Journal articles: 'Influx'

1

Orr, Julie. "Influx." STEAM 1, no. 2 (February 28, 2014): 1–4. http://dx.doi.org/10.5642/steam.20140102.11.

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McCall, Betty L. "“Influx”." ANNALS of the American Academy of Political and Social Science 642, no. 1 (June 4, 2012): 200–209. http://dx.doi.org/10.1177/0002716212438209.

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As a direct result of the 1995 welfare reform legislation, some metropolitan areas relocated women on their welfare rolls through a process called “Greyhound therapy.” Many of these women ended up in rural areas that were not only unprepared to meet their specific needs but also not receptive to their presence. This article tells the story of these women, who were moved almost two hundred miles from a large Pennsylvania city to a small town in a rural region.

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Hallett, M. B., E. J. Pettit, and E. V. Davies. "Capacitative Ca2+ influx and a diffusible influx factor." Biochemical Journal 314, no. 3 (March 15, 1996): 1054–55. http://dx.doi.org/10.1042/bj3141054.

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4

Cheng, Zi Long, Zhi Huai Zhao, and Chun Xia Li. "Prediction of the Location of the Sources of Mine Water Influx Based on Cluster Analyses of the Chemical Characteristics of Water." Advanced Materials Research 962-965 (June 2014): 328–33. http://dx.doi.org/10.4028/www.scientific.net/amr.962-965.328.

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In order to correctly rapidly predict the location of the sources of mine water influx, cluster analysis of the chemical characteristics of water is an effective adjunct way. To contrast hydrochemcial indexes of Mine inflow point and the points of water sampling and draw the A.M.Piper’s three line diagram and observe the area where they are, the location of the sources of mine water influx can be distinguished by analyzing the Similarity of the hydrochemcial indexes of Mine inflow point and the points of water sampling. The results show that the result of predicting the location of the sources of mine water influx through the above method shows high accuracy and has great reference value.

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5

LeBrasseur, Nicole. "STIMulating Ca2+ influx." Journal of Cell Biology 174, no. 6 (September 11, 2006): 736. http://dx.doi.org/10.1083/jcb.1746iti5.

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6

MacDougall, J., and P. T. Jayachandran. "Polar cap influx." Annales Geophysicae 23, no. 5 (July 28, 2005): 1755–61. http://dx.doi.org/10.5194/angeo-23-1755-2005.

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Abstract. This study uses digital ionosonde data from a cusp latitude station (Cambridge Bay, 77° CGM lat.) to study the convection into the polar cap. Days when the IMF magnetic field was relatively steady were used. On many days it was possible to distinguish an interval near noon MLT when the ionosonde data had a different character from that at earlier and later times. Based on our data, and other published measurements, we used the interval 10:00-13:00 MLT as the cusp interval and calculated the convection into the polar cap in this interval. The integrated convection accounted for only ~1/3 of the open polar cap flux. If the convection through the prenoon/postnoon regions on either side of the cusp was calculated the remaining 2/3 of the flux could be accounted for. The characteristics of the prenoon/postnoon regions were different from the cusp region, and we attribute this to transient flank merging versus more steady frontside merging for the cusp. Keywords. Ionosphere (Plasma convection) Magnetospheric physics (Polar cap phenomenon)

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7

Galkina, Elena, and Klaus Ley. "Leukocyte Influx in Atherosclerosis." Current Drug Targets 8, no. 12 (December 1, 2007): 1239–48. http://dx.doi.org/10.2174/138945007783220650.

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8

McCarthy, Nicola. "Calcium influx is moving." Nature Reviews Cancer 9, no. 4 (March 12, 2009): 230–31. http://dx.doi.org/10.1038/nrc2629.

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9

Neher, Erwin. "Controls on calcium influx." Nature 355, no. 6358 (January 1992): 298–99. http://dx.doi.org/10.1038/355298a0.

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10

GIBBONS, SIMON J., JAMES R. BRORSON, DAVID BLEAKMAN, PAUL S. CHARD, and RICHARD J. MILLER. "Calcium Influx and Neurodegeneration." Annals of the New York Academy of Sciences 679, no. 1 Markers of Ne (May 1993): 22–33. http://dx.doi.org/10.1111/j.1749-6632.1993.tb18286.x.

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11

King, Leslie B., and Bruce D. Freedman. "B-lymphocyte calcium inFlux." Immunological Reviews 231, no. 1 (September 2009): 265–77. http://dx.doi.org/10.1111/j.1600-065x.2009.00822.x.

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12

Yaren, Özgür. "The Turkish Sex Influx." Camera Obscura: Feminism, Culture, and Media Studies 33, no. 1 (2018): 1–27. http://dx.doi.org/10.1215/02705346-4336817.

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13

Mazzara, Federica. "Influx: Europe Is Moving." Italian American Review 7, no. 1 (January 1, 2017): 105–8. http://dx.doi.org/10.5406/italamerrevi.7.1.0105.

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14

Edwards, M., A. W. G. John, H. G. Hunt, and J. A. Lindley. "Exceptional influx of oceanic species into the North Sea late 1997." Journal of the Marine Biological Association of the United Kingdom 79, no. 4 (August 1999): 737–39. http://dx.doi.org/10.1017/s0025315498000885.

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Continuous Plankton Recorder records from the North Sea and north-east Atlantic from September 1997 to March 1998 indicate an exceptional influx of oceanic indicator species into the North Sea. These inflow events, according to historical evidence, have only occurred sporadically during this century. This exceptional inflow and previous inflow events are discussed in relation to their similarity in terms of their physical and climatic conditions.

