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Calcium concentration

Calcium is associated in water with carbonates, and more rarely with sulphates. Calcium, as carbonate or bicarbonate, has no influence on the corrosion resistance of aluminium in water, even at concentrations as high as 500 mg-l of calcium carbonate (CaC03), or even higher [15]. [Pg.309]


Calcium sources, such as gypsum and lime, promote cation exchange from sodium clay to a less-sweUing calcium clay. Calcium concentrations ate normally low (<1000 mg/L) and osmotic swelling is only reduced if other salts are present. Calcium chloride has been used infrequently for this purpose but systems are available that allow high calcium chloride levels to be carried in the mud system (98). [Pg.182]

Calcium and Vascular Smooth Muscle Contraction. Calcium acts on a number of sites associated with the control of the cytoplasmic calcium concentration. Vascular smooth muscle contraction can be initiated by the opening of the slow calcium channel aUowing influx of extraceUular calcium through the sarcolemmal membrane into the cytoplasmic compartment. The iatraceUnlar calcium concentration increases to 1 x 10 Af, a threshold concentration necessary to initiate contraction. [Pg.125]

In the presence of calcium, the primary contractile protein, myosin, is phosphorylated by the myosin light-chain kinase initiating the subsequent actin-activation of the myosin adenosine triphosphate activity and resulting in muscle contraction. Removal of calcium inactivates the kinase and allows the myosin light chain to dephosphorylate myosin which results in muscle relaxation. Therefore the general biochemical mechanism for the muscle contractile process is dependent on the avaUabUity of a sufficient intraceUular calcium concentration. [Pg.125]

Co-buHders such as nitnlotriacetic acid or polycarboxylates also may be incorporated into the detergent formulation. Wash performance of detergents decreases with increasing calcium concentration. Protease performance varies, but high calcium concentrations tend to reduce protease performance. Therefore it is an advantage to add a buHder system to the detergent. Proteases need a smaH amount of calcium for the sake of stabHity, but even with the most efficient buHder systems, stabHity during wash is not a problem. [Pg.294]

Another major second messenger in cells is calcium ion. Virtually any mammalian cell line can be used to measure transient calcium currents in fluorescence assays when cells are preloaded with an indicator dye that allows monitoring of changes in cytosolic calcium concentration. These responses can be observed in real time, but a characteristic of these responses is that they are transient. This may lead to problems with hemi-equilibria in antagonist studies whereby the maximal responses to agonists may be depressed in the presence of antagonists. These effects are discussed more fully in Chapter 6. [Pg.83]

Prepare the sample solution in a similar manner to give a fluorescence value falling within the range of the calibration curve, and hence obtain the original calcium concentration in the sample. [Pg.739]

Ashley, C. C. (1970). An estimate of calcium concentration changes during the contraction of single muscle fibres. ]. Physiol. 210 133-134P. [Pg.380]

Hastings, J. W., etal. (1969). Response of aequorin bioluminescence to rapid changes in calcium concentration. Nature 222 1047-1050. [Pg.402]

Llinas, R., Sugimori, M., and Silver, R. B. (1992). Microdomains of high calcium concentration in a presynaptic terminal. Science 256 677-679. [Pg.416]

Woodruff, R. I., Miller, A. L., and Jaffe, L. F. (1991). Difference in free calcium concentration between oocytes and nurse cells revealed by corrected aequorin luminescence. Biol. Bull. 181 349-350. [Pg.453]

The parathyroid glands in FHH are reset to maintain a higher than normal serum calcium concentration owing to impaired suppression of PTH release in the face of hypercalcemia (e.g., resistance to CaQ+) (Fig. 2). Similarly the kidneys show a reduced calciuric response to hypercalcemia, which contributes to the hypercalcemia by promoting inappropriately reabsorption of calcium. Mouse models of FHH and NSHPT result from targeted inactivation of one or both CaR alleles, respectively [1,3]. These animals have provided valuable insights into the alterations in tissue function resulting from loss of the receptor. [Pg.303]

Smooth Muscle Tone Regulation. Figure 2 Membrane mechanisms leading to an increases in cytosolic calcium concentration, depolar, depolarisation of the membrane see text for abbreviations. [Pg.1143]

What potential is expected for a calcium concentration of 5 x 10 4M (Assume activity coefficient of 1.0.)... [Pg.168]

Comparison of results for the first and last entries in Table 7 (AOS 2024 and IOS 2024) was for samples for which the hydrophobe linearity, hydrophobe carbon number, and relative disulfonate content were held nearly constant. The major differences in these surfactants were possible differences in the relative locations of the double bond and the sulfonate group in the alkenesulfonate and in the relative locations of the hydroxy group and the sulfonate group in the hydroxyalkanesulfonate. Analyses to determine these are quite difficult. At calcium ion concentrations below 100-250 ppm, AOS 2024 appeared to be more salt-tolerant than linear IOS 2024. At higher calcium concentrations, the calcium ion tolerance of the two surfactants was similar. [Pg.377]

