Quantifying the origins of population variability in cardiac electrical activity through sensitivity analysis of the electrocardiogram
暂无分享,去创建一个
Luke Domanski | Jamie I Vandenberg | Adam P Hill | Stefan A. Mann | Arash Sadrieh | A. Hill | J. Vandenberg | R. Subbiah | A. Sadrieh | Stefan A Mann | Rajesh N Subbiah | John A Taylor | L. Domanski | John A. Taylor | Arash Sadrieh
[1] H. Bazett,et al. AN ANALYSIS OF THE TIME‐RELATIONS OF ELECTROCARDIOGRAMS. , 1997 .
[2] U. Costabel,et al. Cell number in human heart in atrophy, hypertrophy, and under the influence of cytostatics. , 1975, Recent advances in studies on cardiac structure and metabolism.
[3] Robert Plonsey,et al. Bioelectricity: A Quantitative Approach Duke University’s First MOOC , 2013 .
[4] M. Kageyama,et al. Effects of semotiadil fumarate, a novel Ca2+ antagonist, on cytosolic Ca2+ level and force of contraction in porcine coronary arteries , 1995, British journal of pharmacology.
[5] Y Rudy,et al. Ionic mechanisms of propagation in cardiac tissue. Roles of the sodium and L-type calcium currents during reduced excitability and decreased gap junction coupling. , 1997, Circulation research.
[6] C Antzelevitch,et al. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome. , 1998, Circulation.
[7] James E. Bailey,et al. Lessons from metabolic engineering for functional genomics and drug discovery , 1999, Nature Biotechnology.
[8] S. Priori,et al. Low penetrance in the long-QT syndrome: clinical impact. , 1999, Circulation.
[9] H. Snieder,et al. QT interval in twins , 2000, Journal of Human Hypertension.
[10] Wojciech Zareba,et al. Spectrum of ST-T–Wave Patterns and Repolarization Parameters in Congenital Long-QT Syndrome: ECG Findings Identify Genotypes , 2000, Circulation.
[11] M. Malik,et al. Measurement, interpretation and clinical potential of QT dispersion. , 2000, Journal of the American College of Cardiology.
[12] M. Sanguinetti,et al. Molecular and Cellular Mechanisms of Cardiac Arrhythmias , 2001, Cell.
[13] G. Duker,et al. Instability and Triangulation of the Action Potential Predict Serious Proarrhythmia, but Action Potential Duration Prolongation Is Antiarrhythmic , 2001, Circulation.
[14] 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.
[15] D. Noble. Modeling the Heart--from Genes to Cells to the Whole Organ , 2002, Science.
[16] Hubert Kwiecinski,et al. Functional and clinical characterization of KCNJ2 mutations associated with LQT7 (Andersen syndrome). , 2002, The Journal of clinical investigation.
[17] Y. Rudy,et al. Ionic Current Basis of Electrocardiographic Waveforms: A Model Study , 2002, Circulation research.
[18] J. Brugada,et al. Sudden Death Associated With Short-QT Syndrome Linked to Mutations in HERG , 2003, Circulation.
[19] S. Priori,et al. CaV1.2 Calcium Channel Dysfunction Causes a Multisystem Disorder Including Arrhythmia and Autism , 2004, Cell.
[20] S. Priori,et al. A Novel Form of Short QT Syndrome (SQT3) Is Caused by a Mutation in the KCNJ2 Gene , 2005, Circulation research.
[21] Jens H. Krüger,et al. A Survey of General‐Purpose Computation on Graphics Hardware , 2007, Eurographics.
[22] K. Sampson,et al. Autonomic Control of Cardiac Action Potentials: Role of Potassium Channel Kinetics in Response to Sympathetic Stimulation , 2005, Circulation research.
[23] C. January,et al. Most LQT2 Mutations Reduce Kv11.1 (hERG) Current by a Class 2 (Trafficking-Deficient) Mechanism , 2006, Circulation.
[24] F. Romeo,et al. Distribution and prognostic significance of QT intervals in the lowest half centile in 12,012 apparently healthy persons. , 2006, The American journal of cardiology.
[25] M. Sanguinetti,et al. hERG potassium channels and cardiac arrhythmia , 2006, Nature.
[26] Michel Haïssaguerre,et al. Loss-of-Function Mutations in the Cardiac Calcium Channel Underlie a New Clinical Entity Characterized by ST-Segment Elevation, Short QT Intervals, and Sudden Cardiac Death , 2007, Circulation.
[27] A. Moss,et al. Impaired T‐Amplitude Adaptation to Heart Rate Characterizes IKr Inhibition in the Congenital and Acquired Forms of the Long QT Syndrome , 2007, Journal of cardiovascular electrophysiology.
[28] K. Lunetta. Genetic Association Studies , 2008, Circulation.
[29] D. Roden,et al. A genetic framework for improving arrhythmia therapy , 2008, Nature.
[30] Jamie I Vandenberg,et al. Not All hERG Pore Domain Mutations Have a Severe Phenotype: G584S Has an Inactivation Gating Defect with Mild Phenotype Compared to G572S, Which Has a Dominant Negative Trafficking Defect and a Severe Phenotype , 2009, Journal of cardiovascular electrophysiology.
[31] S. Viskin,et al. The QT interval: too long, too short or just right. , 2009, Heart rhythm.
[32] E. Sobie. Parameter sensitivity analysis in electrophysiological models using multivariable regression. , 2009, Biophysical journal.
[33] Jie Cheng,et al. Programming Massively Parallel Processors. A Hands-on Approach , 2010, Scalable Comput. Pract. Exp..
[34] Ali Akoglu,et al. Cardiac simulation on multi-GPU platform , 2010, The Journal of Supercomputing.
[35] I. Efimov,et al. Transmural Dispersion of Repolarization in Failing and Nonfailing Human Ventricle , 2010, Circulation research.
[36] Wojciech Zareba,et al. T-wave morphology abnormalities in benign, potent, and arrhythmogenic I(kr) inhibition. , 2011, Heart rhythm.
[37] T. Opthof,et al. Counterpoint: M cells do not have a functional role in the ventricular myocardium of the intact heart. , 2011, Heart rhythm.
[38] Jørgen K. Kanters,et al. Heritability of Tpeak-Tend Interval and T-Wave Amplitude: A Twin Study , 2011, Circulation. Cardiovascular genetics.
[39] Eric A Sobie,et al. Quantification of repolarization reserve to understand interpatient variability in the response to proarrhythmic drugs: a computational analysis. , 2011, Heart rhythm.
[40] Yoram Rudy,et al. Simulation of the Undiseased Human Cardiac Ventricular Action Potential: Model Formulation and Experimental Validation , 2011, PLoS Comput. Biol..
[41] D. Rosenbaum,et al. Point: M cells are present in the ventricular myocardium. , 2011, Heart rhythm.
[42] Jacob A. Tennessen,et al. Evolution and Functional Impact of Rare Coding Variation from Deep Sequencing of Human Exomes , 2012, Science.
[43] D. Roden,et al. Blocking Scn10a Channels in Heart Reduces Late Sodium Current and Is Antiarrhythmic , 2012, Circulation research.
[44] Claudio J. Verzilli,et al. An Abundance of Rare Functional Variants in 202 Drug Target Genes Sequenced in 14,002 People , 2012, Science.
[45] D. Roden,et al. Systems biology and cardiac arrhythmias , 2012, The Lancet.
[46] Prashanthan Sanders,et al. Epistatic effects of potassium channel variation on cardiac repolarization and atrial fibrillation risk. , 2012, Journal of the American College of Cardiology.