A computer model of human cardiomyocyte was produced and validated on independent datasets, overcoming shortcomings of its predecessors, also yielding broadly relevant insights and results on major ionic currents.

Mild myelin disruption leads to early axonal pathology, a novel pathological response in neural stem cells, regionally increased oligodendrocytes and altered behavior.

Important mechanistic details on Duchenne Muscular Dystrophy arrhythmogenesis are revealed, providing a crucial lead for investigators interested in developing therapeutic solutions for this deadly disease.

Single-cell sequencing combined with in situ hybridizations reveal dynamic patterns of differentially expressed genes throughout the ventricular and subventricular zone of the embryonic mouse brain, which likely play important roles in cell fate determination.

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.

Production of remyelinating subventricular zone oligodendrocyte progenitors is stimulated by transient abrogation of thyroid hormone signalling in the adult neural stem cell niche.

The functional interaction of Na⁺ and K_ATP channels at the intercalated disk of cardiomyocytes depends on Ankyrin G and is clinically relevant since K_ATP channel mutations affect Na⁺ channel expression.

Genetic mouse models identify a critical mechanism of myogenic vasoconstriction and reveal the in vivo function of myogenic autoregulation in protecting from organ overperfusion and in maintaining vascular resistance.

The Ca²⁺-driven functional coupling of CaV1.2 channels is a mechanism of channel memory that may modulate the amplification of Ca²⁺ influx.

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