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David J. Hosking
Researcher at University of Nottingham
Publications - 134
Citations - 10711
David J. Hosking is an academic researcher from University of Nottingham. The author has contributed to research in topics: Osteoporosis & Bone remodeling. The author has an hindex of 48, co-authored 134 publications receiving 10354 citations. Previous affiliations of David J. Hosking include University of Texas Health Science Center at San Antonio & Nottingham City Hospital.
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Treatment of Metabolic Bone Disease: Management Strategy and Drug Therapy
David J. Hosking,Johann Ringe +1 more
TL;DR: 1. Treatment of Osteomalacia 2. Hypopara-thyroidism 3. Primary Hyperparathyroidism 4. Bone Disease and Malignancy 5. Paget's Disease 6. Renal Bone Disease 7. Transplantation Bone Disease 8. Osteoporosis: Primary Prevention
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Comparison of low-dose intramuscular and intravenous salcatonin in the treatment of primary hyperparathyroidism
TL;DR: The kidney played a pivotal role both in the cause of the hypercalcaemia and in the response to treatment, including the rapid development of resistance which limits the use of salmon calcitonin in primary hyperparathyroidism to short-term reduction of serum calcium.
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The contribution of nutritional factors to osteopenia in the elderly.
Opinder Sahota,David J. Hosking +1 more
TL;DR: Simple deficiency is optimally treated with parent vitamin D, which has a greater safety margin than active vitamin D therapy (1,25 dihydroxyvitamin D), which requires close monitoring in the elderly.
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Vertebral morphometry by DXA: a comparison of supine lateral and decubitus lateral densitometers.
TL;DR: There was good agreement between observers and between the Expert and Prodigy in identifying severe fractures, but lack of agreement in identifying moderate fractures, and measurements of vertebral height are reproducible and patient comfort is not compromised.
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Rescue of trophoblast apoptosis by parathyroid hormone-related protein
TL;DR: Parathyroid hormone‐related protein was found to be a cytotrophoblast apoptosis survival factor and significantly diminished TNFα/IFNγ‐induced apoptosis at 10μM.