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15

Koch, B. D., G. F. Faurot, M. V. Kopanitsa, and D. C. Swinney. "Pharmacology of a Ca2+-influx pathway activated by emptying the intracellular Ca2+ stores in HL-60 cells: evidence that a cytochrome P-450 is not involved." Biochemical Journal 302, no. 1 (August 15, 1994): 187–90. http://dx.doi.org/10.1042/bj3020187.

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In HL-60 cells, inhibition of the endoplasmic-reticular Ca2+ pump by thapsigargin leads to the emptying of this intracellular Ca2+ store and a subsequent activation of plasma-membrane Ca2+ influx through a non-voltage-dependent pathway. The elevated intracellular free Ca2+ concentration ([Ca2+]i) produced and maintained by this Ca2+ inflow was used to examine the potency of various compounds to inhibit this influx mechanism. As expected, specific blockers of known Ca2+ channels, such as nifedipine, omega-conotoxin GVIA and ryanodine were without effect. The less selective inhibitors La3+, SKF-96365 and L-651,582, which are thought to inhibit both voltage-dependent and voltage-independent Ca2+ channels, decreased [Ca2+]i back to resting levels, with pIC50 values of 5.2, 5.9 and 6.2 respectively. It has been proposed that a cytochrome P-450 is involved in activating Ca(2+)-influx pathways in thymocytes, neutrophils and platelets. Consistent with this idea, the imidazole cytochrome P-450 inhibitors miconazole, econazole, clotrimazole and ketoconazole inhibited the thapsigargin-elevated [Ca2+]i with pIC50 values of 7.1, 7.1, 7.1 and 5.8 respectively. The high affinity of imidazoles for cytochromes P-450 is due to co-ordinate binding to the haem. This interaction is greatly decreased in 2-substituted imidazoles. We examined whether the inhibition of Ca2+ influx was due to an interaction of the inhibitor imidazole nitrogen with the haem iron of the putative cytochrome P-450 by comparing the activity of two compounds, identical except that one was methylated at the imidazole 2-position. They were found to block thapsigargin-activated Ca2+ influx with equal potency. These results strongly suggest that a cytochrome P-450 is not involved in the activation of the Ca2+ influx produced by emptying the intracellular Ca2+ stores.

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16

Heimann, Kirsten, Georg Kreimer, Michael Melkonian, and Erwin Latzko. "Light-Induced Ca2+ Influx into Spinach Protoplasts." Zeitschrift für Naturforschung C 42, no. 3 (March 1, 1987): 283–87. http://dx.doi.org/10.1515/znc-1987-0319.

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Protoplasts from spinach leaves exhibit a light-induced Ca2+ influx. The half maximum rate of Ca2+ influx is achieved at ~ 5 Wm-2. The action spectrum of this influx is similar to that of photosynthesis. Furthermore, light-induced Ca2+ influx is abolished by DCMU (≥ 0.5 μᴍ) and is sensitive to the uncoupler FCCP. Vanadate up to 3 μᴍ enhances light-induced Ca2+ influx. These data indicate that photosynthetic electron transport is involved in light-induced Ca2+ influx into spinach protoplasts.

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17

Bell, J. E., K. E. Begg, Y. Sin, J. D. Biggers, and D. J. Benos. "Neutral amino acid influx in developing rabbit blastocysts." American Journal of Physiology-Cell Physiology 251, no. 2 (August 1, 1986): C285—C292. http://dx.doi.org/10.1152/ajpcell.1986.251.2.c285.

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The influx of the neutral amino acids glycine, aminoisobutyric acid (AIB), and leucine into rabbit blastocysts was measured. In day 6 postcoitus (pc) embryos, glycine influx was Na+ independent, whereas AIB and leucine influx involved both Na+-dependent and independent components. From days 5 to 7 pc, the leucine and AIB influx remained constant, although the Na+-dependent fraction decreased and the Na+-independent fraction increased with age. None of the Na+-independent influx was inhibited by methylaminoisobutyric acid (MeAIB), an amino acid analogue specific for the system A of neutral amino acid uptake. In addition, MeAIB influx was Na+ independent, implying that system A is not involved in leucine or AIB uptake. All Na+-dependent influx is thus considered to occur via system ASC. System L contributed only to the influx of leucine at days 6 and 7 pc, as measured by inhibition of Na+-independent influx by 2-amino-bicyclo-(2,2,1)-heptane-2-carboxylic acid.

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18

Taylor, Phillip S. "An Unparalleled Influx of Monarchs." Blue Jay 70, no. 2 (June 25, 2012): 122–26. http://dx.doi.org/10.29173/bluejay283.

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19

Wang, Chunmin, and Zoltan Machaty. "Calcium influx in mammalian eggs." REPRODUCTION 145, no. 4 (April 2013): R97—R105. http://dx.doi.org/10.1530/rep-12-0496.

