High-performance plasmonic polymer modulators through mode hybridization and electro-thermomechanical effects.

In this work, an electro-optical polymer modulator with double-layered gold nanostrips, a polymer nanograting, and a metal substrate is proposed and designed. Interestingly, mode hybridization between the Fabry-Pérot (F-P) and anti-bonding modes is formed, and strongly depends on the nanograting size, which can be controllably modulated by an injection current. The simulation and calculation results show that the temperature sensitivity and large structural sensitivity for the polymer modulator could remain constant during the current-tuning process, and a near-zero reflectance and a low linewidth of 13.

Multiplexed chemogenetics in astrocytes and motoneurons restore blood-spinal cord barrier in ALS.

Blood-spinal cord barrier (BSCB) disruption is thought to contribute to motoneuron (MN) loss in amyotrophic lateral sclerosis (ALS). It is currently unclear whether impairment of the BSCB is the cause or consequence of MN dysfunction and whether its restoration may be directly beneficial. We revealed that , , , and ALS mouse models commonly shared alterations in the BSCB, unrelated to motoneuron loss.

Synaptic restoration by cAMP/PKA drives activity-dependent neuroprotection to motoneurons in ALS.

Excessive excitation is hypothesized to cause motoneuron (MN) degeneration in amyotrophic lateral sclerosis (ALS), but actual proof of hyperexcitation in vivo is missing, and trials based on this concept have failed. We demonstrate, by in vivo single-MN electrophysiology, that, contrary to expectations, excitatory responses evoked by sensory and brainstem inputs are reduced in MNs of presymptomatic mutSOD1 mice. This impairment correlates with disrupted postsynaptic clustering of Homer1b, Shank, and AMPAR subunits.

NF-κB activation in astrocytes drives a stage-specific beneficial neuroimmunological response in ALS.

Astrocytes are involved in non-cell-autonomous pathogenic cascades in amyotrophic lateral sclerosis (ALS); however, their role is still debated. We show that astrocytic NF-κB activation drives microglial proliferation and leukocyte infiltration in the SOD1 (G93A) ALS model. This response prolongs the presymptomatic phase, delaying muscle denervation and decreasing disease burden, but turns detrimental in the symptomatic phase, accelerating disease progression.

Two nonsense mutations cause protein C deficiency by nonsense-mediated mRNA decay.

Introduction: Protein C deficiency is a genetic disorder caused by mutations in the protein C gene (PROC). More than 10% of nonsense and frameshift mutations carrying premature termination codons have been identified in PROC, but the exact molecular mechanisms of these mutations on the pathogenesis of protein C deficiency remain unclear.

Objective: The aim of this study is to investigate whether nonsense-mediated mRNA decay (NMD) can be a mechanism accounting for protein C deficiency.

Pressure-induced structural change in orthorhombic perovskite GdMnO3.

Structural stability of the perovskite-type GdMnO(3) has been investigated by the synchrotron angle-dispersive x-ray diffraction technique up to 63 GPa in a diamond anvil cell. GdMnO(3) stays in an orthorhombic structure but undergoes an isostructural phase transition with ~5% volume reduction at 50 GPa. In the parent orthorhombic phase, the compressions along a, b and c axes exhibit a large anisotropic behavior.