367 research outputs found
Goos-Haenchen induced vector eigenmodes in a dome cavity
We demonstrate numerically calculated electromagnetic eigenmodes of a 3D dome
cavity resonator that owe their shape and character entirely to the
Goos-Haenchen effect. The V-shaped modes, which have purely TE or TM
polarization, are well described by a 2D billiard map with the Goos-Haenchen
shift included. A phase space plot of this augmented billiard map reveals a
saddle-node bifurcation; the stable periodic orbit that is created in the
bifurcation corresponds to the numerically calculated eigenmode, dictating the
angle of its "V". A transition from a fundamental Gaussian to a TM V mode has
been observed as the cavity is lengthened to become nearly hemispherical.Comment: 4 pages, 4 figure
Expression of a Cu,Zn superoxide dismutase typical for familial amyotrophic lateral sclerosis increases the vulnerability of neuroblastoma cells to infectious injury
<p>Abstract</p> <p>Background</p> <p>Infections can aggravate the course of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Mutations in the anti-oxidant enzyme Cu,Zn superoxide dismutase (EC 1.15.1.1, SOD1) are associated with familial ALS. Streptococcus pneumoniae, the most frequent respiratory pathogen, causes damage by the action of the cholesterol-binding virulence factor pneumolysin and by stimulation of the innate immune system, particularly via Toll-like-receptor 2.</p> <p>Methods</p> <p>SH-SY5Y neuroblastoma cells transfected with the G93A mutant of SOD1 typical for familial ALS (G93A-SOD1) and SH-SY5Y neuroblastoma cells transfected with wildtype SOD1 were both exposed to pneumolysin and in co-cultures with cultured human macrophages treated with the Toll like receptor 2 agonist N-palmitoyl-S-[2,3-bis(palmitoyloxy)-(2RS)-propyl]-[R]-cysteinyl-[S]-seryl-[S]-lysyl-[S]-lysyl-[S]-lysyl-[S]-lysyl-[S]-lysine × 3 HCl (Pam<sub>3</sub>CSK<sub>4</sub>). Cell viability and apoptotic cell death were compared morphologically and by in-situ tailing. With the help of the WST-1 test, cell viability was quantified, and by measurement of neuron-specific enolase in the culture supernatant neuronal damage in co-cultures was investigated. Intracellular calcium levels were measured by fluorescence analysis using fura-2 AM.</p> <p>Results</p> <p>SH-SY5Y neuroblastoma cells transfected with the G93A mutant of SOD1 typical for familial ALS (G93A-SOD1) were more vulnerable to the neurotoxic action of pneumolysin and to the attack of monocytes stimulated by Pam<sub>3</sub>CSK<sub>4</sub> than SH-SY5Y cells transfected with wild-type human SOD1. The enhanced pneumolysin toxicity in G93A-SOD1 neuronal cells depended on the inability of these cells to cope with an increased calcium influx caused by pores formed by pneumolysin. This inability was caused by an impaired capacity of the mitochondria to remove cytoplasmic calcium. Treatment of G93A-SOD1 SH-SY5Y neuroblastoma cells with the antioxidant N-acetylcysteine reduced the toxicity of pneumolysin.</p> <p>Conclusion</p> <p>The particular vulnerability of G93A-SOD1 neuronal cells to hemolysins and inflammation may be partly responsible for the clinical deterioration of ALS patients during infections. These findings link infection and motor neuron disease and suggest early treatment of respiratory infections in ALS patients.</p
Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease
<p>Abstract</p> <p>Background</p> <p>Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons (MN) in the brain stem and spinal cord. Intracellular disruptions of cytosolic and mitochondrial calcium have been associated with selective MN degeneration, but the underlying mechanisms are not well understood. The present evidence supports a hypothesis that mitochondria are a target of mutant SOD1-mediated toxicity in familial amyotrophic lateral sclerosis (fALS) and intracellular alterations of cytosolic and mitochondrial calcium might aggravate the course of this neurodegenerative disease. In this study, we used a fluorescence charged cool device (CCD) imaging system to separate and simultaneously monitor cytosolic and mitochondrial calcium concentrations in individual cells in an established cellular model of ALS.</p> <p>Results</p> <p>To gain insights into the molecular mechanisms of SOD1<sup>G93A </sup>associated motor neuron disease, we simultaneously monitored cytosolic and mitochondrial calcium concentrations in individual cells. Voltage – dependent cytosolic Ca<sup>2+ </sup>elevations and mitochondria – controlled calcium release mechanisms were monitored after loading cells with fluorescent dyes fura-2 and rhod-2. Interestingly, comparable voltage-dependent cytosolic Ca<sup>2+ </sup>elevations in WT (SH-SY5Y<sup>WT</sup>) and G93A (SH-SY5Y<sup>G93A</sup>) expressing cells were observed. In contrast, mitochondrial intracellular Ca<sup>2+ </sup>release responses evoked by bath application of the mitochondrial toxin FCCP were significantly smaller in G93A expressing cells, suggesting impaired calcium stores. Pharmacological experiments further supported the concept that the presence of G93A severely disrupts mitochondrial Ca<sup>2+ </sup>regulation.