Leonard A. Harris

The paper presents a coupled fluid-structure and systems biology model to simulate aortic valve calcification dynamics, showing fibrosis-induced stiffening accelerates calcification through altered biomechanical and biochemical pathways.

This paper develops a computational model of tumor-bone interactions to predict how different tumor types respond to perturbations, showing that bone-adapted tumors are less dependent on bone-derived growth factors and less responsive to OC-targeted therapy.

The paper uses Bayesian multimodel inference to analyze tumor growth mechanisms in SCLC, finding that high lineage plasticity, not rare stem-like populations, drives tumor evolution.

This paper introduces a method using real-time luminescence to estimate drug response in cell lines, avoiding the need for cell counting and fluorescent labeling.

The paper identifies heterogeneous drug-tolerant persisters (DTPs) as population-level states with distinct division and death rates, showing increased ferroptosis susceptibility.

This paper introduces an unsupervised logic-based method to infer mechanistic hypotheses of cellular processes from state transitions, recovering dynamics and biochemical species concentration changes.

This study disentangles genetic, epigenetic, and stochastic factors contributing to drug-response variability in an in vitro tumor heterogeneity model using PC9 cell lines.

The paper introduces MAGINE, a framework for analyzing multi-omics time-course data to build mechanistic hypotheses of cellular responses to perturbations.

The paper presents GPU-SSA, a GPU-accelerated implementation of the Stochastic Simulation Algorithm, showing significant speedup over CPU implementations for chemical reaction simulations.