Affiliation: University of California
- A novel computational model of the human ventricular action potential and Ca transientEleonora Grandi
Department of Pharmacology, University of California, 451 Health Sciences Drive, GBSF Room 3513, Davis, CA 95616 8636, USA
J Mol Cell Cardiol 48:112-21. 2010..We conclude that this model provides a useful framework to explore excitation-contraction coupling mechanisms and repolarization abnormalities at the single myocyte level...
- Interplay of voltage and Ca-dependent inactivation of L-type Ca currentEleonora Grandi
Department of Pharmacology, University of California, Davis, 451 Health Sciences Drive, GBSF 3506, Davis, CA 95616, USA
Prog Biophys Mol Biol 103:44-50. 2010..This complicates VDI analysis experimentally, but raises intriguing new questions about how the molecular mechanisms of VDI differ for divalent and monovalent currents through LTCCs...
- Theoretical study of L-type Ca(2+) current inactivation kinetics during action potential repolarization and early afterdepolarizationsStefano Morotti
Department of Pharmacology, University of California, Davis, CA 95616 8636, USA
J Physiol 590:4465-81. 2012..Our model accurately describes ECC and allows dissection of the relative contributions of different Ca(2+) sources to total CDI, and the relative roles of CDI and VDI, during normal and abnormal repolarization...
- Post-translational modifications of the cardiac Na channel: contribution of CaMKII-dependent phosphorylation to acquired arrhythmiasAnthony W Herren
Department of Pharmacology, University of California Davis, Davis, California
Am J Physiol Heart Circ Physiol 305:H431-45. 2013..Understanding the mechanisms of altered NaV1.5 expression and function is crucial for gaining insight into arrhythmogenesis and developing novel therapeutic strategies. ..
- β-adrenergic stimulation activates early afterdepolarizations transiently via kinetic mismatch of PKA targetsYuanfang Xie
Department of Pharmacology, University of California Davis, Davis, CA, USA
J Mol Cell Cardiol 58:153-61. 2013..5) RyR phosphorylation has little effect on either transient EAD type. Our study emphasizes the importance of understanding non-steady state kinetics of several systems in mediating β-adrenergic-induced EADs and arrhythmias...
- Human atrial action potential and Ca2+ model: sinus rhythm and chronic atrial fibrillationEleonora Grandi
Department of Pharmacology, University of California, Davis, 451 Health Sciences Dr, GBSF Room 3513, Davis, CA 95616 8636, USA
Circ Res 109:1055-66. 2011..Understanding atrial fibrillation (AF) requires integrated understanding of ionic currents and Ca2+ transport in remodeled human atrium, but appropriate models are limited...
- How does β-adrenergic signalling affect the transitions from ventricular tachycardia to ventricular fibrillation?Yuanfang Xie
Department of Pharmacology, University of California Davis, 451 Health Sciences Drive, GBSF Room 3502, Davis, CA 95616 8636, USA
Europace 16:452-7. 2014..In this study, we aimed at investigating how βAR signalling affects the transition from VT to VF...
- Human atrial fibrillation: insights from computational electrophysiological modelsDonald M Bers
Department of Pharmacology, University of California at Davis, Davis, CA 95616 8636, USA
Trends Cardiovasc Med 21:145-50. 2011..Potential new avenues of investigation and model development are suggested...
- Calcium/calmodulin-dependent kinase II regulation of cardiac ion channelsDonald M Bers
Department of Pharmacology, University of California, Davis, Davis, CA 95616 8636, USA
J Cardiovasc Pharmacol 54:180-7. 2009..In this review, we summarize the modulatory effects of CaMKII on cardiac ion channel function and expression and illustrate potential implications in the onset of arrhythmias via a computer model...
- Nonequilibrium reactivation of Na+ current drives early afterdepolarizations in mouse ventricleAndrew G Edwards
From the Department of Bioengineering A G E, S P, J H O, A D M, Department of Pharmacology S M, J H B, University of California, San Diego, La Jolla Department of Pharmacology, University of California, Davis E G, D M B and Simula Research Laboratory, Center for Biomedical Computing, Lysaker, Oslo, Norway J E H, P L
Circ Arrhythm Electrophysiol 7:1205-13. 2014..We investigated these dynamics in myocytes from arrhythmia-susceptible calcium calmodulin-dependent protein kinase II delta C (CaMKIIδC)-overexpressing mice (Tg), and via computational simulations...