Computer simulation of wild-type and mutant human cardiac Na+ current
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Stefano Severi | Carlo Napolitano | Silvia G. Priori | Silvio Cavalcanti | Stefania Vecchietti | Ilaria Rivolta | S. Severi | S. Vecchietti | S. Cavalcanti | S. Priori | C. Napolitano | I. Rivolta
[1] J. Schwarz,et al. The effect of temperature on Na currents in rat myelinated nerve fibres , 1986, Pflügers Archiv European Journal of Physiology.
[2] R. Barr,et al. Cell size and communication: role in structural and electrical development and remodeling of the heart. , 2004, Heart rhythm.
[3] S. Priori,et al. Inherited Brugada and Long QT-3 Syndrome Mutations of a Single Residue of the Cardiac Sodium Channel Confer Distinct Channel and Clinical Phenotypes* , 2001, The Journal of Biological Chemistry.
[4] C. Antzelevitch. Late potentials and the Brugada syndrome. , 2002, Journal of the American College of Cardiology.
[5] A. Wilde,et al. Cardiac sodium channel and inherited arrhythmia syndromes. , 2001, Cardiovascular research.
[6] A O Grant,et al. Molecular biology of sodium channels and their role in cardiac arrhythmias. , 2001, The American journal of medicine.
[7] B. Hille. Ionic channels of excitable membranes , 2001 .
[8] C Antzelevitch,et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. , 1999, Circulation research.
[9] J. Brugada,et al. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. , 1992, Journal of the American College of Cardiology.
[10] Action potential changes due to Y1795H mutation in Brugada syndrome patients: a simulation study , 2003, Computers in Cardiology, 2003.
[11] P. C. Viswanathan,et al. Effects of IKr and IKs heterogeneity on action potential duration and its rate dependence: a simulation study. , 1999, Circulation.
[12] A. Wilde,et al. Delay in Right Ventricular Activation Contributes to Brugada Syndrome , 2004, Circulation.
[13] R. Kass,et al. Stimulation of Protein Kinase C Inhibits Bursting in Disease-Linked Mutant Human Cardiac Sodium Channels , 2003, Circulation.
[14] E. Marbán. Cardiac channelopathies , 2020, Nature.
[15] Y Rudy,et al. Action potential and contractility changes in [Na(+)](i) overloaded cardiac myocytes: a simulation study. , 2000, Biophysical journal.
[16] P. Schwartz,et al. Multiple mechanisms of Na+ channel--linked long-QT syndrome. , 1996, Circulation research.
[17] B. Nilius,et al. Inactivation of sodium channels in isolated myocardial mouse cells , 2004, European Biophysics Journal.
[18] Y. Rudy,et al. Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia , 1999, Nature.
[19] J. Towbin,et al. Brugada syndrome: 1992-2002: a historical perspective. , 2003, Journal of the American College of Cardiology.
[20] K.H.W.J. ten Tusscher,et al. Comments on 'A model for human ventricular tissue' : reply , 2005 .
[21] Colleen E Clancy,et al. Insights into the molecular mechanisms of bradycardia-triggered arrhythmias in long QT-3 syndrome. , 2002, The Journal of clinical investigation.
[22] Colleen E. Clancy,et al. Na+ Channel Mutation That Causes Both Brugada and Long-QT Syndrome Phenotypes: A Simulation Study of Mechanism , 2002, Circulation.
[23] J. Balser,et al. The cardiac sodium channel: gating function and molecular pharmacology. , 2001, Journal of molecular and cellular cardiology.
[24] Y. Rudy,et al. Ionic Current Basis of Electrocardiographic Waveforms: A Model Study , 2002, Circulation research.
[25] J. Brugada,et al. Brugada syndrome: a decade of progress. , 2002, Circulation research.
[26] Jeffrey C. Lagarias,et al. Convergence Properties of the Nelder-Mead Simplex Method in Low Dimensions , 1998, SIAM J. Optim..
[27] C Antzelevitch,et al. Sodium channel block with mexiletine is effective in reducing dispersion of repolarization and preventing torsade des pointes in LQT2 and LQT3 models of the long-QT syndrome. , 1997, Circulation.
[28] H A Fozzard,et al. Kinetic analysis of single sodium channels from canine cardiac Purkinje cells , 1990, The Journal of general physiology.
[29] F Bezanilla,et al. A sodium channel gating model based on single channel, macroscopic ionic, and gating currents in the squid giant axon. , 1991, Biophysical journal.
[30] Silvia G Priori,et al. A novel SCN5A mutation associated with long QT-3: altered inactivation kinetics and channel dysfunction. , 2002, Physiological genomics.
[31] A G Hawkes,et al. Relaxation and fluctuations of membrane currents that flow through drug-operated channels , 1977, Proceedings of the Royal Society of London. Series B. Biological Sciences.
[32] Lawrence F. Shampine,et al. The MATLAB ODE Suite , 1997, SIAM J. Sci. Comput..
[33] C. Antzelevitch,et al. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. , 1999, Circulation.
[34] G. Bett,et al. Computer model of action potential of mouse ventricular myocytes. , 2004, American journal of physiology. Heart and circulatory physiology.
[35] S. Severi,et al. Markovian model for wild-type and mutant (Y1795C and Y1795H) human cardiac Na/sup +/ channel , 2003, Computers in Cardiology, 2003.
[36] F. Lehmann-Horn,et al. Voltage-gated ion channels and hereditary disease. , 1999, Physiological reviews.
[37] R Horn,et al. Statistical properties of single sodium channels , 1984, The Journal of general physiology.
[38] P. C. Viswanathan,et al. Two distinct congenital arrhythmias evoked by a multidysfunctional Na(+) channel. , 2000, Circulation research.
[39] R L Winslow,et al. Cardiac sodium channel Markov model with temperature dependence and recovery from inactivation. , 1999, Biophysical journal.