Dissertations / Theses on the topic 'Calcium'

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1

Poitras, Marc. "Mécanisme de régulation du Ca(2+) intracellulaire dans le cortex surrénalien bovin." Sherbrooke : Université de Sherbrooke, 1998.

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2

Chatterjee, Sabyasachi. "Calcite and Calcium Oxalate Sequestration of Heavy Metals." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/50093.

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Engineering
Ph.D.
Heavy metals like cadmium, lead and zinc pose a significant threat to human health and environment. Several factors such as pH, EH, organic matter and clay content of the soil affect the bioavailability of such heavy metals in the environment. The presence of several naturally occurring minerals such as calcite (calcium carbonate, CaCO3) and calcium oxalate (CaC2O4.) in the environment significantly influence the fate and transport of some of the heavy metal cations. Sequestration of heavy metals such as cadmium (Cd) and zinc (Zn) from solution by calcite has been clearly demonstrated in the literature. However, studies on heavy metal sequestration by calcite and calcium oxalate from a multi-metal environmental that represents real world situations are rare. In this contribution, column flow studies of Cd and Zn sequestration by calcite exposed to influent solutions saturated or non-saturated with calcite and containing either 1 mg/L of Cd, 1 mg/L of Zn or combined 1 mg/L of Zn and Cd, followed by desorption of the sequestered metals were conducted. Complementary scanning electron microscopy (SEM) coupled with electron dispersive x-ray spectroscopy (EDS) data were generated. Kinetic studies show that reaction rates of Cd and Zn with calcite are governed by a simple rate law with reaction orders of less than 1 (0.02 - 0.07) indicating at least mathematically, the occurrence of reactions that went to completion if the reaction orders did not change. When the influent solution contains a single cation, the rate of Zn removal from solution by calcite and calcium oxalate is greater than Cd removal rate. However in a multi-cation environment, cadmium removal rate was greater than zinc removal rate. MINTEQA2 a geochemical equilibrium speciation model was used to compute the equilibrium between the various species in the cation-calcite environment. Complimentary desorption studies and surface SEM/EDS analysis indicate that the removal of Cd and Zn from solution by calcite and calcium oxalate is probably due to precipitation/complexation reaction. The SEM and EDS results appear to confirm the presence of a precipitate on the mineral surface in the case of the influent solution containing Zn. The current research also examines the effect of citrate, a commonly present urinary tract species on calcium oxalate dissolution. The dissolution studies indicate that citrate solution is capable of dissolving sodium oxalate at high pH. The dissolution of calcium oxalate results in the release of heavy metals that were previously sequestered within the mineral. Results show that a greater percentage of zinc was removed than cadmium, from calcium oxalate due to its dissolution by citrate.
Temple University--Theses
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3

Roberts, Dewi. "Calcium-dependent inactivation of Cav1.3 calcium channels." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446186.

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4

Lee, Sui-Chen. "Calcium Equilibria in Calcium Fortified Milk Systems /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487934589974558.

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5

Stephens, Christopher James. "On the transformation of amorphous calcium carbonate into calcite." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534898.

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6

Gilchrist, James Stuart Charles. "Calcium regulation of calcium transport by sarcoplasmic reticulum." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30880.

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The sarcoplasmic reticulum (SR) of skeletal muscle is an intracellular membraneous network that, through the cyclical release and re-uptake of Ca²⁺ into and from, respectively, the cytoplasmic space, regulates myofilament shortening and, therefore, muscle contraction. SR derived from the terminal cisternae (HSR) demonstrates the property of Ca²⁺-induced Ca²⁺ release. Upon attainment of a threshold intralumenal Ca²⁺ load, application of a small pulse of extralumenal Ca²⁺ stimulates the release of a pool of intralumenal Ca²⁺ via the ligand gated Ca²⁺ permeable pore of the Ca²⁺ release channel/ryanodine receptor complex. It was hypothesised that intralumenal Ca²⁺ regulates the opening of the release channel. HSR vesicles were purified from skeletal and cardiac muscle by a novel technique. Structural characterisation of these membranes demonstrated an enrichment of harvested fractions in the Ca²⁺ release channel and the intralumenal Ca²⁺ binding protein, calsequestrin. In radiometric studies, skeletal HSR vesicles were shown to bind ryanodine with high capacity at both low and high affinity sites, with 2 fold stimulation of Ca²⁺ accumulation by the polyorganic cation Ca²⁺ channel blocker, ruthenium red. HSR vesicles passively loaded Ca²⁺. Passive loading of HSR vesicles with Ca²⁺ was found to be non-linearly dependent upon the concentration of Ca²⁺ within the loading medium. This suggested the presence of 2 intralumenal Ca²⁺ binding sites with different affinities for Ca²⁺. A spectroscopic dual-wavelength assay of Ca²⁺ release was developed that took advantage of peculiar spectral properties of the metallochromic sensitive dye Antipyrylazo III. In the presence of mM MgATP and mM Mg2+ the initial fast phase of HSR Ca²⁺ was well resolved. Evidence was presented that initial rapid uptake was associated with high affinity binding to an intralumenal compartment. Ca²⁺ -induced Caz+ release was shown to occur with a threshold loading of intralumenal Ca²⁺. The intralumenal Ca²⁺ threshold for Ca²⁺-induced Ca²⁺ release was decreased in the presence of ryanodine. Ryanodine induced Ca²⁺ release was also dependent upon the amount of intralumenal Ca²⁺. Ryanodine was also shown to inhibit sustained Ca²⁺-induced Ca²⁺ release by apparent inhibition of the binding of Ca²⁺ to intralumenal sites. These results suggested that junctional state transitions of the Ca²⁺ channel and calsequestrin were interdependent. Purified mM and mM Ca²⁺ activated neutral protease isoforms selectively cleaved the Ca²⁺ channel into 410 and 150kDa peptides with limited proteolysis. This was demonstrated in both HSR vesicles and the purified Ca²⁺ release channel. A novel 88kDa protein was also shown to be fragmented by both CANP isoforms. The identity of this prominent HSR associated protein remains obscure. CANP fragmentation of HSR protein elevated passive and active 4^Ca²⁺ loading in vesicles. This indicated that selective structural modification of the cytoplasmic portion of the release channel modified the comformational states of a intralumenal Ca²⁺ binding compartment in HSR vesicles. In spectroscopic studies, CANP proteolysis of HSR proteins increased the sensitivity to Ca²⁺ and ryanodine-induced Ca²⁺ release through decreases in the required intralumenal Ca²⁺ threshold for release. These functional alterations coincided with apparent single site cleavage of the release channel. Further proteolysis of the initial 410 and 150kDa peptides was without further significant effect upon function. Based upon the hypothesis that primary sequences rich in proline (P), glutamate (E), aspartate (D), serine (S) and threonine (T) (PEST regions) are recognition sites for CANP binding to substrates, a search for PEST regions within the Ca²⁺ channel was undertaken. It was tentatively proposed that two PEST regions near the N-terminal of the Caz release channel may represent sites close to the CANP cleavage site. The results of this work were discussed in relation to a possible role of Ca²⁺-induced Ca²⁺ release in regulating the patterning of Ca²⁺ cytosolic transients. The frequency and amplitude of cytosolic Ca²⁺ transients appear to be important in regulating protein expression. The requirement of intralumenal Ca²⁺-induced Ca²⁺ release may be a means by which the cyclical uptake and release of Ca²⁺ during muscle relaxation and contraction can be coordinated. This coordination may define the patterning of cytosolic Ca²⁺ transients. The increased sensitivity to Ca²⁺-induced Ca²⁺ release by HSR after CANP treatment may represent a means by which the patterning of cytosolic Ca²⁺ transients can be altered to effect changes in protein synthesis.
Graduate and Postdoctoral Studies
Graduate
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7

