 vs PTH 0.061±0.004 p<0.005), identified as LSK Flt3+ Thy1.1low cells, LSK Flt3− Thy1.1int (VEH 0.056±0.005 vs PTH 0.077±0.004 p<0.01), enriched for ST-HSCs, and the LT-HSC enriched LSK Flt3− Thy1.1int subset (VEH 0.042±0.004 vs PTH 0.054±0.002 p<0.05). Taken together, these data suggest that systemic PTH treatment not only expands the most quiescent HSCs, but also increases ST-HSC/MPPs. Since PTH treatment increased all phenotypic HSC subsets, transplantation of hematopoietic bone marrow cells from PTH treated mice would be expected to have superior engraftment both in the short and long term. Accordingly, a significant increase in both early and late hematopoietic reconstitution was observed in primary transplant recipients of bone marrow from PTH-treated animals, as well as secondary and tertiary transplant recipients. These results also suggest that PTH treatment equally expands all HSC subsets. The novel finding that the less quiescent, multipotent ST-HSC and MPPs are also expanded by PTH may be of great therapeutic relevance, as it supports the use of osteoblastic stimulation by PTH not only to increase long term repopulation, but also to critically improve accelerated hematopoietic recovery after myeloablation. Thus, manipulation of the HSC niche may result in beneficial effects beyond their ability to increase the most quiescent HSCs. Further studies will elucidate the specific mechanisms causing this novel global increase of multipotent primitive hematopoietic cells. Disclosures No relevant conflicts of interest to declare.
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Kawashima, H. "Altered vitamin D metabolism in the kidney of the spontaneously hypertensive rat." Biochemical Journal 237, no. 3 (August 1, 1986): 893–97. http://dx.doi.org/10.1042/bj2370893.
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A decrease in plasma Ca2+ and increases in plasma immunoreactive parathyroid hormone (PTH) have been reported in spontaneously hypertensive (SH) rats as compared with normotensive Wistar-Kyoto (WKy) rats. These changes should lead to a higher plasma 1,25(OH)2D (1,25-dihydroxycholecalciferol/1,25-dihydroxyergocalciferol) concentration in SH rat if the kidney responds appropriately. Plasma 1,25(OH)2D, however, has been reported to be normal in SH rats, suggesting possible impairments of vitamin D metabolism in this animal model of hypertension. To test this possibility, we studied the effect of PTH on renal production of 1,25(OH)2D in SH rats before (4 weeks of age) and after (12 weeks of age) the onset of hypertension. Basal serum levels of 1,25(OH)2D were normal in SH rats at both ages. At 4 weeks of age, the rise in serum 1,25(OH)2D after PTH injection (50 units subcutaneously every 2 h; four times) was also normal in SH rats. By contrast, at 12 weeks of age, the rise in serum 1,25(OH)2D was approximately one-half of that in WKy rats, despite the similar rises in serum Ca2+ levels in both groups by PTH injection. The attenuated rise in serum 1,25(OH)2D in SH rats was consistent with the impaired response of renal 1-hydroxylase (25-hydroxycholecalciferol 1 alpha-hydroxylase) activity to PTH. Basal 1,25(OH)2D production by the kidney in SH rat was higher than that in WKy rats both at 4 and 12 weeks of age. These data suggest that, in SH rats: serum 1,25(OH)2D is inappropriately low in relation to the elevated PTH and this may be due, at least in part, to the impaired responsiveness to PTH of renal 1-hydroxylase and to the enhanced metabolism of 1,25(OH)2D, and elevated PTH or other agents may stimulate the 1-hydroxylase in the kidney even before the onset of hypertension.
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Weinstein, Robert S., Robert L. Jilka, Maria Almeida, Paula K. Roberson, and Stavros C. Manolagas. "Intermittent Parathyroid Hormone Administration Counteracts the Adverse Effects of Glucocorticoids on Osteoblast and Osteocyte Viability, Bone Formation, and Strength in Mice." Endocrinology 151, no. 6 (April 21, 2010): 2641–49. http://dx.doi.org/10.1210/en.2009-1488.
