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 13.8 nm in the red region corresponding to a high quality (Q) factor of 51 is achieved. In addition, a large redshift of 60.7 nm and a super-high modulation depth of 424 are obtained at only 8 µA.

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. METHODS: PROC of genomic DNA was amplified and sequenced. Recombinant plasmids expressing wild-type (wt) and mutant EGFP-protein C (EGFP-PC) cDNA were constructed and transiently transfected into human embryonic kidney cells using lipofectamine. Expression of mRNAs and proteins of EGFP-PC and NMD factor UPF1 were analyzed by qPCR and Western blot. RESULTS: DNA sequencing revealed a novel heterozygous nonsense mutation (p.Trp247*) in patient 1 and two compound heterozygous mutations (p.Phe181Val and p.Arg199*) in patient 2. Expression studies showed that cells transfected with the mutant plasmids expressed significantly lower levels of EGFP-PC mRNAs and proteins compared to cells transfected with the wt plasmid. A translation inhibitor cycloheximide and UPF1 small interfering RNA (UPF1 siRNA) significantly increased mRNA or protein expression of EGFP-PC in cells transfected with the mutant plasmids. CONCLUSION: Two PROC nonsense mutations (p.Trp247* and p.Arg199*) trigger NMD, resulting in protein C deficiency.