592 research outputs found
Surface induced disorder in body-centered cubic alloys
We present Monte Carlo simulations of surface induced disordering in a model
of a binary alloy on a bcc lattice which undergoes a first order bulk
transition from the ordered DO3 phase to the disordered A2 phase. The data are
analyzed in terms of an effective interface Hamiltonian for a system with
several order parameters in the framework of the linear renormalization
approach due to Brezin, Halperin and Leibler. We show that the model provides a
good description of the system in the vicinity of the interface. In particular,
we recover the logarithmic divergence of the thickness of the disordered layer
as the bulk transition is approached, we calculate the critical behavior of the
maxima of the layer susceptibilities, and demonstrate that it is in reasonable
agreement with the simulation data. Directly at the (110) surface, the theory
predicts that all order parameters vanish continuously at the surface with a
nonuniversal, but common critical exponent. However, we find different
exponents for the order parameter of the DO3 phase and the order parameter of
the B2 phase. Using the effective interface model, we derive the finite size
scaling function for the surface order parameter and show that the theory
accounts well for the finite size behavior of the DO3 ordering but not for that
of B2 ordering. The situation is even more complicated in the neighborhood of
the (100) surface, due to the presence of an ordering field which couples to
the B2 order.Comment: To appear in Physical Review
Patient Care in High-Level Containment Care Units: In a Resourced Setting
Vasa, A., Boulter, K., Horihan, Cates, D., Piquette, C., Sullivan, J., Johnson, D, & Hewlett, A. (2019). Patient Care in High-Level Containment Care Units. In T. Cieslak, M. Kortepeter, C. Kratochvil, & J. Lawler (Eds.), Nebraska Isolation and Quarantine Manual (pp. 87-101). Lincoln, NE: University of Nebraska Press.https://digitalcommons.unmc.edu/nm_books/1000/thumbnail.jp
Nucleation and Growth of the Superconducting Phase in the Presence of a Current
We study the localized stationary solutions of the one-dimensional
time-dependent Ginzburg-Landau equations in the presence of a current. These
threshold perturbations separate undercritical perturbations which return to
the normal phase from overcritical perturbations which lead to the
superconducting phase. Careful numerical work in the small-current limit shows
that the amplitude of these solutions is exponentially small in the current; we
provide an approximate analysis which captures this behavior. As the current is
increased toward the stall current J*, the width of these solutions diverges
resulting in widely separated normal-superconducting interfaces. We map out
numerically the dependence of J* on u (a parameter characterizing the material)
and use asymptotic analysis to derive the behaviors for large u (J* ~ u^-1/4)
and small u (J -> J_c, the critical deparing current), which agree with the
numerical work in these regimes. For currents other than J* the interface
moves, and in this case we study the interface velocity as a function of u and
J. We find that the velocities are bounded both as J -> 0 and as J -> J_c,
contrary to previous claims.Comment: 13 pages, 10 figures, Revte
Dynamics of Wetting Fronts in Porous Media
We propose a new phenomenological approach for describing the dynamics of
wetting front propagation in porous media. Unlike traditional models, the
proposed approach is based on dynamic nature of the relation between capillary
pressure and medium saturation. We choose a modified phase-field model of
solidification as a particular case of such dynamic relation. We show that in
the traveling wave regime the results obtained from our approach reproduce
those derived from the standard model of flow in porous media. In more general
case, the proposed approach reveals the dependence of front dynamics upon the
flow regime.Comment: 4 pages, 2 figures, revte
Effects of confinement and surface enhancement on superconductivity
Within the Ginzburg-Landau approach a theoretical study is performed of the
effects of confinement on the transition to superconductivity for type-I and
type-II materials with surface enhancement. The superconducting order parameter
is characterized by a negative surface extrapolation length . This leads to
an increase of the critical field and to a surface critical
temperature in zero field, , which exceeds the bulk . When the
sample is {\em mesoscopic} of linear size the surface induces
superconductivity in the interior for .