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Glucocorticoids act directly on bone cells to decrease production of osteoblasts and osteoclasts, increase osteoblast and osteocyte apoptosis, and prolong osteoclast life span. Conversely, daily injections of PTH decrease osteoblast and osteocyte apoptosis and increase bone formation and strength. Using a mouse model, we investigated whether the recently demonstrated efficacy of PTH in glucocorticoid-induced bone disease results from the ability of this therapeutic modality to counteract at least some of the direct effects of glucocorticoids on bone cells. Glucocorticoid administration to 5- to 6-month-old Swiss-Webster mice for 28 d increased the prevalence of osteoblast and osteocyte apoptosis and decreased osteoblast number, activation frequency, and bone formation rate, resulting in reduced osteoid, wall and trabecular width, bone mineral density, and bone strength. In contrast, daily injections of PTH caused a decrease in osteoblast and osteocyte apoptosis and an increase in osteoblast number, activation frequency, bone formation rate, bone mineral density, and bone strength. The decreased osteocyte apoptosis was associated with increased bone strength. When the two agents were combined, all the adverse effects of glucocorticoid excess on bone were prevented. Likewise, in cultured osteoblastic cells, PTH attenuated the adverse effects of glucocorticoids on osteoblast survival and Wnt signaling via an Akt phosphorylation-dependent mechanism. We conclude that intermittent PTH administration directly counteracts the key pathogenetic mechanisms of glucocorticoid excess on bone, thus providing a mechanistic explanation of its efficacy against glucocorticoid-induced osteoporosis.
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Kiebzak, G. M., A. N. Yusufi, E. Kusano, J. Braun-Werness, and T. P. Dousa. "ATP and cAMP system in the in vitro response of microdissected cortical tubules to PTH." American Journal of Physiology-Renal Physiology 248, no. 1 (January 1, 1985): F152—F159. http://dx.doi.org/10.1152/ajprenal.1985.248.1.f152.
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Responsiveness of proximal convoluted tubule (PCT) and distal convoluted tubule (DCT) microdissected from mouse kidney to PTH, in terms of cAMP accumulation and stimulation of adenylate cyclase, was examined. In both PCT and DCT, the cell-free adenylate cyclase was stimulated at least 10-fold by the same dose (10 U/ml) of PTH, and activity of cAMP phosphodiesterase was about 80% higher in DCT than in PCT. In intact tubules, while the incubation with PTH increased cAMP content in DCT more than 10-fold, it failed to increase the cAMP levels in PCT. To explain discrepancies between cell-free and intact cell incubations, ATP content in microdissected tubules was determined with use of a microbioluminescence assay. ATP content in PCT (4.0 +/- 1.3 fmol/mm, n = 30) was dramatically lower than ATP content of DCT (376.8 +/- 54.3 fmol/mm, n = 25). Incubation with 1 microM rotenone reduced markedly (delta -98%) the ATP content in DCT. In DCT, with ATP depleted by 1 microM rotenone, PTH failed to increase the cAMP, although 1 microM rotenone did not inhibit the adenylate cyclase activity. When 0.1 mM of 1-methyl-3-isobutylxanthine (MIX) was added to the incubation medium, PTH caused a marked elevation in tubular cAMP in PCT and to even a greater degree in DCT. Present results show that various segments of microdissected tubules differ greatly in their ability to maintain adequate ATP levels for cAMP generation in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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Paillard, M., and M. Bichara. "Peptide hormone effects on urinary acidification and acid-base balance: PTH, ADH, and glucagon." American Journal of Physiology-Renal Physiology 256, no. 6 (June 1, 1989): F973—F985. http://dx.doi.org/10.1152/ajprenal.1989.256.6.f973.
