Relevant bibliographies by topics / Calcium fluxes

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Calcium fluxes'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Calcium fluxes"

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Ogasawara, Tomoyasu, Ken-ichi Mori, Teruo Tominaga, Fumitaka Tsukihashi, and Nobuo Sano. "The Activity of Calcium in Calcium-Calcium Halide Fluxes." ISIJ International 36, Suppl (1996): S30—S33. http://dx.doi.org/10.2355/isijinternational.36.suppl_s30.

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von Tscharner, V., D. A. Deranleau, and M. Baggiolini. "Calcium fluxes and calcium buffering in human neutrophils." Journal of Biological Chemistry 261, no. 22 (August 1986): 10163–68. http://dx.doi.org/10.1016/s0021-9258(18)67505-2.

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Donnadieu, E., G. Bismuth, and A. Trautmann. "Calcium fluxes in T lymphocytes." Journal of Biological Chemistry 267, no. 36 (December 1992): 25864–72. http://dx.doi.org/10.1016/s0021-9258(18)35689-8.

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LANGER, G. "Calcium fluxes and cardiac contractility." Journal of Molecular and Cellular Cardiology 18 (1986): 42. http://dx.doi.org/10.1016/s0022-2828(86)80156-0.

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Ochifuji, Yuichiro, Fumitaka Tsukihashi, and Nobuo Sano. "The activity of calcium in calcium-metal-fluoride fluxes." Metallurgical and Materials Transactions B 26, no. 4 (August 1995): 789–94. http://dx.doi.org/10.1007/bf02651725.

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Shkryl, V. M. "Intracellular Calcium Fluxes in Excitable Cells." Neurophysiology 49, no. 5 (October 2017): 384–92. http://dx.doi.org/10.1007/s11062-018-9698-2.

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Rengel, Z., M. Pi�eros, and M. Tester. "Transmembrane calcium fluxes during Al stress." Plant and Soil 171, no. 1 (April 1995): 125–30. http://dx.doi.org/10.1007/bf00009574.

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THOMPSON, Neil T., and Michael C. SCRUTTON. "Intracellular calcium fluxes in human platelets." European Journal of Biochemistry 147, no. 2 (March 1985): 421–27. http://dx.doi.org/10.1111/j.1432-1033.1985.tb08766.x.

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Dennison, Kirsten L., and Edgar P. Spalding. "Glutamate-Gated Calcium Fluxes in Arabidopsis." Plant Physiology 124, no. 4 (December 1, 2000): 1511–14. http://dx.doi.org/10.1104/pp.124.4.1511.

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Hou, Susan H., Jia Zhao, Carol F. Ellman, Jie Hu, Zelma Griffin, David M. Spiegel, and James E. Bourdeau. "Calcium and Phosphorus Fluxes During Hemodialysis With Low Calcium Dialysate." American Journal of Kidney Diseases 18, no. 2 (August 1991): 217–24. http://dx.doi.org/10.1016/s0272-6386(12)80882-1.

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Dissertations / Theses on the topic "Calcium fluxes"

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Gould, Gwyn William. "Calcium fluxes in sarcoplasmic reticulum." Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259665.

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Koorts, Alida Maria. "Intracellular calcium and transmembrane calcium fluxes in chronic renal failure patients." Diss., University of Pretoria, 2000. http://hdl.handle.net/2263/28059.

