131 research outputs found
Numerical Study on Aging Dynamics in the 3D Ising Spin-Glass Model. II. Quasi-Equilibrium Regime of Spin Auto-Correlation Function
Using Monte Carlo simulations, we have studied isothermal aging of
three-dimensional Ising spin-glass model focusing on quasi-equilibrium behavior
of the spin auto-correlation function. Weak violation of the time translational
invariance in the quasi-equilibrium regime is analyzed in terms of {\it
effective stiffness} for droplet excitations in the presence of domain walls.
Within the range of computational time window, we have confirmed that the
effective stiffness follows the expected scaling behavior with respect to the
characteristic length scales associated with droplet excitations and domain
walls, whose growth law has been extracted from our simulated data. Implication
of the results are discussed in relation to experimental works on ac
susceptibilities.Comment: 18 pages, 6 figure
Universality, frustration and conformal invariance in two-dimensional random Ising magnets
We consider long, finite-width strips of Ising spins with randomly
distributed couplings. Frustration is introduced by allowing both ferro- and
antiferromagnetic interactions. Free energy and spin-spin correlation functions
are calculated by transfer-matrix methods. Numerical derivatives and
finite-size scaling concepts allow estimates of the usual critical exponents
, and to be obtained, whenever a second-order
transition is present. Low-temperature ordering persists for suitably small
concentrations of frustrated bonds, with a transition governed by pure--Ising
exponents. Contrary to the unfrustrated case, subdominant terms do not fit a
simple, logarithmic-enhancement form. Our analysis also suggests a vertical
critical line at and below the Nishimori point. Approaching this point along
either the temperature axis or the Nishimori line, one finds non-diverging
specific heats. A percolation-like ratio is found upon analysis of
the uniform susceptibility at the Nishimori point. Our data are also consistent
with frustration inducing a breakdown of the relationship between
correlation-length amplitude and critical exponents, predicted by conformal
invariance for pure systems.Comment: RevTeX code for 10 pages, 9 eps figures, to appear in Physical Review
B (September 1999
Scaling properties in off equilibrium dynamical processes
In the present paper, we analyze the consequences of scaling hypotheses on
dynamic functions, as two times correlations . We show, under general
conditions, that must obey the following scaling behavior , where the scaling variable is
and , two
undetermined functions. The presence of a non constant exponent
signals the appearance of multiscaling properties in the dynamics.Comment: 6 pages, no figure
Dynamics of ghost domains in spin-glasses
We revisit the problem of how spin-glasses ``heal'' after being exposed to
tortuous perturbations by the temperature/bond chaos effects in
temperature/bond cycling protocols. Revised scaling arguments suggest the
amplitude of the order parameter within ghost domains recovers very slowly as
compared with the rate it is reduced by the strong perturbations. The parallel
evolution of the order parameter and the size of the ghost domains can be
examined in simulations and experiments by measurements of a memory
auto-correlation function which exhibits a ``memory peak'' at the time scale of
the age imprinted in the ghost domains. These expectations are confirmed by
Monte Calro simulations of an Edwards-Anderson Ising spin-glass model.Comment: 17 pages, 3 figure
Domain growth by isothermal aging in 3d Ising and Heisenberg spin glasses
Non-equilibrium dynamics of three dimensional model spin glasses - the Ising
system FeMnTiO and the Heisenberg like system Ag(11 at%
Mn) - has been investigated by measurements of the isothermal time decay of the
low frequency ac-susceptibility after a quench from the paramagnetic to the
spin glass phase. It is found that the relaxation data measured at different
temperatures can be scaled according to predictions from the droplet scaling
model, provided that critical fluctuations are accounted for in the analyzes.Comment: 5 pages, 3 figure
Efficiency of Exciton and Charge Carrier Photogeneration in a Semiconducting Polymer
Euan Hendry, Juleon M. Schins, L. P. Candeias, L. D. A. Siebbeles, and Mischa Bonn, Physical Review Letters, Vol. 92, article 196601 (2004). "Copyright © 2004 by the American Physical Society."We determine the efficiencies for the formation of excitons and charge carriers following ultrafast photoexcitation of a semiconducting polymer (MEH-PPV). The simultaneous, quantitative determination of exciton and charge photoyields is achieved through subpicosecond studies of both the real and the imaginary components of the complex conductivity over a wide frequency range. Predominantly excitons, with near-unity quantum efficiency, are generated on excitation, while only a very small fraction (<10-2) of free charges are initially excited, consistent with rapid (∼100  fs) hot exciton dissociation. These initial charges are very short lived, decaying on subpicosecond time scales
Ultrafast supercontinuum spectroscopy of carrier multiplication and biexcitonic effects in excited states of PbS quantum dots
We examine the multiple exciton population dynamics in PbS quantum dots by
ultrafast spectrally-resolved supercontinuum transient absorption (SC-TA). We
simultaneously probe the first three excitonic transitions over a broad
spectral range. Transient spectra show the presence of first order bleach of
absorption for the 1S_h-1S_e transition and second order bleach along with
photoinduced absorption band for 1P_h-1P_e transition. We also report evidence
of the one-photon forbidden 1S_{h,e}-1P_{h,e} transition. We examine signatures
of carrier multiplication (multiexcitons for the single absorbed photon) from
analysis of the first and second order bleaches, in the limit of low absorbed
photon numbers (~ 10^-2), at pump energies from two to four times the
semiconductor band gap. The multiexciton generation efficiency is discussed
