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Journal articles on the topic 'Calcium fluxes'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Bruno, Luciana, Guillermo Solovey, Alejandra C. Ventura, Sheila Dargan, and Silvina Ponce Dawson. "Quantifying calcium fluxes underlying calcium puffs in Xenopus laevis oocytes." Cell Calcium 47, no. 3 (March 2010): 273–86. http://dx.doi.org/10.1016/j.ceca.2009.12.012.

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12

Sneyd, J., K. Tsaneva-Atanasova, D. I. Yule, J. L. Thompson, and T. J. Shuttleworth. "Control of calcium oscillations by membrane fluxes." Proceedings of the National Academy of Sciences 101, no. 5 (January 20, 2004): 1392–96. http://dx.doi.org/10.1073/pnas.0303472101.

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13

Serres, C., J. Yang, and P. Jouannet. "RU486 and Calcium Fluxes in Human Spermatozoa." Biochemical and Biophysical Research Communications 204, no. 3 (November 1994): 1009–15. http://dx.doi.org/10.1006/bbrc.1994.2563.

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14

Nilius, B. "Regulation of Transmembrane Calcium Fluxes in Endothelium." Physiology 6, no. 3 (June 1, 1991): 110–14. http://dx.doi.org/10.1152/physiologyonline.1991.6.3.110.

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Endothelial cells form and secrete mediators that modulate tone of underlying smooth muscle. The signal for their release or synthesis is increased intracellular Ca activity resulting from intracellular Ca release and transmembrane Ca fluxes. Ca influx can occur via different Ca-permeable ion channels, including Ca-activated K channels.

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15

Fournier, N., G. Ducet, and A. Crevat. "Action of cyclosporine on mitochondrial calcium fluxes." Journal of Bioenergetics and Biomembranes 19, no. 3 (June 1987): 297–303. http://dx.doi.org/10.1007/bf00762419.

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16

Mockel, J., C. Delcroix, F. Rodesch, and J. E. Dumont. "Regulation of calcium fluxes in the thyroid." Molecular and Cellular Endocrinology 51, no. 1-2 (May 1987): 95–104. http://dx.doi.org/10.1016/0303-7207(87)90123-7.

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17

Reiss, Michael, Lewis R. Lipsey, and Zhao-Ling Zhou. "Extracellular calcium-dependent regulation of transmembrane calcium fluxes in murine keratinocytes." Journal of Cellular Physiology 147, no. 2 (May 1991): 281–91. http://dx.doi.org/10.1002/jcp.1041470213.

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18

Moreau, Robert, Lucie Simoneau, and Julie Lafond. "Calcium fluxes in human trophoblast (BeWo) cells: Calcium channels, calcium-ATPase, and sodium-calcium exchanger expression." Molecular Reproduction and Development 64, no. 2 (December 24, 2002): 189–98. http://dx.doi.org/10.1002/mrd.10247.

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19

Holder, Anthony A., Mohd A. Mohd Ridzuan, and Judith L. Green. "Calcium dependent protein kinase 1 and calcium fluxes in the malaria parasite." Microbes and Infection 14, no. 10 (August 2012): 825–30. http://dx.doi.org/10.1016/j.micinf.2012.04.006.

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20

Ghosh, Santibrata, Hea-Young Kim, and Nirmalendu Das. "Cerebral calcium fluxes and calcium homeostasis in the rat: A minimal model." Neurological Research 19, no. 4 (August 1997): 403–8. http://dx.doi.org/10.1080/01616412.1997.11740833.

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21

Juška, Alfonsas, Pedro C. Redondo, Juan A. Rosado, and Ginés M. Salido. "Dynamics of calcium fluxes in human platelets assessed in calcium-free medium." Biochemical and Biophysical Research Communications 334, no. 3 (September 2005): 779–86. http://dx.doi.org/10.1016/j.bbrc.2005.07.040.

