Nonlinear terahertz metamaterials via field-enhanced carrier dynamics in GaAs

We demonstrate nonlinear metamaterial split ring resonators (SRRs) on GaAs at terahertz frequencies. For SRRs on doped GaAs films, incident terahertz radiation with peak fields of ~20 - 160 kV/cm drives intervalley scattering. This reduces the carrier mobility and enhances the SRR LC response due to a conductivity decrease in the doped thin film. Above ~160 kV/cm, electric field enhancement within the SRR gaps leads to efficient impact ionization, increasing the carrier density and the conductivity which, in turn, suppresses the SRR resonance. We demonstrate an increase of up to 10 orders of magnitude in the carrier density in the SRR gaps on semi-insulating GaAs substrate. Furthermore, we show that the effective permittivity can be swept from negative to positive values with increasing terahertz field strength in the impact ionization regime, enabling new possibilities for nonlinear metamaterials.Comment: 5 pages, 4 figure

Role of Aβ-RAGE interaction in oxidative stress and cPLA2 activation in astrocytes and cerebral endothelial cells

Blood–brain barrier (BBB) dysfunctions have been implicated in the progression of Alzheimer's disease. Cerebral endothelial cells (CECs) and astrocytes are the main cell components of the BBB. Although amyloid-β oligomers (Aβ42) have been reported to mediate oxidative damage to the CECs and astrocytes and trigger the downstream mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, the cell surface binding site for Aβ42 and exact sequence of these events have yet to be elucidated. In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Aβ42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). We found that Aβ42 competed with the anti-RAGE antibody (AbRAGE) to bind to RAGE on the surfaces of CECs and primary astrocytes. In addition, AbRAGE abrogate Aβ42-induced ROS production and the colocalization between the cytosolic (p47-phox) and membrane (gp91-phox) subunits of NADPH oxidase in both cell types. AbRAGE as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aβ42-induced ERK1/2 and cPLA2 phosphorylation in CECs. At the same time, only AbRAGE, but neither NADPH oxidase inhibitor nor ROS scavenger, inhibited the ERK1/2 pathway and cPLA2 phosphorylation in primary astrocytes. Therefore, this study demonstrates that NADPH oxidase complex assembly and ROS production are not required for Aβ42 binding to RAGE at astrocytic surface leading to sequential phosphorylation of ERK1/2 and cPLA2, and suggests the presence of two different RAGE-dependent downstream pathways in the CECs and astrocytes

Role of Aβ-RAGE interaction in oxidative stress and cPLA2 activation in astrocytes and cerebral endothelial cells

Blood–brain barrier (BBB) dysfunctions have been implicated in the progression of Alzheimer's disease. Cerebral endothelial cells (CECs) and astrocytes are the main cell components of the BBB. Although amyloid-β oligomers (Aβ42) have been reported to mediate oxidative damage to the CECs and astrocytes and trigger the downstream mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, the cell surface binding site for Aβ42 and exact sequence of these events have yet to be elucidated. In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Aβ42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). We found that Aβ42 competed with the anti-RAGE antibody (AbRAGE) to bind to RAGE on the surfaces of CECs and primary astrocytes. In addition, AbRAGE abrogate Aβ42-induced ROS production and the colocalization between the cytosolic (p47-phox) and membrane (gp91-phox) subunits of NADPH oxidase in both cell types. AbRAGE as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aβ42-induced ERK1/2 and cPLA2 phosphorylation in CECs. At the same time, only AbRAGE, but neither NADPH oxidase inhibitor nor ROS scavenger, inhibited the ERK1/2 pathway and cPLA2 phosphorylation in primary astrocytes. Therefore, this study demonstrates that NADPH oxidase complex assembly and ROS production are not required for Aβ42 binding to RAGE at astrocytic surface leading to sequential phosphorylation of ERK1/2 and cPLA2, and suggests the presence of two different RAGE-dependent downstream pathways in the CECs and astrocytes

Low energy laser light (632.8 nm) suppresses amyloid-β peptide-induced oxidative and inflammatory responses in astrocytes

Oxidative stress and inflammation are important processes in the progression of Alzheimer's disease (AD). Recent studies have implicated the role of amyloid β-peptides (Aβ) in mediating these processes. In astrocytes, oligomeric Aβ induces the assembly of NADPH oxidase complexes resulting in its activation to produce anionic superoxide. Aβ also promotes production of pro-inflammatory factors in astrocytes. Since low energy laser has previously been reported to attenuate oxidative stress and inflammation in biological systems, the objective of this study was to examine whether this type of laser light was able to abrogate the oxidative and inflammatory responses induced by Aβ. Primary rat astrocytes were exposed to Helium-Neon laser (λ=632.8 nm), followed by the treatment with oligomeric Aβ. Primary rat astrocytes were used to measure Aβ-induced production of superoxide anions using fluorescence microscopy of dihydroethidium (DHE), assembly of NADPH oxidase subunits by the colocalization between the cytosolic p47phox subunit and the membrane gp91phox subunit using fluorescent confocal microscopy, phosphorylation of cytosolic phospholipase A2 (cPLA2), and expressions of pro-inflammatory factors including interleukin-1β (IL-1β) and inducible nitric-oxide synthase (iNOS) using Western blot Analysis. Our data showed that laser light at 632.8 nm suppressed Aβ-induced superoxide production, colocalization between NADPH oxidase gp91phox and p47phox subunits, phosphorylation of cPLA2, and the expressions of IL-1β and iNOS in primary astrocytes. We demonstrated for the first time that 632.8 nm laser was capable of suppressing cellular pathways of oxidative stress and inflammatory responses critical in the pathogenesis in AD. This study should prove to provide the groundwork for further investigations for the potential use of laser therapy as a treatment for AD

