The free energy in the Derrida--Retaux recursive model

We are interested in a simple max-type recursive model studied by Derrida and Retaux (2014) in the context of a physics problem, and find a wide range for the exponent in the free energy in the nearly supercritical regime

Provable first-order transitions for liquid crystal and lattice gauge models with continuous symmetries

We consider various sufficiently nonlinear sigma models for nematic liquid crystal ordering of RP^{N-1} type and of lattice gauge type with continous symmetries. We rigorously show that they exhibit a first-order transition in the temperature. The result holds in dimension 2 or more for the RP^{N-1} models and in dimension 3 or more for the lattice gauge models. In the two-dimensional case our results clarify and solve a recent controversy about the possibility of such transitions. For lattice gauge models our methods provide the first proof of a first-order transition in a model with a continuous gauge symmetry

Inside-Out Evacuation of Transitional Protoplanetary Disks by the Magneto-Rotational Instability

How do T Tauri disks accrete? The magneto-rotational instability (MRI) supplies one means, but protoplanetary disk gas is typically too poorly ionized to be magnetically active. Here we show that the MRI can, in fact, explain observed accretion rates for the sub-class of T Tauri disks known as transitional systems. Transitional disks are swept clean of dust inside rim radii of ~10 AU. Stellar coronal X-rays ionize material in the disk rim, activating the MRI there. Gas flows from the rim to the star, at a rate limited by the depth to which X-rays ionize the rim wall. The wider the rim, the larger the surface area that the rim wall exposes to X-rays, and the greater the accretion rate. Interior to the rim, the MRI continues to transport gas; the MRI is sustained even at the disk midplane by super-keV X-rays that Compton scatter down from the disk surface. Accretion is therefore steady inside the rim. Blown out by radiation pressure, dust largely fails to accrete with gas. Contrary to what is usually assumed, ambipolar diffusion, not Ohmic dissipation, limits how much gas is MRI-active. We infer values for the transport parameter alpha on the order of 0.01 for GM Aur, TW Hyd, and DM Tau. Because the MRI can only afflict a finite radial column of gas at the rim, disk properties inside the rim are insensitive to those outside. Thus our picture provides one robust setting for planet-disk interaction: a protoplanet interior to the rim will interact with gas whose density, temperature, and transport properties are definite and decoupled from uncertain initial conditions. Our study also supplies half the answer to how disks dissipate: the inner disk drains from the inside out by the MRI, while the outer disk photoevaporates by stellar ultraviolet radiation.Comment: Accepted to Nature Physics June 7, 2007. The manuscript for publication is embargoed per Nature policy. This arxiv.org version contains more technical details and discussion, and is distributed with permission from the editors. 10 pages, 4 figure

Mycolactone-dependent depletion of endothelial cell thrombomodulin is strongly associated with fibrin deposition in Buruli ulcer lesions

A well-known histopathological feature of diseased skin in Buruli ulcer (BU) is coagulative necrosis caused by the Mycobacterium ulcerans macrolide exotoxin mycolactone. Since the underlying mechanism is not known, we have investigated the effect of mycolactone on endothelial cells, focussing on the expression of surface anticoagulant molecules involved in the protein C anticoagulant pathway. Congenital deficiencies in this natural anticoagulant pathway are known to induce thrombotic complications such as purpura fulimans and spontaneous necrosis. Mycolactone profoundly decreased thrombomodulin (TM) expression on the surface of human dermal microvascular endothelial cells (HDMVEC) at doses as low as 2ng/ml and as early as 8hrs after exposure. TM activates protein C by altering thrombin's substrate specificity, and exposure of HDMVEC to mycolactone for 24 hours resulted in an almost complete loss of the cells' ability to produce activated protein C. Loss of TM was shown to be due to a previously described mechanism involving mycolactone-dependent blockade of Sec61 translocation that results in proteasome-dependent degradation of newly synthesised ER-transiting proteins. Indeed, depletion from cells determined by live-cell imaging of cells stably expressing a recombinant TM-GFP fusion protein occurred at the known turnover rate. In order to determine the relevance of these findings to BU disease, immunohistochemistry of punch biopsies from 40 BU lesions (31 ulcers, nine plaques) was performed. TM abundance was profoundly reduced in the subcutis of 78% of biopsies. Furthermore, it was confirmed that fibrin deposition is a common feature of BU lesions, particularly in the necrotic areas. These findings indicate that there is decreased ability to control thrombin generation in BU skin. Mycolactone's effects on normal endothelial cell function, including its ability to activate the protein C anticoagulant pathway are strongly associated with this. Fibrin-driven tisischemia could contribute to the development of the tissue necrosis seen in BU lesions