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Calcium (Ca2+) signals are involved in the regulation of oocyte maturation and play a critical role during fertilization. In the egg, Ca2+is stored in the lumen of the endoplasmic reticulum and a signal is generated when the stored Ca2+is released through specialized channels in the membrane of the endoplasmic reticulum to elevate the free Ca2+concentration in the cytoplasm. Extracellular Ca2+is also important, indicated by the fact that the mobilization of luminal Ca2+is typically followed by Ca2+entry across the plasma membrane. The transmembrane Ca2+flux replenishes the endoplasmic reticulum, and thus, it is essential to sustain prolonged Ca2+signals. It also seems to be responsible for the stimulation of important signaling cascades required for complete egg activation. Characterization of the pathway that mediates Ca2+entry implies that its major components include STIM1, a protein that senses the filling status of the stores, and ORAI1, a channel protein located in the plasma membrane. Defining the mechanism and functions of Ca2+entry will not only lead to a better understanding of egg physiology but may also help improving the efficiency of a number of assisted reproductive technologies.

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20

Tetradis, N. "Cosmological acceleration from energy influx." Physics Letters B 569, no. 1-2 (September 2003): 1–6. http://dx.doi.org/10.1016/j.physletb.2003.07.003.

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21

Perlman, Lisa. "Soviet influx opens new era." Nature 343, no. 6259 (February 1990): 583. http://dx.doi.org/10.1038/343583b0.

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22

Brown, Rebecca M. "InFlux: Contemporary Art in Asia." South Asian Studies 30, no. 2 (July 3, 2014): 282–83. http://dx.doi.org/10.1080/02666030.2014.964111.

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23

Clapham, David E. "A mysterious new influx factor?" Nature 364, no. 6440 (August 1993): 763–64. http://dx.doi.org/10.1038/364763a0.

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24

Morales, Narkis S., and Ignacio C. Fernández. "Chile unprepared for Ph.D. influx." Science 356, no. 6343 (June 15, 2017): 1131.2–1132. http://dx.doi.org/10.1126/science.aan5376.

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25

Parekh, A. B., and R. Penner. "Store depletion and calcium influx." Physiological Reviews 77, no. 4 (October 1, 1997): 901–30. http://dx.doi.org/10.1152/physrev.1997.77.4.901.

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Calcium influx in nonexcitable cells regulates such diverse processes as exocytosis, contraction, enzyme control, gene regulation, cell proliferation, and apoptosis. The dominant Ca2+ entry pathway in these cells is the store-operated one, in which Ca2+ entry is governed by the Ca2+ content of the agonist-sensitive intracellular Ca2+ stores. Only recently has a Ca2+ current been described that is activated by store depletion. The properties of this new current, called Ca2+ release-activated Ca2+ current (ICRAC), have been investigated in detail using the patch-clamp technique. Despite intense research, the nature of the signal that couples Ca2+ store content to the Ca2+ channels in the plasma membrane has remained elusive. Although ICRAC appears to be the most effective and widespread influx pathway, other store-operated currents have also been observed. Although the Ca2+ release-activated Ca2+ channel has not yet been cloned, evidence continues to accumulate that the Drosophila trp gene might encode a store-operated Ca2+ channel. In this review, we describe the historical development of the field of Ca2+ signaling and the discovery of store-operated Ca2+ currents. We focus on the electrophysiological properties of the prototype store-operated current ICRAC, discuss the regulatory mechanisms that control it, and finally consider recent advances toward the identification of molecular mechanisms involved in this ubiquitous and important Ca2+ entry pathway.

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26

Carraro, L., E. Casarotto, R. Pasqualotto, M. E. Puiatti, P. Scarin, and M. Valisa. "Impurity influx diagnostics on RFX." Review of Scientific Instruments 66, no. 1 (January 1995): 610–12. http://dx.doi.org/10.1063/1.1146302.

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27

Dickman, Steven. "Student influx hits German universities." Nature 335, no. 6188 (September 1988): 288. http://dx.doi.org/10.1038/335288c0.

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28

Meldolesi, Jacopo, Emilio Clementi, Cristina Fasolato, Daniele Zacchetti, and Tullio Pozzan. "Ca2+ influx following receptor activation." Trends in Pharmacological Sciences 12 (January 1991): 289–92. http://dx.doi.org/10.1016/0165-6147(91)90577-f.

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29

Garcia-Sancho, Javier, Javier Alvarez, Mayte Montero, and Carlos Villalobos. "Ca2+ influx following receptor activation." Trends in Pharmacological Sciences 13 (January 1992): 12–13. http://dx.doi.org/10.1016/0165-6147(92)90007-s.

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30

Sage, Stewart O., Paul Sargeant, Susanne Jenner, and Richard W. Farndale. "Tyrosine phosphorylation and Ca2+ influx." Trends in Pharmacological Sciences 15, no. 8 (August 1994): 282. http://dx.doi.org/10.1016/0165-6147(94)90007-8.

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31

Robinson, Lisbeth C., and Jonathan S. Marchant. "Calcium Influx: Beyond ‘Current’ Biology." Current Biology 16, no. 14 (July 2006): R548—R550. http://dx.doi.org/10.1016/j.cub.2006.06.036.

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32

Stamp, M. F., K. H. Behringer, M. J. Forrest, P. D. Morgan, and H. P. Summers. "Impurity influx behaviour in JET." Journal of Nuclear Materials 145-147 (February 1987): 236–40. http://dx.doi.org/10.1016/0022-3115(87)90334-5.

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33

LaManna, Joseph C., J. Frederick Harrington, Lisa M. Vendel, Kamal Abi-Saleh, W. David Lust, and Sami I. Harik. "Regional blood-brain lactate influx." Brain Research 614, no. 1-2 (June 1993): 164–70. http://dx.doi.org/10.1016/0006-8993(93)91030-v.