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22

Chambers, Chris, Fiona Smith, Christine Williams, Sandra Marcos, Zhen Liu, Paul Hayter, Giuseppe Ciaramella, Wilma Keighley, Phil Gribbon, and Andreas Sewing. "Measuring Intracellular Calcium Fluxes in High Throughput Mode." Combinatorial Chemistry & High Throughput Screening 6, no. 4 (June 1, 2003): 355–62. http://dx.doi.org/10.2174/138620703106298446.

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23

de Mattia, Fabrizio, Caroline Gubser, Michiel M. T. van Dommelen, Henk-Jan Visch, Felix Distelmaier, Antonio Postigo, Tomas Luyten, et al. "Human Golgi Antiapoptotic Protein Modulates Intracellular Calcium Fluxes." Molecular Biology of the Cell 20, no. 16 (August 15, 2009): 3638–45. http://dx.doi.org/10.1091/mbc.e09-05-0385.

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Golgi antiapoptotic protein (GAAP) is a novel regulator of cell death that is highly conserved in eukaryotes and present in some poxviruses, but its molecular mechanism is unknown. Given that alterations in intracellular Ca2+ homeostasis play an important role in determining cell sensitivity to apoptosis, we investigated if GAAP affected Ca2+ signaling. Overexpression of human (h)-GAAP suppressed staurosporine-induced, capacitative Ca2+ influx from the extracellular space. In addition, it reduced histamine-induced Ca2+ release from intracellular stores through inositol trisphosphate receptors. h-GAAP not only decreased the magnitude of the histamine-induced Ca2+ fluxes from stores to cytosol and mitochondrial matrices, but it also reduced the induction and frequency of oscillatory changes in cytosolic Ca2+. Overexpression of h-GAAP lowered the Ca2+ content of the intracellular stores and decreased the efficacy of IP3, providing possible explanations for the observed results. Opposite effects were obtained when h-GAAP was knocked down by siRNA. Thus, our data demonstrate that h-GAAP modulates intracellular Ca2+ fluxes induced by both physiological and apoptotic stimuli.

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24

Grasso, A., and A. Mastrogiacomo. "Î±-Latrotoxin: preparation and effects on calcium fluxes." FEMS Microbiology Letters 105, no. 1-3 (September 1992): 131–37. http://dx.doi.org/10.1111/j.1574-6968.1992.tb05895.x.

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25

Hartung, Hans-Peter. "Calcium fluxes and calmodulin inhibitors in macrophage activation." Cellular Immunology 100, no. 2 (July 1986): 586. http://dx.doi.org/10.1016/0008-8749(86)90058-4.

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26

Grasso, A. "α-Latrotoxin: preparation and effects on calcium fluxes." FEMS Microbiology Letters 105, no. 1-3 (September 1992): 131–37. http://dx.doi.org/10.1016/0378-1097(92)90083-z.

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27

Demaurex, Nicolas, Damon Poburko, and Maud Frieden. "Regulation of plasma membrane calcium fluxes by mitochondria." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1787, no. 11 (November 2009): 1383–94. http://dx.doi.org/10.1016/j.bbabio.2008.12.012.

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28

Simeone, Diane M., Beth C. Kimball, and Michael W. Mulholland. "Bombesin-mediated calcium fluxes in myenteric plexus neurons." Peptides 16, no. 7 (January 1995): 1307–11. http://dx.doi.org/10.1016/0196-9781(95)02021-n.

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29

Perry, S. F., and G. Flik. "Characterization of branchial transepithelial calcium fluxes in freshwater trout, Salmo gairdneri." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 3 (March 1, 1988): R491—R498. http://dx.doi.org/10.1152/ajpregu.1988.254.3.r491.