Harris, Nicole Andrea. "Rydberg spectroscopy of calcium monofluoride and calcium monochloride." Thesis, Massachusetts Institute of Technology, 1995. http://hdl.handle.net/1721.1/33539.

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8

Hailey, Rebecca Anne 1965. "Laser spectroscopy of calcium monohydroxide and calcium monodeuteroxide." Thesis, The University of Arizona, 1991. http://hdl.handle.net/10150/277856.

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CaOH and CaOD were studied in the gas phase using dye laser spectroscopy. The molecules were produced in a Broida-type oven. Laser excitation spectroscopy was used to study the Ḃ²Σ⁺-X²Σ⁺ transition of CaOD near 5500 Å. The 000-000 band was rotationally analyzed and r₀ structures were established for both states. Like other alkaline earth monohydroxides, CaOD is a linear molecule. For the Ḃ²Σ⁺ state the following bond lengths were found: r(Ca-O) = 1.9697Å and r(O-H) = 0.9179Å, while for the X²Σ⁺ state, r(Ca-O) = 1.9849 and r(O-H) = 0.9207Å. Optical-optical double resonance (OODR) was used to investigate the upper electronic states of CaOH. A ²Π electronic state and three ²Σ vibronic states were observed for the first time in the region 2990 - 3070 Å. For the ²Π state the rotational constant, B°, and the band origin energy, T₀, were calculated: B° = 0.347 cm⁻¹ and T = 32360 cm⁻¹.
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9

Altay, Esra Shahwan Talal R. A. "Effect of reaction conditions and organic additives on the morphologies of synthetic calcium carbonates/." [s.l.]: [s.n.], 2006. http://library.iyte.edu.tr/tezler/master/kimya/T000383.pdf.

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10

Dhulipala, Gangadhar. "Conformational dynamics associated with calcium binding to calcium transducers." FIU Digital Commons, 2010. http://digitalcommons.fiu.edu/etd/2794.

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The Ca2+ association to calcium binding proteins (CaBPs) represents an essential step in Ca2+ signal transduction. This study presents a characterization of Ca interactions with two CaBPs, calmodulin and DREAM, using time-resolved photothermal and fluorescence techniques. Calcium binding to the calmodulin C-terminal domain is associated with a volume change of 40 mL mol-1and an enthalpy change of 35 ± 16 kcal mol-1. These parameters are consistent with the Ca2+ triggered exposure of hydrophobic patches on the calmodulin surface. Also, the rate limiting step for Ca2+ binding to calmodulin is the closed-to-open transition of the C-terminal domain that occurs with a lifetime of 400 μs. Unlike calmodulin, DREAM exists in a dynamic equilibrium of two conformations and Ca2+ binding shifts the equilibrium towards a more compact conformation. These data clearly demonstrate that conformational dynamics play a crucial role in the transmission of Ca2+ signals.
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11

Southall, Tony David. "Calcium signalling and calcium pools in a Drosophila epithelium." Thesis, University of Glasgow, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439203.

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12

Sargeant, Paul. "Calcium signalling in human platelets : stored-regulated calcium entry." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318268.

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13

Thomas, Balbir. "A model of mitochonrial [sic] calcium induced calcium release." The Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1190053132.

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14

Latifzadeh, Lida 1956. "Raman spectroscopic studies of calcium-phosphate, aluminum metaphosphate-sodium fluoride and calcium metaphosphate-calcium fluoride glasses." Thesis, The University of Arizona, 1990. http://hdl.handle.net/10150/278549.

