Titlebook: Calcium Metabolism, Bone and Metabolic Bone Diseases; Proceedings of the 1 Friedrich Kuhlencordt (Professor of Internal Medic Conference pr

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https://doi.org/10.1007/978-3-662-55426-5tic drugs which influence the hydroxylation of cholecalciferol by induction of hepatic microsomal enzymes (HAHN et al., 1972). It is unlikely, however, to be only mechanism responsible for the development of anticonvulsant osteomalacia. This communication describes the study of a single case of anti

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https://doi.org/10.1007/978-3-662-55426-5ism and vitamin D action. The usual model (cf. . 2, 301, 1968) depicts Ca entering the epithelial cell across the brush border, moving through the cytoplasma as the free ion or in association with a complexer, and then being extruded from the cell across the basal membrane by a Ca pump or by a Na-Ca

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On Calcium Metabolism during Immobilizationretion of calcium in the urine and feces increased, resulting in a negative calcium balance. This has been confirmed by among others, MACK (1965), ROSE (1966) and LYNCH et al. (1967), and a corresponding loss of calcium from the skeleton has been demonstrated through densitometric measurements (MACK, 1965).

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The Effect of Estrogen on Calcium Binding Protein Activity in Odentogenic Epithelium of the Rate steroids is the induction of CaBP (Calcium Binding Protein) in the intestine (TAYLOR and WASSERMAN, 1972). Relevance of this protein to calcium transport in the intestine was assessed (WASSERMAN and TAYLOR, 1966).

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J. Pirschel,P. Huppert,W. Lauchartstudy of human bone physiology and pathophysiology. This data could be used, for example, to diagnose and follow up various bone diseases. Summarized briefly in this paper are some of the significant results obtained with these methods.

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U. T. Seyfert,W. Hauck,M. Köhler,E. Wenzeland calcitonin. With each of these regulators, outstanding developments and advances have been made in recent years. It is the purpose of this article to outline some of the developments that have occured, specifically with regard to our understanding of the mechanism of action of vitamin D in terms of its intervention in calcium homeostasis.