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Experiments were performed to determine whether gill transepithelial calcium fluxes in the freshwater trout (Salmo gairdneri) are passive or require active transport and to characterize the mechanisms involved. A comparison of the in vivo unidirectional flux ratios with the flux ratios calculated according to the transepithelial electrochemical gradients revealed that calcium uptake from the water requires active transport of Ca2+. The inhibition of calcium uptake by external lanthanum, the specific deposition of lanthanum on the apical surface of chloride cells, and the favorable electrochemical gradient for calcium across the apical membrane suggest that the initial step in branchial calcium uptake is the passive entry of calcium into the cytosol of chloride cells through apical channels that are permeable to calcium. The study of gill basolateral plasma membrane vesicles demonstrated the existence of a high-affinity calmodulin-dependent calcium-transporting system [half-maximal Ca2+ concentration (K0.5) = 160 nM, Vmax = 1.86 nmol.min-1.mg protein-1]. This system actively transports calcium from the cytosol of chloride cells into the plasma against a sizeable electrochemical gradient, thereby completing the transepithelial uptake of calcium. Calcium efflux occurs passively through paracellular pathways between chloride cells and adjacent pavement cells or between neighboring pavement cells.

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30

Grunze, H. C. R., J. Langosch, C. Normann, D. Rujescu, B. Amann, and J. Waiden. "Dysregulation of ion fluxes in bipolar affective disorder." Acta Neuropsychiatrica 12, no. 3 (September 2000): 81–85. http://dx.doi.org/10.1017/s0924270800035468.

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ABSTRACTBipolar disorder has attracted numerous research from different neurobiological angles. This review will summarize selected findings focusing on the role of disturbed transmem-braneous ion fluxes. Several mood stabilizers exhibit a distinct profile including effects on sodium, calcium and potassium conductance. In summary, some decisive mechanisms of action as calcium antagonism and modulation of potassium currents may play a crucial role in the success of any given mood stabilizer in bipolar disorder.

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31

Schmitt, Anne-Désirée, François Chabaux, and Peter Stille. "The calcium riverine and hydrothermal isotopic fluxes and the oceanic calcium mass balance." Earth and Planetary Science Letters 213, no. 3-4 (August 2003): 503–18. http://dx.doi.org/10.1016/s0012-821x(03)00341-8.

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32

Gold, G. H. "Plasma membrane calcium fluxes in intact rods are inconsistent with the "calcium hypothesis"." Proceedings of the National Academy of Sciences 83, no. 4 (February 1, 1986): 1150–54. http://dx.doi.org/10.1073/pnas.83.4.1150.

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33

Wadhwani, K. C., H. Levitan, and S. I. Rapoport. "Calcium diffusion through perineurium of frog sciatic nerve." American Journal of Physiology-Cell Physiology 254, no. 1 (January 1, 1988): C141—C149. http://dx.doi.org/10.1152/ajpcell.1988.254.1.c141.

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Calcium and sucrose permeabilities (PCa or Psucrose) were calculated from the fluxes of 45Ca and [3H]sucrose across perfused everted and normal configurations of the perineurial cylinder isolated from the frog sciatic nerve and from fluxes into an intact nerve segment bathed in Ringer. Mean PCa for influx across the isolated perineurium equaled 10.2 +/- 0.6 X 10(-7) cm/s (n = 16) compared with Psucrose = 7.4 +/- 0.4 X 10(-7) cm/s. For efflux, PCa = 27.5 +/- 5.0 X 10(-7) cm/s and Psucrose = 23.2 +/- 4.7 X 10(-7) cm/s. The mean ratio of PCa for efflux to PCa for influx (2.7 +/- 0.5) was not significantly different from the flux ratio for sucrose (3.1 +/- 0.7). No effect on PCa or Psucrose was observed when the calcium concentration in the bath was varied from 0.5 to 20 mM, when Na-free Ringer was perfused, or when ouabain, La3+, or 2,4-dinitrophenol was applied. Asymmetrical fluxes across the perineurial cylinder were due presumably to bulk flow and resultant solvent drag out of the lumen caused by perfusion pressure. Calcium accumulated in the perineurial tissue in a saturable manner with a Km of 80 microM and a Bmax of 0.22 mumol/g wet wt. The half time for calcium exchange from the external medium to the nerve was calculated as 3 h. This long half time and the calcium-sequestering ability of the perineurium suggest that the perineurium can stabilize endoneurial calcium during transient changes in the calcium concentration of plasma.

