TBX5-loss associated cardiomyocyte ectopy and atrial fibrillation is prevented by augmentation of SERCA2 activity, establishing a mechanism underlying the genetic basis for a Ca²⁺-dependent pathway for AF risk.

Excitability gradients in heart tissue, imposed by structured sub-threshold optogenetic stimulation, induce drift and termination of spiral waves, thus providing an explanation for successful optogenetic defibrillation in small animal hearts.

Customization of ion channel gating enhances homeostatic regulation through automatic detection and correction of abnormal physiological changes, as illustrated by self-restoration of excitation rhythm in cardiac arrhythmias.

Enhancing mitochondrial Ca²⁺ uptake effectively suppresses aberrant Ca²⁺ induced arrhythmogenic events in zebrafish, mouse and human cardiomyocytes, demonstrating a critical role for mitochondria in the regulation of cardiac rhythmicity.

An integrative approach, combining genetic mouse and large-scale human genetics studies, was used to reveal a novel role for the Bcl-2 protein Bid in maintenance of mitochondrial function that alters susceptibility to myocardial infarction.

Inter-molecular cross-seeding between phenol-soluble modulins facilitates rapid and efficient self-assembly in Staphylococcus aureus biofilms revealing a complex molecular interplay between distinct phenol-soluble modulins orchestrating functional amyloid formation.

Computer simulations show how low-intensity illumination can be used to terminate cardiac arrhythmias.

Polyunsaturated fatty acid analogues show selectivity for different cardiac ion channels, suggesting their potential use for the treatment of different subtypes of Long QT Syndrome.

Neural ensemble activity in the human motor cortex contains dynamical structure that is independent of movement parameters and is not well-explained by current models.

New computer algorithms have allowed people with paralysis to achieve the highest reported typing performance using a brain-computer interface.