Chemically-synthesised, atomically-precise gold clusters deposited and activated on titania

Synchrotron XPS was used to investigate a series of chemically-synthesised, atomically-precise gold clusters Au(n)(PPh₃)(y) (n = 8, 9, 11 and 101, with y depending on cluster size) immobilized on titania nanoparticles. The gold clusters were washed with toluene at 100 °C or calcined at 200 °C to remove the organic ligand. From the position of the Au 4f₇/₂ peak it is concluded that cluster size is not altered through the deposition. From the analysis of the phosphorous spectra, it can be concluded that the applied heat treatment removes the organic ligands. Washing and calcination leads to partial oxidation and partial agglomeration of the clusters. Oxidation of the clusters is most likely due to the interaction of the cluster core with the oxygen of the titania surface after removal of ligands. The position of the Au 4f₇/₂ peak indicates that the size of the agglomerated clusters is still smaller than that of Au₁₀₁.David P. Anderson, Jason F. Alvino, Alexander Gentleman, Hassan Al Qahtani, Lars Thomsen, Matthew I. J. Polson, Gregory F. Metha, Vladimir B. Golovko and Gunther G. Andersso

Altered DNA Methylation in Leukocytes with Trisomy 21

The primary abnormality in Down syndrome (DS), trisomy 21, is well known; but how this chromosomal gain produces the complex DS phenotype, including immune system defects, is not well understood. We profiled DNA methylation in total peripheral blood leukocytes (PBL) and T-lymphocytes from adults with DS and normal controls and found gene-specific abnormalities of CpG methylation in DS, with many of the differentially methylated genes having known or predicted roles in lymphocyte development and function. Validation of the microarray data by bisulfite sequencing and methylation-sensitive Pyrosequencing (MS-Pyroseq) confirmed strong differences in methylation (p<0.0001) for each of 8 genes tested: TMEM131, TCF7, CD3Z/CD247, SH3BP2, EIF4E, PLD6, SUMO3, and CPT1B, in DS versus control PBL. In addition, we validated differential methylation of NOD2/CARD15 by bisulfite sequencing in DS versus control T-cells. The differentially methylated genes were found on various autosomes, with no enrichment on chromosome 21. Differences in methylation were generally stable in a given individual, remained significant after adjusting for age, and were not due to altered cell counts. Some but not all of the differentially methylated genes showed different mean mRNA expression in DS versus control PBL; and the altered expression of 5 of these genes, TMEM131, TCF7, CD3Z, NOD2, and NPDC1, was recapitulated by exposing normal lymphocytes to the demethylating drug 5-aza-2′deoxycytidine (5aza-dC) plus mitogens. We conclude that altered gene-specific DNA methylation is a recurrent and functionally relevant downstream response to trisomy 21 in human cells

Level Set Method for the Evolution of Defect and Brane Networks

A theory for studying the dynamic scaling properties of branes and relativistic topological defect networks is presented. The theory, based on a relativistic version of the level set method, well-known in other contexts, possesses self-similar ``scaling'' solutions, for which one can calculate many quantities of interest. Here, the length and area densities of cosmic strings and domain walls are calculated in Minkowski space, and radiation, matter, and curvature-dominated FRW cosmologies with 2 and 3 space dimensions. The scaling exponents agree the naive ones based on dimensional analysis, except for cosmic strings in 3-dimensional Minkowski space, which are predicted to have a logarithmic correction to the naive scaling form. The scaling amplitudes of the length and area densities are a factor of approximately 2 lower than results from numerical simulations of classical field theories. An expression for the length density of strings in the condensed matter literature is corrected.Comment: 46pp LaTeX, revtex4(preprint), 1 eps figure, revised for publication. Note title chang