Search Results - "Mørk, Halvor K."

Slow Ca2+ sparks de-synchronize Ca2+ release in failing cardiomyocytes: Evidence for altered configuration of Ca2+ release units? by Louch, William E., Hake, Johan, Mørk, Halvor K., Hougen, Karina, Skrbic, Biljana, Ursu, Daniel, Tønnessen, Theis, Sjaastad, Ivar, Sejersted, Ole M.

“…In heart failure, cardiomyocytes exhibit slowing of the rising phase of the Ca2+ transient which contributes to the impaired contractility observed in this…”
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T-tubule disorganization and reduced synchrony of Ca2+ release in murine cardiomyocytes following myocardial infarction by Louch, William E., Mørk, Halvor K., Sexton, Joseph, Strømme, Tævje A., Laake, Petter, Sjaastad, Ivar, Sejersted, Ole M.

“…In cardiac myocytes, initiation of excitation–contraction coupling is highly localized near the T-tubule network. Myocytes with a dense T-tubule network…”
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Control of Ca2+ Release by Action Potential Configuration in Normal and Failing Murine Cardiomyocytes by Louch, William E., Hake, Johan, Jølle, Guro Five, Mørk, Halvor K., Sjaastad, Ivar, Lines, Glenn T., Sejersted, Ole M.

“…Cardiomyocytes from failing hearts exhibit spatially nonuniform or dyssynchronous sarcoplasmic reticulum (SR) Ca2+ release. We investigated the contribution of…”
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Increased cardiomyocyte function and Ca2+ transients in mice during early congestive heart failure by Mørk, Halvor K, Sjaastad, Ivar, Sande, Jørn B, Periasamy, Muthu, Sejersted, Ole M, Louch, William E

“…Abstract End-stage heart failure is believed to involve depressed cardiomyocyte contractility and Ca2+ transients. However, the time course of these…”
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Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout by Louch, William E., Hougen, Karina, Mørk, Halvor K., Swift, Fredrik, Aronsen, Jan M., Sjaastad, Ivar, Reims, Henrik M., Roald, Borghild, Andersson, Kristin B., Christensen, Geir, Sejersted, Ole M.

“…Alterations in trans-sarcolemmal and sarcoplasmic reticulum (SR) Ca 2+ fluxes may contribute to impaired cardiomyocyte contraction and relaxation in heart…”
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Tamoxifen administration routes and dosage for inducible Cre-mediated gene disruption in mouse hearts by Andersson, Kristin B, Winer, Lisbeth H, Mørk, Halvor K, Molkentin, Jeffery D, Jaisser, Frédéric

“…Tissue-specific and time-dependent control of in vivo gene disruption may be achieved using conditional knockout strategies in transgenic mice. Fusion of…”
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Slowing of cardiomyocyte Ca2+ release and contraction during heart failure progression in postinfarction mice by Mørk, Halvor K, Sjaastad, Ivar, Sejersted, Ole M, Louch, William E

“…Deterioration of cardiac contractility during congestive heart failure (CHF) is believed to involve decreased function of individual cardiomyocytes and may…”
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Myocardial infarction in mice induces hypertrophy and heart failure without reduced contraction of viable myocytes by Mørk, Halvor K, Sjaastad, Ivar, Sejersted, Ole M, Louch, William E

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Progressive slowing of calcium transient decline and development of diastolic heart failure in SERCA2 knockout mice by Louch, William E, Aronsen, Magnus, Sjaastad, Ivar, Mørk, Halvor K, Andersson, Kristin B, Hougen, Karina, Christensen, Geir, Sejersted, Ole M

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Increased transsarcolemmal calcium flux and myofilament responsiveness in cardiomyocytes from SERCA2null mice by Louch, William E, Birkeland, Jon A.K, Andersson, Kristin B, Sjaastad, Ivar, Mørk, Halvor K, Sejersted, Ole M

