"Dissertation présentée devant la Faculté de médecine, épreuve de l'agrégation de l'enseignement supérieur." / At head of title: Université catholique de Louvain. Chaire de chirurgie orthopédique, Professeur P. Lacroix, et Institut interuniversitaire des sciences nucléaires. Includes bibliographical references.

Thesis (Ph.D.) - University of Queensland, 2005. / Includes bibliography.

Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.

The plasma calcium level is one of the most precisely regulated constants of the internal environment, and the large reservoir of calcium in the skeleton is primarily responsible for this homeostasis. The experiments presented in this thesis were designed to study quantitatively the regulation of plasma calcium. Acute hypocalcemia was induced by continuous intravenous EDTA infusion (a calcium chelating agent) at a known rate, and hypercalcemia was induced by intravenous calcium gluconate infusion. The rate used in most cases was 10 mg. calcium per kg. for one hour. Both mobilization and storage of calcium appeared to depend on equilibrium with a labile calcium storage pool in bone. The rate of storage or mobilization was shown to be proportional to the amount of blood coming in contact with this labile pool in bone (bone blood flow), and the plasma/bone difference in Ca++ activity. Bone blood flow was measured using the Pick Principle for calcium storage, and it was calculated to be 6.46 ± 0.60% of the cardiac output (14 dogs). The extracellular fluid calcium was also estimated and found to be 15.73 ± 0.72 mg/kg (14 dogs), corresponding to an extracellular fluid volume of approximately 20% of body weight. Less than 5% of the injected calcium was excreted in the urine. The labile calcium storage pool in bone was estimated from the changes in the bone-blood equilibrium after calcium was injected, and was found to be 2 - 5 times greater than the extracellular calcium. The net loss of calcium from the plasma after calcium injection, which is assumed to equal the rate at which calcium is used for bone mineralization less calcium released by resorption, was estimated as 1 - 2 mg. Ca/kg/hr. or 0.15 - 0.35% of the total bone calcium per day. The methods described provide a means of assessing quantitatively the factors involved in acute regulation of the plasma calcium level. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

No description available.

3 pp. / Originally published: 2002 / It is important to know how much calcium you need to consume each day as more than 2500 mg of calcium each day can be harmful. Calcium should be obtained from foods and beverages first, then from supplements if necessary. Taking more than 500 mg of calcium at one time should be avoided. If you choose to take a calcium supplement, calcium citrate or calcium carbonate should be chosen.

Thèses (M.Sc.)--Université de Sherbrooke (Canada), 2002. / Titre de l'écran-titre (visionné le 20 juin 2006). Publié aussi en version papier.

Thesis (M.S.)--University of Michigan, 1993.

Muscle contraction and relaxation are controlled by the intracellular free Ca²⁺ concentration. The sarcoplasmic reticulum (SR) is an intracellular membrane system which regulates this internal free Ca²⁺ concentration. Responding to an electrical excitation of the cell surface membrane, the SR releases Ca²⁺ through a specific Ca²⁺ release channel, thus elevating the Ca²⁺ concentration inside muscle cell and causing the muscle to contract. Subsequent sequestration of Ca²⁺ by the SR Ca²⁺ pumps restores the resting state of the muscle cell. This research focuses on the Ca²⁺ release channel from skeletal muscle SR. The planar lipid bilayer technique was used to study the channel at the single channel level. The SR Ca²⁺ release channel was identified and isolated via its interaction with specific sulfhydryl oxidizing agents. This protein of a molecular mass of 106 kDa was then incorporated into a planar lipid bilayer membrane (BLM). In an asymmetrical Ca²⁺ solution, the channel protein demonstrates a single channel conductance of 107 ± 13 pS and a permeability ratio of Ca²⁺ versus Tris⁺ of 7.4 ± 3.3. In a symmetrical 250 mM NaCl solution, the channel protein displays a large single channel conductance of 400 ± 20 pS, and a weak voltage-dependence. The channel is activated by millimolar ATP and inhibited by micromolar ruthenium red. Nanomolar concentrations of ryanodine modify the channel by changing it from a rapidly gating full conductance state to a long-lived subconductance state. These results demonstrate that the isolated 106 kDa protein channel has properties similar to those observed following fusion of SR vesicles to a BLM. The bilayer system was also used to examine the effect of Ag⁺ on the SR Ca²⁺ release channel. Ag⁺ (0.2-1. 0 μM ) activates the SR Ca²⁺ release channel. Activation by Ag⁺ does not require the presence of Ca²⁺, Mg²⁺, or ATP. Ag⁺ activates the channel by increasing the open probability Po. Ag⁺ activation is always followed by a spontaneous inactivation. The channel is still sensitive to ruthenium red inhibition after exposure to Ag⁺. Isolated SR vesicles were fused to a BLM to study the effect of the photooxidizing dye, rose bengal, on the gating characteristics of the reconstituted SR Ca²⁺ release channel. Rose bengal activates the Ca²⁺ release channel in the presence of light by increasing the channel open probability and leaving the single channel conductance unchanged. This photoactivation is independent of the myoplasmic Ca²⁺ concentration, and can be achieved from either side of the membrane. In addition, the effect is inhibited by addition of 10-20 μM ruthenium red. When modified to its subconducting state by ryanodine, subsequent addition of rose Bengal reactivates the channel to a rapidly fluctuating full conducting state. These studies carried out at the single channel level utilizing the planar lipid bilayer technique have not only enhanced our understanding of the Ca²⁺ release mechanism of skeletal muscle SR, but also provided information about the toxic effects on biological membrane systems caused by heavy metals and oxidizing agents.

Calcium ions are important mediators in the mechanism of contraction and relaxation of muscle fibers. Depolarization of sarcolemma and transverse tubule causes an increase of myoplasmic ca2+ concentration which induces contraction of the myofibrils. In skeletal muscle fibers, the intracellular Ca2+ concentraton is regulated by an extensive membrane system, the sarcoplasmic reticulum (SR). Ca2+-release from SR is initiated by depolarization of the transverse tubule via a process referred to as excitation-contraction coupling. The Ca2+ - release channel located in the junctional SR plays an important role in this mechanism.