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Intracellular calcium is a major determinant of a wide variety of cell functions and thus of organ function. In order to get a clear picture of the intracellular calcium status it is preferable to assess the content of the various intracellular calcium pools as well as the characteristics of the transmembrane calcium movements, Le., the magnitude of the transmembrane Ca2+ flux upon stimulation and the rate of the subsequent return to baseline levels. The first aim of this study was to establish and evaluate the methods in the laboratory. The methods investigated include atomic absorption spectrometry, graphite furnace atomic absorption spectrometry and inductively coupled plasma mass spectrometry for the determination of the total cell calcium content, fluorescence spectrophotometry for the determinations of intracellular free Ca2+ and transmembrane Ca2+ movements and transmission electron microscopy for the localisation of intracellular calcium. The methods eventually identified as feasible included fluorescence spectrophotometry for the determination of intracellular free Ca2+ and transmembrane Ca2+ movements and transmission electron microscopy for the localisation of intracellular calcium. The newly developed fluorescent calcium indicator, fura-PE3, was presently shown to be the most reliable fluorescent indicator for the intracellular free Ca2+ determinations. The best method for the calcium localisation by transmission electron microscopy was an adaptation of the antimonate precipitation technique. The following objectives were set in order to contribute to the knowledge in chronic renal failure; examination of the intracellular free Ca2+ content in the neutrophils of end stage renal failure patients on maintenance haemodialysis treatment, as the result of renal failure, dialysis treatment and medication combined; examination of the characteristics of the transmembrane Ca2+ movements; investigation of the intracellular calcium distribution in the neutrophils; exploration of a possible link between the alterations in intracellular calcium status and factors known to influence the calcium status, including the lipid composition of the membrane, the oxidative status as reflected by anti-oxidant vitamin levels, as well as the levels of parathyroid hormone, and ionised serum calcium. This study involved 14 chronic renal failure patients on maintenance haemodialysis. An increase in intracellular free Ca2+, the magnitude of the transmembrane Ca2+ flux upon fMLP stimulation and an increase in the rate of the subsequent decrease in intracellular free calcium were found. In separating the patients into those receiving rHuEPO and those not receiving rHuEPO, it was seen that the significance in the increase in intracellular free Ca2+ could be ascribed to the values obtained in those patients receiving rHuEPO - despite the fact that they were the only patients receiving calcium channel blockers. No overt indications of oxidative stress could be detected by anti-oxidant vitamin levels. Nevertheless, a decrease in the content of specific membrane fatty acids occurred, supporting the previous suggestions of the presence of a mild chronic inflammatory condition in the chronic renal failure patient on maintenance haemodialysis treatment. These results suggest that factors other than those associated with uraemia, such as rHuEPO administration, might result in an increase in intracellular free Ca2+ in cells of CRF/MHT patients. The magnitude of the rHuEPD-induced increase in intracellular free Ca2+ and the effects of the various calcium channel blockers need urgent further investigation as ineffective counteraction of the rHuEPO effect, as indicated by the relative ineffectivity of Norvasc, may have serious side-effects.
Dissertation (MSc)--University of Pretoria, 2010.
Physiology
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Pelc, Radek. "Calcium mobilisation and uptake in smooth muscle cells : role of intracellular calcium stores." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275402.

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Diaz, Mary E. "Sarcoplasmic reticulum calcium content and sarcolemmal fluxes in single ventricular myocytes under varying calcium loads." Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243213.

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Marshall, Jacqueline. "Calcium fluxes at the plasma membrane Zea Mays L. roots." Thesis, University of York, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304172.

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Collins, P. "Endothelium-derived relaxant factor and calcium fluxes in vascular smooth muscle." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597863.

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Uhlén, Per. "Signal transduction via ion fluxes : a cell imaging study with emphasis on calcium oscillations /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-188-8.

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Du, Toit Eugene Francois. "The pharmacological modification of reperfusion injury with particular reference to calcium fluxes in the isolated rat heart." Doctoral thesis, University of Cape Town, 1994. http://hdl.handle.net/11427/27125.