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34

Marshall, W. S., S. E. Bryson, and C. M. Wood. "Calcium transport by isolated skin of rainbow trout." Journal of Experimental Biology 166, no. 1 (May 1, 1992): 297–316. http://dx.doi.org/10.1242/jeb.166.1.297.

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The skin overlying the cleithrum bone of freshwater-acclimated rainbow trout contains numerous mitochondria-rich (MR) cells, as detected by DASPEI fluorescence. This tissue was mounted in vitro in an Ussing-style chamber with fresh water on the mucosal surface and saline supplemented with bovine serum albumin on the serosal surface. The preparation developed a high transepithelial resistance and a small transepithelial potential (Vt), positive on the serosal side. Radioisotopic flux measurements indicated that the preparation actively transported Ca2+ from the mucosal to the serosal surface, as assessed by the Ussing flux ratio criterion. Ca2+ transport was positively correlated with MR cell density. Cortisol pretreatment in vivo reduced MR cell density and increased Vt but did not significantly alter Ca2+ fluxes. Ca2+ transport was unaffected by adrenergic agonists (10(−5) mol l-1 adrenaline, clonidine, isoprenaline) or cyclic AMP stimulants (10(−3) mol l-1 dibutyryl cyclic adenosine monophosphate, db-cAMP, plus 10(−4) mol l-1 isobutylmethylxanthine, IBMX) applied to the serosal surface. The Ca2+ ionophore ionomycin (1 × 10(−6)-3.2 × 10(−6) mol l-1 on the mucosal surface) increased both unidirectional Ca2+ fluxes and caused Ca2+ to accumulate within the epithelium. Lanthanum (10(−4) mol l-1) did not inhibit unidirectional Ca2+ fluxes, but apparently displaced Ca2+ from binding sites on the mucosal surface. Unlike Ca2+, movements of Na+ and Cl- across the epithelium were passive, as assessed by the flux ratio criterion, and neither adrenaline nor db-cAMP plus IBMX had any effect on Na+ or Cl- fluxes or electrical properties. These results indicate that ion transport across the skin mediated by MR cells (‘chloride cells’) contributes to Ca2+ but not to NaCl balance in freshwater trout.

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35

Kaiser, J., T. Lemaire, S. Naili, V. Sansalone, and S. V. Komarova. "Do calcium fluxes within cortical bone affect osteocyte mechanosensitivity?" Journal of Theoretical Biology 303 (June 2012): 75–86. http://dx.doi.org/10.1016/j.jtbi.2012.03.001.

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36

Kortus, S., G. Dayanithi, and M. Zapotocky. "Computational estimation of calcium fluxes in isolated magnocellular neurons." BMC Neuroscience 16, Suppl 1 (2015): P299. http://dx.doi.org/10.1186/1471-2202-16-s1-p299.

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37

Guérold, B., R. Massarelli, V. Forster, L. Freysz, and H. Dreyfus. "Exogenous gangliosides modulate calcium fluxes in cultured neuronal cells." Journal of Neuroscience Research 32, no. 1 (May 1992): 110–15. http://dx.doi.org/10.1002/jnr.490320113.

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38

Bers, Donald M. "Calcium Fluxes Involved in Control of Cardiac Myocyte Contraction." Circulation Research 87, no. 4 (August 18, 2000): 275–81. http://dx.doi.org/10.1161/01.res.87.4.275.

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39

Williams, R. J. P. "Calcium fluxes in cells: new views on their significance." Cell Calcium 13, no. 5 (May 1992): 273–75. http://dx.doi.org/10.1016/0143-4160(92)90061-v.

