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Defining candidate drug characteristics for Long-QT (LQT3) syndrome
1. | Center for Biomedical Computing, Simula Research Laboratory, P.O. Box 134, Lysaker 1325, Norway, Norway |
2. | Cardiac Bioelectricity & Arrhythmia Center, Washington University, St. Louis, MO 63130-4899, United States |
3. | Department of Bioengineering, University of California San Diego, United States |
References:
[1] |
C. Antzelevitch, Ionic, molecular, and cellular bases of qt-interval prolongation and torsade de pointes,, Europace, 4 (2007), 4. Google Scholar |
[2] |
T. Brennan, M. Fink and B. Rodriguez, Multiscale modelling of drug-induced effects on cardiac electrophysiological activity,, European Journal of Pharmaceutical Sciences, 36 (2009), 62.
doi: 10.1016/j.ejps.2008.09.013. |
[3] |
A. Burashnikov and C. Antzelevitch, A unique mechanism contributing to initiation of atrial fibrillation,, Pacing Clin Electrophysiol, 29 (2006), 290.
doi: 10.1111/j.1540-8159.2006.00336.x. |
[4] |
C. E. Clancy and Y. Rudy, Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia,, Nature, 400 (1999).
doi: 10.1038/23034. |
[5] |
C. E. Clancy, Z. I. Zhu and Y. Rudy, Pharmacogenetics and anti-arrhythmic drug therapy: A theoretical investigation,, Am. J. Physiol. Heart Circ. Physiol., 292 (2007), 66.
doi: 10.1152/ajpheart.00312.2006. |
[6] |
L. Hondeghem and B. G. Katzung, Test of a model of antiarrhythmic drug action. Effects of quinidine and lidocaine on myocardial conduction,, Circulation, 61 (1980), 1217. Google Scholar |
[7] |
J. Keener and J. Sneyd, "Mathematical Physiology,", Springer, (2009). Google Scholar |
[8] |
L. M. Livshitz and Y. Rudy, Regulation of Ca2+ and electrical alternans in cardiac myocytes: Role of CAMKII and repolarizing currents,, Am. J. Physiol. Heart Circ. Physiol., 292 (2007), 2854.
doi: 10.1152/ajpheart.01347.2006. |
[9] |
J. A. Nelder and R. Mead, A simplex method for function minimization,, Computer Journal, 7 (1965), 308. Google Scholar |
[10] |
Denis Noble, Jeremy Levin and William Scott, Biological simulations in drug discovery,, Drug Discovery Today, 4 (1999), 10.
doi: 10.1016/S1359-6446(98)01277-X. |
[11] |
Y. Rudy, Modelling the molecular basis of cardiac repolarization,, Europace, 9 (2007).
doi: 10.1093/europace/eum202. |
[12] |
A. Tveito and G. T. Lines, A note on a method for determining advantageous properties of an anti-arrhythmic drug based on a mathematical model of cardiac cells,, Mathematical Biosciences, 217 (2009), 167.
doi: 10.1016/j.mbs.2008.12.001. |
[13] |
S. Vecchietti, E. Grandi, S. Severi, I. Rivolta, C. Napolitano, S. G. Priori and S. Cavalcanti, In silico assessment of Y1795C and Y1795H SCN5A mutations: Implication for inherited arrhythmogenic syndromes,, Am. J. Physiol. Heart Circ. Physiol., 292 (2007), 56.
doi: 10.1152/ajpheart.00270.2006. |
[14] |
D. W. Wang, K. Yazawa, N. Makita, Jr. A. L. George and P. B. Bennett, Pharmacological targeting of long qt mutant sodium channels,, Journal of Clinical Investigation, 99 (1997), 1714.
doi: 10.1172/JCI119335. |
[15] |
Zheng I. Zhu and Colleen E. Clancy, Genetic mutations and arrhythmia: Simulation from DNA to electrocardiogram,, Journal of Electrocardiology, 40 (2007). Google Scholar |
show all references
References:
[1] |
C. Antzelevitch, Ionic, molecular, and cellular bases of qt-interval prolongation and torsade de pointes,, Europace, 4 (2007), 4. Google Scholar |
[2] |
T. Brennan, M. Fink and B. Rodriguez, Multiscale modelling of drug-induced effects on cardiac electrophysiological activity,, European Journal of Pharmaceutical Sciences, 36 (2009), 62.
doi: 10.1016/j.ejps.2008.09.013. |
[3] |
A. Burashnikov and C. Antzelevitch, A unique mechanism contributing to initiation of atrial fibrillation,, Pacing Clin Electrophysiol, 29 (2006), 290.
doi: 10.1111/j.1540-8159.2006.00336.x. |
[4] |
C. E. Clancy and Y. Rudy, Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia,, Nature, 400 (1999).
doi: 10.1038/23034. |
[5] |
C. E. Clancy, Z. I. Zhu and Y. Rudy, Pharmacogenetics and anti-arrhythmic drug therapy: A theoretical investigation,, Am. J. Physiol. Heart Circ. Physiol., 292 (2007), 66.
doi: 10.1152/ajpheart.00312.2006. |
[6] |
L. Hondeghem and B. G. Katzung, Test of a model of antiarrhythmic drug action. Effects of quinidine and lidocaine on myocardial conduction,, Circulation, 61 (1980), 1217. Google Scholar |
[7] |
J. Keener and J. Sneyd, "Mathematical Physiology,", Springer, (2009). Google Scholar |
[8] |
L. M. Livshitz and Y. Rudy, Regulation of Ca2+ and electrical alternans in cardiac myocytes: Role of CAMKII and repolarizing currents,, Am. J. Physiol. Heart Circ. Physiol., 292 (2007), 2854.
doi: 10.1152/ajpheart.01347.2006. |
[9] |
J. A. Nelder and R. Mead, A simplex method for function minimization,, Computer Journal, 7 (1965), 308. Google Scholar |
[10] |
Denis Noble, Jeremy Levin and William Scott, Biological simulations in drug discovery,, Drug Discovery Today, 4 (1999), 10.
doi: 10.1016/S1359-6446(98)01277-X. |
[11] |
Y. Rudy, Modelling the molecular basis of cardiac repolarization,, Europace, 9 (2007).
doi: 10.1093/europace/eum202. |
[12] |
A. Tveito and G. T. Lines, A note on a method for determining advantageous properties of an anti-arrhythmic drug based on a mathematical model of cardiac cells,, Mathematical Biosciences, 217 (2009), 167.
doi: 10.1016/j.mbs.2008.12.001. |
[13] |
S. Vecchietti, E. Grandi, S. Severi, I. Rivolta, C. Napolitano, S. G. Priori and S. Cavalcanti, In silico assessment of Y1795C and Y1795H SCN5A mutations: Implication for inherited arrhythmogenic syndromes,, Am. J. Physiol. Heart Circ. Physiol., 292 (2007), 56.
doi: 10.1152/ajpheart.00270.2006. |
[14] |
D. W. Wang, K. Yazawa, N. Makita, Jr. A. L. George and P. B. Bennett, Pharmacological targeting of long qt mutant sodium channels,, Journal of Clinical Investigation, 99 (1997), 1714.
doi: 10.1172/JCI119335. |
[15] |
Zheng I. Zhu and Colleen E. Clancy, Genetic mutations and arrhythmia: Simulation from DNA to electrocardiogram,, Journal of Electrocardiology, 40 (2007). Google Scholar |
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