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Myocardial reperfusion injury is thought to be caused by reperfusion induced i) cytosolic Ca²⁺ overload and/or, ii) the formation of oxygen derived freeradicals. At the start of this study, data implicating cytosolic Ca²⁺ overload in the genesis of reversible reperfusion injury were inconclusive. Although several workers have approached this problem by measurements of cytosolic calcium ions, it was my aim to examine the potential sources of such calcium overload. The experiments reported in this thesis were therefore designed to examine the role of altered intracellular and transsarcolemmal Ca²⁺ fluxes in the genesis of reperfusion stunning and arrhythmias. The study was also aimed at elucidating the possible sources and entry pathways contributing to this proposed cytosolic Ca²⁺ overload. In order to investigate the possible role of altered reperfusion Ca²⁺ fluxes in reperfusion injury, we exposed the isolated working, and Langendorff perfused rat heart model to ischaemia and reperfusion to induce reperfusion stunning and arrhythmias. Hearts were pre-treated (before ischaemia) or reperfused with pharmacological compounds, or by interventions known to enhance or inhibit intracellular or transsarcolemmal Ca²⁺ fluxes. The severity of reperfusion stunning (mechanical dysfunction) was measured by reperfusion aortic output, coronary flow and left ventricular pressure. The incidence of reperfusion ventricular arrhythmias was measured by the incidence of ventricular tachycardia and/ or fibrillation. In selected studies, the metabolic status of hearts was evaluated using biochemical assays performed on myocardial tissue samples. Data obtained in these studies indicate that increased Ca²⁺ fluxes through sarcolemmal L-type Ca²⁺ channels during early reperfusion exacerbate stunning, while inhibition of these fluxes with the Ca²⁺ antagonist drug nisoldipine or by Mg²⁺ or Mn²⁺ improve reperfusion function. These data also suggest that although interventions increasing Ca²⁺ fluxes early in reperfusion exacerbate reperfusion stunning, these same interventions improve reperfusion function when performed later. The data also indicate that Ca²⁺ may enter the myocyte indirectly via activation of the Na⁺/H⁺ and Na⁺/Ca²⁺ exchanger during reperfusion. Inhibition of Na⁺/H⁺ exchange activity by HOE 694 during reperfusion attenuated reperfusion stunning and arrhythmias. Both activation of the Na⁺/H⁺ (and Na⁺/Ca²⁺) exchanger and Ca²⁺ influx via the Ca²⁺ channel could contribute to reperfusion induced Ca²⁺ overload and subsequent injury. The study also showed that altered intracellular Ca²⁺ oscillations play a role in reperfusion stunning and arrhythmias as shown by the use of the SR Ca²⁺ release channel blocker, ryanodine. Inhibition of the sarcoplasmic reticulum Ca²⁺ A TP-ase pump by two novel inhibitors, thapsigargin and cyclopiazonic acid, during ischaemia and early reperfusion improved reperfusion function and reduced the incidence of ventricular arrhythmias. function when unphysiologically high concentrations of the peptide were infused into the heart during reperfusion. Taken together, these data suggest that: 1) Ca²⁺ fluxes during early reperfusion (intracellular and transsarcolemmal) play a role in reperfusion injury, 2) that both the Ca²⁺ channel and Na⁺/H⁺ exchange activity contribute to reperfusion injury by possibly contributing to cytosolic Ca²⁺ overload and that, 3) altered intracellular Ca²⁺ oscillations through the SR play a role in both stunning and arrhythmias. Thus the proposal is that modulation of Ca²⁺ fluxes through either the sarcolemma or the sarcoplasmic reticulum, lessen reperfusion injury (stunning and arrhythmias). Although these data do not provide direct evidence of reperfusion Ca²⁺ overload, they support the concept that calcium ions play a role in the genesis of reversible reperfusion injury.
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MacKenzie, Wendy Marlene. "The effects of acid-base disturbances on branchial and renal calcium fluxes in the freshwater rainbow trout (Oncorhynchus mykiss)." Thesis, University of Ottawa (Canada), 1996. http://hdl.handle.net/10393/9995.

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Whole body calcium influx, branchial calcium efflux, and renal Ca$\sp{2+}$ excretion were measured in rainbow trout (Oncorhynchus mykiss) either exposed to environmental hypercapnia or infused intra-arterially with NaHCO$\sb3$. These experiments were performed to assess the potential impact on Ca$\sp{2+}$ balance of the changes in gill morphology that are known to accompany acid-base disturbances in this species. After 48 hours of environmental hypercapnia, gill filamental chloride cell fractional area was significantly reduced. Despite this reduction, and the presumed involvement of the chloride cell in calcium influx, whole body calcium influx was increased after 12 hours of hypercapnia and remained elevated for 48 hours. Branchial calcium efflux was unaltered during hypercapnia exposure, whereas renal Ca$\sp{2+}$ excretion was elevated over preflux values only at 6 hours of hypercapnia. Measurement of the kinetics of whole body calcium influx after 48 hours of hypercapnia revealed a significant increase in the maximal uptake rate of Ca$\sp{2+}$ yet the affinity constant of Ca$\sp{2+}$ uptake was unaffected. Measurements of high-affinity. Ca$\sp{2+}$-ATPase activities and ATP-dependent Ca$\sp{2+}$ transport of gill basolateral membrane vesicles revealed that the ATP-dependent Ca$\sp{2+}$ extrusion mechanism of the gills was not affected by hypercapnia. The results of this study clearly show that the reduced chloride cell surface area that accompanies hypercapnia in trout does not impair calcium homeostasis. Whole body Ca$\sp{2+}$ influx was significantly increased after 6 hours of NaHCO$\sb3$ infusion and remained elevated throughout the duration of the experiment. Branchial and renal Ca$\sp{2+}$ effluxes were largely unaffected by NaHCO$\sb3$ infusion. Plasma total Ca$\sp{2+}$ concentrations were significantly decreased after 6 hours of NaHCO$\sb3$ infusion and remained so until 48 hours. (Abstract shortened by UMI.)
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Dufore, Christopher Michael. "Spatial and Temporal Variations in the Air-Sea Carbon Dioxide Fluxes of Florida Bay." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4031.

