Research Topics
| JAMES N contact WEISSSummaryAffiliation: University of California Country: USA Publications
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Publications
"Good enough solutions" and the genetics of complex diseasesJames N Weiss
Cardiovascular Research Laboratory and Atherosclerosis Research Unit, Department of Medicine Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
Circ Res 111:493-504. 2012..If validated, GMAS may imply that common polygenic diseases are related as much to group interactions between normal genes, as to multiple gene mutations...- Deducing topology of protein-protein interaction networks from experimentally measured sub-networksLing Yang
Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, California 90095, USA
BMC Bioinformatics 9:301. 2008..However, whether topological information reaped from these experimentally-measured sub-networks can be extrapolated to complete protein-protein interaction networks is unclear... 
Role of the mitochondrial permeability transition in myocardial diseaseJames N Weiss
Cardiovascular Research Laboratory, Department of Medicine Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, Calif 90095 1760, USA
Circ Res 93:292-301. 2003..Investigations into this area are beginning to unravel some of the mechanistic links between cardioprotective signaling and mitochondria...- Novel approaches to identifying antiarrhythmic drugsJames N Weiss
Departments of Medicine Cardiology and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095 1760, USA
Trends Cardiovasc Med 13:326-30. 2003..However, new insights into the mechanisms of ventricular fibrillation, particularly the role of dynamic factors that cause wave instability, are providing conceptual advances toward developing effective new pharmacotherapy... - Beyond the implantable cardioverter-defibrillator: are we making progress?James N Weiss
UCLA Cardiovascular Research Laboratory, Department of Medicine Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Heart Rhythm 5:S45-7. 2008..This brief review summarizes some of the recent progress in this direction... - Ventricular fibrillation: new insights into mechanismsJames N Weiss
David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA
Ann N Y Acad Sci 1015:122-32. 2004..New insights into the mechanisms of ventricular fibrillation, particularly the role of dynamic factors causing wave instability, are providing a promising avenue for developing novel therapies to prevent sudden cardiac death... - Systems biology approaches to metabolic and cardiovascular disorders: network perspectives of cardiovascular metabolismJames N Weiss
Cardiovascular Research Laboratory, Departments of Medicine Cardiology and Physiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
J Lipid Res 47:2355-66. 2006..We speculate how this state of "metabolic fibrillation" leads to cell death if not corrected and discuss the implications for cardioprotection... - Short-term cardiac memory and mother rotor fibrillationAli Baher
David Geffen School of Medicine at UCLA, Division of Cardiology, 47 123 CHS, 10833 LeConte Ave, Los Angeles, CA 90095 1679, USA
Am J Physiol Heart Circ Physiol 292:H180-9. 2007..This was due to progressive acceleration and stabilization of rotors as accumulation of memory shortened APD and flattened APD restitution slope nonuniformly throughout the tissue... - From pulsus to pulseless: the saga of cardiac alternansJames N Weiss
Department of Medicine Cardiology, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA
Circ Res 98:1244-53. 2006..These insights have illuminated the mechanistic basis underlying the clinical association of cardiac alternans (eg, T wave alternans) with arrhythmia risk, which may lead to novel therapeutic approaches to avert sudden cardiac death... - Factors determining the transition from ventricular tachycardia to ventricular fibrillationJames N Weiss
Cardiovascular Research Laboratory, Department of Medicine (Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Heart Rhythm 2:1008-10. 2005 - Chaos and the transition to ventricular fibrillation: a new approach to antiarrhythmic drug evaluationJ N Weiss
Department of Medicine, UCLA Cardiovascular Research Laboratory, UCLA School of Medicine and Cedars Sinai Medical Center, Los Angeles, CA, USA
Circulation 99:2819-26. 1999.... - The dynamics of cardiac fibrillationJames N Weiss
Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095 1760, USA
Circulation 112:1232-40. 2005..As global properties, rather than local electrophysiological characteristics, dynamic factors represent an attractive target for novel therapies to prevent ventricular fibrillation... - Ventricular fibrillation: how do we stop the waves from breaking?J N Weiss
Cardiovascular Research Laboratory and the Departments of Medicine Cardiology, Physiology and Physiological Science, UCLA School of Medicine and Cedars Sinai Medical Center, Los Angeles, CA 90095 1760, USA
