Simultaneous three-photon-excited violet upconversion luminescence of Ce3+: Lu2Si2O7 single crystals by femtosecond laser irradiation

We found that Ce3+:Lu2Si2O7 single crystals could be excited at 800 nm by using a femtosecond Ti:sapphire laser. The emission spectra of Ce3+:Lu2Si2O7 crystals were the same for one-photon excitation at 267 nm as for excitation at 800 nm. The emission intensity of Ce3+: Lu2Si2O7 crystals was found to depend on the cube of the laser power at 800 nm, consistent with simultaneous absorption of three 800 nm photons. The measured value of the three-photon absorption cross section is sigma'(3) = 2.44 x 10(-77) cm(6) s(2). (c) 2006 Optical Society of America.

Blue upconversion luminescence generation in Ce3+: Gd2SiO5 crystals by infrared femtosecond laser irradiation

Blue frequency-upconversion fluorescence emission has been observed in Ce3+-doped Gd2SiO5 single crystals, pumped with 120-fs 800 nm IR laser pulses. The observed fluorescence emission peaks at about 440nm is due to 5d -> 4f transition of Ce3+ ions. The intensity dependence of the blue fluorescence emission on the IR excitation laser power obeys the cubic law, demonstrating three-photon absorption process. Analysis suggested that three-photon simultaneous absorption induced population inversion should be the predominant frequency upconversion mechanism. (c) 2006 Optical Society of America.

Color centers and charge state change in Ce : YAG crystals grown by temperature gradient techniques

Color centers and impurity defects of Ce:YAG crystals grown in reduction atmosphere by temperature gradient techniques have been investigated by means of gamma irradiation and thermal treatments. Four absorption bands associated with color centers or impurity defects at 235, 255, 294 and 370 nm were observed in as-grown crystals. Changes in optical intensity of the 235 and 370 nm bands after gamma irradiation indicate that they are associated with F+-type color center. Charge state change processes of Fe3+ impurity and Ce3+ ions take place in the irradiation process. The variations of Ce3+ ions concentration clearly indicate that Ce4+ ions exist in Ce:YAG crystals and gamma irradiations could increase the concentration of Ce3+ ions. Annealing treatments and the changes in optical density suggest that a heterovalent impurity ion associated with the 294 nm band seems to be present in the crystals. (c) 2005 Elsevier B.V. All rights reserved.

High quantum fluorescence yield of Er3+ at 1.5 mu m in an Yb3+, Ce3+-codoped CaF2 crystal

For the first time, a quaternary doping system of Er3+, Yb3+, Ce3+, Na+:CaF2 single crystal was demonstrated to have high fluorescence yield in the eye-safe 1.5 mu m region under 980 nm laser diode pumping, with relatively broad and flat gain curves. A simplified model was established to illustrate the effect of Ce3+ on the branching ratio for the Er3+4I11/2 -> I-4(13/2) transition. With 0.2-at.% Er3+ and 2.0-at.% Ce3+ in the quaternary-doped CaF2 crystal, the branching ratio was estimated to be improved more than 40 times by the deactivating effect of Ce3+ on the Er3+ 4I11/2 level. The quaternary-doped CaF2, system shows great potential to achieve high laser performance in the 1.5 mu m region. (c) 2006 Elsevier B.V. All rights reserved.

Influence of negative ion element impurities on laser induced damage threshold of HfO2 thin film

Negative ion element impurities breakdown model in HfO2 thin film was reported in this paper. The content of negative ion elements were detected by glow discharge mass spectrum analysis (GDMS); HfO2 thin films were deposited by the electron-beam evaporation method. The weak absorption and laser induced damage threshold (LIDT) of HfO2 thin films were measured to testify the negative ion element impurity breakdown model. It was found that the LIDT would decrease and the absorption would increase with increasing the content of negative ion element. These results indicated that negative ion elements were harmful impurities and would speed up the damage of thin film. (c) 2006 Elsevier B.V. All rights reserved.

Investigation on the properties of high reflective mirror prepared by ion-beam sputtering

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.

High laser-induced damage threshold HfO2 films prepared by ion-assisted electron beam evaporation

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.

Preparation of high laser induced damage threshold antireflection film using interrupted ion assisted deposition

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

Influence of oxygen post-treatment on laser-induced damage of antireflection coatings prepared by electron-beam evaporation and ion beam assisted deposition

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.

Calcium-permeable acid-sensing ion channel is a molecular target of the neurotoxic metal ion lead

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

Characterization of acid-sensing ion channels in dorsal horn neurons of rat spinal cord

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.

Coupling between NMDA receptor and acid-sensing ion channel contributes to ischemic neuronal death

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.

Upregulation of acid-sensing ion channel ASIC1a in spinal dorsal horn neurons contributes to inflammatory pain hypersensitivity

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

In vivo studies on the toxic effects of microcystins on mitochondrial electron transport chain and ion regulation in liver and heart of rabbit

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.