Photon tunneling into a single-mode planar silicon waveguide

We demonstrate the direct excitation of a single TE mode in 25 nm thick planar crystalline silicon waveguide by photon tunneling from a layer of fluorescent dye molecules deposited by the Langmuir-Blodgett technique. The observed photon tunneling rate as a function of the dye- silicon separation is well fitted by a theoretical tunneling rate, which is obtained via a novel approach within the framework of quantum mechanics. We suggest that future ultrathin crystalline silicon solar cells can be made efficient by simple light trapping structures consisting of molecules on silicon

Forming-free resistive switching of tunable ZnO films grown by atomic layer deposition

Undoped ZnO thin films with tunable electrical properties have been achieved by adjusting the O2 plasma time in the plasma enhanced atomic layer deposition process. The structural, compositional and electrical properties of the deposited ZnO films were investigated by various characterization techniques. By tuning the plasma exposure from 2 to 8 s, both resistivities and carrier concentrations of the resultant ZnO films can be modulated by up to 3 orders of magnitude. Forming-free TiN/ZnO/TiN resistive memory devices have been achieved by choosing the ZnO film with the plasma exposure time of 6 s. This deposition method offers a great potential for producing other un-doped metal oxides with tunable properties as well as complex multilayer structures in a single deposition

Forming-free resistive switching of tunable ZnO films grown by atomic layer deposition

Undoped ZnO thin films with tunable electrical properties have been achieved by adjusting the O2 plasma time in the plasma enhanced atomic layer deposition process. The structural, compositional and electrical properties of the deposited ZnO films were investigated by various characterization techniques. By tuning the plasma exposure from 2 to 8 s, both resistivities and carrier concentrations of the resultant ZnO films can be modulated by up to 3 orders of magnitude. Forming-free TiN/ZnO/TiN resistive memory devices have been achieved by choosing the ZnO film with the plasma exposure time of 6 s. This deposition method offers a great potential for producing other un-doped metal oxides with tunable properties as well as complex multilayer structures in a single deposition

Tunable on-chip optical traps for levitating particles based on single-layer metasurface

Optically levitated multiple nanoparticles have emerged as a platform for studying complex fundamental physics such as non-equilibrium phenomena, quantum entanglement, and light-matter interaction, which could be applied for sensing weak forces and torques with high sensitivity and accuracy. An optical trapping landscape of increased complexity is needed to engineer the interaction between levitated particles beyond the single harmonic trap. However, existing platforms based on spatial light modulators for studying interactions between levitated particles suffered from low efficiency, instability at focal points, the complexity of optical systems, and the scalability for sensing applications. Here, we experimentally demonstrated that a metasurface which forms two diffraction-limited focal points with a high numerical aperture (~0.9) and high efficiency (31%) can generate tunable optical potential wells without any intensity fluctuations. A bistable potential and double potential wells were observed in the experiment by varying the focal points’ distance, and two nanoparticles were levitated in double potential wells for hours, which could be used for investigating the levitated particles’ nonlinear dynam-ics, thermal dynamics, and optical binding. This would pave the way for scaling the number of levitated optomechanical devices or realizing paralleled levitated sensors

A Quasi-Concertina force-displacement MEMS probe for measuring biomechanical properties

In this work the development of a novel Quasi-Concertina (QC) microelectromechanical systems (MEMS) force - displacement (F-D) sensor is presented. The developed sensor has a resolution as small as 5.6 nN and 1.25 nm and a range of as much as 5.5 mN and 1000 μm. The performance of the microfabricated proof-of-concept QC MEMS device is in good agreement with our analytical and numerical estimates. Force sensors with these attributes will enable the mechanical properties of biological phenomena to be continuously measured over large F-D ranges without the need to change the measurement instrument. Thus, this sensor will appeal to biologists, biochemists, life scientists, clinicians, engineers, and physicist researchers working to understand the fundamentals of cell biology, the onset and progression of diseases such as cancer, and for the development of tools for the diagnostics, prophylactics and therapeutics of diseases

Metabolic adaptation to a disruption in oxygen supply during myocardial ischemia and reperfusion is underpinned by temporal and quantitative changes in the cardiac proteome

Despite decades of intensive research, there is still no effective treatment for ischemia/reperfusion (I/R) injury, an important corollary in the treatment of ischemic disease. I/R injury is initiated when the altered biochemistry of cells after ischemia is no longer compatible with oxygenated microenvironment (or reperfusion). To better understand the molecular basis of this alteration and subsequent incompatibility, we assessed the temporal and quantitative alterations in the cardiac proteome of a mouse cardiac I/R model by an iTRAQ approach at 30 min of ischemia, and at 60 or 120 min reperfusion after the ischemia using sham-operated mouse heart as the baseline control. Of the 509 quantified proteins identified, 121 proteins exhibited significant changes (p-value < 0.05) over time and were mostly clustered in eight functional groups: Fatty acid oxidation, Glycolysis, TCA cycle, ETC (electron transport chain), Redox Homeostasis, Glutathione S-transferase, Apoptosis related, and Heat Shock proteins. The first four groups are intimately involved in ATP production and the last four groups are known to be important in cellular antioxidant activity. During ischemia and reperfusion, the short supply of oxygen precipitates a pivotal metabolic switch from aerobic metabolism involving fatty acid oxidation, TCA, and phosphorylation to anaerobic metabolism for ATP production and this, in turn, increases reactive oxygen species (ROS) formation. Therefore the implication of these 8 functional groups suggested that ischemia-reperfusion injury is underpinned in part by proteomic alterations. Reversion of these alterations to preischemia levels took at least 60 min, suggesting a refractory period in which the ischemic cells cannot adjust to the presence of oxygen. Therefore, therapeutics that could compensate for these proteomic alterations during this interim refractory period could alleviate ischemia-reperfusion injury to enhance cellular recovery from an ischemic to a normoxic microenvironment. Among the perturbed proteins, Park7 and Ppia were selected for further investigation of their functions under hypoxia. The results show that Park7 plays a key role in regulating antioxidative stress and cell survival, and Ppia may function in coping with the unfolded protein stress in the I/R condition