Circ Res 87:1103-7. 2000..Developing therapies that favorably alter electrical restitution properties have promise as a new paradigm for preventing fibrillation... - Understanding biological complexity: lessons from the pastJames N Weiss
The UCLA Cardiovascular Research Laboratory, and Department of Medicine Cardiology, UCLA School of Medicine, Los Angeles, California 90095 1760, USA
FASEB J 17:1-6. 2003..When combined, they are highly synergistic in analyzing the mechanisms underlying the behavior of complex biological systems. Their effective integration will be essential for unraveling the physical basis of the mysteries of life... - Alternans and arrhythmias: from cell to heartJames N Weiss
Department of Medicine, University of California at Los Angeles, 90095, USA
Circ Res 108:98-112. 2011..Throughout, we emphasize the qualitatively novel properties that emerge at each new scale of integration... - Early afterdepolarizations and cardiac arrhythmiasJames N Weiss
UCLA Cardiovascular Research Laboratory, Departments of Medicine Cardiology, Physiology and Integrative Biology and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Heart Rhythm 7:1891-9. 2010.... - Electrical restitution and cardiac fibrillationJames N Weiss
Department of Medicine, UCLA School of Medicine, Cedars Sinai Medical Center, Los Angeles, California 90095 1760, USA
J Cardiovasc Electrophysiol 13:292-5. 2002..Developing therapies that favorably alter these cardiac electrical restitution properties are a promising new approach to preventing fibrillation... - Increased susceptibility of aged hearts to ventricular fibrillation during oxidative stressNorishige Morita
Translational Arrhythmia Research Laboratory and Cardiovascular Research Laboratory, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, USA
Am J Physiol Heart Circ Physiol 297:H1594-605. 2009..We conclude that in aged ventricles exposed to oxidative stress, fibrosis facilitates the ability of cellular EADs to emerge and generate TA, VT, and VF at the tissue level... - Remodelling of action potential and intracellular calcium cycling dynamics during subacute myocardial infarction promotes ventricular arrhythmias in Langendorff-perfused rabbit heartsChung Chuan Chou
Division of Cardiology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA, USA
J Physiol 580:895-906. 2007.... - Molecular mechanism for ATP-dependent closure of the K+ channel Kir6.2Scott A John
UCLA Cardiovascular Research Laboratory, Department of Physiology, UCLA School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA
J Physiol 552:23-34. 2003..Binding of the alpha phosphate group of ATP to R201 then stabilizes the closed state. R50 on the N-terminus controls ATP binding by facilitating the interaction of the beta phosphate group of ATP with K185 to destabilize the open state... - Cardiac alternans in embryonic mouse ventriclesCarlos de Diego
Division of Cardiology, David Geffen School of Medicine at UCLA, University of California Los Angeles, CA 90095, USA
Am J Physiol Heart Circ Physiol 294:H433-40. 2008..5 and older hearts. Embryonic mouse ventricles can develop cardiac alternans, which generally is well correlated with APD restitution slope and does not depend on fully functional SR Ca(i) cycling... - Effects of early afterdepolarizations on reentry in cardiac tissue: a simulation studyRay B Huffaker
Department of Computer Science, David Geffen School of Medicine at University of California, Los Angeles, CA 90095 1596, USA
Am J Physiol Heart Circ Physiol 292:H3089-102. 2007..These findings may explain many features of Torsades des pointes, such as perpetuation by focal excitations, rapidly changing electrical axis, frequent self-termination, and occasional degeneration to fibrillation... - Virtual electrodes and the induction of fibrillation in Langendorff-perfused rabbit ventricles: the role of intracellular calciumHideki Hayashi
Division of Cardiology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California, USA
Am J Physiol Heart Circ Physiol 295:H1422-8. 2008..However, the inhibition of the sarcoplasmic reticulum function also reduced VFT, indicating that the [Ca(2+)](i) dynamics modulate, but are not essential, to ventricular vulnerability... - Calcium transient dynamics and the mechanisms of ventricular vulnerability to single premature electrical stimulation in Langendorff-perfused rabbit ventriclesHideki Hayashi
Division of Cardiology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California, USA
Heart Rhythm 5:116-23. 2008..We hypothesize that Ca current-mediated slow-response action potentials (APs) play a key role in the propagation in the central common pathway (CCP) of the reentry... - Cardiac alternans induced by fibroblast-myocyte coupling: mechanistic insights from computational modelsYuanfang Xie
Department of Medicine Cardiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
Am J Physiol Heart Circ Physiol 297:H775-84. 2009..Thus, through their coupling with myocytes, fibroblasts alter repolarization and Ca(i) cycling alternans at both the cellular and tissue scales, which may play important roles in arrhythmogenesis in diseased cardiac tissue with fibrosis... 
