RESUMO
The flexible control of surface plasmon polaritons (SPPs) is important and intriguing due to its wide application in novel plasmonic devices. Transformation optics (TO) offers the capability either to confine the SPP propagation on rigid curved/uneven surfaces, or to control the flow of SPPs on planar surfaces. However, TO has not permitted us to confine, manipulate, and control SPP waves on flexible curved surfaces. Here, we propose to confine and freely control flexible SPPs using TO and graphene. We show that SPP waves can be naturally confined and propagate on curved or uneven graphene surfaces with little bending and radiation losses, and the confined SPPs are further manipulated and controlled using TO. Flexible plasmonic devices are presented, including the bending waveguides, wave splitter, and Luneburg lens on curved surfaces. Together with the intrinsic flexibility, graphene can be served as a good platform for flexible transformation plasmonics.
Assuntos
Grafite/química , Lentes , Nanopartículas/química , Refratometria/instrumentação , Ressonância de Plasmônio de Superfície/instrumentação , Desenho Assistido por Computador , Módulo de Elasticidade , Desenho de Equipamento , Análise de Falha de EquipamentoRESUMO
Atrial fibrillation (AF) is a common cardiac arrhythmia whose molecular etiology is poorly understood. We studied a family with hereditary persistent AF and identified the causative mutation (S140G) in the KCNQ1 (KvLQT1) gene on chromosome 11p15.5. The KCNQ1 gene encodes the pore-forming alpha subunit of the cardiac I(Ks) channel (KCNQ1/KCNE1), the KCNQ1/KCNE2 and the KCNQ1/KCNE3 potassium channels. Functional analysis of the S140G mutant revealed a gain-of-function effect on the KCNQ1/KCNE1 and the KCNQ1/KCNE2 currents, which contrasts with the dominant negative or loss-of-function effects of the KCNQ1 mutations previously identified in patients with long QT syndrome. Thus, the S140G mutation is likely to initiate and maintain AF by reducing action potential duration and effective refractory period in atrial myocytes.