both in terms of a broadband global fit and the ratio between early- to
long-time transient absorption signals.. Analysis of population dynamics shows
that the bleach peak due to the biexciton population is red-shifted respect the
single exciton one, indicating a positive binding energy.Comment: 16 pages, 5 figure
Identification of a Common Gene Expression Response in Different Lung Inflammatory Diseases in Rodents and Macaques
To identify gene expression responses common to multiple pulmonary diseases we collected microarray data for acute lung inflammation models from 12 studies and used these in a meta-analysis. The data used include exposures to air pollutants; bacterial, viral, and parasitic infections; and allergic asthma models. Hierarchical clustering revealed a cluster of 383 up-regulated genes with a common response. This cluster contained five subsets, each characterized by more specific functions such as inflammatory response, interferon-induced genes, immune signaling, or cell proliferation. Of these subsets, the inflammatory response was common to all models, interferon-induced responses were more pronounced in bacterial and viral models, and a cell division response was more prominent in parasitic and allergic models. A common cluster containing 157 moderately down-regulated genes was associated with the effects of tissue damage. Responses to influenza in macaques were weaker than in mice, reflecting differences in the degree of lung inflammation and/or virus replication. The existence of a common cluster shows that in vivo lung inflammation in response to various pathogens or exposures proceeds through shared molecular mechanisms
Allergen particle binding by human primary bronchial epithelial cells is modulated by surfactant protein D
<p>Abstract</p> <p>Background</p> <p>Allergen-containing subpollen particles (SPP) are released from whole plant pollen upon contact with water or even high humidity. Because of their size SPP can preferentially reach the lower airways where they come into contact with surfactant protein (SP)-D. Our previous work demonstrated that SP-D increases the uptake of SPP by alveolar macrophages. In the present study, we investigated the uptake of SPP in human primary epithelial cells and the potential modulation by SP-D. The patho-physiological consequence was evaluated by measurement of pro-inflammatory mediators.</p> <p>Methods</p> <p>SPP were isolated from timothy grass and subsequently fluorescently labelled. Human primary bronchial epithelial cells were incubated with SPP or polystyrene particles (PP) in the presence and absence of surfactant protein D. In addition, different sizes and surface charges of the PP were studied. Particle uptake was evaluated by flow cytometry and confocal microscopy. Soluble mediators were measured by enzyme linked immunosorbent assay or bead array.</p> <p>Results</p> <p>SPP were taken up by primary epithelial cells in a dose dependent manner. This uptake was coincided with secretion of Interleukin (IL)-8. SP-D increased the fraction of bronchial epithelial cells that bound SPP but not the fraction of cells that internalized SPP. SPP-induced secretion of IL-8 was further increased by SP-D. PP were bound and internalized by epithelial cells but this was not modulated by SP-D.</p> <p>Conclusions</p> <p>Epithelial cells bind and internalize SPP and PP which leads to increased IL-8 secretion. SP-D promotes attachment of SPP to epithelial cells and may thus be involved in the inflammatory response to inhaled allergen.</p
Systemic Inhibition of NF-κB Activation Protects from Silicosis
Background: Silicosis is a complex lung disease for which no successful treatment is available and therefore lung transplantation is a potential alternative. Tumor necrosis factor alpha (TNFα) plays a central role in the pathogenesis of silicosis. TNFα signaling is mediated by the transcription factor, Nuclear Factor (NF)-κB, which regulates genes controlling several physiological processes including the innate immune responses, cell death, and inflammation. Therefore, inhibition of NF-κB activation represents a potential therapeutic strategy for silicosis. Methods/Findings: In the present work we evaluated the lung transplant database (May 1986-July 2007) at the University of Pittsburgh to study the efficacy of lung transplantation in patients with silicosis (n = 11). We contrasted the overall survival and rate of graft rejection in these patients to that of patients with idiopathic pulmonary fibrosis (IPF, n = 79) that was selected as a control group because survival benefit of lung transplantation has been identified for these patients. At the time of lung transplantation, we found the lungs of silica-exposed subjects to contain multiple foci of inflammatory cells and silicotic nodules with proximal TNFα expressing macrophage and NF-κB activation in epithelial cells. Patients with silicosis had poor survival (median survival 2.4 yr; confidence interval (CI): 0.16-7.88 yr) compared to IPF patients (5.3 yr; CI: 2.8-15 yr; p = 0.07), and experienced early rejection of their lung grafts (0.9 yr; CI: 0.22-0.9 yr) following lung transplantation (2.4 yr; CI:1.5-3.6 yr; p<0.05). Using a mouse experimental model in which the endotracheal instillation of silica reproduces the silica-induced lung injury observed in humans we found that systemic inhibition of NF-κB activation with a pharmacologic inhibitor (BAY 11-7085) of IκBα phosphorylation decreased silica-induced inflammation and collagen deposition. In contrast, transgenic mice expressing a dominant negative IκBα mutant protein under the control of epithelial cell specific promoters demonstrate enhanced apoptosis and collagen deposition in their lungs in response to silica. Conclusions: Although limited by its size, our data support that patients with silicosis appear to have poor outcome following lung transplantation. Experimental data indicate that while the systemic inhibition of NF-κB protects from silica-induced lung injury, epithelial cell specific NF-κB inhibition appears to aggravate the outcome of experimental silicosis. © 2009 Di Giuseppe et al
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