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That the adaptation of the kidney to the acid-base status may be controlled by peptide hormones is considered. In the proximal tubule parathyroid hormone (PTH) inhibits reabsorption of both bicarbonate and phosphate. The former effect is compensated for by an increase in bicarbonate absorption in Henle's loop, and the latter effect serves to augment phosphate concentration in the distal tubular fluid, which stimulates proton secretion in collecting ducts, the net effect of PTH administration being an enhancement of urinary acidification. In the thick ascending limb, both antidiuretic hormone (ADH) and glucagon inhibit bicarbonate absorption. In distal and cortical collecting tubules ADH stimulates net bicarbonate absorption and glucagon net bicarbonate secretion, which results in stimulation and inhibition of final urine acidification, respectively. Acute acid loading stimulates endogenous PTH secretion, which, by enhancing urinary acidification, constitutes a homeostatic response of the parathyroid glands. The major effects of ADH on urinary acidification serve at least to counterbalance disturbing consequences on urinary ammonia excretion of physiological variations in the urinary flow rate. The physiological significance of the effects of glucagon is unclear at present. Thus other peptide hormones may add to PTH and corticosteroid hormones to modulate urinary acidification, which leads to the concept of a pluri-hormonal control of acid-base balance.
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Windfuhr, Jochen P., Jens C. Deck, and Stephan Remmert. "Hemorrhage following Coblation Tonsillectomy." Annals of Otology, Rhinology & Laryngology 114, no. 10 (October 2005): 749–56. http://dx.doi.org/10.1177/000348940511401003.
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Objectives: We performed a prospective study to evaluate the incidence of post-tonsillectomy hemorrhage (PTH) in adults and children who underwent Coblation tonsillectomy (CTE) under general anesthesia. Methods: The data of 63 adults and children (mean age, 21.8 years) were analyzed. Results: There were 7 episodes of considerable bleeding (11.1%) that required surgical treatment under general anesthesia in 6 patients, of whom 5 experienced secondary bleeding (>24 hours). Moreover, bleeding and massive swelling of the pharynx required surgical treatment and prolonged intubation (35 hours) in 1 patient. None of the patients received blood transfusions. There was no case with a lethal outcome. Less intense bleeding (clots; blood-tinged sputum) was observed in 17 patients (27%) who required readmission or prolonged inpatient observation, 1 of whom had previously undergone surgical treatment of PTH. However, these 17 patients had an uneventful clinical course. In total, 22 patients experienced minor or major forms of PTH (34.9%). Conclusions: At least in our hands, CTE dramatically increased the frequency of PTH. The high rate of secondary bleeding contrasts with our documented experience using conventional methods, ie, cold dissection and suture ligation, to achieve hemostasis (7.9% with CTE versus <0.8% with conventional methods). Therefore, at our institution, tonsillectomy with conventional instruments remains the method of choice.
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Fuentes, Juan, Pedro M. Guerreiro, Teresa Modesto, Josep Rotllant, Adelino V. M. Canario, and Deborah M. Power. "A PTH/PTHrP receptor antagonist blocks the hypercalcemic response to estradiol-17β." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 2 (August 2007): R956—R960. http://dx.doi.org/10.1152/ajpregu.00111.2007.
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Estradiol (E2) increases circulating calcium and phosphate levels in fish, thus acting as a hypercalcemic and hyperphosphatemic factor during periods of high calcium requirements, such as during vitellogenesis. Since parathyroid hormone (PTH)-related protein (PTHrP) has been shown to be calciotropic in fish, we hypothesized that the two hormones could be mediating the same process. Sea bream ( Sparus auratus) juveniles receiving a single intraperitoneal injection of piscine PTHrP(1-34) showed an elevation in calcium plasma levels within 24 h. In contrast, injections of the PTH/PTHrP receptor antagonist PTHrP(7-34) decreased circulating levels of calcium in the same period. Intraperitoneal implants of estradiol-17β (E2; 10 μg/g) evoked significant increases of circulating plasma levels of calcium and phosphorus and a sustained increases of circulating plasma levels of PTHrP. However, a combined treatment of E2 and PTHrP(7-34) evoked a markedly lower calcium response compared with E2 alone. We conclude that PTHrP or a related peptide that binds the PTH/PTHrP receptor mediates, at least in part, the hypercalcemic effect of E2 in calcium and phosphate balance in fish.
