The combination therapy of colistin, artesunate, and EDTA could serve as a promising approach to combat colistin-resistant Salmonella infections by disrupting bacterial membranes, collapsing proton motive force, and increasing reactive oxygen species levels.

FMT alleviated the intestinal barrier damage caused by enterotoxigenic Escherichia coli infection in antibiotic-induced microbiome-disordered model through increasing the relative abundance of A. muciniphila in the intestine.

A mechanistic model based on the interaction of activity-independent cues from potential synaptic partners and local activity-dependent synaptic plasticity generates growing dendritic morphologies and non-random synaptic organization during development.