The Pseudomonas aeruginosa secreted signaling molecule 2'-aminoacetophenone modulates cellular immunometabolism to promote persistence in infected tissues.

Applied and computational results show how dimensionality reduction approaches can help in grouping correlated genetic variant-exposure associations and improve causal inference in the Mendelian randomisation framework.

Release site heterogeneity represents a previously unknown level of structural and functional organization within individual active zones in central synapses, which determines the spatiotemporal dynamics of multi-vesicular release.

The number of neurotransmitter vesicles released into the synaptic cleft is regulated by the size of the readily-releasable pool upstream of release probability.

A cystic fibrosis (CF) lung microbiome-informed in vitro polymicrobial system allows for a mechanistic understanding of community-specific tolerance of Pseudomonas aeruginosa to a front-line CF antimicrobial.

The integration of signals via the pleiotropic NF-kappaB (NF-κB) system enables microenvironmental cues to tune cellular responses to pathogenic substances.

A novel Mendelian randomisation framework unravels one gene expression component, correlated with proliferation and genome stability-related features, associated with telomere length in lung adenocarcinoma tumours, which provides insights into how telomere length influences the genetic basis of lung cancer aetiology.

Autism-associated iPSC-derived neurons mutant in CNTN5 or EHMT2 are hyperactive.

Phenome-wide estimation of causality between plasma triglyceride levels and disease risk highlights associations with atherosclerotic disease and other unrelated diseases.

Asynchronous release is not uniform, but comprises two subpopulations of events, one occurring inside the active zone and another occurring ectopically, which are characterized by distinctive spatiotemporal dynamics in hippocampal synapses.