Research
Our research develops the theoretical and computational tools to predict instability in complex material systems: statistical precursors to fracture in disordered solids, failure mode selection in soft and porous media, and force-driven shape changes in living cells. The common language is mechanics and statistical physics.
Criticality & Statistical Failure
Catastrophic failure is not a single event — it is the culmination of countless interacting micro-failures that organize into an avalanche. We use tools from statistical physics to understand how disorder shapes the collective mechanics of failure, and to identify universal statistical signatures that precede catastrophe. Our long-term goal is a predictive science of failure: forecasting structural collapse from early acoustic signals, long before any macroscopic damage is visible. The open questions are rich — how does disorder shape the statistics of failure? How do fluctuations scale with sample size, crystalline symmetry, and loading rate?
Instability & Fracture in Soft Solids
Gels, elastomers, and biological tissues fail by breaking symmetry, not just propagating a crack. We have shown that damage localization in soft solids is itself a bifurcation — and that the resulting fracture patterns depend critically on geometry, confinement, and material nonlinearity. Going forward, we aim to extend this framework to fluid-driven failure: blistering, hydraulic uplift in soft soils, and fracture in porous biological media. The unifying goal is a regime map — predicting which failure mode a pressurized or loaded soft solid will select, and when.
Mechanics of Living Matter
The cell surface — a composite of the actomyosin cortex and plasma membrane — is an active material that generates, senses, and transmits forces to drive division, motility, and tissue morphogenesis. We have built the first viscous active shell theory of the cell cortex and shown how protrusions and contractions propagate long-range membrane tension. Ahead, we aim to understand 3D amoeboid migration through stochastic cortex–membrane detachment, model tissue remodeling during wound healing, and ultimately connect single-cell mechanics to organ-scale developmental processes.