A note on anti-coordination and social interactions

This note confirms a conjecture of [Bramoull\'{e}, Anti-coordination and social interactions, Games and Economic Behavior, 58, 2007: 30-49]. The problem, which we name the maximum independent cut problem, is a restricted version of the MAX-CUT problem, requiring one side of the cut to be an independent set. We show that the maximum independent cut problem does not admit any polynomial time algorithm with approximation ratio better than $n^{1-\epsilon}$, where $n$ is the number of nodes, and $\epsilon$ arbitrarily small, unless P=NP. For the rather special case where each node has a degree of at most four, the problem is still MAXSNP-hard.Comment: 7 page

Low energy laser light (632.8 nm) suppresses amyloid-β peptide-induced oxidative and inflammatory responses in astrocytes

Oxidative stress and inflammation are important processes in the progression of Alzheimer's disease (AD). Recent studies have implicated the role of amyloid β-peptides (Aβ) in mediating these processes. In astrocytes, oligomeric Aβ induces the assembly of NADPH oxidase complexes resulting in its activation to produce anionic superoxide. Aβ also promotes production of pro-inflammatory factors in astrocytes. Since low energy laser has previously been reported to attenuate oxidative stress and inflammation in biological systems, the objective of this study was to examine whether this type of laser light was able to abrogate the oxidative and inflammatory responses induced by Aβ. Primary rat astrocytes were exposed to Helium-Neon laser (λ=632.8 nm), followed by the treatment with oligomeric Aβ. Primary rat astrocytes were used to measure Aβ-induced production of superoxide anions using fluorescence microscopy of dihydroethidium (DHE), assembly of NADPH oxidase subunits by the colocalization between the cytosolic p47phox subunit and the membrane gp91phox subunit using fluorescent confocal microscopy, phosphorylation of cytosolic phospholipase A2 (cPLA2), and expressions of pro-inflammatory factors including interleukin-1β (IL-1β) and inducible nitric-oxide synthase (iNOS) using Western blot Analysis. Our data showed that laser light at 632.8 nm suppressed Aβ-induced superoxide production, colocalization between NADPH oxidase gp91phox and p47phox subunits, phosphorylation of cPLA2, and the expressions of IL-1β and iNOS in primary astrocytes. We demonstrated for the first time that 632.8 nm laser was capable of suppressing cellular pathways of oxidative stress and inflammatory responses critical in the pathogenesis in AD. This study should prove to provide the groundwork for further investigations for the potential use of laser therapy as a treatment for AD

Entanglement in spin-one Heisenberg chains

By using the concept of negativity, we study entanglement in spin-one Heisenberg chains. Both the bilinear chain and the bilinear-biquadratic chain are considered. Due to the SU(2) symmetry, the negativity can be determined by two correlators, which greatly facilitate the study of entanglement properties. Analytical results of negativity are obtained in the bilinear model up to four spins and the two-spin bilinear-biquadratic model, and numerical results of negativity are presented. We determine the threshold temperature before which the thermal state is doomed to be entangled.Comment: 7 pages and 4 figure

Free energy of the Fr\"ohlich polaron in two and three dimensions

We present a novel Path Integral Monte Carlo scheme to solve the Fr\"ohlich polaron model. At intermediate and strong electron-phonon coupling, the polaron self-trapping is properly taken into account at the level of an effective action obtained by a preaveraging procedure with a retarded trial action. We compute the free energy at several couplings and temperatures in three and two dimensions. Our results show that the accuracy of the Feynman variational upper bound for the free energy is always better than 5% although the thermodynamics derived from it is not correct. Our estimates of the ground state energies demonstrate that the second cumulant correction to the variational upper bound predicts the self energy to better than 1% at intermediate and strong coupling.Comment: RevTeX 7 pages 3 figures, revised versio

Fully Automatic Expression-Invariant Face Correspondence

We consider the problem of computing accurate point-to-point correspondences among a set of human face scans with varying expressions. Our fully automatic approach does not require any manually placed markers on the scan. Instead, the approach learns the locations of a set of landmarks present in a database and uses this knowledge to automatically predict the locations of these landmarks on a newly available scan. The predicted landmarks are then used to compute point-to-point correspondences between a template model and the newly available scan. To accurately fit the expression of the template to the expression of the scan, we use as template a blendshape model. Our algorithm was tested on a database of human faces of different ethnic groups with strongly varying expressions. Experimental results show that the obtained point-to-point correspondence is both highly accurate and consistent for most of the tested 3D face models