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34

Brock, T. A., C. Brugnara, M. Canessa, and M. A. Gimbrone. "Bradykinin and vasopressin stimulate Na+-K+-Cl- cotransport in cultured endothelial cells." American Journal of Physiology-Cell Physiology 250, no. 6 (June 1, 1986): C888—C895. http://dx.doi.org/10.1152/ajpcell.1986.250.6.c888.

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We have characterized a Na+-K+-Cl- cotransporter in vascular endothelial cells (EC) cultured from different blood vessels and species that is inhibited by the diuretics furosemide and bumetanide (50% inhibitory concentration for 86Rb influx approximately 20 microM and 0.5 microM, respectively). Inward 86Rb influx mediated via this pathway is greater than 86Rb influx transported by the Na+-K+ pump in cultured EC from bovine and pig aorta, bovine vena cava, and baboon cephalic vein but not in human umbilical or saphenous vein EC. External Na+ or Cl- -stimulated, ouabain-insensitive 86Rb influx is equal to furosemide or bumetanide-sensitive 86Rb influx. Ouabain-insensitive 22Na influx is also partially inhibited by these drugs and stimulated by increasing external K+ or Cl-. Net Na+ extrusion occurs via the Na+-K+-Cl- cotransporter in the absence of external K+, whereas net Na+ influx occurs at higher external K+ (greater than 1 mM). Maximal concentrations (100 nM) of bradykinin and vasopressin increase the initial rate of bumetanide-sensitive 86Rb influx by approximately 60 and 70% (50% effective concentration approximately 1 and 0.6 nM, respectively). Addition of either ethyleneglycol-bis(beta-aminotethylether)-N,N'-tetraacetic acid or LaCl3 (to block calcium influx) prevents bradykinin-stimulated 86Rb influx. When intracellular calcium is elevated using ionomycin (100 nM), a Ca2+ ionophore, bumetanide-sensitive 86Rb influx increases approximately twofold. In contrast, isoproterenol (100 microM) and forskolin (50 microM), adenylate cyclase stimulators, decrease furosemide-sensitive 86Rb influx.(ABSTRACT TRUNCATED AT 250 WORDS)

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35

Lee, D. B., M. W. Walling, and D. B. Corry. "Phosphate transport across rat jejunum: influence of sodium, pH, and 1,25-dihydroxyvitamin D3." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 1 (July 1, 1986): G90—G95. http://dx.doi.org/10.1152/ajpgi.1986.251.1.g90.

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Inorganic phosphate (Pi) transport in intact, rat jejunal epithelium was measured in vitro under short-circuited conditions. Transepithelial net absorptive Pi flux increased linearly with increases in extracellular sodium concentration ([Na]) up to 144 mM. Transmucosal border Pi influx, in contrast, displayed a biphasic Na dependency. Pi influx increased as [Na] was raised from 0 to 100 mM. A further increase in [Na] to 144 mM caused unanticipated reduction in Pi influx. The reason for this dissociation between transmucosal border influx and transepithelial absorptive flux is not clear. We then examined the effect of changes in extracellular pH on Pi influx. Reduction in pH from 7.4 to 6.0 was associated with 150% increase in Pi influx, an observation consistent with the reported reciprocal relation between intestinal brush-border membrane vesicles (BBMV) Pi uptake and extravesicular pH. In contrast to BBMV data, however, a smaller increase (50%) in mucosal Pi influx was noted in intact epithelium when pH was increased from 7.4 to 8.5. Under optimized conditions for Pi influx, i.e., [Na] = 90 mM and pH 6.0, the effect of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on Pi influx was measured. The total influx could be resolved into a saturable, Na-dependent and a nonsaturable, Na-independent component. 1,25(OH)2D3 stimulated the saturable component of Pi influx.

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36

Demaurex, N., A. Monod, D. P. Lew, and K. H. Krause. "Characterization of receptor-mediated and store-regulated Ca2+ influx in human neutrophils." Biochemical Journal 297, no. 3 (February 1, 1994): 595–601. http://dx.doi.org/10.1042/bj2970595.

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1. It is not known to what extent the emptying of intracellular Ca2+ stores participates in the mediation of chemoattractant-induced Ca2+ influx in human neutrophils. To study this question, we compared the properties of bivalent-cation influx in response to the chemoattractant N-formyl-L-methionyl-L-leucyl-L-phenyl-alanine (f-MLP) and to the microsomal Ca(2+)-ATPase inhibitor thapsigargin. 2. The influx pathway activated by f-MLP and thapsigargin had identical properties of permeation. Mn2+ influx became saturated at around 1 mM extracellular Mn2+, whereas Ca2+ influx did not become saturated up to concentrations of 10 mM. 3. The influx of the two bivalent cations, Mn2+ and Ca2+, was activated to a similar extent and with identical kinetics of activation. 4. The Mn2+ influx activated by f-MLP and thapsigargin was blocked, with identical dose-inhibition curves, by four imidazole analogues. 5. The same relationship between the emptying of Ca2+ stores and bivalent-cation influx was observed for f-MLP and thapsigargin, with a half-maximal activation of the influx at 40% emptying of intracellular stores. 6. In conclusion, neutrophils possess a single type of Ca(2+)-influx pathway that is activated by receptor agonists and by store depletion. Receptor agonists activate this influx pathway to a large extent, if not completely, through the depletion of intracellular Ca2+ stores.

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Frame, M. D., and M. A. Milanick. "Mn and Cd transport by the Na-Ca exchanger of ferret red blood cells." American Journal of Physiology-Cell Physiology 261, no. 3 (September 1, 1991): C467—C475. http://dx.doi.org/10.1152/ajpcell.1991.261.3.c467.