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The role of modifier on the molecular structure of Ca-phosphate, sodium fluorophosphate and sodium aluminophosphate glasses have been investigated by Raman spectroscopy. Ca-phosphate glasses for this study have the molar ratio of CaO/P₂O₅ from 1.00 to 1.50. Curve fitting procedures have been used to resolve the overlapped peaks for accurate interpretation. Amorphous species with varying chain lengths and two crystalline phases of γ- and α-Ca₂P₂O₇ have been identified. Sodium fluorophosphate glasses have been prepared from the reaction between Al(PO₃)₃ and NaF. The molar ratio of Na/P is varied from 0.900 to 2.00 and the F/P ratio is from 0.510 to 1.61. By studying the vibrational frequency shifts, species with varying phosphorus and fluorine contents and aluminophosphate compounds have been identified.
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15

Patel, Jitandrakumar Ramanbhai. "The kinetics of calcium-induced calcium release in the heart." Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294077.

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16

Swainsbury, David. "Decoding calcium spiking : the calcium ion-binding properties of CCaMK." Thesis, University of East Anglia, 2011. https://ueaeprints.uea.ac.uk/39151/.

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17

Farrington, Jasmine. "Calcium release activated calcium channels in human lung mast cells." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6609/.

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18

Beaurain-Buttez, Dominique. "Canaux calciques : agonistes et antagonistes." Lille 2, 1992. http://www.theses.fr/1992LIL2P003.

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19

Lowry, Austin William. "Calcium and hypertension." Thesis, Kansas State University, 1985. http://hdl.handle.net/2097/9866.

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20

Leroy, Pierre. "Calcium et corrosion." Paris 5, 1991. http://www.theses.fr/1991PA05P623.

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21

Houtkooper, Linda, and Vanessa A. Farrell. "Calcium Supplement Guidelines." College of Agriculture, University of Arizona (Tucson, AZ), 2017. http://hdl.handle.net/10150/625294.

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4 pp.
Calcium is an essential mineral found in great abundance in the body. Ninety-nine percent of all the calcium in the body is found in the bones and teeth. The remaining one percent is in the blood. Calcium plays important roles in nerve conduction, muscle contraction, and blood clotting. If calcium levels in the blood drop below normal, calcium will be taken from bone and put into the blood in order to maintain blood calcium levels. Therefore, it is important to consume enough calcium to maintain adequate blood and bone calcium levels. Revised 2017, Revised 2011, Original 2004
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22

Houtkooper, Linda, and Vanessa Farrell. "Calcium Supplement Guidelines." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2011. http://hdl.handle.net/10150/146429.

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23

Grignon, Sylvain. "Effets des drogues psychotropes sur les canaux calciques neuronaux : etude in vitro et perspectives therapeutiques." Aix-Marseille 2, 1990. http://www.theses.fr/1990AIX20953.

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24

BOUTARFA, SALIHA. "Une methode de mesure de l'absorption calcique chez les patients hemodialyses." Amiens, 1989. http://www.theses.fr/1989AMIEM024.

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25

Morris, Jennifer Toni. "The role of calcium stores in calcium signalling in human sperm." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5068/.

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Calcium (Ca\(^{2+}\)) signalling is implicated in the regulation of numerous sperm processes elemental for fertilisation including the acrosome reaction, hyperactivated motility (HA) and capacitation. A number of studies have identified components of Ca\(^{2+}\) storage organelles in human sperm, including inositol-1,4,5 triphosphate receptors IP3Rs, secretory pathway calcium ATPases (SPCA), ryanodine receptors (RyR) and the store operated calcium entry (SOCE) channels STIM and Orai, all of which are associated with the acrosome and posterior head/neck region of the sperm (PHN). In 2005, Herrick et al., characterised the Ca\(^{2+}\) storage capacity of mammalian acrosomes; however the identity of the PHN Ca\(^{2+}\) store is less clear. The aim of this study was to characterise the PHN Ca\(^{2+}\) store to determine the relationship between store mobilisation and HA in human sperm. We observed localisation of high Ca\(^{2+}\) at the PHN and midpiece of human sperm. Treatment with mitochondrial uncouplers CCCP and DNP elevated [Ca\(^{2+}\)]\(_i\) and depolarised the mitochondrial membrane potential (MMP) consistent with mobilisation of mitochondrial Ca\(^{2+}\) stores. However pre-treatment with mitochondrial uncouplers had no significant effect on the characteristic biphasic [Ca\(^{2+}\)]\(_i\) increase associated with progesterone. Conversely prior mobilisation of stored Ca\(^{2+}\) with thimerosal (IP3R activator) or pre-treatment with SKF-96365 (SOCE inhibitor) significantly reduced the sustained component of the biphasic [Ca\(^{2+}\)]\(_i\) response, whilst treatment with 2-APB or SKF (SOCE modulators) enhanced the progesterone induced [Ca\(^{2+}\)]\(_i\) transient. In addition treatment with novel Orai targeted bioportides results in a significant prolongation of the progesterone-induced [Ca\(^{2+}\)]\(_i\), apparently due to non-reversible SOCE activation, initiated during the transient. These results indicate the presence of at least two discrete Ca\(^{2+}\) stores at the PHN which contribute separately to the biphasic progesterone [Ca\(^{2+}\)]\(_i\) increase and a role for STIM/Orai mediated SOCE in both transient and sustained components of the progesterone-induced [Ca\(^{2+}\)]\(_i\) signal in human sperm.
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26

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
unrestricted
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27

Frye, Hannah. "Eggshell calcium regulates calcium transport protein expression in an oviparous snake." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/honors/237.