</p> <p>Conclusion</p> <p>In this study, by fluorescence measurement of cytosolic calcium and using simultaneous [Ca<sup>2+</sup>]i and [Ca<sup>2+</sup>]<sub>mito </sub>measurements, we are able to separate and simultaneously monitor cytosolic and mitochondrial calcium concentrations in individual cells an established cellular model of ALS. The primary goals of this paper are (1) method development, and (2) screening for deficits in mutant cells on the single cell level. On the technological level, our method promises to serve as a valuable tool to identify mitochondrial and Ca<sup>2+</sup>-related defects during G93A-mediated MN degeneration. In addition, our experiments support a model where a specialized interplay between cytosolic calcium profiles and mitochondrial mechanisms contribute to the selective degeneration of neurons in ALS.</p
Fresnel filtering in lasing emission from scarred modes of wave-chaotic optical resonators
We study lasing emission from asymmetric resonant cavity (ARC) GaN
micro-lasers. By comparing far-field intensity patterns with images of the
micro-laser we find that the lasing modes are concentrated on three-bounce
unstable periodic ray orbits, i.e. the modes are scarred. The high-intensity
emission directions of these scarred modes are completely different from those
predicted by applying Snell's law to the ray orbit. This effect is due to the
process of ``Fresnel filtering'' which occurs when a beam of finite angular
spread is incident at the critical angle for total internal reflection.Comment: 4 pages, 3 figures (eps), RevTeX 3.1, submitted to Phys. Rev. Lett;
corrected a minor (transcription) erro
Goos-H\"{a}nchen-like shifts for Dirac fermions in monolayer graphene barrier
We investigate the Goos-H\"{a}nchen-like shifts for Dirac fermions in
transmission through a monolayer graphene barrier. The lateral shifts, as the
functions of the barrier's width and the incidence angle, can be negative and
positive in Klein tunneling and classical motion, respectively. Due to their
relations to the transmission gap, the lateral shifts can be enhanced by the
transmission resonances when the incidence angle is less than the critical
angle for total reflection, while their magnitudes become only the order of
Fermi wavelength when the incidence angle is larger than the critical angle.
These tunable beam shifts can also be modulated by the height of potential
barrier and the induced gap, which gives rise to the applications in
graphene-based devices.Comment: 5 pages, 5 figure
Bayesian D-Optimal Choice Designs for Mixtures
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\nConsumer products and services can often be described as mixtures of ingredients. Examples are the mixture of ingredients in a cocktail and the mixture of different components of waiting time (e.g., in-vehicle and out-of-vehicle travel time) in a transportation setting. Choice experiments may help to determine how the respondents\' choice of a product or service is affected by the combination of ingredients. In such studies, individuals are confronted with sets of hypothetical products or services and they are asked to choose the most preferred product or service from each set.
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\nHowever, there are no studies on the optimal design of choice experiments involving mixtures. We propose a method for generating an optimal design for such choice experiments. To this end, we first introduce mixture models in the choice context and next present an algorithm to construct optimal experimental designs, assuming the multinomial logit model is used to analyze the choice data. To overcome the problem that the optimal designs depend on the unknown parameter values, we adopt a Bayesian D-optimal design approach. We also consider locally D-optimal designs and compare the performance of the resulting designs to those produced by a utility-neutral (UN) approach in which designs are based on the assumption that individuals are indifferent between all choice alternatives. We demonstrate that our designs are quite different and in general perform better than the UN designs
Work, life and time in the new economy: an introduction
International audienc
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