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Ca influx via the Na-Ca exchanger into ferret red blood cells is easily measured from a Na-free solution; the intracellular Na concentration is normally approximately 150 mM in ferret red blood cells. We have found that Mn and Cd competitively inhibit Ca influx. Mn influx and Cd influx were a saturable function of the divalent cation concentration, consistent with a carrier mechanism. Indeed, the Km (approximately 10 microM) and the Vmax (usually 1-3 mmol.l packed cells-1.h-1) were similar for Ca, Cd, and Mn. Extracellular Na inhibited divalent cation influx, and intracellular Na stimulated influx. These results are consistent with Na-Cd and Na-Mn influx pathways in ferret red blood cells. Ca (1 mM) almost completely inhibited Mn influx and Cd influx, whereas 1 mM Mg inhibited 5-15%. These results strongly support the notion that Mn and Cd are alternative substrates for Ca on the ferret red cell Na-Ca exchanger. The similarity in the behavior of all three divalent cation places important constraints on kinetic and structural models of the exchanger.

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38

Longo, N., L. D. Griffin, and L. J. Elsas. "Influx and efflux of 3-O-methyl-D-glucose by cultured human fibroblasts." American Journal of Physiology-Cell Physiology 254, no. 5 (May 1, 1988): C628—C633. http://dx.doi.org/10.1152/ajpcell.1988.254.5.c628.

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We measured the initial rates of 3-O-methyl-D-glucose (OMG) fluxes by cultured human fibroblasts. D-Glucose (300 mM) and cytochalasin B (5 microM) inhibited approximately 80% of OMG (1 mM) influx. OMG rapidly entered human fibroblasts, and influx was linear up to 20 s. OMG influx and efflux were about equal. Cytochalasin B inhibited OMG (1 mM) influx and efflux within 20 s of exposure. Cytochalasin B half maximally inhibited OMG influx and efflux at 0.51 and 0.75 microM, respectively. In zero trans conditions, the kinetics of OMG influx and efflux were similar. However, when OMG was present on the trans side of the membrane, OMG influx but not OMG efflux was stimulated. Trans stimulation of OMG influx increased the maximal velocity of this transport process, without affecting its Km. These results suggest that 1) OMG influx and efflux occur through the same transporter, and 2) the glucose transporter of cultured human fibroblasts presents a functional asymmetry when substrate is present on the trans side of the membrane.

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39

Wei, Mingqiang, Keyi Ren, Yonggang Duan, Qingxuan Chen, and Morteza Dejam. "Production Decline Behavior Analysis of a Vertical Well with a Natural Water Influx/Waterflood." Mathematical Problems in Engineering 2019 (September 2, 2019): 1–9. http://dx.doi.org/10.1155/2019/1683989.

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The production decline type curves are considered as a robust technique to interpret the production data and obtain the flow parameters, the original gas in place, etc. However, most of the previous models have focused on the primary depletion with a closed boundary, rather than on the secondary depletion with a water influx/waterflood. Therefore, in this study, a transient flow model considering the water influx/waterflood is developed. Subsequently, the functions of the production decline type curves for a vertical well with a water influx/waterflood are derived based on the material balance equation. In other words, the theory of Blasingame production decline analysis is extended to the water influx/waterflood reservoir. Further advanced Blasingame production decline type curves for a vertical well in water influx/waterflood reservoirs are generated. Compared with Blasingame type curves without a water influx/waterflood, the behavior of the ones presented in this study is quite different at the boundary. Thereafter, the effects of the relevant parameters, including the dimensionless maximum water influx, the dimensionless beginning time of the water influx, and the dimensionless external boundary radius, are studied on type curves. Finally, Blasingame type curves for a vertical well in water influx/waterflood reservoirs are verified through a field case study. This work provides very meaningful references for reservoir engineers working on the evaluation of the water influx and the estimation of the beginning time of the water influx by matching the developed type curves with the actual field data.

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40

Wallnofer, A., C. Cauvin, T. W. Lategan, and U. T. Ruegg. "Differential blockade of agonist- and depolarization-induced 45Ca2+ influx in smooth muscle cells." American Journal of Physiology-Cell Physiology 257, no. 4 (October 1, 1989): C607—C611. http://dx.doi.org/10.1152/ajpcell.1989.257.4.c607.

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ATP stimulated 45Ca2+ influx in rat aortic smooth muscle cells in a concentration-dependent manner (EC50 = 3.6 +/- 0.5 X 10(-7) M). ADP and GTP were less effective than ATP in stimulating 45Ca2+ influx; AMP was weakly active and the adenosine agonist 5'-(N-ethyl-carboxamido)-adenosine (NECA) had no effect. ATP gamma S was about equieffective with ATP, whereas alpha,beta-methylene-ATP (APCPP) did not induce 45Ca2+ influx. Stimulation of 45Ca2+ influx by ATP was not abolished by the dihydropyridine Ca2+ channel antagonist darodipine (PY 108-068), which completely blocked depolarization-induced 45Ca2+ influx. Inorganic cations (La3+, Cd2+, Co2+, Ni2+, Mn2+, and Mg2+) were able to inhibit both agonist- and depolarization-induced 45Ca2+ influx. Cd2+, however, was approximately 20 times more selective in blocking K+-stimulated than agonist-stimulated 45Ca2+ influx. These data indicate that ATP-stimulated Ca2+ influx in rat aortic smooth muscle cells is resistant to darodipine but is reduced by La3+, Cd2+, and other inorganic blockers of Ca2+ channels.