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One hypothesis explaining the numerous independent evolutionary transitions from oviparity to viviparity among squamates (snakes and lizards) proposed that squamate embryonic development is independent of eggshell calcium. Recent research showed at least 25% of the calcium in hatchling oviparous squamates is extracted from the shell. Though not a direct test, these results are inconsistent with the hypothesis. To directly test the hypothesis, we removed eggshell calcium (through peeling) early in development of Pantherophis guttatus (corn snake) eggs. Survivorship to hatching did not differ between peeled and intact eggs. Yet hatchlings from peeled eggs were shorter (273.6 ± 3.4 vs. 261.0 ± 3.7 mm, p=0.0028, n=16), lighter (6.36 ±0.22 vs. 5.75 ± 0.23 g, p=0.0158, n=16), and had reduced calcium (40.8 ± 1.7 vs. 30.5 ± 1.8 mg, p
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28

Wang, Fang. "DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?" Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/214814.

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Physiology
Ph.D.
Cardiovascular disease remains the number one cause or mortally in the western world. Heart failure is the most rapidly growing cardiovascular disease (Hobbs, 2004; Levy, et al., 2002). Heart failure, by definition, is progressive deteriorating function of the heart due to progressive cardiac myocytes loss. Though after decades of endeavor of searching the pathophysiology and treatments for heart failure, it remains highly lethal. Therefore, it is vital to find novel therapies to help treat such chronic disease. Replace the lost cardiomyocyte with new ones could restore cardiac function and reduce mortality. The purpose of this study is to investigate on how TTCCs (T-type calcium channels) affect cardiomyocyte proliferation. In mice after birth, the major TTCC expressed in the heart is Cav3.1/α1G, and therefore we used Cav3.1/α1G transgenic (TG), knockout (-/-) and wild type mice respectively to define the role of TTCC in cardiomyocyte proliferation. In neonatal mouse ventricular myocyte (NMVMs) right after birth, there is almost no TTCC after birth in α1G-/- NMVMs, whereas there are around 35% NMVMs in wild type (WT) show TTCC. On day 7 after birth, there are no T-type calcium currents in both α1G-/- NMVMs and WT NMVMs. Using BrdU, a DNA synthesis marker, we identified plenty of BrdU positive cardiomyocyte during the first seven days after birth. Cardiomyocyte is special due to its double nucleation property. Our cell cycle studies showed that there is significant difference in cell cycle distribution between α1G-/- and WT NMVMs on day seven after birth. Significantly more NMVMs are arrested in G1 phase in α1G-/-, compared to WT NMVMs. Even until 2 month old, there are still significantly more mono-nucleated cardiomyocyte in α1G-/- than in WT. In conclusion, all these evidence showed that blocking T-type calcium channel could partially prevent binucleation from happening and stop cardiomyocytes withdrawal from cell cycle. Mononucleated cardiomyocyte is still able to proliferate. Hence, mononucleated cardiomyocytes in adult still have potential to proliferation because these cardiomyoctes are arrested in their cell-cycle before their terminal differentiation, which could offer a novel approach for cardiac repair.
Temple University--Theses
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29

Zhang, Fengrui. "Digestibility of Calcium in Feed Ingredients and Digestible Calcium Requirements for Pigs." Thesis, Purdue University, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10635881.

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The objective of this research was to compare different expressions for the digestibility of Ca in both pigs and chickens, and to determine the true total tract digestible (TTTD) Ca requirement for 10- to 20-kg and 20- to 40-kg pigs.

In the first study, two experiments were conducted to compare apparent ileal digestibility (AID) and apparent total tract digestibility (ATTD) of Ca in pigs. In Exp. 1, three semi-purified diets with soybean meal, canola meal or sunflower meal as the sole source of Ca were formulated. Eighteen cannulated pigs (initial BW = 66 ± 5 kg) were assigned in a randomized complete block design to 3 treatments and 6 replicates per treatment. Results indicated that for either Ca or P, the ATTD was not different from AID in three diets. In Exp. 2, diets with four Ca concentrations were formulated with calcium carbonate as the Ca source. Sixteen cannulated pigs (initial BW = 73 ± 4 kg) were assigned in a randomized complete block design to 4 treatments in 2 experimental periods. The results indicated that the ATTD of Ca was not different from AID for all diets, and the Ca digestibility was not affected by the dietary Ca concentration. The results of these two experiments indicated that both AID and ATTD can be used to describe the digestibility of Ca for growing-finishing pigs. Total tract digestibility was used to express digestibility of Ca in later studies.

