Systemic pharmacological suppression of neural activity reverses learning impairment in a mouse model of Fragile X syndrome.

The enhancement of associative synaptic plasticity often results in impaired rather than enhanced learning. Previously, we proposed that such learning impairments can result from saturation of the plasticity mechanism (Nguyen-Vu et al., 2017), or, more generally, from a history-dependent change in the threshold for plasticity.

Cytokines drive the formation of memory-like NK cell subsets via epigenetic rewiring and transcriptional regulation.

Activation of natural killer (NK) cells with the cytokines interleukin-12 (IL-12), IL-15, and IL-18 induces their differentiation into memory-like (ML) NK cells; however, the underlying epigenetic and transcriptional mechanisms are unclear. By combining ATAC-seq, CITE-seq, and functional analyses, we discovered that IL-12/15/18 activation results in two main human NK fates: reprogramming into enriched memory-like (eML) NK cells or priming into effector conventional NK (effcNK) cells. eML NK cells had distinct transcriptional and epigenetic profiles and enhanced function, whereas effcNK cells resembled cytokine-primed cNK cells.

Discovering Pyramidal Treasures: Multi-Scale Design of High Strength-Ductility Titanium Alloys.

Mechanical properties of titanium alloys, one of humankind's most essential structural materials, suffer from the lack of 〈c + a〉 dislocations on pyramidal slip planes, failing homogeneous plastic strain accommodation. This mechanical treasure is not easily accessible in titanium alloys because of the required excessively high stress levels. The present work demonstrates that such a dilemma may be overcome by meticulously tuning the c/a ratio, the simplest crystallographic parameter of the hexagonal close-packed lattice, through Sn alloying.