Spatially discordant alternans in cardiomyocyte monolayersCarlos de Diego
Cardiovascular Research Laboratory, Department of Medicine, Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
Am J Physiol Heart Circ Physiol 294:H1417-25. 2008....- Diastolic intracellular calcium-membrane voltage coupling gain and postshock arrhythmias: role of purkinje fibers and triggered activityMitsunori Maruyama
Krannert Institute of Cardiology and the Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, USA
Circ Res 106:399-408. 2010..Recurrent ventricular arrhythmias after initial successful defibrillation are associated with poor clinical outcome... - Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventriclesGyo-Seung Hwang
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
Circulation 114:2595-603. 2006..The Ca(i) prefluorescence at the first postshock early site suggests that reverse excitation-contraction coupling might be responsible for the initiation of postshock activations that lead to ventricular fibrillation... - A rabbit ventricular action potential model replicating cardiac dynamics at rapid heart ratesAman Mahajan
UCLA Cardiovascular Research Laboratory, Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Biophys J 94:392-410. 2008.... - Influence of channel subunit composition on L-type Ca2+ current kinetics and cardiac wave stabilityVadim Gudzenko
Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California Los Angeles 90095 7115, USA
Am J Physiol Heart Circ Physiol 293:H1805-15. 2007..These results imply that subunit modification of L-type Ca(2+) channels can potentially be used as an antifibrillatory strategy... - A tale of two fibrillationsPeng-Sheng Chen
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, Calif, USA
Circulation 108:2298-303. 2003 - Bifurcation and chaos in a model of cardiac early afterdepolarizationsDiana X Tran
Department of Medicine, Cardiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
Phys Rev Lett 102:258103. 2009..During period pacing, chaos always occurs at the transition from no EAD to EADs as the stimulation frequency decreases, providing a distinct explanation for the irregular EAD behavior frequently observed in experiments... - Two types of ventricular fibrillation in isolated rabbit hearts: importance of excitability and action potential duration restitutionTsu Juey Wu
Division of Cardiology, Department of Medicine, Taichung Veterans General Hospital and Institute of Clinical Medicine, Cardiovascular Research Center, National Yang Ming University School of Medicine, Taipei, Taiwan
Circulation 106:1859-66. 2002..The combined effects of excitability and action potential duration (APD) restitution on wavefront dynamics remain unclear... - Vulnerability to re-entry in simulated two-dimensional cardiac tissue: effects of electrical restitution and stimulation sequenceDiana X Tran
Cardiovascular Research Laboratories, Department of Physiological Science, David Geffen School of Medicine at UCLA, University of California, Los Angeles, California 90095, USA
Chaos 17:043115. 2007..When APD restitution is even steeper, the vulnerable window is reduced due to collision of the spiral tips... - A simulation study of the effects of cardiac anatomy in ventricular fibrillationFagen Xie
Department of Medicine (Cardiology, Cardiovascular Research Laboratory, University of California, Los Angeles (UCLA, Los Angeles, California 90095-1679, USA
J Clin Invest 113:686-93. 2004..Thus, interventions that promote dynamical wave stability show promise as an antifibrillatory strategy in this more realistic setting... - Effects of metabolic inhibition on conduction, Ca transients, and arrhythmia vulnerability in embryonic mouse heartsFuhua Chen
Cardiovascular Research Laboratory, David Geffen School of Medicine at University of California, Los Angeles, California 90095 1760, USA
Am J Physiol Heart Circ Physiol 293:H2472-8. 2007..These data support the idea that both glycolysis and oxidative phosphorylation play critical metabolic roles in regulating cardiac function in the embryonic mouse heart... - Intracellular Ca dynamics in ventricular fibrillationChikaya Omichi
Division of Cardiology, Cedars-Sinai Medical Center and Center for Health Sciences, University of California-Los Angeles Cardiovascular Research Laboratory, David Geffen School of Medicine, UCLA, Los Angeles, California 90095-1760, USA
Am J Physiol Heart Circ Physiol 286:H1836-44. 2004..Cai is closely associated with Vm closely during pacing and VT but not during VF. These findings suggest that during VF, non-voltage-gated Cai release events occur and may influence wavebreak by altering Vm and APD locally... - Glycolytic oscillations in isolated rabbit ventricular myocytesJun Hai Yang