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40

Oelberg, David G., Leslie B. Wang, Jeffrey W. Sackman, Eugene W. Adcock, Roger Lester, and William P. Dubinsky. "Bile salt-induced calcium fluxes in artificial phospholipid vesicles." Biochimica et Biophysica Acta (BBA) - Biomembranes 937 (1988): 289–99. http://dx.doi.org/10.1016/0005-2736(88)90251-9.

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41

Juška, Alfonsas. "Dynamics of Calcium Fluxes in Nonexcitable Cells: Mathematical Modeling." Journal of Membrane Biology 211, no. 2 (May 2006): 89–99. http://dx.doi.org/10.1007/s00232-005-7019-3.

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42

Amnattanakul, Suwimol, Narattaphol Charoenphandhu, Liangchai Limlomwongse, and Nateetip Krishnamra. "Endogenous prolactin modulated the calcium absorption in the jejunum of suckling rats." Canadian Journal of Physiology and Pharmacology 83, no. 7 (July 1, 2005): 595–604. http://dx.doi.org/10.1139/y05-045.

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Prolactin has been reported to stimulate intestinal calcium absorption in young and mature, but not aging rats. The present study was performed on suckling rats to elucidate the actions of endogenous prolactin on calcium absorption in various intestinal segments. Before measuring the calcium fluxes, 9-day-old rats were administered for 7 days with 0.9% NaCl, s.c. (control), 3 mg/kg bromocriptine, i.p., twice daily to abolish secretion of endogenous pro lac tin, or bromocriptine plus exogenous 2.5 mg/kg prolactin, s.c. Thereafter, the 16-day-old rats were experimented upon by instilling the 45Ca-containing solution into the intestinal segments. The results showed that, under a physiological condition, the jejunum had the highest rate of calcium absorption compared with other segments (1.4 ± 0.35 µmol·h1·cm1, p < 0.05). The duodenum and ileum also manifested calcium absorption, whereas the colon showed calcium secretion. Lack of endogenous prolactin decreased lumen-to-plasma and net calcium fluxes in jejunum from 2.07 ± 0.31 to 1.19 ± 0.12 and 1.40 ± 0.35 to 0.88 ± 0.18 µmol·h1·cm1 (p < 0.05), respectively, and exogenous prolactin restored the jejunal calcium absorption to the control value. Endogenous prolactin also had an effect on the duodenum but, in this case, exogenous prolactin did not reverse the effect of bromocriptine. However, neither ileal nor colonic calcium fluxes were influenced by prolactin. Because luminal sodium concentration has been demonstrated to affect calcium absorption in mature rats, the effect of varying luminal sodium concentrations on calcium fluxes in suckling rats was evaluated. The jejunum was used due to its highest rate of calcium absorption. After filling the jejunal segments with 124 (control), 80, 40 mmol/L Na+-containing or Na+-free solution, increases in calcium absorption were found to be inversely related to luminal sodium concentrations in both control and bromocriptine-treated rats. The plasma concentration of 45Ca under luminal sodium free condition was also higher than that of the control condition (2.26% ± 0.07% vs. 2.01% ± 0.09% administered dose, p < 0.05). However, 3H-mannitol, a marker of the widening of tight junction that was introduced into the lumen, had a stable level in the plasma during an increase in plasma 45Ca, suggesting that the widening of tight junction was not required for enhanced calcium absorption. In conclusion, calcium absorption in suckling rats was of the highest rate in the jejunum where endogenous prolactin modulated calcium absorption without increasing the paracellular transport of mannitol. Key words: calcium absorption, intestinal segments, prolactin, suckling rats.

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43

Gorczynska, E., and D. J. Handelsman. "Requirement for transmembrane sodium flux in maintenance of cytosolic calcium levels in rat Sertoli cells." American Journal of Physiology-Endocrinology and Metabolism 264, no. 6 (June 1, 1993): E863—E867. http://dx.doi.org/10.1152/ajpendo.1993.264.6.e863.

