1000 resultados para BF2 ion


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In this study, a collimating lens is introduced at the output facet of a tapered waveguide laser to compensate for the divergence of the optical mode. The collimating lens is shown to enhance the laser efficiency while simultaneously reducing the far field divergence.

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We have investigated the use of focused ion beam (FIB) etching for the fabrication of GaN-based devices. Although work has shown that conventional reactive ion etching (RIE) is in most cases appropriate for the GaN device fabrication, the direct write facility of FIB etching - a well-established technique for optical mask repair and for IC failure analysis and repair - without the requirement for depositing an etch mask is invaluable. A gallium ion beam of about 20nm diameter was used to sputter GaN material. The etching rate depends linearly on the ion dose per area with a slope of 3.5×10 -4μm3/pC. At a current of 3nA, for example, this corresponds to an etch rate of 1.05μm3/s. Good etching qualities have been achieved with a side wall roughness significantly below 0.1μm. Changes in the roughness of the etched surface plane stay below 8nm.

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An alternative method for seeding catalyst nanoparticles for carbon nanotubes and nanowires growth is presented. Ni nanoparticles are formed inside a 450 nm SiO2 film on (100) Si wafers through the implantation of Ni ions at fluences of 7.5×1015 and 1.7×1016 ions.cm-2 and post-annealing treatments at 700, 900 and 1100°C. After exposed to the surface by HF dip etching, the Ni nanoparticles are used as catalyst for the growth of vertically aligned carbon nanotubes by direct current plasma enhanced chemical vapor deposition. © 2007 Materials Research Society.

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A number of alternative designs are presented for Penning ion traps suitable for quantum information processing (QIP) applications with atomic ions. The first trap design is a simple array of long straight wires, which allows easy optical access. A prototype of this trap has been built to trap Ca+ and a simple electronic detection scheme has been employed to demonstrate the operation of the trap. Another trap design consists of a conducting plate with a hole in it situated above a continuous conducting plane. The final trap design is based on an array of pad electrodes. Although this trap design lacks the open geometry of the other traps described above, the pad design may prove useful in a hybrid scheme in which information processing and qubit storage take place in different types of trap. The behaviour of the pad traps is simulated numerically and techniques for moving ions rapidly between traps are discussed. Future experiments with these various designs are discussed. All of the designs lend themselves to the construction of multiple trap arrays, as required for scalable ion trap QIP.

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Acid-sensing ion channels (ASICs) are emerging as fundamental players in the regulation of neural plasticity and in pathological conditions. Here we showed that lead (Pb2+), a well known neurotoxic metal ion, reversibly and concentration-dependently inhib

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Acid-sensing ion channels (ASICs) are ligand-gated cation channels activated by extracellular protons. In periphery, they contribute to sensory transmission, including that of nociception and pain. Here we characterized ASIC-like currents in dorsal horn neurons of the rat spinal cord and their functional modulation in pathological conditions. Reverse transcriptase-nested PCR and Western blotting showed that three ASIC isoforms, ASIC1a, ASIC2a, and ASIC2b, are expressed at a high level in dorsal horn neurons. Electrophysiological and pharmacological properties of the proton-gated currents suggest that homomeric ASIC1a and/or heteromeric ASIC1a + 2b channels are responsible for the proton-induced currents in the majority of dorsal horn neurons. Acidification-induced action potentials in these neurons were compatible in a pH-dependent manner with the pH dependence of ASIC-like current. Furthermore, peripheral complete Freund's adjuvant-induced inflammation resulted in increased expression of both ASIC1a and ASIC2a in dorsal horn. These results support the idea that the ASICs of dorsal horn neurons participate in central sensory transmission/modulation under physiological conditions and may play important roles in inflammation-related persistent pain.

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Acid-sensing ion channels (ASICs) composed of ASIC1a subunit exhibit a high Ca2+ permeability and play important roles in synaptic plasticity and acid-induced cell death. Here, we show that ischemia enhances ASIC currents through the phosphorylation at Ser478 and Ser479 of ASIC1a, leading to exacerbated ischemic cell death. The phosphorylation is catalyzed by Ca2+/calmodulin-dependent protein kinase II (CaMKII) activity, as a result of activation of NR2B-containing N-methyl-D-aspartate subtype of glutamate receptors (NMDARs) during ischemia. Furthermore, NR2B-specific antagonist, CaMKII inhibitor, or overexpression of mutated form of ASIC1a with Ser478 or Ser479 replaced by alanine (ASICla-S478A, ASIC1a-S479A) in cultured hippocampal neurons prevented ischemia-induced enhancement of ASIC currents, cytoplasmic Ca2+ elevation, as well as neuronal death. Thus, NMDAR-CaMKII cascade is functionally coupled to ASICs and contributes to acidotoxicity during ischemia. Specific blockade of NMDAR/CaMKII-ASIC coupling may reduce neuronal death after ischemia and other pathological conditions involving excessive glutamate release and acidosis.