In analogy with adsorbed fluids, superconductivity in thin films of type-I
materials is akin to {\em capillary condensation} and competes with the
interface delocalization or "wetting" transition. The finite-size scaling
properties of capillary condensation in superconductors are scrutinized in the
limit that the ratio of magnetic penetration depth to superconducting coherence
length, , goes to zero, using analytic
calculations. While standard finite-size scaling holds for the transition in
non-zero magnetic field , an anomalous critical-point shift is found for
H=0. The increase of for H=0 is calculated for mesoscopic films,
cylindrical wires, and spherical grains of type-I and type-II materials.
Surface curvature is shown to induce a significant increase of ,
characterized by a shift inversely proportional to the
radius .Comment: 37 pages, 5 figures, accepted for PR
Bone marrow injection stimulates hepatic ductular reactions in the absence of injury via macrophage-mediated TWEAK signaling
Tissue progenitor cells are an attractive target for regenerative therapy. In various organs, bone marrow cell (BMC) therapy has shown promising preliminary results, but to date no definite mechanism has been demonstrated to account for the observed benefit in organ regeneration. Tissue injury and regeneration is invariably accompanied by macrophage infiltration, but their influence upon the progenitor cells is incompletely understood, and direct signaling pathways may be obscured by the multiple roles of macrophages during organ injury. We therefore examined a model without injury; a single i.v. injection of unfractionated BMCs in healthy mice. This induced ductular reactions (DRs) in healthy mice. We demonstrate that macrophages within the unfractionated BMCs are responsible for the production of DRs, engrafting in the recipient liver and localizing to the DRs. Engrafted macrophages produce the cytokine TWEAK (TNF-like weak inducer of apoptosis) in situ. We go on to show that recombinant TWEAK activates DRs and that BMC mediated DRs are TWEAK dependent. DRs are accompanied by liver growth, occur in the absence of liver tissue injury and hepatic progenitor cells can be isolated from the livers of mice with DRs. Overall these results reveal a hitherto undescribed mechanism linking macrophage infiltration to DRs in the liver and highlight a rationale for macrophage derived cell therapy in regenerative medicine
Wetting films on chemically heterogeneous substrates
Based on a microscopic density functional theory we investigate the
morphology of thin liquidlike wetting films adsorbed on substrates endowed with
well-defined chemical heterogeneities. As paradigmatic cases we focus on a
single chemical step and on a single stripe. In view of applications in
microfluidics the accuracy of guiding liquids by chemical microchannels is
discussed. Finally we give a general prescription of how to investigate
theoretically the wetting properties of substrates with arbitrary chemical
structures.Comment: 56 pages, RevTeX, 20 Figure
Metabolic and Innate Immune Cues Merge into a Specific Inflammatory Response via the UPR
Erratum in : Metabolic and Innate Immune Cues Merge into a Specific Inflammatory Response via the UPR. [Cell. 2019]International audienceInnate immune responses are intricately linked with intracellular metabolism of myeloid cells. Toll-likereceptor (TLR) stimulation shifts intracellular metabolism toward glycolysis, while anti-inflammatorysignals depend on enhanced mitochondrial respiration. How exogenous metabolic signals affect theimmune response is unknown. We demonstrate that TLR-dependent responses of dendritic cells (DC)are exacerbated by a high fatty acid (FA) metabolic environment. FA suppress the TLR-inducedhexokinase activity and perturb tricarboxylic acid cycle metabolism. These metabolic changesenhance mitochondrial reactive oxygen species (mtROS) production and, in turn, the unfolded proteinresponse (UPR) leading to a distinct transcriptomic signature, with IL-23 as hallmark. Interestingly,chemical or genetic suppression of glycolysis was sufficient to induce this specific immune response.Conversely, reducing mtROS production or DC-specific deficiency in XBP1 attenuated IL-23expression and skin inflammation in an IL-23-dependent model of psoriasis. Thus, fine-tuning of innateimmunity depends on optimization of metabolic demands and minimization of mtROS-induced UPR
Paracrine cellular senescence exacerbates biliary injury and impairs regeneration
Senescence has been suggested as causing biliary cholangiopathies but how this is regulated is unclear. Here, the authors generate a mouse model of biliary senescence by deleting Mdm2 in bile ducts and show that inhibiting TGFÎČ limits senescence-dependent aggravation of cholangiopathies
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