Director, Basic Research Programs; Director, Cardiology Fellowship
Cardiology
Dr. Joshua I. Goldhaber, MD
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Joshua Goldhaber practices Cardiology. He went to medical school at Harvard Medical School. Harvard Medical School is a one of the best medicals schools. Harvard Medical School is ranked 1 in research and 12 in primary care medicine He received awards:"Fellow (FACC)", "Super Doctor" and "Fellow". Joshua Goldhaber is also published. He has 68 publications published. The lastest publication: "Connexin-43 hemichannels opened by metabolic inhibition.' He is registered with Medicare and accepts Medicare payments.
Publications
- A modified local control model for Ca(2+) transients in cardiomyocytes: Junctional flux is accompanied by release from adjacent non-junctional RyRs.
- Na/Ca exchange and contraction of the Heart.
- 20 years from NCX purification and cloning: milestones.
- Cardiac sodium-calcium exchange and efficient excitation-contraction coupling: implications for heart Disease.
- The role of E2F-1 and downstream target genes in mediating ischemia/reperfusion injury in vivo.
- Sodium-calcium exchange is essential for effective triggering of calcium release in mouse Heart.
- Role of inotropic agents in the treatment of Heart failure.
- Loss of intracellular and intercellular synchrony of calcium release in systolic Heart failure.
- Novel features of the rabbit transverse tubular system revealed by quantitative analysis of three-dimensional reconstructions from confocal images.
- Reprogrammed mouse fibroblasts differentiate into cells of the cardiovascular and hematopoietic lineages.
- Effect of metabolic inhibition on couplon behavior in rabbit ventricular myocytes.
- Gi alpha 1-mediated cardiac electrophysiological remodeling and arrhythmia in hypertrophic Cardiomyopathy.
- Homozygous overexpression of the Na+-Ca2+ exchanger in mice: evidence for increased transsarcolemmal Ca2+ fluxes.
- Na+/Ca2+ exchanger knockout mice: plasticity of cardiac excitation-contraction coupling.
- Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger.
- Mechanism of shortened action potential duration in Na+-Ca2+ exchanger knockout mice.
- Is the ryanodine receptor a target for antiarrhythmic therapy?
- Excitation-contraction coupling in Na+-Ca2+ exchanger knockout mice: reduced transsarcolemmal Ca2+ flux.
- Mutation in sodium-calcium exchanger 1 (NCX1) causes cardiac Fibrillation in zebrafish.
- Cardiac-specific ablation of the Na+-Ca2+ exchanger confers protection against ischemia/reperfusion injury.
- Effects of Na+-Ca2+ exchange expression on excitation-contraction coupling in genetically modified mice.
- Metabolic inhibition alters subcellular calcium release patterns in rat ventricular myocytes: implications for Defective excitation-contraction coupling during cardiac...
- Action potential duration restitution and alternans in rabbit ventricular myocytes: the key role of intracellular calcium cycling.
- Genetic manipulation of cardiac Na+/Ca2+ exchange expression.
- Functional adult myocardium in the absence of Na+-Ca2+ exchange: cardiac-specific knockout of NCX1.
- Return of calcium: manipulating intracellular calcium to prevent cardiac pathologies.
- Knockout mice for pharmacological screening: testing the specificity of Na+-Ca2+ exchange inhibitors.
- The Na+-Ca2+ exchanger is essential for the action of cardiac glycosides.
- Oxygen free radicals and cardiac reperfusion abnormalities.
- Effects of lysophosphatidylcholine on electrophysiological properties and excitation-contraction coupling in isolated guinea pig ventricular myocytes.
- Mechanisms of excitation-contraction coupling Failure during metabolic inhibition in guinea-pig ventricular myocytes.
- Effects of exogenous free radicals on electromechanical function and metabolism in isolated rabbit and guinea pig ventricle. Implications for ischemia and reperfusion ...
- Excitation-contraction coupling in single guinea-pig ventricular myocytes exposed to hydrogen peroxide.
- Lactate transport in mammalian ventricle. General properties and relation to K+ fluxes.
- Effects of physical exercise training in Syndrome X.
- Endothelium-dependent vasodilators do not cause propagated intercellular Ca2+ waves in vascular endothelial monolayers.