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The flux of CO2 between the ocean and the atmosphere is an important measure in determining local, global, and regional, as well as short term and long term carbon budgets. In this study, air-sea CO2 fluxes measured using a floating chamber were used to examine the spatial and temporal variability of CO2 fluxes in Florida Bay. Measurements of dissolved inorganic carbon and total alkalinity obtained concurrently with chamber measurements of CO2 flux allowed calculation of ΔpCO2 from flux measurements obtained at zero wind velocity. Floating chamber measurements of ΔpCO2 were subsequently coupled with wind speed data to provide a simple yet reliable means of predicting absolute flux values. Florida Bay is a marine-dominated, sub-tropical estuary located at the southern tip of the Florida peninsula. Spatial variability within the bay reveals four distinct regions that appear to be affected by a variety of physical, chemical and biological processes. In the eastern part of the bay, the waters tend to be oversaturated with respect to CO2, likely due to the input of freshwater from Taylor Slough. The central portion of the bay is characterized by a number of extremely shallow semi-isolated basins with limited exchange with the rest of the bay. This area is typically undersaturated with respect to CO2 and provides a sink for atmospheric CO2. Both the northern and southern regions were highly variable both spatially and temporally.
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Books on the topic "Calcium fluxes"

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Walker, Lesley Margaret. The effect of mechanical and hormonal stimuli on femur derived osteoblasts; intracellular calcium fluxes and calcium channels. Birmingham: University of Birmingham, 1998.

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United States International Trade Commission. Calcium aluminate flux from France. Washington, DC: U.S. International Trade Commission, 1994.

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Commission, United States International Trade. Calcium aluminate flux from France. Washington, DC: U.S. International Trade Commission, 1994.

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Spenlé, Daniel. Guide du calcul en mécanique: Pour maîtriser la performance des systèmes industriels. Paris: Hachette, 1998.

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McKague, Alan Ross *. Dephosphorization of carbon saturated iron using lime-calcium halide fluxes. 1988.

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Hahn, Robert G. Fluid and electrolyte physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0003.

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The maintenance of body fluid homeostasis is an essential task in perioperative care. Body fluid volumes are tightly controlled by the nervous system, by hormones, and by the kidneys. All these systems are affected by anaesthesia and surgery in ways that must be appreciated by the anaesthetist. Administration of infusion fluids is the key tool to prevent major derangements of the body fluid volumes during before, during, and after surgery. By varying its composition, an infusion fluid can be made to selectively expand or shrink a body fluid compartment. The total osmolality determines whether the infused volume distributes over the total body water or over the extracellular fluid volume, or even attracts fluid from intracellular space. Infusion fluid is the first-line tool in the management of the vasodilation that is induced by both general and regional anaesthesia. Fluids are also an essential component in the treatment of haemorrhage, in which a reduction in arterial pressure implies that 20% of the blood volume has been lost. Capillary refill restores the blood volume, but too slowly to prevent haemorrhagic shock. In this situation, prompt intravenous fluid therapy is life-saving. Electrolyte derangements may be induced by disease and/or medication. The most essential ones to consider during anaesthesia are sodium, potassium, calcium, and bicarbonate.
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Molecular and Cellular Mechanisms in Disease : 1: Bioenergetics · Cell Specificity · Inborn Errors of Metabolism · Malnutrition · Calcium and ... · Hormones Body Fluids and Electrolytes. Springer, 2011.

