about
Transgenic overexpression of caveolin-3 in the heart induces a cardiomyopathic phenotypeStudy familial hypertrophic cardiomyopathy using patient-specific induced pluripotent stem cellsHomozygous missense N629D hERG (KCNH2) potassium channel mutation causes developmental defects in the right ventricle and its outflow tract and embryonic lethality.Clinical and molecular heterogeneity in the Brugada syndrome: a novel gene locus on chromosome 3.Adrenergic stimulation promotes T-wave alternans and arrhythmia inducibility in a TNF-alpha genetic mouse model of congestive heart failure.Targeting device therapy: genomics of sudden death.Statins Decrease Oxidative Stress and ICD Therapies.Systems approach to understanding electromechanical activity in the human heart: a national heart, lung, and blood institute workshop summary.Upsurge in T-wave alternans and nonalternating repolarization instability precedes spontaneous initiation of ventricular tachyarrhythmias in humans.Left ventricular diameter and risk stratification for sudden cardiac death.Effect of angiotensin-converting enzyme inhibitors and receptor blockers on appropriate implantable cardiac defibrillator shock in patients with severe systolic heart failure (from the GRADE Multicenter Study).Mechanism of automaticity in cardiomyocytes derived from human induced pluripotent stem cells.Survival benefit of implantable cardioverter-defibrillators in left ventricular assist device-supported heart failure patients.Mathematical modeling mechanisms of arrhythmias in transgenic mouse heart overexpressing TNF-αNocturnal peak in atrial tachyarrhythmia occurrence as a function of arrhythmia burden.Left Ventricular Dilatation Increases the Risk of Ventricular Arrhythmias in Patients With Reduced Systolic FunctionNighttime instabilities of neurophysiological, cardiovascular, and respiratory activity: integrative modeling and preliminary results.Genetic variation in the alternative splicing regulator RBM20 is associated with dilated cardiomyopathy.Prevention of adverse electrical and mechanical remodeling with biventricular pacing in a rabbit model of myocardial infarction.Angiotensin receptor type 1 single nucleotide polymorphism 1166A/C is associated with malignant arrhythmias and altered circulating miR-155 levels in patients with chronic heart failure.Ventricular arrhythmia risk after subarachnoid hemorrhage.The many faces of repolarization instability: which one is prognostic?Cardiac implantable electronic device infections: Who is at greatest risk?Effect of right ventricular versus biventricular pacing on electrical remodeling in the normal heart.Dissection of the voltage-activated potassium outward currents in adult mouse ventricular myocytes: I(to,f), I(to,s), I(K,slow1), I(K,slow2), and I(ss).N-(6-chloro-pyridin-3-yl)-3,4-difluoro-benzamide (ICA-27243): a novel, selective KCNQ2/Q3 potassium channel activator.Targeted replacement of KV1.5 in the mouse leads to loss of the 4-aminopyridine-sensitive component of I(K,slow) and resistance to drug-induced qt prolongation.Serum amine-based metabolites and their association with outcomes in primary prevention implantable cardioverter-defibrillator patients.Isolated right ventricular failure and abnormal hemodynamics caused by right ventricular pacing are reversed with cardiac resynchronization therapy.Searching for sudden death snps in calcium handling genes.Detecting instabilities of cardiac rhythm.Cardiac autonomic modulation by estrogen in female mice undergoing ambulatory monitoring and in vivo electrophysiologic testing.Myocarditis following adeno-associated viral gene expression of human soluble TNF receptor (TNFRII-Fc) in baboon hearts.Design of a phase 1/2 trial of intracoronary administration of AAV1/SERCA2a in patients with heart failure.Amiodarone and atrial fibrillation.Cloning and characterization of an olfactory cyclic nucleotide-gated channel expressed in mouse heart.Sirtuin 1 regulates cardiac electrical activity by deacetylating the cardiac sodium channel.The transient outward current in mice lacking the potassium channel gene Kv1.4.A common variant alters SCN5A-miR-24 interaction and associates with heart failure mortality.Emerging Potential Benefits of Modulating NAD+ Metabolism in Cardiovascular Disease.
P50
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P50
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onderzoeker
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researcher ORCID ID = 0000-0003-1506-3947
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name
Barry London
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Barry London
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Barry London
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Barry London
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Barry London
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Barry London
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Barry London
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Barry London
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Barry London
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Barry London
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Barry London
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Barry London
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0000-0003-1506-3947