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Items: 1 to 20 of 119

1.

Quantification of repolarization reserve to understand interpatient variability in the response to proarrhythmic drugs: a computational analysis.

Sarkar AX, Sobie EA.

Heart Rhythm. 2011 Nov;8(11):1749-55. doi: 10.1016/j.hrthm.2011.05.023. Epub 2011 Jun 7.

2.

Preclinical cardiac safety assessment of pharmaceutical compounds using an integrated systems-based computer model of the heart.

Bottino D, Penland RC, stamps A, Traebert M, Dumotier B, Georgiva A, Helmlinger G, Lett GS.

Prog Biophys Mol Biol. 2006 Jan-Apr;90(1-3):414-43.

PMID:
16321428
3.

Refining repolarization reserve.

Roden DM, Abraham RL.

Heart Rhythm. 2011 Nov;8(11):1756-7. doi: 10.1016/j.hrthm.2011.06.024. Epub 2011 Jun 24. No abstract available.

4.
5.

Antiarrhythmic effect of IKr activation in a cellular model of LQT3.

Diness JG, Hansen RS, Nissen JD, Jespersen T, Grunnet M.

Heart Rhythm. 2009 Jan;6(1):100-6. doi: 10.1016/j.hrthm.2008.10.020. Epub 2008 Oct 17.

PMID:
19121808
6.

I(Ks) restricts excessive beat-to-beat variability of repolarization during beta-adrenergic receptor stimulation.

Johnson DM, Heijman J, Pollard CE, Valentin JP, Crijns HJ, Abi-Gerges N, Volders PG.

J Mol Cell Cardiol. 2010 Jan;48(1):122-30. doi: 10.1016/j.yjmcc.2009.08.033. Epub 2009 Sep 8.

PMID:
19744496
7.

Determinants of beat-to-beat variability of repolarization duration in the canine ventricular myocyte: a computational analysis.

Heijman J, Zaza A, Johnson DM, Rudy Y, Peeters RL, Volders PG, Westra RL.

PLoS Comput Biol. 2013;9(8):e1003202. doi: 10.1371/journal.pcbi.1003202. Epub 2013 Aug 22.

8.

In silico risk assessment for drug-induction of cardiac arrhythmia.

Suzuki S, Murakami S, Tsujimae K, Findlay I, Kurachi Y.

Prog Biophys Mol Biol. 2008 Sep;98(1):52-60. doi: 10.1016/j.pbiomolbio.2008.05.003. Epub 2008 May 29. Review.

PMID:
18635251
9.

In silico screening of the impact of hERG channel kinetic abnormalities on channel block and susceptibility to acquired long QT syndrome.

Romero L, Trenor B, Yang PC, Saiz J, Clancy CE.

J Mol Cell Cardiol. 2014 Jul;72:126-37. doi: 10.1016/j.yjmcc.2014.02.018. Epub 2014 Mar 11. Corrected and republished in: J Mol Cell Cardiol. 2015 Oct;87:271-82.

10.

IKs blockade reduces dispersion of repolarization in heart failure.

Pajouh M, Wilson LD, Poelzing S, Johnson NJ, Rosenbaum DS.

Heart Rhythm. 2005 Jul;2(7):731-8.

PMID:
15992730
11.

Quantitative comparison of cardiac ventricular myocyte electrophysiology and response to drugs in human and nonhuman species.

O'Hara T, Rudy Y.

Am J Physiol Heart Circ Physiol. 2012 Mar 1;302(5):H1023-30. doi: 10.1152/ajpheart.00785.2011. Epub 2011 Dec 9.

12.
13.

Pharmacological modulation of I(Ks): potential for antiarrhythmic therapy.

Salataa JJ, Selnickb HG, Lynch JJ Jr.

Curr Med Chem. 2004 Jan;11(1):29-44. Review.

PMID:
14754424
14.

Feedback remodeling of cardiac potassium current expression: a novel potential mechanism for control of repolarization reserve.

Xiao L, Xiao J, Luo X, Lin H, Wang Z, Nattel S.

Circulation. 2008 Sep 2;118(10):983-92. doi: 10.1161/CIRCULATIONAHA.107.758672. Epub 2008 Aug 18.

15.

Impaired Inactivation of L-Type Ca2+ Current as a Potential Mechanism for Variable Arrhythmogenic Liability of HERG K+ Channel Blocking Drugs.

Kim JG, Sung DJ, Kim HJ, Park SW, Won KJ, Kim B, Shin HC, Kim KS, Leem CH, Zhang YH, Cho H, Bae YM.

PLoS One. 2016 Mar 1;11(3):e0149198. doi: 10.1371/journal.pone.0149198. eCollection 2016.

16.

Electrophysiologic effects of SB-237376: a new antiarrhythmic compound with dual potassium and calcium channel blocking action.

Xu X, Yan GX, Wu Y, Liu T, Kowey PR.

J Cardiovasc Pharmacol. 2003 Mar;41(3):414-21.

PMID:
12605020
17.

Experimentally-Based Computational Investigation into Beat-To-Beat Variability in Ventricular Repolarization and Its Response to Ionic Current Inhibition.

Pueyo E, Dangerfield CE, Britton OJ, Virág L, Kistamás K, Szentandrássy N, Jost N, Varró A, Nánási PP, Burrage K, Rodríguez B.

PLoS One. 2016 Mar 28;11(3):e0151461. doi: 10.1371/journal.pone.0151461. eCollection 2016.

18.

The plateau outward current in canine ventricle, sensitive to 4-aminopyridine, is a constitutive contributor to ventricular repolarization.

Sridhar A, da Cunha DN, Lacombe VA, Zhou Q, Fox JJ, Hamlin RL, Carnes CA.

Br J Pharmacol. 2007 Nov;152(6):870-9. Epub 2007 Aug 13.

19.

Diastolic spontaneous calcium release from the sarcoplasmic reticulum increases beat-to-beat variability of repolarization in canine ventricular myocytes after β-adrenergic stimulation.

Johnson DM, Heijman J, Bode EF, Greensmith DJ, van der Linde H, Abi-Gerges N, Eisner DA, Trafford AW, Volders PG.

Circ Res. 2013 Jan 18;112(2):246-56. doi: 10.1161/CIRCRESAHA.112.275735. Epub 2012 Nov 13.

20.

Mechanistic basis for type 2 long QT syndrome caused by KCNH2 mutations that disrupt conserved arginine residues in the voltage sensor.

McBride CM, Smith AM, Smith JL, Reloj AR, Velasco EJ, Powell J, Elayi CS, Bartos DC, Burgess DE, Delisle BP.

J Membr Biol. 2013 May;246(5):355-64. doi: 10.1007/s00232-013-9539-6. Epub 2013 Apr 2.

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