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Bettoun, J. David, Masanori Minagawa, Mei Yee Kwan, Han S. Lee, Toshiyuki Yasuda, Geoffrey N. Hendy, David Goltzman, and John H. White. "Cloning and Characterization of the Promoter Regions of the Human Parathyroid Hormone (PTH)/PTH-Related Peptide Receptor Gene: Analysis of Deoxyribonucleic Acid from Normal Subjects and Patients with Pseudohypoparathyroidism Type 1b*." Journal of Clinical Endocrinology & Metabolism 82, no. 4 (April 1, 1997): 1031–40. http://dx.doi.org/10.1210/jcem.82.4.3906.
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Abstract Expression of the PTH/PTH-related peptide (PTHrP) receptor (PTHR) in the mouse is controlled by at least two promoters. The downstream promoter (P2) is ubiquitously expressed, whereas expression of the upstream promoter (P1) is largely restricted to kidney. These observations may provide a genetic basis for a human PTH resistance syndrome, pseudohypoparathyroidism type 1b (PHP1b), in which renal, but not osseous, signaling by PTH is defective. We, therefore, cloned and characterized the 5′-end of the human PTHR gene and found that its organization is very similar to that of the mouse. Transcription initiation sites of human P1 and P2 promoters are in similar, but not identical, positions to those of the mouse gene. The identification of a human P2 promoter is significant because no P2-specific human PTHR complementary DNAs have been isolated to date. Southern analysis of genomic DNA from seven PHP1b patients did not reveal any rearrangements in proximal promoter regions or exons encoding 5′-untranslated region sequences. No significant sequence differences were found in clones of normal and patient DNAs encompassing proximal promoter sequences, and untranslated region and signal sequence exons. Thus, in the seven PHP1b patients analyzed, no defects were identified that would influence initiation site selection, stability, or splicing of renal PTHR transcripts. These data indicate that the genetic defect(s) in PHP1b in these patients lies in distal enhancer elements of the gene, in an essential transcriptional regulator, or in some as yet unidentified cofactor required for renal PTH signaling.
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Werchowski, J. L., M. H. Sanders, J. P. Costantino, F. C. Sciurba, and R. M. Rogers. "Inductance plethysmography measurement of CPAP-induced changes in end-expiratory lung volume." Journal of Applied Physiology 68, no. 4 (April 1, 1990): 1732–38. http://dx.doi.org/10.1152/jappl.1990.68.4.1732.
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The respiratory inductance plethysmograph (RIP) has recently gained popularity in both the research and clinical arenas for measuring tidal volume (VT) and changes in functional residual capacity (delta FRC). It is important however, to define the likelihood that individual RIP measurements of VT and delta FRC would be acceptably accurate (+/- 10%) for clinical and investigational purposes in spontaneously breathing individuals on continuous positive airway pressure (CPAP). Additionally, RIP accuracy has not been compared in these regards after calibration by two commonly employed techniques, the least squares (LSQ) and the quantitative diagnostic calibration (QDC) methods. We compared RIP with pneumotachographic (PTH) measurements of delta FRC and VT during spontaneous mouth breathing on 0-10 cmH2O CPAP. Comparisons were made after RIP calibration with both the LSQ (6 subjects) and QDC (7 subjects) methods. Measurements of delta FRC by RIPLSQ and RIPQDC were highly correlated with PTH measurements (r = 0.94 +/- 0.04 and r = 0.98 +/- 0.01 (SE), respectively). However, only an average of 30% of RIPQDC determinations per subject and 31.4% of RIPLSQ determinations per subject were accurate to +/- 10% of PTH values. An average of 55.2% (QDC) and 68.8% (LSQ) of VT determinations per subject were accurate to +/- 10% of PTH values. We conclude that in normal subjects, over a large number of determinations, RIP values for delta FRC and VT at elevated end-expiratory lung volume correlate well with PTH values. However, regardless of whether QDC or LSQ calibration is used, only about one-third of individual RIP determinations of delta FRC and one-half of two-thirds of VT measurements will be sufficiently accurate for clinical and investigational use.
