Shaul G. Massry
University of Southern California
431 Papers
7.6K Citations
Shaul G. Massry is an academic researcher from University of Southern California. The author has contributed to research in topics: Parathyroid hormone & Calcium. The author has an hindex of 74, co-authored 431 publications. Previous affiliations of Shaul G. Massry include University of Florida & Saint Louis University.
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Papers
Phosphate depletion increases cytosolic calcium of brain synaptosomes.
TL;DR: The data indicate that PD raises [Ca2+]i in brain synaptosomes and suggest that PD increases calcium entry into synaptoomes, which would inhibit mitochondrial ATP production, with a consequent fall in ATP content of synaptOSomes.
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Reduced activity of Na(+)-K+ ATPase of pancreatic islets in chronic renal failure: role of secondary hyperparathyroidism.
TL;DR: The data indicate that the chronic excess blood levels of PTH in CRF initiates events that lead to the reduction in ATP content and in Vmax of Na(+)-K+ ATPase of pancreatic islets.
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Elevation of [Ca2+]i of renal proximal tubular cells and down-regulation of mRNA of PTH-PTHrP, Via and AT1 receptors in kidney of diabetic rats
TL;DR: The results show that the hyperglycemia of IDDM in rats causes a significant elevation in the basal levels of [Ca2+]i of the renal proximal tubular cells and down-regulation of their mRNAs of the PTH-PTHrP, V1a and AT1 receptors; these effects occurred in the presence of normal renal function and normal blood of PTH and phosphorus.
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Relationship between the concentrations of calcium and phosphorus in blood and cerebrospinal fluid.
TL;DR: The integrity of the blood-brain barrier is disrupted in certain clinical conditions, such as hyperparathyroidism, resulting in an increase in brain calcium content, and the mechanism(s) of this phenomenon is examined to evaluate the regulation of calcium and phosphorus by theBlood-cerebrospinal fluid (CSF) interface of theblood- brain barrier in humans and animals.
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Short-term effects of 1,25-dihydroxycholecalciferol on disordered calcium metabolism of renal failure
TL;DR: The steroid corrected the "vitamin D resistance" of uremia, suggesting that the renal production of 1,25-(OH) 2 D 3 in Uremia is defective.
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