Human neuroimaging with time-evolving network analysis reveals dynamic interactions among multiple functional brain networks in response to sustained pain.

Imaging of structure and function in the brain from thousands of participants was used along with genetics and biophysical measures to study many different aspects of how the brain ages.

Ex vivo, in vitro, and computational modeling studies indicate a persistence of myofibroblast senescence in the infarct border zone with age which can disrupt conduction and promote arrhythmias via senescent myofibroblast-cardiomyocyte coupling.

Integrated stress response-induced expression of ATF4 and its transactivation of SOX9 causes aberrant chondrocyte differentiation and skeletal defects which can be alleviated by modulating initiation-factor eIF2α phosphorylation translation control.

Indomethacin, a nonsteroidal anti-inflammatory drug, alters the composition of the intestinal microbiota, and the intestinal microbiota affect the pharmacokinetics of indomethacin.

Although cellular organelles show a functional deterioration in aging, genetic loci associated with common age-associated disease instead nominate nuclear transcription factors across several age-related diseases.

Mechanosensitive channels Piezo1/2 are required for osteoblast differentiation from progenitors by sensing fluid sheer stress and matrix rigidity and regulating NFATc1, YAP1 and ß-catenin activities through Ca²⁺ stimulated phosphatase calcineurin.

The loading-induced temperature evolution phenomenon in the knee joint modulates chondrogenic cells response to loading and accordingly opens a new paradigm that is coined 'thermo-mechanobiology'.