Cardiovascular Research Laboratory, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095 1760, USA
J Biol Chem 283:36321-7. 2008.... - Multisite phosphorylation and network dynamics of cyclin-dependent kinase signaling in the eukaryotic cell cycleLing Yang
Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095, USA
Biophys J 86:3432-43. 2004..In summary, our findings suggest that multisite phosphorylation of proteins is a critical biological mechanism in generating the essential dynamics and ensuring robust behavior of the cell cycle... - Intracellular calcium cycling, early afterdepolarizations, and reentry in simulated long QT syndromeRay Huffaker
Department of Computer Science, University of California, Los Angeles, 90095, USA
Heart Rhythm 1:441-8. 2004..CONCLUSIONS: These computer simulations suggest that EADs related to spontaneous SR Ca(2+) release can enhance arrhythmogenesis in LQT syndromes by reinitiating reentry... - Arrhythmogenic consequences of intracellular calcium wavesLai Hua Xie
Cardiovascular Research Laboratory, Department of Medicine Cardiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
Am J Physiol Heart Circ Physiol 297:H997-H1002. 2009..These findings link Ca(i)(2+) waves directly to a variety of arrhythmogenic phenomena relevant to the intact heart... - Long polyamines act as cofactors in PIP2 activation of inward rectifier potassium (Kir2.1) channelsLai-Hua Xie
Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, CA 90095, USA
J Gen Physiol 126:541-9. 2005..Sustained pore block by polyamines was neither sufficient nor necessary for this effect. We conclude that long polyamines serve a dual role as both blockers and coactivators (with PIP2) of Kir2.1 channels... - Dynamic origin of spatially discordant alternans in cardiac tissueHideki Hayashi
Division of Cardiology, Cedars Sinai Medical Center, Los Angeles, California, USA
Biophys J 92:448-60. 2007..Our results support the viewpoint that spatially discordant alternans in the heart can be formed via a dynamical pattern formation process which does not require tissue heterogeneity... - Frequency analysis of ventricular fibrillation in Swine ventriclesMiguel Valderrabano
Division of Cardiology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA, USA
Circ Res 90:213-22. 2002..In conclusion, stable intramural reentry as the engine of fibrillation was not observed. Our findings support the idea that dynamic wavebreak plays a fundamental role in the generation and maintenance of ventricular fibrillation... - Intracellular Ca alternans: coordinated regulation by sarcoplasmic reticulum release, uptake, and leakLai Hua Xie
Cardiovascular Research Laboratory, Department of Medicine Cardiology, David Geffen School of Medicine at the University of California, Los Angeles, California 90095, USA
Biophys J 95:3100-10. 2008..Thus, BayK8644 promotes, whereas Ad-SERCA2a overexpression, ryanodine, and FK506 suppress, Ca(i) alternans under AP clamp conditions... - Dispersion of refractoriness and induction of reentry due to chaos synchronization in a model of cardiac tissueYuanfang Xie
Department of Medicine Cardiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
Phys Rev Lett 99:118101. 2007..These regions of increased refractoriness create localized conduction block, which induces spiral wave reentry... - Protection of cardiac mitochondria by diazoxide and protein kinase C: implications for ischemic preconditioningPaavo Korge
University of California Cardiovascular Research Laboratory and Department of Medicine (Cardiology, University of California School of Medicine, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 99:3312-7. 2002.... - Superiority of biphasic over monophasic defibrillation shocks is attributable to less intracellular calcium transient heterogeneityGyo Seung Hwang
Division of Cardiology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California, USA
J Am Coll Cardiol 52:828-35. 2008..The purpose of this study was to test the hypothesis that superiority of biphasic waveform (BW) over monophasic waveform (MW) defibrillation shocks is attributable to less intracellular calcium (Ca(i)) transient heterogeneity... - Spark-induced sparks as a mechanism of intracellular calcium alternans in cardiac myocytesRobert Rovetti
Department of Mathematics, Loyola Marymount University, Los Angeles, Calif, USA