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Contribution of the Na+/Ca2+ exchanger to rapid Ca2+ release in cardiomyocytes by Lines, Glenn T, Sande, Jørn B, Louch, William E, Mørk, Halvor K, Grøttum, Per, Sejersted, Ole M

“…Trigger Ca(2+) is considered to be the Ca(2+) current through the L-type Ca(2+) channel (LTCC) that causes release of Ca(2+) from the sarcoplasmic reticulum…”
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Slow Ca 2 + sparks de-synchronize Ca 2 + release in failing cardiomyocytes: Evidence for altered configuration of Ca 2 + release units? by Louch, William E, Hake, Johan, Mørk, Halvor K, Hougen, Karina, Skrbic, Biljana, Ursu, Daniel, Tønnessen, Theis, Sjaastad, Ivar, Sejersted, Ole M

“…Abstract In heart failure, cardiomyocytes exhibit slowing of the rising phase of the Ca 2 + transient which contributes to the impaired contractility observed…”
Get full text

Alterations in Ca2+ Sparks and T-Tubules Promote Slowed, Dyssynchronous Ca2+ Release in Failing Cardiomyocytes by Louch, William E., Mørk, Halvor K., Hougen, Karina, Sjaastad, Ivar, Sejersted, Ole M.

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Control of Ca^sup 2+^ Release by Action Potential Configuration in Normal and Failing Murine Cardiomyocytes by Louch, William E, Hake, Johan, Jølle, Guro Five, Mørk, Halvor K, Sjaastad, Ivar, Lines, Glenn T, Sejersted, Ole M

“…Cardiomyocytes from failing hearts exhibit spatially nonuniform or dyssynchronous sarcoplasmic reticulum (SR) Ca... release. We investigated the contribution…”
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SERCA2 Knockout Mice Exhibit Impaired Control of Ca2+ Current but not Ventricular Arrhythmias by Mørk, Halvor K., Richard, Sylvain, Stokke, Mathis K., Sjaastad, Ivar, Andersson, Kristin B., Christensen, Geir, Sejersted, Ole M., Louch, William E.

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SERCA2 Knockout Mice Exhibit Impaired Control of Ca 2+ Current but not Ventricular Arrhythmias by Mørk, Halvor K., Richard, Sylvain, Stokke, Mathis K., Sjaastad, Ivar, Andersson, Kristin B., Christensen, Geir, Sejersted, Ole M., Louch, William E.

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Control of Ca Release Synchrony by Action Potential Configuration in Murine Cardiomyocytes by Hake, Johan, Jølle, Guro F., Mørk, Halvor K., Sjaastad, Ivar, Sejersted, Ole M., Louch, William E., Lines, Glenn T.

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Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout: SERCA loss and Na + gain promote diastolic dysfunction in heart failure by Louch, William E., Hougen, Karina, Mørk, Halvor K., Swift, Fredrik, Aronsen, Jan M., Sjaastad, Ivar, Reims, Henrik M., Roald, Borghild, Andersson, Kristin B., Christensen, Geir, Sejersted, Ole M.

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Contribution of the Na+/Ca^sup 2+^ Exchanger to Rapid Ca^sup 2+^ Release in Cardiomyocytes by Lines, Glenn T, Sande, Jørn B, Louch, William E, Mørk, Halvor K

“…Trigger Ca^sup 2+^ is considered to be the Ca^sup 2+^ current through the L-type Ca^sup 2+^ channel (LTCC) that causes release of Ca^sup 2+^ from the…”
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Increased cardiomyocyte function and Ca 2+ transients in mice during early congestive heart failure by Mørk, Halvor K., Sjaastad, Ivar, Sande, Jørn B., Periasamy, Muthu, Sejersted, Ole M., Louch, William E.

“…End-stage heart failure is believed to involve depressed cardiomyocyte contractility and Ca 2+ transients. However, the time course of these alterations is…”
Get full text