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Fast ignition is an interesting scheme for nuclear fusion reaction. Here the authors show electron generation using intense short laser pulses and energy transport by coupling the laser energy to the imploded plasma core as in the ICF conditions.

Fast ignition (FI) is a promising approach for high-energy-gain inertial confinement fusion in the laboratory. To achieve ignition, the energy of a short-pulse laser is required to be delivered efficiently to the pre-compressed fuel core via a high-energy electron beam. Therefore, understanding the transport and energy deposition of this electron beam inside the pre-compressed core is the key for FI. Here we report on the direct observation of the electron beam transport and deposition in a compressed core through the stimulated Cu Kα emission in the super-penetration scheme. Simulations reproducing the experimental measurements indicate that, at the time of peak compression, about 1% of the short-pulse energy is coupled to a relatively low-density core with a radius of 70 μm. Analysis with the support of 2D particle-in-cell simulations uncovers the key factors improving this coupling efficiency. Our findings are of critical importance for optimizing FI experiments in a super-penetration scheme.

Organic-based solar cells potentially offer a photovoltaic module with low production costs and low hazard risk of the components. We report organic dye-sensitized solar cells, fabricated with molecular designed indoline dyes in conjunction with highly reactive but robust nitroxide radical molecules as redox mediator in a quasi-solid gel form of the electrolyte. The cells achieve conversion efficiencies of 10.1% at 1 sun, and maintain the output performance even under interior lighting. The indoline dyes, customized by introducing long alkyl chains, specifically interact with the radical mediator to suppress a charge-recombination process at the dye interface. The radical mediator also facilitates the charge-transport with remarkably high electron self-exchange rate even in the quasi-solid state electrolyte to lead to a high fill factor.

Purpose: To investigate the physiological role of a protein kinase, PKN, and its relation to apoptosis in vivo., Methods: An ischemia/reperfusion model of the rat retina was created by elevating the intraocular pressure. Retinal samples were obtained after ischemic insult (15-45 minutes) followed by reperfusion (1-7 days). The effect of ischemia on the fragmentation of PKN was examined by immunoblotting and immunocytochemical procedures using the antibody against PKN. N-methyl-D-aspartate (NMDA) or a caspase-3 inhibitor (DEVD-CHO) was administered intravitreally to investigate its effect on the induction of PKN fragmentation. The retinal cell loss in each sample was evaluated by toluidine blue staining., Results: Ischemia induced a 55-kDa PKN cleavage fragment corresponding to the molecular size of the constitutively active fragment of PKN. The appearance of the cleavage fragment depended on the duration of reperfusion and correlated with the occurrence of retinal cell loss. Immunocytochemical analysis revealed that ischemia increased PKN immunoreactivity in the inner layers of the retina. DEVD-CHO significantly inhibited the appearance of the 55-kDa fragment and protected against retinal cell loss. The administration of NMDA also induced cleavage of PKN., Conclusions: PKN is specifically cleaved by caspase-3 or a related protease during apoptosis in vivo, and PKN cleavage is at least partially initiated by activation of the NMDA receptor.