Series expansions without diagrams

We discuss the use of recursive enumeration schemes to obtain low and high temperature series expansions for discrete statistical systems. Using linear combinations of generalized helical lattices, the method is competitive with diagramatic approaches and is easily generalizable. We illustrate the approach using the Ising model and generate low temperature series in up to five dimensions and high temperature series in three dimensions. The method is general and can be applied to any discrete model. We describe how it would work for Potts models.Comment: 24 pages, IASSNS-HEP-93/1

Specific Heat Exponent for the 3-d Ising Model from a 24-th Order High Temperature Series

We compute high temperature expansions of the 3-d Ising model using a recursive transfer-matrix algorithm and extend the expansion of the free energy to 24th order. Using ID-Pade and ratio methods, we extract the critical exponent of the specific heat to be alpha=0.104(4).Comment: 10 pages, LaTeX with 5 eps-figures using epsf.sty, IASSNS-93/83 and WUB-93-4

Series studies of the Potts model. I: The simple cubic Ising model

The finite lattice method of series expansion is generalised to the $q$-state Potts model on the simple cubic lattice. It is found that the computational effort grows exponentially with the square of the number of series terms obtained, unlike two-dimensional lattices where the computational requirements grow exponentially with the number of terms. For the Ising ($q=2$) case we have extended low-temperature series for the partition functions, magnetisation and zero-field susceptibility to $u^{26}$ from $u^{20}$. The high-temperature series for the zero-field partition function is extended from $v^{18}$ to $v^{22}$. Subsequent analysis gives critical exponents in agreement with those from field theory.Comment: submitted to J. Phys. A: Math. Gen. Uses preprint.sty: included. 24 page

New extended high temperature series for the N-vector spin models on three-dimensional bipartite lattices

High temperature expansions for the susceptibility and the second correlation moment of the classical N-vector model (O(N) symmetric Heisenberg model) on the sc and the bcc lattices are extended to order $\beta^{19}$ for arbitrary N. For N= 2,3,4.. we present revised estimates of the critical parameters from the newly computed coefficients.Comment: 11 pages, latex, no figures, to appear in Phys. Rev.

Improved high-temperature expansion and critical equation of state of three-dimensional Ising-like systems

High-temperature series are computed for a generalized $3d$ Ising model with arbitrary potential. Two specific ``improved'' potentials (suppressing leading scaling corrections) are selected by Monte Carlo computation. Critical exponents are extracted from high-temperature series specialized to improved potentials, achieving high accuracy; our best estimates are: $\gamma=1.2371(4)$, $\nu=0.63002(23)$, $\alpha=0.1099(7)$, $\eta=0.0364(4)$, $\beta=0.32648(18)$. By the same technique, the coefficients of the small-field expansion for the effective potential (Helmholtz free energy) are computed. These results are applied to the construction of parametric representations of the critical equation of state. A systematic approximation scheme, based on a global stationarity condition, is introduced (the lowest-order approximation reproduces the linear parametric model). This scheme is used for an accurate determination of universal ratios of amplitudes. A comparison with other theoretical and experimental determinations of universal quantities is presented.Comment: 65 pages, 1 figure, revtex. New Monte Carlo data by Hasenbusch enabled us to improve the determination of the critical exponents and of the equation of state. The discussion of several topics was improved and the bibliography was update

Correction: Detrimental ELAVL-1/HuR-dependent GSK3β mRNA stabilization impairs resolution in acute respiratory distress syndrome.

[This corrects the article DOI: 10.1371/journal.pone.0172116.]

A novel population of repair cells identified in the stroma of the human cornea

A

Detrimental ELAVL-1/HuR-dependent GSK3β mRNA stabilization impairs resolution in acute respiratory distress syndrome

<div><p>A hallmark of acute respiratory distress syndrome (ARDS) is accumulation of protein-rich edema in the distal airspaces and its removal is critical for patient survival. Previous studies have shown a detrimental role of Glycogen Synthase Kinase (GSK) 3β during ARDS via inhibition of alveolar epithelial protein transport. We hypothesized that post-transcriptional regulation of GSK3β could play a functional role in ARDS resolution. To address this hypothesis, we performed an <i>in silico</i> analysis to identify regulatory genes whose expression correlation to GSK3β messenger RNA utilizing two lung cancer cell line array datasets. Among potential regulatory partners of GSK3β, these studies identified the RNA-binding protein ELAVL-1/HuR (Embryonic Lethal, Abnormal Vision, Drosophila-Like) as a central component in a likely GSK3β signaling network. ELAVL-1/HuR is a RNA-binding protein that selectively binds to AU-rich elements of mRNA and enhances its stability thereby increasing target gene expression. Subsequent studies with siRNA suppression of ELAVL-1/HuR demonstrated deceased GSK3β mRNA and protein expression and improved clearance of FITC-albumin in A549 cells. Conversely, stabilization of ELAVL-1/HuR with the proteasome inhibitor MG-132 resulted in induction of GSK3β at mRNA and protein level and attenuated FITC-albumin clearance. Utilizing ventilator-induced lung injury or intra-tracheal installation of hydrochloric acid to induce ARDS in mice, we observed increased mRNA and protein expression of ELAVL-1/HuR and GSK3β. Together, our findings indicate a previously unknown interaction between GSK3β and ELAV-1 during ARDS, and suggest the inhibition of the ELAV-1- GSK3β pathways as a novel ARDS treatment approach.</p></div

Stabilization of ELAVL-1/HUR up regulates GSK3β in vitro and attenuates epithelial albumin clearance.

<p>Cells were incubated with 20 μM of the lysosomal inhibitor MG-132 at indicated time points to stabilize ELAV-1. (A) ELAVL-1/HUR protein expression was determined in the nuclear cell lysate via western blot. (B) mRNA and protein expression of GSK3β in cells treated with MG-132. Binding (C) and uptake (D) of FITC labelled albumin All experiments were conducted in A549 cells, n = 4; data represent the mean ± SEM * p< 0.05, **p<0.01, ***p<0.001, n.s. = non significant.</p