InGaN-based light-emitting diodes with an embedded conical air-voids structure

The conical air-void structure of an InGaN light-emitting diode (LEDs) was formed at the GaN/sapphire interface to increase the light extraction efficiency. The fabrication process of the conical air-void structure consisted of a dry process and a crystallographic wet etching process on an undoped GaN layer, followed by a re-growth process for the InGaN LED structure. A higher light output power (1.54 times) and a small divergent angle (120o) were observed, at a 20mA operation current, on the treated LED structure when compared to a standard LED without the conical air-void structure. In this electroluminescence spectrum, the emission intensity and the peak wavelength varied periodically by corresponding to the conical air-void patterns that were measured through a 100nm-optical-aperture fiber probe. The conical air-void structure reduced the compressed strain at the GaN/sapphire interface by inducing the wavelength blueshift phenomenon and the higher internal quantum efficiency of the photoluminescence spectra for the treated LED structure

Mechanisms of c-Myc Degradation by Nickel Compounds and Hypoxia

Nickel (Ni) compounds have been found to cause cancer in humans and animal models and to transform cells in culture. At least part of this effect is mediated by stabilization of hypoxia inducible factor (HIF1a) and activating its downstream signaling. Recent studies reported that hypoxia signaling might either antagonize or enhance c-myc activity depending on cell context. We investigated the effect of nickel on c-myc levels, and demonstrated that nickel, hypoxia, and other hypoxia mimetics degraded c-myc protein in a number of cancer cells (A549, MCF-7, MDA-453, and BT-474). The degradation of the c-Myc protein was mediated by the 26S proteosome. Interestingly, knockdown of both HIF-1α and HIF-2α attenuated c-Myc degradation induced by Nickel and hypoxia, suggesting the functional HIF-1α and HIF-2α was required for c-myc degradation. Further studies revealed two potential pathways mediated nickel and hypoxia induced c-myc degradation. Phosphorylation of c-myc at T58 was significantly increased in cells exposed to nickel or hypoxia, leading to increased ubiquitination through Fbw7 ubiquitin ligase. In addition, nickel and hypoxia exposure decreased USP28, a c-myc de-ubiquitinating enzyme, contributing to a higher steady state level of c-myc ubiquitination and promoting c-myc degradation. Furthermore, the reduction of USP28 protein by hypoxia signaling is due to both protein degradation and transcriptional repression. Nickel and hypoxia exposure significantly increased the levels of dimethylated H3 lysine 9 at the USP28 promoter and repressed its expression. Our study demonstrated that Nickel and hypoxia exposure increased c-myc T58 phosphorylation and decreased USP28 protein levels in cancer cells, which both lead to enhanced c-myc ubiquitination and proteasomal degradation

Perinatal asphyxia: current status and approaches towards neuroprotective strategies, with focus on sentinel proteins

Delivery is a stressful and risky event menacing the newborn. The mother-dependent respiration has to be replaced by autonomous pulmonary breathing immediately after delivery. If delayed, it may lead to deficient oxygen supply compromising survival and development of the central nervous system. Lack of oxygen availability gives rise to depletion of NAD+ tissue stores, decrease of ATP formation, weakening of the electron transport pump and anaerobic metabolism and acidosis, leading necessarily to death if oxygenation is not promptly re-established. Re-oxygenation triggers a cascade of compensatory biochemical events to restore function, which may be accompanied by improper homeostasis and oxidative stress. Consequences may be incomplete recovery, or excess reactions that worsen the biological outcome by disturbed metabolism and/or imbalance produced by over-expression of alternative metabolic pathways. Perinatal asphyxia has been associated with severe neurological and psychiatric sequelae with delayed clinical onset. No specific treatments have yet been established. In the clinical setting, after resuscitation of an infant with birth asphyxia, the emphasis is on supportive therapy. Several interventions have been proposed to attenuate secondary neuronal injuries elicited by asphyxia, including hypothermia. Although promising, the clinical efficacy of hypothermia has not been fully demonstrated. It is evident that new approaches are warranted. The purpose of this review is to discuss the concept of sentinel proteins as targets for neuroprotection. Several sentinel proteins have been described to protect the integrity of the genome (e.g. PARP-1; XRCC1; DNA ligase IIIα; DNA polymerase β, ERCC2, DNA-dependent protein kinases). They act by eliciting metabolic cascades leading to (i) activation of cell survival and neurotrophic pathways; (ii) early and delayed programmed cell death, and (iii) promotion of cell proliferation, differentiation, neuritogenesis and synaptogenesis. It is proposed that sentinel proteins can be used as markers for characterising long-term effects of perinatal asphyxia, and as targets for novel therapeutic development and innovative strategies for neonatal care