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DeLisle, S., D. Pittet, B. V. Potter, P. D. Lew, and M. J. Welsh. "InsP3 and Ins(1,3,4,5)P4 act in synergy to stimulate influx of extracellular Ca2+ in Xenopus oocytes." American Journal of Physiology-Cell Physiology 262, no. 6 (June 1, 1992): C1456—C1463. http://dx.doi.org/10.1152/ajpcell.1992.262.6.c1456.

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To investigate the role of D-myo-inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4] in the regulation of Ca2+ influx, we injected inositol phosphates into Xenopus oocytes and measured Ca(2+)-gated Cl- current to assay intracellular free Ca2+ concentration ([Ca2+]i). To assess Ca2+ influx, we removed extracellular Ca2+ or added the inorganic Ca2+ channel blocker Mn2+ to the extracellular bath and measured the resulting change in Cl- current. Ins(1,3,4,5)P4 did not cause Ca2+ influx when injected alone or when preceded by an injection of Ca2+. In contrast, Ins(1,3,4,5)P4 stimulated Ca2+ influx when injected after the poorly metabolized inositol trisphosphate (InsP3) analogues D-myo-inositol 1,4,5-trisphosphorothioate [Ins(1,4,5)P3S3] or D-myo-inositol 2,4,5-trisphosphate [Ins(2,4,5)P3]. These results indicate that Ins(1,3,4,5)P4 is not sufficient to stimulate Ca2+ influx but acts in synergy with InsP3s to cause Ca2+ influx. We also studied the effect of Ca2+ influx on the immediate metabolism of D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] in single oocytes. Ca2+ influx shunted the metabolism of Ins(1,4,5)P3 toward the formation of Ins(1,3,4,5)P4 and away from D-myo-inositol 1,4-bisphosphate [Ins(1,4)P2]. These results suggest that there is a positive feedback regulatory mechanism in which Ca2+ influx stimulates Ins(1,3,4,5)P4 production and Ins(1,3,4,5)P4 stimulates further Ca2+ influx.

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Ramagopal, M. V., and S. J. Mustafa. "Effect of adenosine and its analogues on calcium influx in coronary artery." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 6 (December 1, 1988): H1492—H1498. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1492.

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In the present study, we have investigated the changes in calcium influx during the relaxing responses to adenosine and its analogues. Calcium-45 influx was measured in bovine coronary artery rings in the presence of prostaglandin F2 alpha (10(-5) M) and KCl (50 and 100 mM). Prostaglandin F2 alpha and KCl caused increases in calcium influx. Prostaglandin F2 alpha produced a further contraction when added to rings maximally contracted with KCl (100 mM or higher), suggesting two different mechanisms for prostaglandin F2 alpha- and KCl-induced contractions. Similarly, a greater calcium influx was observed when prostaglandin F2 alpha was mixed with KCl (50 or 100 mM). At all the concentrations tested, adenosine and its analogues [5'-(N-ethyl-carboxamidoadenosine, NECA; N6-(L-2-phenylisopropyl)adenosine, L-PIA] significantly inhibited prostaglandin F2 alpha-induced increases in calcium influx. However, only higher concentrations of adenosine, NECA, and L-PIA inhibited 100 mM KCl-induced calcium influx. Previous treatment with 8-phenyltheophylline blocked the inhibitory actions of adenosine, NECA, and L-PIA on calcium influx. The inhibition of calcium influx by adenosine, NECA, and L-PIA correlated well with their relaxing ability in the presence of prostaglandin F2 alpha. The data suggest that prostaglandin F2 alpha-induced calcium influx was more sensitive to the action of adenosine and its analogues than the calcium influx induced by high K+ depolarization.

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BOSE, Diptiman D., Roshanak RAHIMIAN, and David W. THOMAS. "Activation of ryanodine receptors induces calcium influx in a neuroblastoma cell line lacking calcium influx factor activity." Biochemical Journal 386, no. 2 (February 22, 2005): 291–96. http://dx.doi.org/10.1042/bj20040900.

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We have further characterized the Ca2+ signalling properties of the NG115-401L (or 401L) neuroblastoma cell line, which has served as an important cell line for investigating SOC (store-operated channel) influx pathways. These cells possess an unusual Ca2+ signalling phenotype characterized by the absence of Ca2+ influx when Ca2+ stores are depleted by inhibitors of SERCA (sarcoplasmic/endoplasmic reticulum Ca2+-ATPase). Previous studies found that Ca2+-store depletion does not produce a CIF (Ca2+ influx factor) activity in 401L cells. These observations have prompted the question whether 401L cells possess the signalling machinery that permits non-voltage-gated Ca2+ influx to occur. We tested the hypothesis that ryanodine-sensitive Ca2+ pools and activation of RyRs (ryanodine receptors) constitute a signalling pathway capable of inducing Ca2+ influx in 401L cells. We found that 401L cells express mRNA for RyR1 and RyR2 and that RyR activators induced Ca2+ release. Activation of RyRs robustly couples with Ca2+ influx responses in 401L cells, in sharp contrast with absence of Ca2+ influx when cells are treated with SERCA inhibitors. Thus it is clear that 401L cells, despite lacking depletion-induced Ca2+ influx pathways, express the functional components of a Ca2+ influx pathway under the control of RyR function. These findings further support the importance of the 401L cell line as an important cell phenotype for deciphering Ca2+ influx regulation.

