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Mutations along the signaling pathway of the E. coli sensor histidine kinase PhoQ alter signal gain and ligand-sensitivity by altering thermodynamic allosteric coupling between domains.

Two distinct projections from the basolateral amygdala to nucleus accumbens differentially contribute to cue- versus reward-mediated behavioral reinforcement.

Patterns of communication between the thalamus and the cortex are correlated with anesthesia-induced loss of consciousness and recovery.

Skeletal muscle stem cells play important roles in the regeneration of neuromuscular junctions, and so present new targets for therapies to treat neuromuscular decline observed in the context of aging and various neuromuscular diseases.

Anaesthesia and disorders of consciousness both reduce the capacity of the human brain to integrate information, specifically targeting interactions within a shared circuit of regions in the brain’s default network.

Brain recovery after injury can be predicted based on its activity and structure, which may allow us to understand why some brain injuries lead to permanent loss of cognitive function, while others do not.

The protein translocation apparatus of the inner- (Sec) and outer-membrane (BAM) interact to form a trans-periplasmic super-complex capable of long-range, PMF-dependent conformational changes to facilitate efficient outer-membrane protein maturation.

Experimental and computational approaches reveal how ligand binding is coupled to voltage sensing in a HCN channels.

Involuntary eye movements that keep images positioned over the center of the retina are synchronized with blinks to minimize disruption to vision.

Preclinical efficacy experiments testing sunitinib in animal cancer models display a lack of methodological rigour, with trim-and-fill analysis suggesting prominent publication bias that leads to an overestimation of treatment effect.