A second series of studies was conducted to decide whether ATTD or TTTD should be used to estimate Ca digestibility of limestone and dicalcium phosphate (DCP). Two pig experiments were conducted to determine the ATTD and TTTD of limestone and DCP, and their additivity in a semi-purified diet for pigs. In Exp. 1, forty eight barrows with an average initial BW of 19.2 ± 1.1 kg were assigned to 1 of 6 dietary treatments in a 2 × 3 factorial arrangement of two Ca sources, including limestone or DCP, with three dietary Ca concentrations each. Diets were fed for a 5-d adjustment period followed by a total collection period of 5 d. The results indicated that the increased dietary Ca concentration linearly increased Ca intake, digested and retained, but did not affect the ATTD of Ca when using limestone and DCP as Ca sources. In Exp. 2, seventy-two barrows with an average initial BW of 20.8 ± 1.3 kg were used to test the additivity of TTTD for Ca in limestone and dicalcium phosphate (DCP) in pigs. All pigs were assigned to 1 of 9 dietary treatments in a 3 × 3 factorial arrangement of three Ca sources, including limestone, DCP, or a mixed diet at a ratio of 1:1; and three dietary Ca concentrations. Feeding and sample collection procedures were as in Exp. 1. The results indicated that the average ATTD were 66.46, 70.34, and 69.32% for limestone, DCP, and their mixed diet, respectively. By regressing daily digested Ca against daily Ca intake, the TTTD of Ca was determined at 70.06, 76.42, and 73.72% for limestone, DCP, and their mixed diet, respectively. The endogenous losses of was estimated to be between 0.217 to 0.321 g/kg DM intake. The predicted TTTD for Ca in the mixed diet of limestone and DCP was calculated to be 72.67% based upon the Ca contribution coefficient of 0.59 for limestone and 0.41 for DCP. The predicted Ca TTTD (72.67%) in the mixed diet was not statistically different from the determined Ca TTTD (73.72%). It is concluded that although ATTD of limestone and DCP were not affected by the Ca concentration in the diet, TTTD is recommended for evaluation of Ca digestibility because of its additivity in a mixed diet.

A similar additivity experiment was conducted on Ross 708 broiler chickens from d 22 to d 27 post hatch, using true ileal digestibility (TID) for Ca in limestone and dicalcium phosphate (DCP). The birds were fed a standard broiler starter diet from d 1 to 11 post hatching. A total of 504 birds were grouped in a 3 × 3 factorial arrangement of 3 Ca sources including limestone, DCP, and their mixed diet at a ratio of 1:1, and 3 dietary Ca concentration at 3.3, 4.3, and 5.3 g/kg. The results showed that by regressing digested Ca per bird against Ca intake per bird, the TID of Ca was determined at 63.73, 67.14, and 67.79% for limestone, DCP, and the mixed diet, respectively. (Abstract shortened by ProQuest.)

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30

Sher, Anna. "Modelling local calcium dynamics and the sodium/calcium exchanger in ventricular myocytes." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670114.

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31

Jacques, Daniel Jean. "Calcium uptake and translocation effects upon localized calcium deficiency symptoms in poinsettias /." The Ohio State University, 1988. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487592050230111.

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32

Canabady-Rochelle, Laëtitia. "Équilibre en calcium dans les systèmes lactés - Étude des interactions calcium-protéines." Thesis, Vandoeuvre-les-Nancy, INPL, 2008. http://www.theses.fr/2008INPL016N.

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Les équilibres en calcium (Ca) entre la phase soluble et la phase colloïdale ont été étudiés dans des systèmes lactés (laits de vache, de soja Hydrolysé ou Non-Hydrolysé). La supplémentation en Ca (CaCl2, CC, 25 mmoles.kg-1) a été suivie d’un cycle de pH (pHmin 5,5 ou 3,5). Le pH, la concentration en calcium ionisé (Ca2+), la turbidité et la viscosité apparente ont été reliés aux variations de la phase protéique. La concentration en Ca2+, initialement négligeable dans le lait de soja, augmente avec l’addition en Ca, ainsi qu’avec l’acidification et diminue lors de l’alcalinisation. Pour le lait de vache non supplémenté, le cycle de pH à 5,5 n’est réversible ni sur les variations en Ca2+, ni sur les variations de la phase protéique, contrairement au lait de vache supplémenté en Ca. Ceci pourrait être dû à la capture préalable en Ca, entraînant un renforcement des micelles de caséines. Pour des cycles de pH à 5,5, l’agrégation induite par l’acidification est partiellement ou complètement réversible lors de l’alcalinisation pour les laits de soja NH et H, mais l’agrégation induite par le Ca est irréversible. Quelque soit le système, des phénomènes sont irréversibles lors de cycle de pH à 3,5. Les interactions Ca-protéines (de vache ou de soja) étudiées par CTI montrent des signaux endothermiques similaires, probablement dû au relargage de molécules d’eau. La liaison du Ca pourrait être décrite comme un échange H+/Ca2+ étant donné les force électrostatiques impliquées. Les sites de fixation du Ca on été identifiés par IR-TF. L’énergie d’absorption diminue dans les région amides I et II et dans la région carboxylate lors de l’addition de Ca
Ca equilibrium between soluble and colloidal phases was studied in milky systems (milk, Non Hydrolysed, NH, or Hydrolysed, H, soy milks). Calcium chloride supplementation (CC, 25 mmoles.kg-1) was followed by pH cycle (pHmin 5.5 or 3.5). pH, Ca2+, turbidity and apparent viscosity were recorded in situ. Ca equilibria were related to protein phase variations. Contrarily to milk, Ca2+ concentration was initially negligible in soy milks. Yet, whatever the milky system, Ca2+ increased upon CC addition and with acidification, and decreased during alkalinization. For reference milk, pH cycle to 5.5 was reversible neither on Ca2+ variations nor on protein phase contrarily to CC-milk. This could be due to the previous capture of Ca during supplementation, involving casein micelles reinforcement through Ca-protein interactions. For pH cycle to 5.5, acid-induced aggregation was partially and completely reversible upon alkalinization for NH and H-soy milks, respectively. Once CC addition, Ca-induced aggregation was irreversible and pH cycle had minor effects. Whatever the system, the irreversibility of phenomena was observed for pH cycle to 3.5. Ca-(milk or soy) protein interactions studied by ITC showed similar endothermic signals, probably due to the water release occurring upon interaction. Ca binding should rather be described as H+/Ca2+ exchange with respect to the electrostatic forces involved. Finally, Ca-binding sites were identified with FTIR spectroscopy. A decrease of the absorption energy in the amide I and II region and in the carboxylate region occurred upon CC-addition, with higher variations in soy milks
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33

Canabady-Rochelle, Latha-Selvi Desobry-Banon Sylvie Sanchez Christian. "Équilibre en calcium dans les systèmes lactés - Étude des interactions calcium-protéines." S. l. : S. n, 2008. http://www.scd.inpl-nancy.fr/theses/2008_CANABADY-ROCHELLE_L_S.pdf.