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FILARDI, SILVANA, CARLOS A. M. GUERREIRO, LUIS ALBERTO MAGNA, and JOÃO FRANCISCO MARQUES NETO. "Bone mineral density, vitamin D and anticonvulsant therapy." Arquivos de Neuro-Psiquiatria 58, no. 3A (September 2000): 616–20. http://dx.doi.org/10.1590/s0004-282x2000000400003.
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The aim of this study was to assess bone mineral density and vitamin D metabolism in patients on chronic anticonvulsant therapy. METHODS: Sixty-nine men, outpatients on chronic anticonvulsant therapy, who had been treated for at least 5 years, were studied, comparing them to thirty healthy controls. Bone mineral density was measured as well as serum levels of calcium, ionized calcium, alkaline phosphatase, PTH, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. RESULTS: No differences in bone mineral density, serum levels of vitamin D and intact-PTH were observed between patients and controls. Bone mineral density was not associated with chronic anticonvulsant therapy. CONCLUSION: Those adult patients who were on chronic anticonvulsant therapy and who lived in low latitude regions had normal bone mineral density as well as vitamin D serum levels.
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Edwards, Aurélie, and Olivier Bonny. "A model of calcium transport and regulation in the proximal tubule." American Journal of Physiology-Renal Physiology 315, no. 4 (October 1, 2018): F942—F953. http://dx.doi.org/10.1152/ajprenal.00129.2018.
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The objective of this study was to examine theoretically how Ca2+ reabsorption in the proximal tubule (PT) is modulated by Na+ and water fluxes, parathyroid hormone (PTH), Na+-glucose cotransporter (SGLT2) inhibitors, and acetazolamide. We expanded a previously published mathematical model of water and solute transport in the rat PT (Layton AT, Vallon V, Edwards A. Am J Physiol Renal Physiol 308: F1343–F1357, 2015) that did not include Ca2+. Our results indicate that Ca2+ reabsorption in the PT is primarily driven by the transepithelial Ca2+ concentration gradient that stems from water reabsorption, which is itself coupled to Na+ reabsorption. Simulated variations in permeability or transporter activity elicit opposite changes in paracellular and transcellular Ca2+ fluxes, whereas a simulated decrease in filtration rate lowers both fluxes. The model predicts that PTH-mediated inhibition of the apical Na+/H+ exchanger NHE3 reduces Na+ and Ca2+ transport to a similar extent. It also suggests that acetazolamide- and SGLT2 inhibitor-induced calciuria at least partly stems from reduced Ca2+ reabsorption in the PT. In addition, backleak of phosphate (PO4) across tight junctions is predicted to reduce net PO4 reabsorption by ~20% under normal conditions. When transcellular PO4 transport is substantially reduced by PTH, paracellular PO4 flux is reversed and contributes significantly to PO4 reabsorption. Furthermore, PTH is predicted to exert an indirect impact on PO4 reabsorption via its inhibitory action on NHE3. This model thus provides greater insight into the mechanisms that modulate Ca2+ and PO4 reabsorption in the PT.
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BRAUN-MOSCOVICI, YOLANDA, DANIEL E. FURST, DORON MARKOVITS, ALEXANDER ROZIN, PHILIP J. CLEMENTS, ABRAHAM MENAHEM NAHIR, and ALEXANDRA BALBIR-GURMAN. "Vitamin D, Parathyroid Hormone, and Acroosteolysis in Systemic Sclerosis." Journal of Rheumatology 35, no. 11 (November 2008): 2201–5. http://dx.doi.org/10.3899/jrheum.071171.