Circ Res 106:1582-91. 2010..Intracellular calcium (Ca) alternans has been widely studied in cardiac myocytes and tissue, yet the underlying mechanism remains controversial... - Inward rectification by polyamines in mouse Kir2.1 channels: synergy between blocking componentsLai Hua Xie
Cardiovascular Research Laboratory, Department of Medicine Cardiology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095, USA
J Physiol 550:67-82. 2003..1, is consistent with longer polyamines binding at their positively charged ends to the E224 and E299 positions in the same subunit, potentially accommodating four polyamine molecules per channel... - Effects of fibroblast-myocyte coupling on cardiac conduction and vulnerability to reentry: A computational studyYuanfang Xie
Department of Medicine Cardiology, David Geffen School of Medicine at University of California, Los Angeles, California 90095, USA
Heart Rhythm 6:1641-9. 2009.... - Spatiotemporal correlation between phase singularities and wavebreaks during ventricular fibrillationYen-Bin Liu
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA
J Cardiovasc Electrophysiol 14:1103-9. 2003..The close spatiotemporal correlation between PSs and WBs establishes that PSs are a valid alternate representation of WB during VF and further validated the use of phase mapping in the study of VF dynamics... - Irregularly appearing early afterdepolarizations in cardiac myocytes: random fluctuations or dynamical chaos?Daisuke Sato
Department of Medicine Cardiology, David Geffen School of Medicine at University of California, Los Angeles, California, USA
Biophys J 99:765-73. 2010..We conclude that the irregular dynamics of EADs is intrinsically chaotic, with random fluctuations playing a nonessential, auxiliary role potentiating the complex dynamics... - Action potential duration restitution and ventricular fibrillation due to rapid focal excitationMoshe Swissa
Division of Cardiology, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California 90048, USA
Am J Physiol Heart Circ Physiol 282:H1915-23. 2002..In this model of focal source VF, the VT-to-VF transition occurred due to a wave break outside the aconitine site, and drugs that flattened the APD restitution slope converted VF to VT despite continuous activation from aconitine site... - Intracellular calcium dynamics and acceleration of sinus rhythm by beta-adrenergic stimulationBoyoung Joung
Krannert Institute of Cardiology and the Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, USA
Circulation 119:788-96. 2009..Here we test the hypothesis that sinus rate acceleration by beta-adrenergic stimulation involves synergistic interactions between these clock mechanisms... - Atrioventricular ring reentry in embryonic mouse heartsMiguel Valderrabano
Department of Medicine, David Geffen School of Medicine at UCLA, 675 Charles Young Dr So, 3645 MRL, Los Angeles, Calif 90095 1760, USA
Circulation 114:543-9. 2006..We studied AV conduction during this transition and its sensitivity to autonomic modulation... - Nitric oxide donors protect murine myocardium against infarction via modulation of mitochondrial permeability transitionGuangwu Wang
Department of Physiology, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
Am J Physiol Heart Circ Physiol 288:H1290-5. 2005..These data suggest that a critical process during NO donor-induced cardioprotection is to prevent MPT pore opening potentially via targeting of the adenine nucleotide translocator... - Hysteresis and cell cycle transitions: how crucial is it?Zhangang Han
Cardiovascular Research Laboratory, Department of Medicine Cardiology, David Geffen School of Medicine at the University of California, Los Angeles, California 90095, USA
Biophys J 88:1626-34. 2005..Thus, although a hysteretic response is neither necessary nor sufficient, it is in general a much more robust mechanism for generating cell cycle dynamics than nonhysteretic mechanisms... - Autonomic regulation of calcium cycling in developing embryonic mouse heartsFuhua Chen
Department of Pediatrics and the Cardiovascular Research Laboratory, David Geffen School of Medicine at UCLA, 675 Charles Young Drive So. 3754 MRL, Los Angeles, CA 90095-7045, USA
Cell Calcium 39:375-85. 2006..These results define the functional and structural sequence of autonomic regulation of Ca(2+) transient in the embryonic mouse heart... - The pinwheel experiment revisited: effects of cellular electrophysiological properties on vulnerability to cardiac reentryMing Jim Yang
Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California, Los Angeles 90095, USA
