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Books on the topic 'Boues de phosphate'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 September 2024

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1

International Workshop on Phosphate and Other Minerals (7th 1985 Marseille, France). Phosphate and mineral homeostasis. New York: Plenum Press, 1986.

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2

Lewin, Jonathan Stuart. The combined use of Tc-99m-phosphate and Ga-67-citrate imaging in the diagnosis of acute osteomyelitis in children. [New Haven: s.n.], 1985.

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3

Felix, Bronner, and Peterlik Meinrad, eds. Extra- and intracellular calcium and phosphate regulation: From basic research to clinical medicine. Boca Raton: CRC Press, 1992.

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4

Bossche, Hugues Vanden. Devenir du phosphore apporté sur les sols et risques de contamination des eaux de surface: Cas des boues de stations d'épuration. Rennes, France: Géosciences Rennes, UMR 6118, CNRS-Université de Rennes I, Campus de Beaulieu, 2002.

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5

Rogers, Mike, Graham Russell, and Stuart Ralston. Bisphosphonates. Informa Healthcare, 2002.

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6

Barrios, Carlos Gerardo Sanchez. FLUX DE PHOSPHORE ET COLLECTE DES BOUES D’UNE PISCICULTURE. Omniscriptum, 2010.

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7

(Editor), Shaul G. Massry, Michel Olmer (Editor), and Eberhard Ritz (Editor), eds. Phosphate and Mineral Homeostasis (Advances in Experimental Medicine and Biology). Springer, 1987.

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8

Thin calcium phosphate coatings for medical implants. New York: Springer, 2009.

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9

Anderson, Paul, Borje Edgar Christopher Nordin, and Howard Arthur Morris. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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10

Anderson, Paul, Borje Edgar Christopher Nordin, and Howard Arthur Morris. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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11

Anderson, Paul. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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12

Anderson, Paul. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2017.

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13

Bronner, Felix, and Meinrad Peterlik. Extra- and Intracellular Calcium and Phosphate Regulation: From Basic Research to Clinical Medicine. CRC, 1992.

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14

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0144.

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Paget's disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.

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15

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0144_update_001.

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Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.

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16

Bisphosphonates in bone disease: From the laboratory to the patient. 4th ed. San Diego: Academic Press, 2000.

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17

Bisphosphonates in bone disease: From the laboratory to the patient. 3rd ed. New York: Parthenon Pub. Group, 1997.

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18

Bisphosphonates in bone disease: From the laboratory to the patient. 2nd ed. New York: Parthenon Pub. Group, 1995.

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