Electrical stimulation at the lateral habenula causes an instantaneous remission of depressive symptoms in two rat models, with more medial stimulation sites exhibiting greater antidepressant effects than more lateral stimulation sites, as revealed by functional MRI studies.

The rapid antidepressant actions of low dose ketamine occur through the direct relief of suppression of protein synthesis via antagonism of a subset of NMDA receptors containing the GluN2B subunit.

There is substantial individual variation in behavioral and neural responses to acute ketamine administration in healthy controls, which emphasises the need for personalized approaches when harnessing ketamine as a treatment for depression.

Erlotinib-resistant AXL overexpressing cells are present in therapy-naive tumors, and expression of AXL in these cells is regulated through a stochastic mechanism centered on the epigenetic regulation of miR-335.

Sodium selenate is the first treatment with persistent disease-modifying effects reducing seizures and improving cognitive deficits, in chronically epileptic and drug-resistant TLE animals.

A systematic review shows no evidence of harm or benefit of antibiotic combinations on resistance evolution as clinical data lack statistical power to draw definitive conclusions, highlighting a knowledge gap.

The dimer destabilizers cause a dimer-to-monomer equilibrium shift favoring the human thymidylate synthase monomer more degradable by the proteasome, thus breaking the long-standing link between inhibition and enhanced expression of the protein to fight cancer drug resistance.

Most of the mRNAs whose translation is resistant to the stress-induced repression of protein synthesis contain upstream open reading frames that are efficiently translated under normal conditions.

Oncoprotein BCL6 confers tumor adaptive resistance to genotoxic stress through the IFN-BCL6-PTEN axis in solid tumors and presents a promising combinational target for chemo-sensitization.

Breast cancer resistant to either doxorubicin or epirubicin relies on distinct primary metabolic processes, which can be targeted to reduce cancer progression.