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Musch, M. W., and M. Field. "K-independent Na-Cl cotransport in bovine tracheal epithelial cells." American Journal of Physiology-Cell Physiology 256, no. 3 (March 1, 1989): C658—C665. http://dx.doi.org/10.1152/ajpcell.1989.256.3.c658.

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Uptakes of 22Na, 36Cl, and 86Rb into isolated bovine tracheal epithelial cells were measured in the presence and absence of 10 microM bumetanide. Preincubation with ouabain (0.5 mM) did not alter initial rates of Na and Cl uptakes but prolonged from 0.5 or less to 2 min the period in which Na uptake is linear with time. Initial rates of bumetanide-inhibitable Na and Cl uptakes (influxes), measured for 2 min in identical solutions, were similar in magnitude (bumetanide-sensitive Cl influx/bumetanide-sensitive Na influx = 1.2). Omission of K did not affect bumetanide-sensitive Na or Cl influx. Cl influx was not affected by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid. Amiloride (0.1 mM) partially inhibited the bumetanide-insensitive Na influx but had no effect on the bumetanide-sensitive Na influx. Rb influx was not affected by bumetanide but was markedly reduced by ouabain and slightly reduced by Ba, the combination being additive. Half-maximally inhibitory concentration values for inhibition of Cl influx by 4 sulfamoylbenzoic acid derivatives were as follows (in mumol/l): 0.125 benzmetanide; 0.64 bumetanide; 16 piretanide; and 26 furosemide. Affinities of Na and Cl for the bumetanide-inhibitable cotransport process were determined by measuring bumetanide-sensitive Cl influx at varying [Na] and bumetanide-sensitive Na influx at varying [Cl]. Both plots were hyperbolic, and the K0.5 values for Na and Cl were 4.1 and 53.9 mM, respectively. Bumetanide-inhibitable Cl influx was not altered by secretory stimuli (epinephrine, A23187) but was more than doubled by osmotic shrinkage (200 mM mannitol or sucrose).(ABSTRACT TRUNCATED AT 250 WORDS)

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MIYAKAWA, Tomoya, Masatoyo KOJIMA, and Michio UI. "Differential routes of Ca2+ influx in Swiss 3T3 fibroblasts in response to receptor stimulation." Biochemical Journal 329, no. 1 (January 1, 1998): 107–14. http://dx.doi.org/10.1042/bj3290107.

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Ca2+ influx into cells in response to stimulation of various receptors was studied with Swiss 3T3 fibroblasts. The mechanisms involved were found to be so diverse that they were classified into four groups, Type I to IV. Type-I influx occurred, via pertussis toxin-susceptible G-proteins, immediately after internal Ca2+ mobilization by bradykinin, thrombin, endothelin, vasopressin or angiotensin II. Type-II influx induced by bombesin differed from Type I in its insusceptibility to pertussis toxin treatment. Ca2+ influx induced by prostaglandin E1, referred to as Type-III influx, was unique in that phospholipase C was apparently not activated without extracellular Ca2+, strongly suggesting that the Ca2+ influx preceded and was responsible for InsP3 generation and internal Ca2+ mobilization. More Ca2+ entered the cells more slowly via the Type-IV route opened by platelet-derived and other growth factors. These types of Ca2+ influx could be differentiated by their different susceptibilities to protein kinase C maximally activated by 1 h of exposure of cells to PMA, which inhibited phospholipase Cβ coupled to receptors involved in Type-I and -II influx but did not inhibit growth-factor-receptor-coupled phospholipase Cγ. Type-I and -II Ca2+ influxes, together with store-operated influx induced by thapsigargin, were not directly inhibited by exposure of cells to PMA, but Type-III and -IV influxes were completely inhibited. In addition, stimulation of receptors involved in Type-I and -IV Ca2+ influx, but not Type-II and -III influx, led to phospholipase A2 activation in the presence of extracelluar Ca2+. Inhibition of Type-I and -IV Ca2+ influxes by their respective inhibitors, diltiazem and nifedipine, resulted in abolition of phospholipase A2 activation induced by the respective receptor agonists, in agreement with the notion that Ca2+ influx via these routes is responsible for receptor-mediated phospholipase A2 activation.

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Vostal, J. G., and J. C. Fratantoni. "Econazole inhibits thapsigargin-induced platelet calcium influx by mechanisms other than cytochrome P-450 inhibition." Biochemical Journal 295, no. 2 (October 15, 1993): 525–29. http://dx.doi.org/10.1042/bj2950525.

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Cytochrome P-450 has been suggested as a mediator of the signal between depleted platelet calcium stores and an increase in plasma membrane permeability to calcium which follows depletion of the stores. This hypothesis is based on the observations that inhibitors of cytochrome P-450, such as the imidazole antifungal agents, also inhibit influx of a calcium surrogate (manganese) into calcium-depleted platelets. We tested the effects of econazole and of a cytochrome P-450 inhibitor, carbon monoxide (CO), on thapsigargin (TG)-induced platelet 45Ca2+ influx. TG specifically depletes internal calcium stores and activates store-regulated calcium influx. Econazole blocked 45Ca2+ influx when it was added before TG (IC50 11 microM). Econazole at a concentration (20 microM) that inhibited 83% of TG-induced calcium influx was not inhibitory to TG-induced calcium efflux from 45Ca(2+)-loaded platelets, and did not affect calcium fluxes in resting platelets. This econazole concentration was also inhibitory to calcium influx even when it was added after the stores had been calcium-depleted by EGTA and TG for 15 min and the signal to increase calcium influx had already been generated. Inhibition of cytochrome P-450 with CO bubbled through platelet suspensions did not change calcium influx in resting cells and potentiated TG-induced calcium influx (160% of control calcium accumulation at 20 min). This effect appeared to be concentration-dependent, such that a 5 min exposure to CO produced a greater influx potentiation than a 3 min exposure. These observations indicate that (1) cytochrome P-450 does not mediate store-regulated calcium influx, and (2) econazole probably inhibits store-regulated calcium influx by an alternative mechanism, such as interaction with plasma membrane calcium channels.