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Kalinin, A. A., Ye E. Savchenko, and V. Yu Prokofiev. Mineralogy and genesis of the Oleninskoe gold deposit (Kola Peninsula). FRC KSC RAS, 2021. http://dx.doi.org/10.37614/978.5.91137.446.4.

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Data on geology of the Oleninskoe deposit, and results of mineralogical and geochemical investigations of ores and altered rocks are presented. Mineralization is connected with granite porphyry sills, an end member of gabbrodiorite-diorite-granodiorite complex of minor intrusions. The main alteration processes are diopsidization and biotitization, formation of quartz-muscovite-albite, quartz-aresenopyrite-tourmaline, and quartz metasomatic rocks. More than 50 ore minerals (sulfides, sulfosalts, tellurides, and native metals) were identified in the ore, including 20 minerals of silver and gold. Mineral associations in the ore and sequence of mineral formation are defined. Five generations of gold-silver alloys are identified, its composition covers spectrum from native silver to high-grade gold. Mineralized fluids in the deposit are of high salinity (sodium and calcium chlorides), and rich in As, Sb, Pb, Cu, Zn, and Ag. The Oleninskoe deposit is classified as an epithermal metamorphosed gold deposit.The book is of interest for specialists in economic geology, mineralogy and geochemistry of ore deposits.
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Murer, Heini, Jürg Biber, and Carsten A. Wagner. Phosphate homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0025.

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Inorganic phosphate ions (H2PO4−/ HPO42−) (abbreviated as Pi) are involved in formation of bone and generation of high-energy bonds (e.g. ATP), metabolic pathways, and regulation of cellular functions. In addition, Pi is a component of biological membranes and nucleic acids. Only about 1% of total body Pi content is present in extracellular fluids, at a plasma concentration in adults within the range 0.8–1.4 mMol/L (at pH 7.4 mostly as HPO42−), with diurnal variations of approximately 0.2 mM. A small amount of plasma Pi is bound to proteins or forms complexes with calcium. Under normal, balanced conditions, absorption of dietary Pi along the small intestine equals the output of Pi via kidney and faeces. Renal excretion of Pi represents the key determinant for the adjustment of normal Pi plasma concentrations. Renal reabsorption of Pi occurs along the proximal tubules by sodium-dependent Pi cotransporters that are strictly localized at the apical brush border membrane. Parathyroid hormone (PTH) and FGF23 are key regulators amongst a myriad of factors controlling excretion of Pi in urine, mostly by changes of the apical abundance of Na/Pi cotransporters. Hypophosphataemia may result in osteomalacia, rickets, muscle weakness, and haemolysis. Hyperphosphataemia can lead to hyperparathyroidism and severe calcifications in different tissues.
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Barbara, Toole-O'Neil, and Ohio Coal Development Office, eds. Dry scrubbing technologies for flue gas desulfurization. Boston: Kluwer Academic Publishers, 1998.

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Book chapters on the topic "Calcium fluxes"

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Fülöp, T., M. P. Jacob, G. Fòris, Zs Varga, and L. Robert. "Effects of Elastin Peptides on Ion Fluxes." In Cell Calcium Metabolism, 617–22. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_63.

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Grinstein, Sergio, Stephen Macdougall, Roy K. Cheung, and Erwin W. Gelfand. "Role and Properties of Ligand-Induced Calcium Fluxes in Lymphocytes." In Cell Calcium Metabolism, 283–91. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_31.

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Vassort, Guy. "Calcium Ion Fluxes Across Plasma Membranes." In Bioelectrochemistry IV, 29–51. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2576-9_3.

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Fesce, Riccardo, and Daniele Zacchetti. "Calcium Fluxes and Distribution in Neurons." In Bioelectrochemistry IV, 53–68. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2576-9_4.

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Rengel, Z., M. Pineros, and M. Tester. "Transmembrane calcium fluxes during Al stress." In Plant-Soil Interactions at Low pH: Principles and Management, 291–96. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0221-6_39.