- Free radicals enhance Na+/Ca2+ exchange in ventricular myocytes.
- Effects of TNF-alpha on [Ca2+]i and contractility in isolated adult rabbit ventricular myocytes.
- Mechanism of hypoxic K loss in rabbit ventricle.
- Safety and hemodynamic effects of intravenous triiodothyronine in advanced Congestive heart failure.
- Localization and functional effects of adenosine A1 receptors on cardiac vagal afferents in adult rats.
- Beta1 integrins participate in the hypertrophic response of rat ventricular myocytes.
- Connexin-43 hemichannels opened by metabolic inhibition.
- Induction of monocyte binding to endothelial cells by MM-LDL: role of lipoxygenase metabolites.
- High-density lipoprotein increases intracellular calcium levels by releasing calcium from internal stores in human endothelial cells.
- Local regulation of the threshold for calcium sparks in rat ventricular myocytes: role of sodium-calcium exchange.
- Sodium-calcium exchange: the phantom menace.
- Intracellular Ca(2+) dynamics and the stability of ventricular tachycardia.
- Putative ryanodine receptors in the sarcolemma of ventricular myocytes.
- Metabolic inhibition activates a non-selective current through connexin hemichannels in isolated ventricular myocytes.
- Oxygen free radicals and excitation-contraction coupling.
- Phenylarsine oxide induces mitochondrial permeability transition, hypercontracture, and cardiac cell death.
- Complete Atrial-specific knockout of sodium-calcium exchange eliminates sinoAtrial node pacemaker activity.
- Mitochondrial Ca(2+) uptake by the voltage-dependent anion channel 2 regulates cardiac rhythmicity.
- Proarrhythmia in a non-failing murine model of cardiac-specific Na(+)/Ca (2+) exchanger overexpression: whole Heart and cellular mechanisms.
- Activation of reverse Na+-Ca2+ exchange by the Na+ current augments the cardiac Ca2+ transient: evidence from NCX knockout mice.
- Na+ currents are required for efficient excitation-contraction coupling in rabbit ventricular myocytes: a possible contribution of neuronal Na+ channels.
- Recapitulation of the embryonic cardiovascular progenitor cell niche.
- Triple threat: the Na+/Ca2+ exchanger in the pathophysiology of cardiac arrhythmia, ischemia and Heart failure.
- Towards computational modeling of excitation-contraction coupling in cardiac myocytes: reconstruction of structures and proteins from confocal imaging.
- Spontaneously beating cardiomyocytes derived from white mature adipocytes.
- Dysfunction of ouabain-induced cardiac contractility in mice with Heart-specific ablation of Na,K-ATPase beta1-subunit.
- Movement of vault particles visualized by GFP-tagged major vault protein.
- Sub-micrometer anatomical models of the sarcolemma of cardiac myocytes based on confocal imaging.
- Na(+)--Ca2+ exchange in the regulation of cardiac excitation-contraction coupling.
- Cardiac excitation-contraction coupling in the absence of Na(+) - Ca2+ exchange.
- Mice overexpressing the cardiac sodium-calcium exchanger: Defects in excitation-contraction coupling.
Schools
Harvard Medical School
Procedures Preformed
- Cardiac Catheterization (incl. Coronary Angiography)
- Cardiac Imaging
- Cardioversion, Elective
Conditions Treated
- Angina and Acute Coronary Syndrome
- Aortic Ectasia
- Aortic Valve Disease
- Arrhythmias (incl. Atrial Fibrillation)
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Doctors Specialties
- Cardiology
Accepted Insurances
Awards
- Fellow (FACC)
- Super Doctor
- Fellow
Education
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UCLA Medical Center -
Harvard Medical School
Hospital
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Cedars-Sinai Medical Center
Drug Facts
| NPI NUMBER | 1750306940 | |
| NPPES Provider LastName | GOLDHABER | |
| NPPES Provider FirstName | JOSHUA | |
| NPPES Provider ZIPCode | 900481804 | |
| NPPES Provider State | CA | |
| Specialty Description | Cardiology | |
| Total Claim Count | 19.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1750306940 |
| Last Name Of The Provider | GOLDHABER |
| First Name Of The Provider | JOSHUA |
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