Universality of slow decorrelation in KPZ growth

There has been much success in describing the limiting spatial fluctuations of growth models in the Kardar-Parisi-Zhang (KPZ) universality class. A proper rescaling of time should introduce a non-trivial temporal dimension to these limiting fluctuations. In one-dimension, the KPZ class has the dynamical scaling exponent $z=3/2$, that means one should find a universal space-time limiting process under the scaling of time as $t\,T$, space like $t^{2/3} X$ and fluctuations like $t^{1/3}$ as $t\to\infty$. In this paper we provide evidence for this belief. We prove that under certain hypotheses, growth models display temporal slow decorrelation. That is to say that in the scalings above, the limiting spatial process for times $t\, T$ and $t\, T+t^{\nu}$ are identical, for any $\nu<1$. The hypotheses are known to be satisfied for certain last passage percolation models, the polynuclear growth model, and the totally / partially asymmetric simple exclusion process. Using slow decorrelation we may extend known fluctuation limit results to space-time regions where correlation functions are unknown. The approach we develop requires the minimal expected hypotheses for slow decorrelation to hold and provides a simple and intuitive proof which applied to a wide variety of models.Comment: Exposition improved, typos correcte

On universality of local edge regime for the deformed Gaussian Unitary Ensemble

We consider the deformed Gaussian ensemble $H_n=H_n^{(0)}+M_n$ in which $H_n^{(0)}$ is a hermitian matrix (possibly random) and $M_n$ is the Gaussian unitary random matrix (GUE) independent of $H_n^{(0)}$. Assuming that the Normalized Counting Measure of $H_n^{(0)}$ converges weakly (in probability if random) to a non-random measure $N^{(0)}$ with a bounded support and assuming some conditions on the convergence rate, we prove universality of the local eigenvalue statistics near the edge of the limiting spectrum of $H_n$.Comment: 25 pages, 2 figure

Estudo de diferentes alturas de repicagem na produção de biomassa de porta-enxertos cítricos em sistema hidropônico.

A citricultura brasileira é a mais competitiva do mundo, com produção de 19.112.251 toneladas em 2010/11, sendo o Estado de São Paulo o principal produtor, com safra de laranja (2010/11) em torno de 290 milhões de caixas (AGRIANUAL, 2012). Vários são os fatores levados em consideração na ocasião da implantação de um pomar cítrico, porém, é consenso que a escolha de mudas de qualidade atestada é fator preponderante no sucesso da atividade. Pompeu Júnior (2005) enfatiza que os porta-enxertos afetam diversas características das variedades copas, tais como: vigor, produção e sua precocidade, tolerância da planta às adversidades climáticas, além de característica que conferem maior qualidade ao fruto

Impact‐based forecasting for pluvial floods

Pluvial floods in urban areas are caused by local, fast storm events with very high rainfall rates, which lead to inundation of streets and buildings before the storm water reaches a watercourse. An increase in frequency and intensity of heavy rainfall events and an ongoing urbanization may further increase the risk of pluvial flooding in many urban areas. Currently, warnings for pluvial floods are mostly limited to information on rainfall intensities and durations over larger areas, which is often not detailed enough to effectively protect people and goods. We present a proof-of-concept for an impact-based forecasting system for pluvial floods. Using a model chain consisting of a rainfall forecast, an inundation, a contaminant transport and a damage model, we are able to provide predictions for the expected rainfall, the inundated areas, spreading of potential contamination and the expected damage to residential buildings. We use a neural network-based inundation model, which significantly reduces the computation time of the model chain. To demonstrate the feasibility, we perform a hindcast of a recent pluvial flood event in an urban area in Germany. The required spatio-temporal accuracy of rainfall forecasts is still a major challenge, but our results show that reliable impact-based warnings can be forecasts are available up to 5 min before the peak of an extreme rainfall event. Based on our results, we discuss how the outputs of the impact-based forecast could be used to disseminate impact-based early warnings

