Generation of Broadband Emission by Incorporating N\u3csup\u3e3-\u3c/sup\u3e into Ca\u3csub\u3e3\u3c/sub\u3eSc\u3csub\u3e2\u3c/sub\u3eSi\u3csub\u3e3\u3c/sub\u3eO\u3csub\u3e12\u3c/sub\u3e:Ce\u3csup\u3e3+\u3c/sup\u3e Garnet for High Rendering White LEDs

Adding Si3N4 into green emitting Ca3Sc2Si3O12:Ce3+ garnet phosphor generates an additionally red emission band peaking around 610 nm that are assigned to Ce3+ ions having N3− in their local coordination. The excitation spectrum of the red band consists of not only a distinct band at 510 nm of itself but also an intense blue band at 450 nm that belongs to the typical Ce3+ ions with green emission, indicating a notable energy transfer from the green emitting Ce3+ ions to the red ones. The energy transfer significantly enables the achievement of a broad emission spectrum covering a red and green spectral region suitable for generating white light upon a blue light-emitting diode (LED) excitation. The decay patterns of the red and green fluorescence are discussed in relation to the effect of energy transfer. A white LED with high color rendering of 86 and low correlated color temperature of 4700 K is fabricated using the present single garnet phosphor

NR2B-dependent cyclophilin D translocation suppresses the recovery of synaptic transmission after oxygen-glucose deprivation

N-methyl d-aspartate receptor (NMDA) subunit 2B (NR2B)-containing NMDA receptors and mitochondrial protein cyclophilin D (CypD) are well characterized in mediating neuronal death after ischemia, respectively. However, whether and how NR2B and CypD work together in mediating synaptic injury after ischemia remains elusive. Using an ex vivo ischemia model of oxygen–glucose deprivation (OGD) in hippocampal slices, we identified a NR2B-dependent mechanism for CypD translocation onto the mitochondrial inner membrane. CypD depletion (CypD null mice) prevented OGD-induced impairment in synaptic transmission recovery. Overexpression of neuronal CypD mice (CypD +) exacerbated OGD-induced loss of synaptic transmission. Inhibition of CypD-dependent mitochondrial permeability transition pore (mPTP) opening by cyclosporine A (CSA) attenuated ischemia-induced synaptic perturbation in CypD + and non-transgenic (non-Tg) mice. The treatment of antioxidant EUK134 to suppress mitochondrial oxidative stress rescued CypD-mediated synaptic dysfunction following OGD in CypD + slices. Furthermore, OGD provoked the interaction of CypD with P53, which was enhanced in slices overexpressing CypD but was diminished in CypD-null slices. Inhibition of p53 using a specific inhibitor of p53 (pifithrin-μ) attenuated the CypD/p53 interaction following OGD, along with a restored synaptic transmission in both non-Tg and CypD + hippocampal slices. Our results indicate that OGD-induced CypD translocation potentiates CypD/P53 interaction in a NR2B dependent manner, promoting oxidative stress and loss of synaptic transmission. We also evaluate a new ex vivo chronic OGD-induced ischemia model for studying the effect of oxidative stress on synaptic damage

NR2B-dependent cyclophilin D translocation suppresses the recovery of synaptic transmission after oxygen-glucose deprivation

N-methyl d-aspartate receptor (NMDA) subunit 2B (NR2B)-containing NMDA receptors and mitochondrial protein cyclophilin D (CypD) are well characterized in mediating neuronal death after ischemia, respectively. However, whether and how NR2B and CypD work together in mediating synaptic injury after ischemia remains elusive. Using an ex vivo ischemia model of oxygen–glucose deprivation (OGD) in hippocampal slices, we identified a NR2B-dependent mechanism for CypD translocation onto the mitochondrial inner membrane. CypD depletion (CypD null mice) prevented OGD-induced impairment in synaptic transmission recovery. Overexpression of neuronal CypD mice (CypD +) exacerbated OGD-induced loss of synaptic transmission. Inhibition of CypD-dependent mitochondrial permeability transition pore (mPTP) opening by cyclosporine A (CSA) attenuated ischemia-induced synaptic perturbation in CypD + and non-transgenic (non-Tg) mice. The treatment of antioxidant EUK134 to suppress mitochondrial oxidative stress rescued CypD-mediated synaptic dysfunction following OGD in CypD + slices. Furthermore, OGD provoked the interaction of CypD with P53, which was enhanced in slices overexpressing CypD but was diminished in CypD-null slices. Inhibition of p53 using a specific inhibitor of p53 (pifithrin-μ) attenuated the CypD/p53 interaction following OGD, along with a restored synaptic transmission in both non-Tg and CypD + hippocampal slices. Our results indicate that OGD-induced CypD translocation potentiates CypD/P53 interaction in a NR2B dependent manner, promoting oxidative stress and loss of synaptic transmission. We also evaluate a new ex vivo chronic OGD-induced ischemia model for studying the effect of oxidative stress on synaptic damage

Low Friction at the Nanoscale of Hydrogenated Fullerene-Like Carbon Films

Friction force microscopy experiments at the nanometer scale are applied to study low friction of hydrogenated fullerene-like carbon films. The measured friction coefficients indicate that lower hydrogen concentration during preparation is beneficial to enter the low friction regime, especially in combination with only methane as precursor. Furthermore, two regions are found with distinct friction coefficients and surface roughnesses related to different surface structures. One is rich in amorphous carbon and the other is rich in fullerene-like carbon, dispersed on the same surface. Transmission electron microscopy and Raman spectroscopy images verify this observation of the two separated structures, especially with the extracted fullerene-like structures in the wear debris from macro friction experiments. It is speculated that hydrogen may tend to impair the growth of fullerene-like carbon and is therefore detrimental for lubricity

Adaptive Sliding Mode Fault Tolerant Control for Autonomous Vehicle With Unknown Actuator Parameters and Saturated Tire Force Based on the Center of Percussion

With consideration of tire force saturation in vehicle motions, a novel path-following controller is developed for autonomous vehicles with unknown-bound disturbances and unknown actuator parameters. An adaptive sliding-mode fault-tolerant control (ASM-FTC) strategy is designed to stabilize the path-following errors without any information of disturbance boundaries, actuator fault boundaries and steering ratio from the steering wheel to the front wheels. By selecting the distance from the center of gravity to the center of percussion as the preview length, the effects of the lateral rear-tire force are decoupled and cancelled out, and then the preview error, which represents the path-following performance, can be only commanded by the front-tire force. To further address the issue of unknown tire-road friction limits, a modified ASM-FTC strategy is presented to improve the path-following performance as the lateral tire force is saturated. Simulation results show that the modified ASM-FTC controller demonstrates superior tracking performance over the normal ASM-FTC while the autonomous vehicle follows desired paths

Strong Convergence of Monotone Hybrid Algorithm for Hemi-Relatively Nonexpansive Mappings

The purpose of this article is to prove strong convergence theorems for fixed points of closed hemi-relatively nonexpansive mappings. In order to get these convergence theorems, the monotone hybrid iteration method is presented and is used to approximate those fixed points. Note that the hybrid iteration method presented by S. Matsushita and W. Takahashi can be used for relatively nonexpansive mapping, but it cannot be used for hemi-relatively nonexpansive mapping. The results of this paper modify and improve the results of S. Matsushita and W. Takahashi (2005), and some others