Lower limb reaction time discriminates between multiple and single fallers

Despite decades of intensive research, there is still no effective treatment for ischemia/reperfusion (I/R) injury, an important corollary in the treatment of ischemic disease. I/R injury is initiated when the altered biochemistry of cells after ischemia is no longer compatible with oxygenated microenvironment (or reperfusion). To better understand the molecular basis of this alteration and subsequent incompatibility, we assessed the temporal and quantitative alterations in the cardiac proteome of a mouse cardiac I/R model by an iTRAQ approach at 30 min of ischemia, and at 60 or 120 min reperfusion after the ischemia using sham-operated mouse heart as the baseline control. Of the 509 quantified proteins identified, 121 proteins exhibited significant changes (<i>p</i>-value < 0.05) over time and were mostly clustered in eight functional groups: Fatty acid oxidation, Glycolysis, TCA cycle, ETC (electron transport chain), Redox Homeostasis, Glutathione <i>S</i>-transferase, Apoptosis related, and Heat Shock proteins. The first four groups are intimately involved in ATP production and the last four groups are known to be important in cellular antioxidant activity. During ischemia and reperfusion, the short supply of oxygen precipitates a pivotal metabolic switch from aerobic metabolism involving fatty acid oxidation, TCA, and phosphorylation to anaerobic metabolism for ATP production and this, in turn, increases reactive oxygen species (ROS) formation. Therefore the implication of these 8 functional groups suggested that ischemia-reperfusion injury is underpinned in part by proteomic alterations. Reversion of these alterations to preischemia levels took at least 60 min, suggesting a refractory period in which the ischemic cells cannot adjust to the presence of oxygen. Therefore, therapeutics that could compensate for these proteomic alterations during this interim refractory period could alleviate ischemia-reperfusion injury to enhance cellular recovery from an ischemic to a normoxic microenvironment. Among the perturbed proteins, Park7 and Ppia were selected for further investigation of their functions under hypoxia. The results show that Park7 plays a key role in regulating antioxidative stress and cell survival, and Ppia may function in coping with the unfolded protein stress in the I/R condition

Metabolic Adaptation to a Disruption in Oxygen Supply during Myocardial Ischemia and Reperfusion Is Underpinned by Temporal and Quantitative Changes in the Cardiac Proteome

Despite decades of intensive research, there is still no effective treatment for ischemia/reperfusion (I/R) injury, an important corollary in the treatment of ischemic disease. I/R injury is initiated when the altered biochemistry of cells after ischemia is no longer compatible with oxygenated microenvironment (or reperfusion). To better understand the molecular basis of this alteration and subsequent incompatibility, we assessed the temporal and quantitative alterations in the cardiac proteome of a mouse cardiac I/R model by an iTRAQ approach at 30 min of ischemia, and at 60 or 120 min reperfusion after the ischemia using sham-operated mouse heart as the baseline control. Of the 509 quantified proteins identified, 121 proteins exhibited significant changes (<i>p</i>-value < 0.05) over time and were mostly clustered in eight functional groups: Fatty acid oxidation, Glycolysis, TCA cycle, ETC (electron transport chain), Redox Homeostasis, Glutathione <i>S</i>-transferase, Apoptosis related, and Heat Shock proteins. The first four groups are intimately involved in ATP production and the last four groups are known to be important in cellular antioxidant activity. During ischemia and reperfusion, the short supply of oxygen precipitates a pivotal metabolic switch from aerobic metabolism involving fatty acid oxidation, TCA, and phosphorylation to anaerobic metabolism for ATP production and this, in turn, increases reactive oxygen species (ROS) formation. Therefore the implication of these 8 functional groups suggested that ischemia-reperfusion injury is underpinned in part by proteomic alterations. Reversion of these alterations to preischemia levels took at least 60 min, suggesting a refractory period in which the ischemic cells cannot adjust to the presence of oxygen. Therefore, therapeutics that could compensate for these proteomic alterations during this interim refractory period could alleviate ischemia-reperfusion injury to enhance cellular recovery from an ischemic to a normoxic microenvironment. Among the perturbed proteins, Park7 and Ppia were selected for further investigation of their functions under hypoxia. The results show that Park7 plays a key role in regulating antioxidative stress and cell survival, and Ppia may function in coping with the unfolded protein stress in the I/R condition