Combination of pulsed laser ablation and inert gas condensation for the synthesis of nanostructured nanocrystalline, amorphous and composite materials

A new instrument combining pulsed laser ablation and inert gas condensation for the production of nanopowders is presented. It is shown that various nanostructured materials, such as regular metallic, semiconducting, insulating materials, complex high entropy alloys, amorphous alloys, composites and oxides can be synthesized. The unique variability of the experimental set-up is possible due to the reproducible control of laser power (pulse energy and repetition rate), laser ablation pattern on the target, and experimental conditions during the inert gas condensation, all of which can be controlled and optimized independently. Microstructure analysis of the as-prepared composite and amorphous Ni(60)Nb(40) nanopowders establishes the instrument's ability for the synthesis of materials with unique compositions and atomic structure. It is further shown that small variations of the synthesis parameters can influence materials properties of the final product, in terms of particle size, composition and properties. As an example, the laser power has been used to control the magnetic properties of amorphous Ni(60)Nb(40) nanopowders. A few selected examples of the manifold possibilities of the new synthesis apparatus are presented in this report together with detailed structural characterization of the produced nanopowders

Integration of Spin-Coated Nanoparticulate-Based La0.6Sr0.4CoO3-δCathodes into Micro-Solid Oxide Fuel Cell Membranes

Thin cathodes for micro-solid oxide fuel cells (micro-SOFCs) are fabricated by spin-coating a suspension of La0.6Sr0.4CoO3–δ (LSC) nanoparticulates obtained by salt-assisted spray pyrolysis. The resulting 250 nm thin LSC layers exhibit a three-dimensional porous microstructure with a grain size of around 45 nm and can be integrated onto free-standing 3 mol.% yttria-stabilized-zirconia (3YSZ) electrolyte membranes with high survival rates. Weakly buckled micro-SOFC membranes enable a homogeneous distribution of the LSC dispersion on the electrolyte, whereas the steep slopes of strongly buckled membranes do not allow for a perfect LSC coverage. A micro-SOFC membrane consisting of an LSC cathode on a weakly buckled 3YSZ electrolyte and a sputtered Pt anode has an open-circuit voltage of 1.05 V and delivers a maximum power density of 12 mW cm–2 at 500 °C

Reversible Cyclosporin A-sensitive Mitochondrial Depolarization Occurs within Minutes of Stroke Onset in Mouse Somatosensory Cortex in Vivo: A TWO-PHOTON IMAGING STUDY*

Neuronal structure and function are rapidly damaged during global ischemia but can in part recover during reperfusion. Despite apparent recovery in the hours/days following an ischemic episode, delayed cell death can be initiated, making it important to understand how initial ischemic events affect potential mediators of apoptosis. Mitochondrial dysfunction and the opening of the mitochondrial permeability transition pore (mPTP) are proposed to link ischemic ionic imbalance to mitochondrially mediated cell death pathways. Using two-photon microscopy, we monitored mitochondrial transmembrane potential (Δψm) in vivo within the somatosensory cortex during ischemia and reperfusion in a mouse global ischemia model. Our results indicated a synchronous loss of Δψm within 1–3 min of ischemic onset that was linked to within seconds of plasma membrane potential (Δψp) depolarization. Δψm recovered rapidly upon reperfusion, and no delayed depolarization was observed over 2 h. Cyclosporin A treatment largely blocked Δψm collapse during ischemia, suggesting a role for the mPTP. Blocking Δψm depolarization did not affect structural damage to dendrites, indicating that the opening of the mPTP and damage to dendrites are separable pathways that are activated during Δψp depolarization. Our findings using in vivo imaging suggest that mitochondrial dysfunction and specifically the activation of the mPTP are early reversible events during brain ischemia that could trigger delayed cell death