Fano resonances in plasmonic core-shell particles and the Purcell effect

Despite a long history, light scattering by particles with size comparable with the light wavelength still unveils surprising optical phenomena, and many of them are related to the Fano effect. Originally described in the context of atomic physics, the Fano resonance in light scattering arises from the interference between a narrow subradiant mode and a spectrally broad radiation line. Here, we present an overview of Fano resonances in coated spherical scatterers within the framework of the Lorenz-Mie theory. We briefly introduce the concept of conventional and unconventional Fano resonances in light scattering. These resonances are associated with the interference between electromagnetic modes excited in the particle with different or the same multipole moment, respectively. In addition, we investigate the modification of the spontaneous-emission rate of an optical emitter at the presence of a plasmonic nanoshell. This modification of decay rate due to electromagnetic environment is referred to as the Purcell effect. We analytically show that the Purcell factor related to a dipole emitter oriented orthogonal or tangential to the spherical surface can exhibit Fano or Lorentzian line shapes in the near field, respectively.Comment: 28 pages, 10 figures; invited book chapter to appear in "Fano Resonances in Optics and Microwaves: Physics and Application", Springer Series in Optical Sciences (2018), edited by E. O. Kamenetskii, A. Sadreev, and A. Miroshnichenk

Delayed cardioprotection is associated with the sub-cellular relocalisation of ventricular protein kinase C epsilon, but not p42/44MAPK

Both noradrenaline administration to rats and rapid cardiac pacing in dogs induces delayed protection of the heart against ischaemia-induced ventricular arrhythmias. In an attempt to establish molecular mechanisms underlying the delayed cardioprotection, we have examined the potential role of two kinases, PKC epsilon and p42/44MAPK. These protein kinases are expressed in the ventricles of the heart and are characterised by their ability to regulate ion-flux and gene transcription. In the rat p42MAPK is predominantly localised in the high-speed supernatant fraction of the ventricle homogenate, whereas p44MAPK is enriched in the nuclear low speed pellet. A small proportion of the p42MAPK is activated even in hearts from control animals. However, neither kinase is relocalised or activated by noradrenaline administration and this provides preliminary evidence the p42/44MAPK may not play a significant role in delayed protection in this species. In contrast, noradrenaline does induce the translocation of PKC epsilon to cell membranes, a response that is sustained for up to 4 h. However, PKC epsilon is down-regulated from the cytoplasm after 24 h post noradrenaline treatment. PKC epsilon is also translocated to the membrane in dogs that have been classically pre-conditioned and cardiac paced. In the latter case, translocation of PKC epsilon from the cytoplasm to the cell membrane is evident 24 h after pacing. These results indicate that the release of endogenous mediators may either inhibit down-regulation or elicit an increase in PKC epsilon mRNA expression. Therefore, in dog heart the subcellular relocalisation of PKC epsilon persists into the 'second window' and may play a central role in the molecular mechanism governing delayed cardioprotection. It is important in the future to identify either the gene products that are induced or the target protein(s) that are phosphorylated by PKC epsilon