Karoline Horgmo Jæger

TL;DR: It is concluded that collections of cardiac cells can be simulated using the EMI model, and that the E MI model enable greater modeling flexibility than the classical monodomain and bidomain models.

TL;DR: The present work explores the accuracy of the classical models (a) and (b) by comparing them to more accurate models available where the potentials inside and outside the neurons are computed simultaneously in a self-consistent scheme.

TL;DR: It is concluded that a non-uniform sodium channel distribution increases the conduction velocity and decreases the time delays over gap junctions of reduced coupling in the EMI model simulations, and ephaptic coupling can influence the dynamics of the sodium channels and potentially provide cell-to-cell coupling when the gap junction connection is absent.

TL;DR: A computational framework is described to address a limitation in the ability of hiPSC derived cardiomycocytes to predict dangerous drug side effects, and indicates that optically obtained waveforms of voltage and calcium from microphysiological systems can be inverted into information on drug ion channel blockage.

TL;DR: An updated action potential model is utilized to represent both hiPSC-CMs and adult cardiomyocytes, an IC50-based model of dose-dependent drug effects is applied, and a continuation-based optimization algorithm is introduced for analysis of dose escalation measurements using five drugs with known effects.