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34

Horn, Johanna. "Calcium antagonists in stroke." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/58263.

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35

Lawson, Alison C. "Collagen-calcium phosphate composites." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300895.

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36

Melford, Steven K. "Calcium signalling in megakaryocytes." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364104.

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37

Lindqvist, Susanne. "Colonic crypt calcium signalling." Thesis, University of East Anglia, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327537.

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38

Jai-Yoon, Sul. "Calcium signalling in astrocytes." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391921.

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39

Guery, Christine. "Le calcium et l'hypertension." Paris 5, 1988. http://www.theses.fr/1988PA05P212.

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40

Симоненко, Наталія Олександрівна, Наталия Александровна Симоненко, Nataliia Oleksandrivna Symonenko, and A. Borodenko. "Calcium, aspirin and cancer." Thesis, Вид-во СумДУ, 2009. http://essuir.sumdu.edu.ua/handle/123456789/16783.

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41

Andac, Omer. "Calcium sulfoaluminate based cements." Thesis, University of Aberdeen, 1996. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602277.

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Knowledge of energy requirements, solid solutions and phase compatibilities of high temperature cement phases is essential to the economics and performance of cement clinkers. Both chemical engineering and chemical approaches have been used to determine phase compatibilities and solid solutions of calcium sulfoaluminate, C4A3 S, C3S and C2S as well as to develop a new type of cement based on calcium monosulfoaluminate, C4A3S, tricalcium silicate, C3S, and dicalcium silicate, C2S. Investigation of solid solutions, substitution mechanisms and phase compatibilities of C4A3S, C3S and C2S form the basis of this thesis, and the subject is addressed as follows: (i) Investigation of the structures, solid solutions, phase compatibilities, polymorphism and stabilisation of C4A3S (literature review, theoretical and experimental research). This research discloses the existence of a high temperature polymorph (a) of C4A3S. It can be stabilised to ambient temperature by Fe or Na-Si coupled substitution. Limits of Na, Fe, Si and P solubilities in the C4A3S structure were investigated. When limits of Na2O or NaF in C4A3S solid solutions (~3%) is exceeded, C4A3S becomes unstable as a result of Na2SO4 or Na2Ca(SO4)2 formation. C4A3S is compatible with C2S, with CaO, with C3A, with C12A7, with CA, with CA2, with Al2O3, with C2AS and with Ca3(PO4)2 at 1300 C. (ii) Investigation of the microstructure and microchemistry of commercial calcium sulfoaluminate cement (literature review, theoretical and experimental research). Because of extensive A1 and S substitution, a large Si deficiency can occur in C2S solid solutions. The open structured texture of calcium sulfoaluminate cement explains why it is easily ground. (iii) Investigation of A1 and sulfur substitution into C2S solid solutions (literature review, theoretical and experimental research). A1 and S substitute into C2S by several mechanisms, the most important of which are 2A1+S for 3Si and Ca+S for 2Ca+Si. (iv) Investigation of the NaF-CaO-SiO2 phase equilibria and its resultant effect on C3S formation (literature review, theoretical and experimental research). This investigation revealed that NaF not only acts as flux but mainly it has a mineralising effect on C3S formation and results in extensive solid solutions, NaxCa3.xSiO5.xFx. C3Sss, can be obtained as low as ~1000 C in the presence of NaF. In the course of this study, I phase, structurally similar to that of 9 C3S but consisting of 15 and 24 layer variants, has been characterised. (v) Investigation of the NaF-CaO-Al2O3-SiO2-SO3 system and its resultant effect on both C3S and C4A3S formation. Cement based on C3Sss and C4A3S can be made at ~1300 C if F and SO3 concentrations in the raw materials are controlled. SO3 in excess relative to that required for the formation of C4A3S should be added to inhibit C11A7.CaF2 and C3A formation. In the course of this study, large amount of Si deficiency in the C2S structure, such as that of belite in commercial calcium sulfoaluminate cement (as a result of 2A1+S for 3Si substitution), has been found.
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42

Farrell, Vanessa A. "Calcium: A Simple Guide." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2011. http://hdl.handle.net/10150/146446.

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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.
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43

Skupin, Alexander. "How does Calcium oscillate?" Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15969.

