286 resultados para ION IRRADIATION
Resumo:
CO2 laser irradiation experiments on ZnO thin films are reported. The structural, optical, luminescent and vibrational properties of the samples were investigated by X-ray diffraction (XRD), transmittance, photoluminescence (PL) and Raman measurements. XRD results show that the crystalline of the irradiated films was improved. The (002) peaks of irradiated ZnO films shift to. higher 20 angles due to the stress relaxation in the case of laser beam irradiation. From optical transmittance spectra, all films exhibit high transmittance in the visible range, the optical band edge of irradiated films showed a redshift compared with that of as-grown films. Compared with the as-grown films, the photoluminescence emission (in particular the relative intensities of visible emissions) intensities of irradiated samples enhanced. In the Raman scattering spectral both the A I. and E modes exhibited slight Raman blueshift. (c) 2005 Elsevier B.V. All rights reserved.
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The single- and multi-shot damage behaviors of HfO2/SiO2 high-reflecting (HR) coatings under Nd:YAG laser exposure were investigated. Fundamental aspects of multi-shot laser damage, such as the instability due to pulse-to-pulse accumulation of absorption defect and structural defect effect, and the mechanism of laser induced defect generation, are considered. It was found in multi-shot damage, the main factors influencing laser-induced damage threshold (LIDT) are accumulation of irreversible changes of structural defects and thermal stress that induced by thermal density fluctuations.
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The single-sided and dual-sided high reflective mirrors were deposited with ion-beam sputtering (IBS). When the incident light entered with 45 degrees, the reflectance of p-polarized light at 1064 nm exceeded 99.5%. Spectrum was gained by spectrometer and weak absorption of coatings was measured by surface thermal lensing (STL) technique. Laser-induced damage threshold (LIDT) was determined and the damage morphology was observed with Lecia-DMRXE microscope simultaneously. The profile of coatings was measured with Mark III-GPI digital interferometer. It was found that the reflectivity of mirror exceeded 99.9% and its absorption was as low as 14 ppm. The reflective bandwidth of the dual-sided sample was about 43 nm wider than that of single-sided sample, and its LIDT was as high as 28 J/cm2, which was 5 J/cm2 higher than that of single-sided sample. Moreover, the profile of dual-sided sample was better than that of substrate without coatings.
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HfO2 films were deposited by electron beam evaporation with different deposition parameters. The properties such as refractive index, weak absorption, and laser induced damage thresholds (LIDTs) of these films have been investigated. It was found that when pulsed Nd:YAG 1064 nm laser is used to investigate LIDT of films: Metallic character is the main factor that influences LIDTs of films obtained from Hf starting material by ion-assisted reaction, and films prepared with higher momentum transfer parameter P have fewer metallic character; The ion-assisted reaction parameters are key points for preparing high LIDT films and if the parameters are chose properly, high LIDT films can be obtained. (c) 2004 Elsevier B.V. All rights reserved.
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Single layers and antireflection films were deposited by electron beam evaporation, ion assisted deposition and interrupted ion assisted deposition, respectively. Antireflection film of quite high laser damage threshold (18J/cm(2)) deposited by interrupted ion assisted deposition were got. The electric field distribution, weak absorption, and residual stress of films and their relations to damage threshold were investigated. It was shown that the laser induced damage threshold of film was the result of competition of disadvantages and advantages, and interrupted ion assisted deposition was one of the valuable methods for preparing high laser induced damage threshold films. (c) 2007 Optical Society of America
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Antireflection coatings at the center wavelength of 1053 nm were prepared on BK7 glasses by electron-beam evaporation deposition (EBD) and ion beam assisted deposition (IBAD). Parts of the two kinds of samples were post-treated with oxygen plasma at the environment temperature after deposition. Absorption at 1064 nm was characterized based on surface thermal lensing (STL) technique. The laser-induced damage threshold (LIDT) was measured by a 1064-nm Nd:YAG laser with a pulse width of 38 ps. Leica-DMRXE Microscope was applied to gain damage morphologies of samples. The results revealed that oxygen post-treatment could lower the absorption and increase the damage thresholds for both kinds of as-grown samples. However, the improving effects are not the same. (c) 2008 Elsevier B.V. All rights reserved.
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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.
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Development of chronic pain involves alterations in peripheral nociceptors as well as elevated neuronal activity in multiple regions of the CNS. Previous pharmacological and behavioral studies suggest that peripheral acid-sensing ion channels (ASICs) cont
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This study examined the toxic effects of microcystins on mitochondria of liver and heart of rabbit in vivo. Rabbits were injected i.p. with extracted microcystins (mainly MC-RR and -LR) at two doses, 12.5 and 50 MCLReq. mu g/kg bw, and the changes in mitochondria of liver and heart were studied at 1, 3,12, 24 and 48 h after injection. MCs induced damage of mitochondrial morphology and lipid peroxidation in both liver and heart. MCs influenced respiratory activity through inhibiting NADH dehydrogenase and enhancing succinate dehydrogenase (SDH). MCs altered Na+-K+-ATPase and Ca2+-Mg2+-ATPase activities of mitochondria and consequently disrupted ionic homeostasis, which might be partly responsible for the loss of mitochondrial membrane potential (MMP). MCs were highly toxic to mitochondria with more serious damage in liver than in heart. Damage of mitochondria showed reduction at 48 h in the low dose group, suggesting that the low dose of MCs might have stimulated a compensatory response in the rabbits. (C) 2008 Elsevier Inc. All rights reserved.