Regulation of Intracellular Free Calcium Concentration (an n-Compartment System) 183... [Pg.155]

Finally, a 150 kDa calmodulin binding protein, caldesmon is found bound to actin filaments at low calcium concentrations. The ratio of caldesmon to actin molecules seems to vary from 1 20 in the aorta to as much as 1 200 in chicken gizzard. It has been reported and disputed that caldesmon crosslinks actin filaments into large bundles. [Pg.170]

Figure 6. A hypothetical scheme for the control of the number of active crossbridges in smooth muscle. Following the activation of a smooth muscle by an agonist, the concentrations of intermediates along the main route begins to build up transiently. This is shown by the thickened arrows. Also, cAMP is generated which is universally an inhibitor in smooth muscle. Cyclic AMP in turn combines with protein kinase A, which accounts for most of its action. The downstream mechanisms, however, are not well worked out and at least three possibilities are likely in different circumstances. First, protein kinase A is known to catalyze the phosphorylation of MLCK, once phosphorylated MLCK has a relatively lower affinity for Ca-calmodulin so that for a given concentration of Ca-calmodulin, the activation downstream is reduced. The law of mass action predicts that this inhibition should be reversed at high calcium concentrations. Other cAMP inhibitory mechanisms for which there is evidence include interference with the SR Ca storage system, and activation of a MLC phosphatase. Figure 6. A hypothetical scheme for the control of the number of active crossbridges in smooth muscle. Following the activation of a smooth muscle by an agonist, the concentrations of intermediates along the main route begins to build up transiently. This is shown by the thickened arrows. Also, cAMP is generated which is universally an inhibitor in smooth muscle. Cyclic AMP in turn combines with protein kinase A, which accounts for most of its action. The downstream mechanisms, however, are not well worked out and at least three possibilities are likely in different circumstances. First, protein kinase A is known to catalyze the phosphorylation of MLCK, once phosphorylated MLCK has a relatively lower affinity for Ca-calmodulin so that for a given concentration of Ca-calmodulin, the activation downstream is reduced. The law of mass action predicts that this inhibition should be reversed at high calcium concentrations. Other cAMP inhibitory mechanisms for which there is evidence include interference with the SR Ca storage system, and activation of a MLC phosphatase.

See other pages where Calcium concentration is mentioned: [Pg.150]    [Pg.563]    [Pg.121]    [Pg.529]    [Pg.155]    [Pg.242]    [Pg.667]    [Pg.672]    [Pg.351]    [Pg.788]    [Pg.795]    [Pg.31]    [Pg.117]    [Pg.303]    [Pg.304]    [Pg.305]    [Pg.401]    [Pg.488]    [Pg.824]    [Pg.847]    [Pg.1142]    [Pg.1143]    [Pg.1144]    [Pg.1145]    [Pg.1274]    [Pg.1276]    [Pg.1282]    [Pg.1302]    [Pg.341]    [Pg.383]    [Pg.185]    [Pg.194]   
See also in sourсe #XX -- [ Pg.251 ]

See also in sourсe #XX -- [ Pg.124 , Pg.126 ]

See also in sourсe #XX -- [ Pg.479 , Pg.749 ]




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ATPase cytosolic calcium concentration

Adsorption plateau, calcium concentration

Blood plasma, calcium concentration

Calcitriol calcium concentration regulated

Calcium arsenates concentration

Calcium carbonate, reduction concentrations

Calcium channels concentration reductions

Calcium concentration determination

Calcium concentration factor

Calcium concentration ocean

Calcium concentration, urinary

Calcium cytosolic free concentrations

Calcium intracellular concentration regulation

Calcium intracellular concentrations

Calcium ion concentration

Calcium plasma concentrations

Calcium resting cell concentration

Calcium sulfate Concentration

Calcium, absorption plasma concentration

Calcium-ascorbic acid concentration

Chloride calcium concentration

Concentration correlation with calcium

Determination of Calcium Ion Concentration

Effect of Calcium Concentration

Extracellular calcium concentration

Magnesium calcium concentration

Plasma Concentrations of Calcium and Phosphate

Plasma membrane cytosolic calcium concentration

Protein tyrosine kinases intracellular calcium concentration

Proton and calcium concentration

Seawater calcium concentration

Serum calcium concentration

Smooth muscle activation intracellular calcium concentration

Solid-phase calcium concentration

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