Am J Physiol Heart Circ Physiol 293:H1781-90. 2007..We derive an analytical treatment that shows good agreement with numerical simulation results... - Modifying L-type calcium current kinetics: consequences for cardiac excitation and arrhythmia dynamicsAman Mahajan
UCLA Cardiovascular Research Laboratory, Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Biophys J 94:411-23. 2008..These findings provide a proof-of-concept test that I(Ca,L) can be targeted to increase dynamic wave stability without depressing contractility, which may have promise as an antifibrillatory strategy... - Tachycardia-induced early afterdepolarizations: insights into potential ionic mechanisms from computer simulationsRay B Huffaker
Department of Computer Science, University of California, 405 Hilgard Avenue, Los Angeles, CA 90095 1596, USA
Comput Biol Med 38:1140-51. 2008..Using two previously suggested spontaneous release morphologies, we found two distinct tachycardia-induced EAD mechanisms: one mechanistically similar to bradycardia-induced EADs, the other to delayed afterdepolarizations (DADs)... - ATP-sensitive K+ channels: regulation of bursting by the sulphonylurea receptor, PIP2 and regions of Kir6.2Bernard Ribalet
University of California Los Angeles Cardiovascular Research Laboratory, 90095, USA
J Physiol 571:303-17. 2006..In conjunction with this PIP2-dependent process, SUR1 also regulates channel activity via a PIP2-independent, but MgADP-dependent process... - Dynamics of the cell cycle: checkpoints, sizers, and timersZhilin Qu
Cardiovascular Research Laboratory, Departments of Medicine Cardiology and Physiology, David Geffen School of Medicine at University of California, Los Angeles, California 90095, USA
Biophys J 85:3600-11. 2003..This model successfully reproduces sizer, timer, and the restriction point features of the eukaryotic cell cycle, in addition to other experimental findings... - Atrioventricular conduction and arrhythmias at the initiation of beating in embryonic mouse heartsFuhua Chen
UCLA Cardiovascular Research Laboratory, David Geffen School of Medicine, University of California Los Angeles, 675 Charles Young Drive South, Los Angeles, CA 90095, USA
Dev Dyn 239:1941-9. 2010..In summary, at the onset of beating, I(f)-dependent pacemaking drives both AP propagation and Ca(i) transient generation through activation of voltage-dependent Ca channels. Na channels and intracellular Ca cycling have minor roles... - Redox regulation of endogenous substrate oxidation by cardiac mitochondriaPaavo Korge
Cardiovascular Research Laboratory, Department of Medicine, David Geffen University of California Los Angeles, School of Medicine, 3641 MRL Bldg, Los Angeles, CA 90095, USA
Am J Physiol Heart Circ Physiol 291:H1436-45. 2006..Incapacitation of this mechanism may potentially contribute to mitochondrial dysfunction during oxidative stress... - Anisotropic conduction block and reentry in neonatal rat ventricular myocyte monolayersCarlos de Diego
Cardiovascular Research Laboratory, Department of Medicine Cardiology and Physiology, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California 90095, USA
Am J Physiol Heart Circ Physiol 300:H271-8. 2011.... - Phosphatidylinositol-4,5-bisphosphate (PIP2) regulation of strong inward rectifier Kir2.1 channels: multilevel positive cooperativityLai Hua Xie
Cardiovascular Research Laboratory, Rm 3645 MRL Building, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
J Physiol 586:1833-48. 2008..Interaction with additional subunits exerts positive cooperativity at multiple levels to further enhance channel availability and promote the fully open state... - Effects of amiodarone on wave front dynamics during ventricular fibrillation in isolated swine right ventricleChikaya Omichi
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, University of California at Los Angeles School of Medicine, Los Angeles, California 90048-1865, USA
Am J Physiol Heart Circ Physiol 282:H1063-70. 2002..We conclude that amiodarone reduced spontaneous wave breaks. It might terminate VF or convert VF to VT. These effects were associated with the flattening of APD restitution slope and increased core size of reentrant wave fronts... - Coexistence of two types of ventricular fibrillation during acute regional ischemia in rabbit ventricleYen-Bin Liu
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
J Cardiovasc Electrophysiol 15:1433-40. 2004..Both ischemic and nonischemic regions develop proarrhythmic changes during regional ischemia, thus contributing to increased ventricular vulnerability to VF and sudden death during acute coronary occlusion... - Calcium dynamics and ventricular fibrillationMasahiro Ogawa