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The prompt rise in cytosolic calcium induced by follicle-stimulating hormone (FSH) in rat Sertoli cells suggests a role for calcium in FSH signal transduction. To evaluate the requirement for sodium in transmembrane calcium fluxes in Sertoli cells, we measured intracellular calcium concentration under sodium-free conditions and during stimulation by monensin and veratridine, used to elevate cytosolic sodium. Cytosolic calcium levels were measured by dual-wavelength spectrofluorimetry using freshly isolated cells loaded with fura-2 acetoxymethyl ester. Whereas, removal of extracellular sodium lowered cytosolic calcium in unstimulated cells from 89 +/- 4 to 75 +/- 8 nM, treatment with monensin and veratridine increased cytosolic calcium to 142 +/- 19 and 126 +/- 13 nM, respectively. Without extracellular calcium, monensin still produced 47% of the rise in cytosolic calcium observed in the presence of extracellular calcium, indicating approximately equal contributions of calcium from intracellular and extracellular sources. Blockade of voltage-sensitive or/and voltage-insensitive calcium channels by verapamil and ruthenium red was unable to completely prevent the monensin-induced elevation of cytosolic calcium. In addition tetrodotoxin failed to block the FSH-induced rise in cytosolic calcium. These observations, together with the considerable reduction in monensin-induced rise in cytosolic calcium under extracellular sodium-free condition, support the hypothesis that sodium-calcium exchange rather than the specific calcium or sodium channels regulate basal and monensin-induced transmembrane sodium and calcium fluxes in Sertoli cells.

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44

Artalejo, C. R., A. G. García, and D. Aunis. "Chromaffin cell calcium channel kinetics measured isotopically through fast calcium, strontium, and barium fluxes." Journal of Biological Chemistry 262, no. 2 (January 1987): 915–26. http://dx.doi.org/10.1016/s0021-9258(19)75873-6.

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45

Michelangeli, F. "Fluo-3 AN IDEAL CALCIUM INDICATOR FOR MEASURING CALCIUM FLUXES IN SR AND ER." Biochemical Society Transactions 19, no. 2 (April 1, 1991): 183S. http://dx.doi.org/10.1042/bst019183s.

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46

Ding, Xue, Xiuhui Zhang, and Lin Ji. "Contribution of calcium fluxes to astrocyte spontaneous calcium oscillations in deterministic and stochastic models." Applied Mathematical Modelling 55 (March 2018): 371–82. http://dx.doi.org/10.1016/j.apm.2017.11.002.

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47

El Haj, A. J., L. M. Walker, M. R. Preston, and S. J. Publicover. "Mechanotransduction pathways in bone: calcium fluxes and the role of voltage-operated calcium channels." Medical & Biological Engineering & Computing 37, no. 3 (May 1999): 403–9. http://dx.doi.org/10.1007/bf02513320.

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48

Antia, A. N. "Solubilization of particles in sediment traps: revising the stoichiometry of mixed layer export." Biogeosciences 2, no. 2 (August 4, 2005): 189–204. http://dx.doi.org/10.5194/bg-2-189-2005.