死体肺移植におけるrecombinant tissue-field name="type" plasminogen activator(rt-PA)の効果について

[[sponsorship]]物理研究所[[note]]已出版;[SCI];有審查制度;具代表性[[note]]http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Drexel&SrcApp=hagerty_opac&KeyRecord=1434-6044&DestApp=JCR&RQ=IF_CAT_BOXPLO

Search for the Standard Model Higgs boson produced in association with top quarks and decaying into in collisions at with the ATLAS detector

This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecomm ons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Funded by SCOAP3.We acknowledge the support of ANPCyT, Argentina; YerPhI, Armenia; ARC, Australia; BMWFW and FWF, Austria; ANAS, Azerbaijan; SSTC, Belarus; CNPq and FAPESP, Brazil; NSERC, NRC and CFI, Canada; CERN; CONICYT, Chile; CAS, MOST and NSFC, China; COLCIENCIAS, Colombia; MSMT CR, MPO CR and VSC CR, Czech Republic; DNRF, DNSRC and Lundbeck Foundation, Denmark; EPLANET, ERC and NSRF, European Union; IN2P3-CNRS, CEA-DSM/IRFU, France; GNSF, Georgia; BMBF, DFG, HGF, MPG and AvH Foundation, Germany; GSRT and NSRF, Greece; RGC, Hong Kong SAR, China; ISF, MINERVA, GIF, I-CORE and Benoziyo Center, Israel; INFN, Italy; MEXT and JSPS, Japan; CNRST, Morocco; FOM and NWO, Netherlands; BRF and RCN, Norway; MNiSW and NCN, Poland; GRICES and FCT, Portugal; MNE/IFA, Romania; MES of Russia and ROSATOM, Russian Federation; JINR; MSTD, Serbia; MSSR, Slovakia; ARRS and MIZŠ, Slovenia; DST/NRF, South Africa; MINECO, Spain; SRC and Wallenberg Foundation, Sweden; SER, SNSF and Cantons of Bern and Geneva, Switzerland; NSC, Taiwan; TAEK, Turkey; STFC, the Royal Society and Leverhulme Trust, United Kingdom; DOE and NSF, United States of Americ

InGaN light emitting diodes with a laser-treated tapered GaN structure

InGaN light-emitting diode (LED) structures get an air-void structure and a tapered GaN structure at the GaN/sapphire interface through a laser decomposition process and a lateral wet etching process. The light output power of the treated LED structure had a 70% enhancement compared to a conventional LED structure at 20 mA. The intensities and peak wavelengths of the micro-photoluminescence spectra were varied periodically by aligning to the air-void (461.8nm) and the tapered GaN (459.5nm) structures. The slightly peak wavelength blueshift phenomenon of the EL and the PL spectra were caused by a partial compressed strain release at the GaN/sapphire interface when forming the tapered GaN structure. The relative internal quantum efficiency of the treated LED structure (70.3%) was slightly increased compared with a conventional LED (67.8%) caused by the reduction of the piezoelectric field in the InGaN active layer

Gold nanohole arrays with ring-shaped silver nanoparticles for highly efficient plasmon-enhanced fluorescence

To enhance the interaction between electromagnetic fields and reduce photoluminescence (PL) lifetime in plasmon-enhanced fluorescence, this study presents a novel approach involving the fabrication of gold (Au) nanohole arrays (ANA) decorated with ring-shaped silver nanoparticles (AgNPs) on a silicon-dioxide (SiO2)/silver (Ag) substrate. The surface plasmon resonance coupling in terms of the PL reactions of ANA substrates with and without ring-shaped AgNPs is investigated via experiments and numerical simulations. The remarkable enhancement of PL intensity of the proposed substrate is attributed to increased absorption, which enables the tuning of surface-enhanced electromagnetic fields. Specifically, the Raman signal of rhodamine 6G (R6G) dye and the PL intensity of 4-(dicyanomethylene)-2-t-butyl-6-(1,1,7,7-tetramethyljulolidyl-9-enyl)-4H-pyran (DCJTB) molecules are significantly enhanced 3.7 and 2.2 times, respectively, compared to those of the bare ANA substrate. Meanwhile, the PL lifetime is reduced by 46.15%. These results confirm that ANAs decorated with ring-shaped AgNPs can significantly improve plasmon-enhanced fluorescence. The findings presented herein demonstrate the potential to revolutionize biosensing, imaging, and photonics