Circ Res 102:e52. 2008 - Mother rotors and the mechanisms of D600-induced type 2 ventricular fibrillationTsu Juey Wu
Cardiovascular Center, Taichung Veterans General Hospital and Institute of Clinical Medicine, National Yang Ming University School of Medicine, Taipei, Taiwan
Circulation 110:2110-8. 2004..Type 1 VF is characterized by the presence of multiple, wandering wavelets, whereas type 2 VF shows local spatiotemporal periodicity. We hypothesized that a single mother rotor underlies type 2 VF... - Mechanism of inward rectification in Kir channelsScott A John
J Gen Physiol 123:623-5. 2004 - The chicken or the egg? Voltage and calcium dynamics in the heartZhilin Qu
Am J Physiol Heart Circ Physiol 293:H2054-5. 2007 - Molecular basis for Kir6.2 channel inhibition by adenine nucleotidesBernard Ribalet
UCLA Cardiovascular Research Laboratory, Department of Physiology, University of California Los Angeles School of Medicine, 90095, USA
Biophys J 84:266-76. 2003..Based on these results a structural scheme is proposed, which includes features of other recently published models... - Reactive oxygen species production in energized cardiac mitochondria during hypoxia/reoxygenation: modulation by nitric oxidePaavo Korge
Cardiovascular Research Laboratory, Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
Circ Res 103:873-80. 2008.... - Systems approach to understanding electromechanical activity in the human heart: a national heart, lung, and blood institute workshop summaryYoram Rudy
Cardiac Bioelectricity and Arrhythmia Center, The Fred Saigh Distinguished Professor, Washington University, Campus Box 1097, Whitaker Hall Room 290B, One Brookings Dr, St Louis, MO 63130 4899, USA
Circulation 118:1202-11. 2008..The recommendations can be found on the NHLBI Web site at http://www.nhlbi.nih.gov/meetings/workshops/electro.htm... - Electrophysiological characterization of cardiac veins in humansDavid A Cesario
UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, Los Angeles CA
J Interv Card Electrophysiol 10:241-7. 2004..Further, the absence of such differences in pediatric patients could partly explain relative differences in types of supraventricular arrhythmias seen in different age groups... - Regulation of gating by negative charges in the cytoplasmic pore in the Kir2.1 channelLai Hua Xie
Cardiovascular Research Laboratory, Department of Medicine, David Geffen School of Medicine at UCLA, 675 Young Drive South, MRL 3645, Los Angeles, CA 90095, USA
J Physiol 561:159-68. 2004..1 channels. By suppressing fast gating, these negative charges facilitate polyamine block and unblock, which may be their physiologically important role... - Inferring the cellular origin of voltage and calcium alternans from the spatial scales of phase reversal during discordant alternansDaisuke Sato
Biophys J 92:L33-5. 2007..These results show that experimentally accessible measurements of Ca(i) and V(m) in cardiac tissue can be used to shed light on the cellular origin of alternans... - Calsequestrin-mediated mechanism for cellular calcium transient alternansJuan G Restrepo
Physics Department and Center for Interdisciplinary Research in Complex Systems, Northeastern University, Boston, Massachusetts, USA
Biophys J 95:3767-89. 2008..The ability to link microscopic properties of the calcium release units to whole cell behavior makes this model a powerful tool to investigate the arrhythmogenic role of abnormal calcium handling in many pathological settings...
Research Grants
- Metabolic Oscillations in HeartJAMES N contact WEISS; Fiscal Year: 2010..These insights may suggest novel therapies to protect the heart from injury during metabolic stresses such as heart attacks. ..
- Cardiac Fibrillation: Mechanisms and TherapyJames Weiss; Fiscal Year: 2007....
- PROPERTIES OF INWARD RECTIFIER K CHANNELSJames Weiss; Fiscal Year: 2007..Together, these studies in Kir channels will provide important insights into the regulation of excitability in ventricular and atrial cardiac muscle, as well as in other excitable tissues. ..
- Mitochondria and Cardiac Cell DeathJames Weiss; Fiscal Year: 2007....
- CARDIOVASCULAR SCIENTIST TRAINING PROGRAMJames Weiss; Fiscal Year: 2007..D.), the UCLA Cardiology STAR Program provides graduates with the rigorous research background essential to translate advances in molecular health sciences into modern molecular medicine. ..
- Afterdepolarizations and Cardiac ArrhythmiasJames N Weiss; Fiscal Year: 2010..S. citizens each year. The goal is to use this information to develop novel therapies to prevent this deadly manifestation of heart disease. ..