More than a decade of expert testimony in pharmaceutical injury and drug-related death — built on thirty years of UCSF research into how drugs act from molecule to cell to whole organ. Scientific causation that holds up under Rule 702 and Daubert.
Three decades on the faculty of the School of Medicine at the University of California, San Francisco produced more than fifty peer-reviewed publications in journals including Nature, Neuron, and the Journal of Physiology — and a command of drug action across every level a defensible causation analysis must connect.
That record includes the co-discovery of the L- and T-type cardiac calcium channels and the mechanism of dihydropyridine action, and the identification of mechanosensitive TRPV4 channels as a driver of Duchenne muscular dystrophy pathology. In litigation, this is the difference between asserting that a drug caused harm and demonstrating, mechanistically, how.
Seven-time Teacher of the Year at UCSF and two-time AACP Teacher of the Year — the same ability to make ion-channel biophysics clear to first-year students makes molecular causation clear to a jury.
Pharmaceutical product liability, drug-induced injury, and drug-related death — for plaintiff and defense counsel, with national availability.
Early assessment of scientific merit and the viability of a causation theory — before it shapes the rest of the case.
Rule 702–compliant written opinions that lay out reliability step by step, grounded in the primary scientific literature.
Testimony anchored in peer-reviewed science and prepared to withstand cross-examination on methodology.
Jury-accessible explanation of molecular mechanism and causation, without sacrificing scientific precision.
Foundational discoveries in cardiac and neuronal ion channels — the same biology that underlies drug-induced arrhythmia, sudden cardiac death, myopathy, and CNS adverse events.
Discovered the hyperpolarization-activated current responsible for spontaneous rhythm of the sinoatrial node — relevant to drug-induced arrhythmia and sudden cardiac death.
Co-discovered the distinct channel subtypes in ventricular myocytes and how dihydropyridines and beta-adrenergic agonists modulate heart rate and contractility — direct authority on drug action at cardiac ion channels.
First direct measurement of how long a single Ca²⁺ ion resides within the calcium-channel pore — definitive evidence for the two-site model of selectivity.
Identified mechanically-activated channels in vascular endothelial cells as the transducer of blood pressure and shear flow — relevant to drug-induced hypertension and endothelial dysfunction.
Established these channels as the dominant pathway for pathological Ca²⁺ influx in Duchenne muscular dystrophy — relevant to drug-induced myopathy, rhabdomyolysis, and cardiomyopathy.
Characterized functionally distinct L-type Ca²⁺ channels in brain neurons and a novel store-depletion pathway for refilling intracellular Ca²⁺ stores — relevant to CNS adverse events.
Demonstrated electrical remodeling in cerebellar neurodegenerative disease — relevant to drug-induced neurotoxicity and cerebellar ataxia.
Causation analysis that connects molecule to cell to organ — the levels Rule 702 requires a reliable opinion to bridge.
Opinions grounded in the peer-reviewed record, by an author of that record across Nature, Neuron, and the Journal of Physiology.
A seven-time Teacher of the Year who can make ion-channel biophysics — and your causation theory — clear to twelve lay jurors.
A 30-minute call carries no fee and resolves whether the engagement is a fit — for both plaintiff and defense counsel, nationwide.
Initial consultations do not create an engagement and are not legal or medical advice. Information shared before a signed engagement should be non-privileged.
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