Ablation of the G-protein-coupled receptor C3aR1 specifically on macrophages or Kupffer cells does not alter the course of metabolic dysfunction-associated steatotic liver disease in a dietary mouse model.

A single amino acid change in a neuronal ion channel called KCNQ2 blocks ion flow, prevents protein localization on axons, and results in severe epilepsy and slowed neurological development.

Human-based electromechanical simulations reveal electrocardiogram biomarkers are better indicators of pro-arrhythmic substrate after myocardial infarction than ejection fraction.