Live-cell imaging captures the heterogenity of bacterial growth within intracellular bacterial communities and demonstrates that the constituent bacteria are protected from clearance by antibiotics delivered with a physiologically relevant pharmacodynamic profile.

A new role is identified for GLI1 in modulating the inflammatory response of macrophages and the overaction of osteoclasts in collagen-induced arthritis by collaboratively regulating DNMT1 and DNMT3a.

A link between chronic stress and organ dysfunction is explained by the gateway reflex, in which brain micro-inflammation at specific vessels establishes a new neural pathway to induce fatal organ failure particularly in gastrointestine and heart.

Identifying the patient-specific mutation that shifted the antibody light chain to the deadly fibrillar species provides new insight in the molecular pathogenesis of AL amyloidosis.

Analysis of protein interfaces suggests cotranslational assembly can be an adaptive process, likely serving to minimise non-specific interactions with other proteins in the cell.

Activation of TRPV4 induced increases in Ca²⁺ influx, activated CaMKII, enhanced pro-inflammatory NFκB-NLRP3 signaling, and promoted inflammation response, thus contributing to pathological cardiac remodeling.

Kasugamycin potentiates rifampicin killing of Mycobacterium tuberculosis by targeting adaptive mistranslation.