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Cantley, Lewis, Philip M. Rosoff, Robert Levenson, Ian G. Macara, Li-An Yeh, Leona Ling, and Leigh English. "Na+ and Ca2+ Fluxes and Differentiation of Transformed Cells." In Calcium in Biological Systems, 173–78. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2377-8_20.

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Schubert, P., K. Lee, and G. W. Kreutzberg. "Neuromodulation by Adenosine and the Effect on Ion Fluxes." In Calcium Electrogenesis and Neuronal Functioning, 236–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70744-5_22.

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Scharff, Ole, and Birthe Foder. "Calcium Fluxes in Pathologically Altered Red Cells." In The Red Cell Membrane, 423–42. Totowa, NJ: Humana Press, 1989. http://dx.doi.org/10.1007/978-1-4612-4500-1_18.

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Friel, David D. "Mitochondrial and ER Calcium Uptake and Release Fluxes and their Interplay in Intact Nerve Cells." In Understanding Calcium Dynamics, 37–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-540-44878-5_3.

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Bygrave, F. L., P. H. Reinhart, and W. M. Taylor. "Mitochondrial Calcium Fluxes and Their Role in the Regulation of Intracellular Calcium." In Calcium and Cell Physiology, 94–104. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70070-5_4.

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Conference papers on the topic "Calcium fluxes"

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Warren, NJ, EJ Crampin, and MH Tawhai. "Shear Stress, Intracellular Calcium, and Transepithelial Water Fluxes." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1888.

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Tarraf, Bachar, Michael Leguèbe, Yves Coudière, and Philippe Diolez. "Thermodynamical Fluxes for the Modeling of Cardiac Mitochondrial Calcium Handling." In 2019 Computing in Cardiology Conference. Computing in Cardiology, 2019. http://dx.doi.org/10.22489/cinc.2019.274.

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Cannell, Mark B., Marc D. Jacobs, Paul J. Donaldson, and Christian Soeller. "Application of two-photon flash photolysis to measure microscopic diffusion and calcium fluxes." In Lasers and Applications in Science and Engineering, edited by Joseph Neev, Christopher B. Schaffer, Andreas Ostendorf, and Stefan Nolte. SPIE, 2005. http://dx.doi.org/10.1117/12.601431.

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Braverman, Boris, Aleksandr Avramchik, Olga Kryukova, and Yury Maksimov. "Effect of Pressure on the Joint Reduction of ZrO2 and B2O3 with Calcium." In 2020 7th International Congress on Energy Fluxes and Radiation Effects (EFRE). IEEE, 2020. http://dx.doi.org/10.1109/efre47760.2020.9241893.

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Unachukwu, U. J., and J. M. D'Armiento. "ER Stress-Induced Calcium Fluxes Define the Therapeutic Mechanisms of Tyrosine Kinase Inhibitors in Lymphangioleiomyomatosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1199.

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SIMON, M. F., H. CHAP, and L. DOUSTE-BLAZY. "EFFECTS OF SIN 1 ON PLATELET ACTIVATION INDUCED BY THROMBIN IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643423.

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The mechanism of platelet activation is well known. The interaction of agonist such as thrombin, on specific membrane receptor induces phosphatidylinositol-specific phospholipase C activation, with a concomitant formation of two second messengers (from PIP2): inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 is able to induce a rapid discharge of Ca2+ from internal stores and Ca2+ influx through plasma membrane by unidentified Ca2+ channels linked to receptor activation. The increase of cytoplasmic free calcium concentration leads to the activation of the calcium calmodulin dependent myosine light chain kinase which phosphoryla-tes 20 kD proteins (myosine light chain). DAG is a potent activator of protein kinase C, which phosphorylates 40 kD proteins. These different pathways act in synergism.Sin 1 is a platelet aggregating inhibitor. This compound is an active metabolite of molsidomine, which activates platelet guany-late cyclase, inducing a rapid rise in cyclic GMP level. The precise role of cyclic GMP in platelet activation is not yet known. In order to study the mechanism of action of this drug, we tried to determine the effect of Sin 1 on the different steps described above. We measured Ca2+ fluxes and phospholipase C activation in thrombin (0,5 U/ml) stimulated platelets in the presence of different doses of Sin 1 (10™7-10™3M). Serotonin secretion was inhibited by 30 % with Sin 1 (10™4M-10™5m). A parallel inhibition of phospholipase C was detected by measurement of [32P)-PA level. Platelets loaded with Quin 2 and stimulated by thrombin showed a 70 % inhibition of external Ca2+ influx as soon as a concentration of 10™7M of Sin 1 was added. A study on platelet loaded with [45Ca2+) and Quin 2 confirmed these results. On the contrary, discharge of internal Ca2+ store seemed to be unaffected.In conclusion, the major effect of Sin 1 on platelet phospholipase C pathway is an inhibition of Ca2+ influx through plasma membrane. Some further experiments are necessary to shown whether this inhibition is correlated with cyclic GMP formation (the major effect of Sin 1) and try to establish a relation between this inhibition and that exerted on phospholipase C.Sin 1 was a generous gift of Hoechst.
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7