Endothelial cell CD36 regulates membrane ceramide formation, exosome fatty acid transfer and circulating fatty acid levels

Endothelial cell (EC) CD36 controls tissue fatty acid (FA) uptake. Here we examine how ECs transfer FAs. FA interaction with apical membrane CD36 induces Src phosphorylation of caveolin-1 tyrosine-14 (Cav-1Y14) and ceramide generation in caveolae. Ensuing fission of caveolae yields vesicles containing FAs, CD36 and ceramide that are secreted basolaterally as small (80-100 nm) exosome-like extracellular vesicles (sEVs). We visualize in transwells EC transfer of FAs in sEVs to underlying myotubes. In mice with EC-expression of the exosome marker emeraldGFP-CD63, muscle fibers accumulate circulating FAs in emGFP-labeled puncta. The FA-sEV pathway is mapped through its suppression by CD36 depletion, blocking actin-remodeling, Src inhibition, Cav-1Y14 mutation, and neutral sphingomyelinase 2 inhibition. Suppression of sEV formation in mice reduces muscle FA uptake, raises circulating FAs, which remain in blood vessels, and lowers glucose, mimicking prominent Cd3

Tumor-derived exosomes confer antigen-specific immunosuppression in a murine delayed-type hypersensitivity model

Exosomes are endosome-derived small membrane vesicles that are secreted by most cell types including tumor cells. Tumor-derived exosomes usually contain tumor antigens and have been used as a source of tumor antigens to stimulate anti-tumor immune responses. However, many reports also suggest that tumor-derived exosomes can facilitate tumor immune evasion through different mechanisms, most of which are antigen-independent. In the present study we used a mouse model of delayed-type hypersensitivity (DTH) and demonstrated that local administration of tumor-derived exosomes carrying the model antigen chicken ovalbumin (OVA) resulted in the suppression of DTH response in an antigen-specific manner. Analysis of exosome trafficking demonstrated that following local injection, tumor-derived exosomes were internalized by CD11c+ cells and transported to the draining LN. Exosome-mediated DTH suppression is associated with increased mRNA levels of TGF-β1 and IL-4 in the draining LN. The tumor-derived exosomes examined were also found to inhibit DC maturation. Taken together, our results suggest a role for tumor-derived exosomes in inducing tumor antigen-specific immunosuppression, possibly by modulating the function of APCs. © 2011 Yang et al

CD36 maintains the gastric mucosa and associates with gastric disease

The gastric epithelium is often exposed to injurious elements and failure of appropriate healing predisposes to ulcers, hemorrhage, and ultimately cancer. We examined the gastric function of CD36, a protein linked to disease and homeostasis. We used the tamoxifen model of gastric injury in mice null for Cd36 (Cd3

Visceral obesity and insulin resistance associate with CD36 deletion in lymphatic endothelial cells

Disruption of lymphatic lipid transport is linked to obesity and type 2 diabetes (T2D), but regulation of lymphatic vessel function and its link to disease remain unclear. Here we show that intestinal lymphatic endothelial cells (LECs) have an increasing CD36 expression from lymphatic capillaries (lacteals) to collecting vessels, and that LEC CD36 regulates lymphatic integrity and optimizes lipid transport. Inducible deletion of CD36 in LECs in adult mice (Cd36(ΔLEC)) increases discontinuity of LEC VE-cadherin junctions in lacteals and collecting vessels. Cd36(ΔLEC) mice display slower transport of absorbed lipid, more permeable mesenteric lymphatics, accumulation of inflamed visceral fat and impaired glucose disposal. CD36 silencing in cultured LECs suppresses cell respiration, reduces VEGF-C-mediated VEGFR2/AKT phosphorylation and destabilizes VE-cadherin junctions. Thus, LEC CD36 optimizes lymphatic junctions and integrity of lymphatic lipid transport, and its loss in mice causes lymph leakage, visceral adiposity and glucose intolerance, phenotypes that increase risk of T2D