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Wada, A., H. Takara, F. Izumi, H. Kobayashi, and N. Yanagihara. "Influx of 22Na through acetylcholine receptorassociated Na channels: relationship between 22Na influx, 45Ca influx and secretion of catecholamines in cultured bovine adrenal medulla cells." Neuroscience 15, no. 1 (May 1985): 283–92. http://dx.doi.org/10.1016/0306-4522(85)90135-6.

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Ferrier, Jack, Angela Kesthely, Eva Lagan, and Conrad Richter. "An experimental test of a model for repeated Ca2+ spikes in osteoblastic cells." Biochemistry and Cell Biology 69, no. 7 (July 1, 1991): 433–41. http://dx.doi.org/10.1139/o91-066.

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A model for cytosolic Ca2+ spikes is presented that incorporates continual influx of Ca2+, uptake into an intracellular compartment, and Ca2+-induced Ca2+ release from the compartment. Two versions are used. In one, release is controlled by explicit thresholds, while in the other, release is a continuous function of cytosolic and compartmental [Ca2+]. Some model predictions are as follows. Starting with low Ca2+ influx and no spikes: (1) induction of spiking when Ca2+ influx is increased. Starting with spikes: (2) increase in magnitude and decrease in frequency when influx is reduced; (3) inhibition of spiking if influx is greatly reduced; (4) decrease in the root-mean-square value when influx is increased; and (5) elimination of spiking if influx is greatly increased. Since there is good evidence that hyperpolarizing spikes reflect cytosolic Ca2+ spikes, we used electrophysiological measurements to test the model. Each model prediction was confirmed by experiments in which Ca2+ influx was manipulated. However, the original spike activity tended to return within 5–30 min, indicating a cellular resetting process.Key words: calcium, electrophysiology, mathematical modelling.

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Sachs, J. R. "Volume-sensitive K influx in human red cell ghosts." Journal of General Physiology 92, no. 5 (November 1, 1988): 685–711. http://dx.doi.org/10.1085/jgp.92.5.685.

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K influx into resealed human red cell ghosts increases when the ghosts are swollen. The influx demonstrates properties similar to volume-sensitive K fluxes present in other cells. The influx is, for the most part, insensitive to the nature of the major intracellular cation and therefore is not a K-K exchange. The influx is much greater when the major anion is Cl than when the major anion is NO3; Cl stimulates the flux and, at constant Cl, NO3 inhibits it. Increase in the influx rate is rapid when shrunken ghosts are swollen or when NO3 is replaced by Cl. The volume-sensitive K influx requires intracellular MgATP at low concentrations, and ATP cannot be replaced by nonhydrolyzable ATP analogues. The volume-sensitive influx is inhibited by Mg2+ and by high concentrations of vanadate, but is stimulated by low concentrations of vanadate. It is not modified by cAMP, the removal of Ca2+ by EGTA, substances that activate protein kinase C, or by inhibition of phosphatidylinositol kinase. The influx is inhibited by neomycin and by trifluoperazine.

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Masood, Azhar, Man Yi, Rosetta Belcastro, Jun Li, Lianet Lopez, Crystal Kantores, Robert P. Jankov, and A. Keith Tanswell. "Neutrophil elastase-induced elastin degradation mediates macrophage influx and lung injury in 60% O2-exposed neonatal rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 1 (July 1, 2015): L53—L62. http://dx.doi.org/10.1152/ajplung.00298.2014.

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Neutrophil (PMNL) influx precedes lung macrophage (LM) influx into the lung following exposure of newborn pups to 60% O2. We hypothesized that PMNL were responsible for the signals leading to LM influx. This was confirmed when inhibition of PMNL influx with a CXC chemokine receptor-2 antagonist, SB-265610, also prevented the 60% O2-dependent LM influx, LM-derived nitrotyrosine formation, and pruning of small arterioles. Exposure to 60% O2was associated with increased lung contents of neutrophil elastase and α-elastin, a marker of denatured elastin, and a decrease in elastin fiber density. This led us to speculate that neutrophil elastase-induced elastin fragments were the chemokines that led to a LM influx into the 60% O2-exposed lung. Inhibition of neutrophil elastase with sivelestat or elafin attenuated the LM influx. Sivelestat also attenuated the 60% O2-induced decrease in elastin fiber density. Daily injections of pups with an antibody to α-elastin prevented the 60% O2-dependent LM influx, impaired alveologenesis, and impaired small vessel formation. This suggests that neutrophil elastase inhibitors may protect against neonatal lung injury not only by preventing structural elastin degradation, but also by blocking elastin fragment-induced LM influx, thus preventing tissue injury from LM-derived peroxynitrite formation.

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Journal articles on the topic 'Influx'

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