Powling, M. J., and R. M. Hardisty. "THE DEPENDENCE OF PLATELET ATP SECRETION IN RESPONSE TO VARIOUS AGONISTS ON Ca2+ MOBILIZATION AND AGGREGATION IN QUIN 2 LOADED PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644676.

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Thrombin (0.O5 and 0.5 u/ml), ADP (10 uM), PAF. (30 nM), vasopressin (vp, 0.018 u/m1 ), arachidonate (AA, 10 uM), U46619 (0.125 ug/ml) and A23187 (2OO nM) induce aggregation ATP secretion, TxB2 generation and a rapid elevation of intracellular calcium (Ca2+i) concentration provided the medium contains 1 mM extracellular Ca2+. Phorbol ester (TPA) induces aggregation and secretion with no alteration in [Ca2+i]. Pre-incubation with Fab fragments of Ml48, a monoclonal antibody against GPIIb/lIIa, completely abolished aggregation in response to all agonists without affecting Ca2+i flux. ADP and A23187-induced secretion was completely abolished by M148 Fab while that induced by VP, PAF, U46619, AA, thrombin and TPA was inhibited by 70%, 70%, 30%, 25%, 25% and 10% respectively.In the presence of 1 mM EGTA (Ca2+o <100 nM), aggregation was again abolished and the Ca2+i fluxes were about 10-20% of those in the presence of 1 mM Ca2+ o. ADP and A23187 again induced no secretion, but 0.05 u/ml thrombin, PAF, VP, U46619, AA, 0.5 u/ml thrombin and TPA induced respectively 6%, 8%, 12%, 30%, 40%, 57% and 85% of control (1 mM Ca2+ o) levels. Addition of Ml48 Fab and EGTA together had no greater effect than EGTA alone.At the concentrations used, ADP and A23187 are thus completely dependent on aggregation for the induction of ATP secretion, while TPA and thrombin (0.5 u.ml) can actlargely independently of both aggregation and changes in[Ca2+ i]. Low concentrations of thrombin induce secretion in the absence of aggregation provided the stimulated [Ca2+i] is sufficiently high (ie greater than that seen with <100 nM Ca2+ o). VP and PAF appear to be more dependent on aggregation for their secretory responses, while U46619 and AA are more dependent on stimulated [Ca2+i].
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8

Siess, W., and E. G. Lapetina. "SYNERGISM OF Gi-DISSOCIATION AND PROTEIN KINASE C STIMULATION IN PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644511.

