Polyvinylidene Fluoride Core-Shell Nanofiber Membranes with Highly Conductive Shells for Electromagnetic Interference Shielding.

As the demand for wireless sensors and equipment is unprecedentedly increasing, the interest in electromagnetic interference (EMI)-shielding materials that can effectively block accompanying electromagnetic interference is also constantly increasing. In particular, flexible and lightweight EMI-shielding materials that exhibit high EMI-shielding effectiveness (SE) have been more actively investigated as they are applicable to various applications. In this work, we reported the fabrication and performance of conducting polymer nanofiber EMI-shielding material, which was realized using electrospun polyvinylidene fluoride (PVDF) core-shell nanofiber membranes with highly conductive shells.

Persistently Elevated mTOR Complex 1-S6 Kinase 1 Disrupts DARPP-32-Dependent D Dopamine Receptor Signaling and Behaviors.

Background: The serine-threonine kinase mTORC1 (mechanistic target of rapamycin complex 1) is essential for normal cell function but is aberrantly activated in the brain in both genetic-developmental and sporadic diseases and is associated with a spectrum of neuropsychiatric symptoms. The underlying molecular mechanisms of cognitive and neuropsychiatric symptoms remain controversial.

Methods: The present study examines behaviors in transgenic models that express Rheb, the most proximal known activator of mTORC1, and profiles striatal phosphoproteomics in a model with persistently elevated mTORC1 signaling.

A Missense Variant at the Nrxn3 Locus Enhances Empathy Fear in the Mouse.

Empathy is crucial for our emotional experience and social interactions, and its abnormalities manifest in various psychiatric disorders. Observational fear is a useful behavioral paradigm for assessing affective empathy in rodents. However, specific genes that regulate observational fear remain unknown.

Hedgehog agonist therapy corrects structural and cognitive deficits in a Down syndrome mouse model.

Down syndrome (DS) is among the most frequent genetic causes of intellectual disability, and ameliorating this deficit is a major goal in support of people with trisomy 21. The Ts65Dn mouse recapitulates some major brain structural and behavioral phenotypes of DS, including reduced size and cellularity of the cerebellum and learning deficits associated with the hippocampus. We show that a single treatment of newborn mice with the Sonic hedgehog pathway agonist SAG 1.