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Kalzium ist ein wichtiger intrazelluläre Botenstoff, der extrazelluläre Signale in zelluläre Antworten übersetzt. Oft werden externen Signale in wiederholte Anstiege der zytosolischen Kalziumkonzentration übersetzt, die als Oszillationen bezeichnet werden. Diese interdisziplinäre Arbeit kombiniert biologische Experimente, analytische Methoden der theoretischen Physik und Computersimulationen, um den Oszillationsmechanismus zu charakterisieren. Von wesentlicher Bedeutung ist dabei die räumlich inhomogene Verteilung der Kanäle, die Kanalcluster bilden. Dies induziert zusammen mit Pumpen große Konzentrationsgradienten in der Nähe von offenen Clustern, was zu einer hierarchischen Organisation führt. Unter diesem Gesichtspunkt erwartet man, dass Kalziumoszillationen stochastisch sind und auf räumlicher Wechselwirkung beruhen. Diese Hypothese wird im ersten Teil der Arbeit experimentell verifiziert, indem Oszillationen vier verschiedener Zellarten analysiert werden. Der Kalziumsignalweg nutzt thermisches Rauschen konstruktiv um globale Signale zu bilden. Dabei werden molekulare Fluktuationen durch die hierarchische Struktur auf die zelluläre Ebene gehoben. Dies steht im Gegensatz zu der jahrzehntelang weitläufigen Auffassung, dass Kalzium ein repräsentatives Beispiel eines zellulären Oszillators ist. Des weiteren macht dieses Ergebnis Kalzium zu einem ersten natürlichen Beispiel für "array enhanced coherent resonance". Im Modellierungsteil dieser Arbeit wird ein physiologisches Modell für die intrazelluläre Kalziumdynamik entwickelt, das die dreidimensionale Struktur von Zellen berücksichtigt. Es verwendet ein detailliertes Kanalmodell und berücksichtigt sowohl Diffusion als auch Reaktionen mit Puffern. Der entwickelte parallele Green''s cell Algorithmus generiert in Abhängigkeit von physiologischen Parametern das gesamte Spektrum der experimentell bekannten Kalziumsignale und spiegelt die experimentellen Daten des ersten Teils in nahezu perfekter Weise wider.
Calcium is an important second messenger in cells serving as a critical link between extracellular stimuli and their cellular responses. The external signals are translated often into repeated increases of the cytosolic calcium concentration what is referred as oscillations. This work uses an interdisciplinary approach combining experimental techniques from biology, analytical tools from theoretical physics and computer simulations to clarify the question of the oscillation mechanism and how cells can generate globally coordinated calcium signals originated from local stochastic channel dynamics. In this context, the spatial inhomogeneous distribution of channels forming channel clusters plays a key role. Together with calcium pumps and buffers, this induces huge functional concentration gradients close to open clusters, leading to a hierarchical organization of calcium signals. Thus, calcium oscillations are predicted to be stochastic and to have a spatial character. This hypothesis is justified experimentally in the first part of this thesis by analyzing calcium oscillations of four different cell types. Hence, calcium signaling constructively uses thermal noise to build global signals. This contradicts the current opinion of the last decades of calcium being a representative cellular oscillator. Moreover, this makes calcium a first natural example of array enhanced coherent resonance. In the modeling part of this work, a physiological model for intracellular calcium dynamics in three spatial dimensions is developed that takes the spatial arrangement of cells seriously. It uses a detailed channel model for the discrete release sites and takes into account diffusion and buffer interaction of calcium. In dependence on physiologic parameters, the developed parallel Green''s cell algorithm generates in a natural way the whole spectrum of experimentally known calcium signals and fits the experimental data of the first part in an almost perfect manner.
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44

Overend, Catherine Louise. "The effect of modulating calcium-induced calcium release on the properties of spontaneous and systolic calcium release in rat ventricular myocytes." Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366686.

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The effects of modulation of CICR on spontaneous and systolic Ca2+ release were investigated in isolated rat ventricular myocytes. Spontaneous waves of Ca2 + release were initially abolished and then resumed at a lower frequency during exposure to 100 J.LMtetracaine. Both the duration of the initial quiescent period and oscillation frequency in tetracaine were dependent on the control oscillation frequency and the concentration of tetracaine applied. Electrophysiological quantification of the SR Ca2+ content of myocytes revealed a significant increase during exposure to tetracaine. The amplitude of spontaneous Ca2 + release was also increased such that despite decreased frequency, efflux per unit time activated by Ca2+ waves was not changed significantly. Using confocal microscopy, the spatial and temporal properties of Ca2+ waves were studied revealing that tetracaine inhibits the propagation of Ca2 + release. The increased SR Ca2+ content and the increased amplitude of Ca2+ release can reverse this effect. Application of 100 J.LMtetracaine to electrically stimulated cells transiently depressed systolic Ca2+ release and contraction but had no effect in the steady state. Removal of tetracaine was associated with potentiation of systolic Ca2+ release followed by gradual recove~. Quantification of the SR Ca2+ content revealed that in tetracaine the SR Ca + content was significantly increased in the steady state. This increase was accounted for by inhibition of systolic Ca2+ release activating less Ca2+ efflux in the presence of the same or increased Ca2+ influx on the L-type Ca2+ current. As the SR Ca2+ content increases, more efflux is activated until eventually efflux and influx balance in the steady state. The transient potentiation of contraction on removal of tetracaine is due to the increased SR Ca2 + content, which increases the gain of CICR in the absence of inhibition of Ca2 + release. The mechanism of post rest potentiation in rat cardiac tissue has not been conclusively elucidated by previous studies. This investigation provides evidence that changes in SR Ca2 + content and recovery of channels from inactivation could contribute to the potentiation of contraction observed in rat ventricle after a period of rest. Tetracaine enhances the degree of potentiation of contraction, which can only partially be attributed to its ability to enhance SR Ca2+ accumulation. During myocardial ischaemia dramatic changes in the substrate and metabolite levels in cells occur and a number of these changes are known to affect the RyR. However, the overall effects of metabolic blockade on the sensitivity CICR in intact cells have been overlooked. Experiments were carried out to investigate the effect of metabolic inhibition on spontaneous Ca2+ release and SR Ca2+ content in isolated rat ventricular myocytes. The results show that CICR is inhibited during metabolic inhibition. This could contribute to the degree of damaging and potentially fatal Ca2+ overload experienced on reperfusion of ischaemic tissue.
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45

Yassine, Maya. "Calcium, Calcium-permeable channels and autophagy modulators in control of autophagy and cancer." Thesis, Lille 1, 2013. http://www.theses.fr/2013LIL10159/document.

