Cell biology analysis demonstrated for the first time the effect of chronic ethanol consumption in neutrophil impaired migration by CXCR2 downregulation and neutrophil function during acute Aspergillus fumigatus infection.

Prenatal ethanol exposure results in aberrant tangential migration by altering NKCC1-mediated chloride homeostasis that can be mitigated by bumetanide.

Maternally experienced environmental stress leads to multigenerational inheritance of ethanol preference and an altered rewards pathway in Drosophila melanogaster.

Electrophysiology, optogenetics, and imaging in a mouse model of Dravet syndrome reveals dentate gyrus circuit dysfunction driven by hyperexcitability of the perforant path input from entorhinal cortex that can be modulated by recruitment of parvalbumin-expressing inhibitory interneurons.

Dissection of a cis-regulatory element (CRM) in its native chromosomal context using CRISPR/Cas9 editing and novel 'Active Genetics' reveals new features of CRM function and insights into how such regulatory elements change during evolution.

MreB filaments bind, orient, and move along the direction of greatest membrane curvature, thus orienting the insertion of new glycan strands around the cell circumference in a manner that may help establish and maintain rod shape.

HNF1A, a risk factor gene for pancreatic ductal adenocarcinoma, is critical to maintaining pancreatic cancer stem cell properties through regulating POU5F1 (OCT4) expression, providing a novel role for HNF1A in maintenance of the disease.

Mice that successfully avoid developing tinnitus despite exposure to excessive noise show spontaneous recovery of KCNQ2/3 potassium channel activity associated with a reduction in HCN channel activity in auditory brainstem neurons.

Population mutation rates are highly flexible and evolvable under extreme stress conditions, matching changes in selective pressure to avoid extinction of the entire population.

Biochemical and microscopy-based approaches in mouse and human macrophages reveal that glycine cytoprotection acts at the level of the newly identified pan-death protein NINJ1 to inhibit multiple lytic cell death pathways, thereby resolving a long-standing mechanism of glycine cytoprotection.