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Abstract. Sinking particles, once caught in sediment trap jars, release dissolved elements into the surrounding medium through leaching from their pore fluids, chemical dissolution and the activity of free exoenzymes. This results in an increase in dissolved elements in the trap jar supernatant. Elemental fluxes as traditionally measured by sediment traps underestimate total export when this particle-associated dissolved flux is not considered. The errors introduced are variable and alter both the absolute levels of flux as well as the stoichiometry of export. These errors have been quantified and corrections applied for samples from sediment traps in the North Atlantic based on measurements of excess dissolved carbon, nitrogen, phosphorus, silica and calcium in the supernatant of the collection cups. At the base of the winter mixed layer, on average 90±6% of phosphorus fluxes are found as excess phosphate whereas for carbon and nitrogen dissolved concentrations account for 30 (±8)% and 47(±11)% of total fluxes respectively. Excess dissolved silica is on average 61 (±17)% of total biogenic silica flux. Little (<10%) of calcium is solubilized. The proportion of dissolved to total flux decreases with trap deployment depth. Calculations of the C:N:P ratios for particles only are well above the Redfield ratios of 106:16:1 (Redfield et al., 1963), although the mid-water dissolved N:P and N:Si values as well as the C:N:P ratios of remineralisation along isopycnals conform to the Redfield ratios at this site. Accounting for dissolved fluxes of all these elements brings the stoichiometry of export in agreement with the Redfield Ratio and with other geochemical estimates of winter mixed layer export. A factor of 3 to 4 higher ratios of organic: inorganic carbon export also implies that the net atmospheric CO2 sequestration by the biological pump is about 50% higher at this site when the dissolved elemental fluxes are considered. Solubilization is thus a process that should be accounted for in protocols used to measure vertical fluxes with sediment traps.

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49

Li, Wen Ping, Jun Hong Chen, Christoph Wohrmeyer, Hong Yan Guan, and Jia Lin Sun. "Effect of Premelted Calcium-Magnesium-Aluminate Flux on Magnesia Carbon Brick." Advanced Materials Research 683 (April 2013): 639–42. http://dx.doi.org/10.4028/www.scientific.net/amr.683.639.

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The novel Calcium-Magnesium-Aluminate (CMA) based premelted fluxes with different concentrations of MgO are developed and their corrosion to MgO/C brick is compared with traditional fluxing practice based on CaF2 addition. Results show that the corrosion of the MgO/C brick can be reduced obviously with initial high content of MgO employed in CMA. Additionally, the corrosion could be decreased correspondingly with the increase of MgO content in CMA fluxes, and the working lifetime of ladle slag zone can be extended by adding CMA flux.

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Ship, J. A., L. L. Patton, and R. B. Wellner. "Muscarinic regulation of potassium transport in a human submandibular epithelial cell line." American Journal of Physiology-Cell Physiology 259, no. 2 (August 1, 1990): C340—C348. http://dx.doi.org/10.1152/ajpcell.1990.259.2.c340.

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Results of previous studies suggest that the transport of K+ by salivary ducts is under muscarinic control. The mechanisms by which this regulation occurs have not been well defined, however. In this paper, we describe mechanisms involved in the muscarinic regulation of K+ (86Rb) transport in HSG-PA, an epithelial cell line derived from human submandibular gland duct. Stimulation of HSG-PA cells by carbachol, a muscarinic agonist, increases both 86Rb influx and efflux, which results in a decrease in the equilibrium content of 86Rb within the cells. Increases in both fluxes are dose dependent with respect to carbachol concentration, and both responses can be blocked by atropine, a muscarinic antagonist. The carbachol-stimulated 86Rb fluxes appear to be calcium dependent since 1) the calcium ionophore A23187 increases 86Rb fluxes in these cells, 2) cells loaded with 1,2-bis(2-aminophenoxy)ethane- N,N,N',N'-tetraacetic acid (BAPTA; a calcium chelator) exhibit a reduced ability to respond to carbachol stimulation, and 3) removal of extracellular calcium concentration reduces the carbachol-stimulated effects. Treatment of HSG-PA cells with 10(-7) M phorbol myristate acetate (PMA) partially blocks the carbachol-stimulated changes in 86Rb fluxes, suggesting that protein kinase C plays a role in this response. PMA also partially blocks A23187-stimulated 86Rb influx, suggesting that activation of protein kinase C inhibits muscarinic-stimulated K+ influx by blocking either the Ca2+ signal (X. He, X. Wu, and B.J. Baum. Biochem. Biophys. Res. Commun. 152: 1062-1069, 1988), steps subsequent to this effect, or both.(ABSTRACT TRUNCATED AT 250 WORDS)

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