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Epinephrine or UK 14304 (a specific (α2-adrenoceptor agonist) synergizes with phorbol esters (phorbol 12,13-dibutyrate, PdBu) or bioactive diacylglycerols (sn-1,2-dioctanoylglycerol, DiC8) to induce aggregation and ATP-secretion of platelets. The effect on aggregation is more pronounced than on secretion, and it is observed in aspirinized platelet-rich plasma or suspensions of washed platelets containing ADP-scavengers. No prior shape change is found. In the presence of epinephrine, DiCg induces reversible aggregation and PdBu evokes irreversible aggregation that correlates with the effects, on protein phosphorylation. Epinephrine and UK 14304 neither induce nor enhance the phosphorylation of myosin light chain (20kDa), the substrate of protein kinase C (47kDa), or a 38kDa protein evoked by DiCg) or PdBu. Epinephrine does not cause, stimulation of phospholipase C as reflected by the production of inositol mono-, bis- and tris-phosphate or phosphatidic acid. Even under conditions of maximal aggregation induced by epinephrine plus PdBu, formation of 32p-phOSphatidic acid is not observed. The synergistic action of epinephrine and PdBu does not depend on extracellular Ca2+. Primary aggregation induced by epinephrine, but not platelet aggregation induced by PdBu plus epinephrine, is inhibited by high intracellular concentrations of the calcium chelator quin2. Prostacyclin prevents platelet aggregation but does not affect protein phosphorylation induced by PdBu plus epinephrine.The experiments indicate that α2-adrenoceptor agonists may induce primary aggregation by a mechanism involving release of membrane-bound Ca2+. The synergism with protein kinase C is, however, caused by a mechanism that occurs distally to protein phosphorylation and is not related to Phospholipase C activation and Ca2+-fluxes across the Dlasma membrane or in the cvtosol. Evidence is presented suoportina the view that this mechanism miqht be related to the dissociation of Gi caused by α2-adrenoceptor activation.
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Zhang, Nan, Amy T. Kan, and Mason B. Tomson. "Attchment/Release of Phosphonate to/from a CaCO3 Surface in Supersaturated Brines." In SPE International Oilfield Scale Conference and Exhibition. SPE, 2014. http://dx.doi.org/10.2118/spe-169772-ms.

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Abstract One of the most intractable concerns when engineers try to reuse the produced water as frac fluid in the Bakken and some other shale plays is the scale formation caused by the incompatibility of produced water with additives in the frac fluids and with the formation. In order to obtain a more efficient scale treatment for a successful hydraulic fracing that handles the extraordinary amount of water with high supersaturation level, the better understanding of inhibitor retention and release in the production system is urgent. To explore the mechanism of attachment/release of phosphonate to/from a mineral surface, calcite supersaturated feed solutions with different diethylenetriamine penta (DTPMP) concentrations were introduced into the steel tubing that was internally pre-coated with a thin layer of CaCO3. It is unveiled that DTPMP attachment was dominated by the precipitation of calcium phosphonate solid once the solution is supersaturated with Ca3H4DTPMP (pKsp=53.5), and the total amount of DTPMP attached on the calcite surface added up with the increasing supersaturation of Ca3H4DTPMP. The co-precipitation of CaCO3 and Ca3H4DTPMP has facilitated the attachment of the inhibitor with the increase of supersaturation of CaCO3. The retained phosphonate was released from the surface with a steady and low level inhibitor concentration over extended period of time. Combining with the kinetics of calcium carbonate precipitation in the presence of inhibitor, a 1500 gram of calcium phosphonate precipitation can protect the scaling for about 100 days (100 bbl/day) when the saturation index of calcium carbonate (SIcalcite) is as high as 1.3. The results provide a better understanding of calcium-phosphonate-carbonate interaction, and show the phosphonate inhibitor can continuously accumulate on the carbonate and slowly dissolve. We anticipate this study can shed a light on how much inhibitor can be delivered to the unconventional reservoir as well as the theoretical limitation of inhibitor return in the flowback water.
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WANG, XUEZHAO, RONG SHEN, WEIJIA WEN, and KUNQUAN LU. "HIGH PERFORMANCE CALCIUM TITANATE NANOPARTICAL ER FLUIDS." In Proceedings of the Ninth International Conference. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702197_0008.

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Reports on the topic "Calcium fluxes"

1

Dilley, R. A. (Calcium gating of proton fluxes in chloroplasts). Office of Scientific and Technical Information (OSTI), January 1991. http://dx.doi.org/10.2172/5618821.

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2

Dilley, R. (Calcium gated proton fluxes in energy transducing membranes). Office of Scientific and Technical Information (OSTI), December 1989. http://dx.doi.org/10.2172/7192297.

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Dilley, R. A. [Calcium gating of proton fluxes in chloroplasts]. Progress report, April 1989--April 1991. Office of Scientific and Technical Information (OSTI), December 1991. http://dx.doi.org/10.2172/10134843.

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4

McConkey, David J. Regulation of Calcium Fluxes and Apoptosis by BCL-2 Family Proteins in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada435122.

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5

McConkey, David J. Regulation of Calcium Fluxes and Apoptosis by BCL-2 Family Proteins in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada472063.

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