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ObjectiveSclerodactyly with acroosteolysis (AO) and calcinosis are prominent features of systemic sclerosis (SSc), but the pathogenesis of these findings is poorly understood. Vitamin D and parathyroid hormone (PTH) have a crucial role in bone metabolism and resorption and may affect AO and calcinosis. We assessed vitamin D and PTH in patients with SSc.MethodsMedical records of 134 consecutive patients with SSc (American College of Rheumatology criteria) followed at the rheumatology department during the years 2003–2006 were reviewed for clinical assessment, laboratory evaluation [including 25(OH) vitamin D, calcium, phosphorus, alkaline phosphatase, PTH, creatinine, and albumin]; imaging data confirming AO and/or calcinosis. Patients followed routinely at least once a year were included (81 patients). Of these, 60 patients’ medical records were found to have complete, relevant clinical, laboratory, and radiographic imaging.ResultsThirteen patients had diffuse disease and 47 limited disease — 51 women and 9 men, 44 Jews and 16 Arabs; mean age 55 ± 14 years; disease duration 8 ± 6 years. AO with or without calcinosis was observed in 42 patients (70%). Vitamin D deficiency was found in 46% of patients (16 out of 44 Jewish patients, 10 out of 16 Arab patients). PTH was elevated in 21.7% of patients. Significant correlations were observed between acroosteolysis and PTH (p = 0.015), calcinosis (p = 0.009), and disease duration (p = 0.008), and between PTH and vitamin D levels (p = 0.01). All patients had normal serum concentrations of calcium, phosphorus, magnesium, and albumin, and liver and kidney functions.ConclusionIn this group of Mediterranean patients with SSc, the incidence of vitamin D deficiency and secondary hyperparathyroidism was surprisingly high. This finding correlated with the occurrence of AO and calcinosis. Low levels of vitamin D may reflect silent malabsorption and might be a risk factor for secondary hyperparathyroidism and bone resorption. Traditional dress habits and low exposure to sun may contribute to vitamin D deficiency in an Arab population but do not explain all the findings. The pathogenesis of these findings needs to be corroborated in other SSc populations.
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Allas, Soraya, Michel Ovize, Michael D. Culler, Clarisse Geraul, Jeroen van de Wetering, and Michael Mannstadt. "A Single Administration of AZP-3601, a Novel, Long-Acting PTH Analog, Induces a Significant and Sustained Calcemic Response: Preliminary Data From a Randomized, Double-Blind, Placebo-Controlled Phase 1 Study." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A254. http://dx.doi.org/10.1210/jendso/bvab048.516.
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Abstract Hypoparathyroidism is a rare disease characterized by a deficiency in parathyroid hormone (PTH) that results in hypocalcemia and hyperphosphatemia. Current treatment approaches, including high dose oral calcium and active vitamin D, as well as recombinant human PTH (1–84), do not provide adequate or consistent control of either serum calcium or clinical symptoms over a full 24-hour period. AZP-3601 is a novel 36 amino-acid PTH analog that has been designed to potently bind to the R0 conformation of the PTH1 receptor, which results in prolonged signaling responses in vitro and prolonged calcemic responses in animals despite having a short circulating half-life. A Phase 1 double-blind, placebo-controlled, single and multiple ascending dose study is being conducted to evaluate the safety, tolerability and pharmacodynamics of AZP-3601 in healthy adults. Here we report data from the first cohorts of the single ascending dose portion of the study. Sequential cohorts of 4 (cohort 1) to 8 (cohort 2 to 4) healthy male subjects aged 18–60 years, with a body mass index of 19–28 kg/m2, were assigned to receive 5, 10, 20 or 40μg of AZP-3601 or placebo at a ratio of 3:1. The study drug was administered in the morning by subcutaneous injection in the abdominal wall and was well tolerated with no remarkable adverse events. As compared with placebo controls, AZP-3601 treatment produced a clear, dose-dependent increase in mean albumin-adjusted serum calcium values from baseline. The normal physiological diurnal variation of albumin-adjusted serum calcium was gradually attenuated with 5 and 10μg AZP-3601, and was completely eliminated with 20μg. With the dose of 40μg AZP-3601, mean albumin-adjusted serum calcium values were significantly increased but stayed within normal laboratory range and remained elevated through at least 24 hours post-administration. We observed a dose-dependent decrease in mean endogenous serum PTH that was significantly correlated with the concomitant increase in mean serum calcium. These data provide initial evidence of the pharmacodynamic effect of AZP-3601 in healthy humans characterized by a sustained calcemic response for at least 24 hours following a single administration.