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L'autophagie est une voie cellulaire strictement régulée dont le but principal est la dégradation lysosomale et le recyclage ultérieur du matériel cytoplasmique afin de maintenir l'homéostasie cellulaire normale. Des défauts dans l'autophagie sont liés à une variété d'états pathologiques, dont le cancer. Le cancer est une maladie associée aux modifications des processus cellulaires fondamentaux tels que l'apoptose et l'autophagie. Le calcium régule une série de processus physiologiques et pathologiques tels que le vieillissement, la neurodégénérescence et le cancer. Si le rôle du calcium et des canaux calciques dans le cancer est bien établi, l'information sur la nature moléculaire des canaux régulant l’autophagie ainsi que les mécanismes de cette régulation reste encore limitée. Le rôle de l'autophagie dans le cancer est complexe. En effet, elle peut favoriser à la fois la prévention tumorale et la résistance aux traitements. Elle est souvent détectée dans les cellules cancéreuses en réponse aux expositions aux rayons et la chimiothérapie. Elle semble contribuer à la résistance thérapeutique de certains cancers. Il est maintenant bien établi que sa modulation peut potentiellement contribuer à la mise en œuvre des méthodes de traitement du cancer. Dans cette étude, nos travaux ont permis d’identifier le calcium intracellulaire, comme un régulateur important de l'autophagie. Ainsi, nous proposons un lien possible entre le calcium, les canaux calciques, l’autophagie et la progression du cancer. De plus, nous avons mis en évidence un nouveau modulateur de l’autophagie, le ML-9. Cet outil pourrait cibler l'autophagie et être utilise dans le traitement des cancers
Autophagy is a tightly regulated cellular pathway the main purpose of which islysosomal degradation and subsequent recycling of cytoplasmic material to maintain normal cellular homeostasis. Defects in autophagy are linked to a variety of pathological states,including cancer. Cancer is the disease associated with abnormal tissue growth following an alteration in such fundamental cellular processes as apoptosis, proliferation, differentiation,migration and autophagy. Calcium is a ubiquitous secondary messenger which regulates plethora of physiological and pathological processes such as aging, neurodegeneration and cancer. The role of calcium and calcium-permeable channels in cancer is well-established, whereas theinformation about molecular nature of channels regulating autophagy and the mechanisms of this regulation is still limited. The role of autophagy in cancer is complex, as it can promoteboth tumor prevention and survival/treatment resistance. Elevated autophagy is often detected in cancer cells in response to radiation and chemotherapy. Furthermore, autophagy seems to contribute to the therapeutic resistance of some cancers. It's now clear that modulation of autophagy has a great potential in cancer diagnosis and treatment. Our findings identified intracellular calcium as an important regulator of autophagy. We propose a possible link between calcium, calcium permeable ion channels, autopohagy and cancer progression. Further, our results revealed a new autophagy modulator ML-9 as an attractive tool for targeting autophagy in cancer therapy
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46

Gelli, Angie Cristina. "The electrophysiological characterization of plant calcium channels and their role in calcium signaling." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0007/NQ27928.pdf.

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47

Hagen, Brian M. "Regulation of calcium-activated potassium channels by localized calcium transients in murine colon." abstract and full text PDF (free order & download UNR users only), 2005. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3209955.

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48

Lagnado, Leon. "Electrogenic sodium-calcium exchange and the regulation of free calcium in vertebrate photoreceptors." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303119.

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49

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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50

Ayar, Ahmet. "An investigation of calcium-induced calcium-release (CICR) in cultured rat sensory neurones." Thesis, University of Aberdeen, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285521.

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In this study the mechanisms of Ca2+-induced-Ca2+-release, effects of membrane depolarizations and the actions of pharmacological intracellular Ca2+-modulators were examined in cultured rat dorsal root ganglion (DRG) neurones. The whole cell configuration of the patch clamp technique was used to record action potentials, action potential after-potentials and voltage-activated calcium currents, (ICa), calcium-activated chloride currents, (ICI(Ca)), and non-selective cation currents, (ICAN), under current and voltage clamp recording conditions, respectively. A sub population of DRG neurones expressed action potential after-depolarizations and ICI(Ca) tail currents which were due to activation of Ca2+-activated Cl- channels as a result of Ca2+ entry. ICAN was dominantly activated due to Ca2+ release from intracellular stores evoked by pharmacological Ca2+-releasing agents such as caffeine, ryanodine and dihydrosphingosine. Calcium-activated conductances were identified by estimating reversal potentials of the activated currents, using selective pharmacological blockers and extracellular ionic replacement studies. Calcium-dependence of activated currents was also examined by using high concentration of intracellular Ca2+ buffer, EGTA, to prevent elevation of intracellular Ca2+-levels and by rapidly buffering raised intracellular Ca2+ using intracellular 'caged Ca2+ chelator', diazo-2. The involvement of intracellular Ca2+- stores was examined by performing experiments in Ca2+-free extracellular recording medium and pharmacologically inhibiting release of Ca2+ from intracellular stores, using dantrolene. Ryanodine had complex actions on DRG neurones, which reflected its ability to mobilize Ca2+, deplete Ca2+ stores, and inhibit Ca2+ release channels. Ryanodine inhibited action potential after-depolarizations and ICI(Ca) tail currents by interacting with intracellular stores and preventing amplification of Ca2+ signalling by CICR. It was found that CICR observed under physiological conditions in rat DRG neurones involves intracellular Ca2+ stores which were sensitive to ryanodine. In addition to ryanodine sensitivity these intracellular Ca2+ stores could be mobilized by caffeine and dihydrosphingosine.
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