Shock conditions and shock wave structures in a steady flow in a dissipative fluid

More precisely, calling xi the reciprocal of the Reynolds number based on the shock wave curvature radius, the xi terms of the first order are systematically taken into account. The most important result is a system of formulas giving a correction of order xi for the various RANKINE-HUGONIOT conditions. The suggested formulas may for instance have to be used instead of the conventional ones to evaluate the loss of the total pressure across the detached shock wave which is found at the nose of a very small probe in supersonic flow

Global Solutions for the Gravity Water Waves Equation in Dimension 3

We show existence of global solutions for the gravity water waves equation in dimension 3, in the case of small data. The proof combines energy estimates, which yield control of L^2 related norms, with dispersive estimates, which give decay in L^\infty. To obtain these dispersive estimates, we use an analysis in Fourier space; the study of space and time resonances is then the crucial point

Joint superexchange--Jahn-Teller mechanism for A-type antiferromagnetism in LaMnO3LaMnO_3

We propose a mechanism for A-type antiferromagnetism in orthorombic LaMnO_3, compatible with the large Jahn-Teller splitting inferred from structural data. Orbital ordering resulting from Jahn-Teller distortions effectively leads to A-type ordering (antiferromagnetic in the c axis and ferromagnetic in the ab plane) provided the in-plane distorsion Q_2 is large enough, a condition generally fulfilled in existing data.Comment: 4 pages Late

A spatially-organized multicellular innate immune response in lymph nodes limits systemic pathogen spread

The lymphatic network that transports interstitial fluid and antigens to lymph nodes constitutes a conduit system that can be hijacked by invading pathogens to achieve systemic spread unless dissemination is blocked in the lymph node itself. Here, we show that a network of diverse lymphoid cells (natural killer cells, γδ T cells, natural killer T cells, and innate-like CD8+ T cells) are spatially prepositioned close to lymphatic sinus-lining sentinel macrophages where they can rapidly and efficiently receive inflammasome-generated IL-18 and additional cytokine signals from the pathogen-sensing phagocytes. This leads to rapid IFNγ secretion by the strategically positioned innate lymphocytes, fostering antimicrobial resistance in the macrophage population. Interference with this innate immune response loop allows systemic spread of lymph-borne bacteria. These findings extend our understanding of the functional significance of cellular positioning and local intercellular communication within lymph nodes while emphasizing the role of these organs as highly active locations of innate host defense

Fabry disease

Fabry disease (FD) is a progressive, X-linked inherited disorder of glycosphingolipid metabolism due to deficient or absent lysosomal α-galactosidase A activity. FD is pan-ethnic and the reported annual incidence of 1 in 100,000 may underestimate the true prevalence of the disease. Classically affected hemizygous males, with no residual α-galactosidase A activity may display all the characteristic neurological (pain), cutaneous (angiokeratoma), renal (proteinuria, kidney failure), cardiovascular (cardiomyopathy, arrhythmia), cochleo-vestibular and cerebrovascular (transient ischemic attacks, strokes) signs of the disease while heterozygous females have symptoms ranging from very mild to severe. Deficient activity of lysosomal α-galactosidase A results in progressive accumulation of globotriaosylceramide within lysosomes, believed to trigger a cascade of cellular events. Demonstration of marked α-galactosidase A deficiency is the definitive method for the diagnosis of hemizygous males. Enzyme analysis may occasionnally help to detect heterozygotes but is often inconclusive due to random X-chromosomal inactivation so that molecular testing (genotyping) of females is mandatory. In childhood, other possible causes of pain such as rheumatoid arthritis and 'growing pains' must be ruled out. In adulthood, multiple sclerosis is sometimes considered. Prenatal diagnosis, available by determination of enzyme activity or DNA testing in chorionic villi or cultured amniotic cells is, for ethical reasons, only considered in male fetuses. Pre-implantation diagnosis is possible. The existence of atypical variants and the availability of a specific therapy singularly complicate genetic counseling. A disease-specific therapeutic option - enzyme replacement therapy using recombinant human α-galactosidase A - has been recently introduced and its long term outcome is currently still being investigated. Conventional management consists of pain relief with analgesic drugs, nephroprotection (angiotensin converting enzyme inhibitors and angiotensin receptors blockers) and antiarrhythmic agents, whereas dialysis or renal transplantation are available for patients experiencing end-stage renal failure. With age, progressive damage to vital organ systems develops and at some point, organs may start to fail in functioning. End-stage renal disease and life-threatening cardiovascular or cerebrovascular complications limit life-expectancy of untreated males and females with reductions of 20 and 10 years, respectively, as compared to the general population. While there is increasing evidence that long-term enzyme therapy can halt disease progression, the importance of adjunctive therapies should be emphasized and the possibility of developing an oral therapy drives research forward into active site specific chaperones

Tuning of antigen sensitivity by T cell receptor-dependent negative feedback controls T cell effector function inflammed tissues

Activated T cells must mediate effector responses sufficient to clear pathogens while avoiding excessive tissue damage. Here we have combined dynamic intravital microscopy with ex vivo assessments of T cell cytokine responses to generate a detailed spatiotemporal picture of CD4+ T cell effector regulation in the skin. In response to antigen, effector T cells arrested transiently on antigen presenting cells, briefly producing cytokine and then resuming migration. Antigen recognition led to PD-1 upregulation of the programmed death-1 (PD-1) glycoprotein by T cells and blocking its canonical ligand, programmed death-ligand 1 (PD-L1), lengthened the duration of migration arrest and cytokine production, showing that PD-1 interaction with PD-L1 is a major negative feedback regulator of antigen responsiveness. We speculate that the immune system employs a mechanism involving T cell recruitment, transient activation, and rapid desensitization, allowing the T cell response to rapidly adjust to changes in antigen presentation and minimize collateral injury to the host

James Sdrales and Virginia Zambukos v. Sam Rondos : Brief of Respondents

This paper deals with shape optimization for anisotropic elastoplasticity in logarithmic strain space. We aim to find an appropriate undeformed configuration of a workpiece knowing in advance its deformed configuration, the boundary conditions and the applied loads. The node coordinates of the finite element (FE) domain are chosen as design variables. A discrete sensitivity analysis is presented and analytical gradients are performed. A numerical example illustrates the theoretical aspects

On a recursive algorithm for avoiding mesh distortion in inverse form finding

A challenge in the design of functional parts is the determination of the initial, undeformed shape such that under a given load a part will obtain the desired deformed shape. A shape optimization formulation might be used to determine the initial shape in the sense of an inverse problem via successive iterations of a direct mechanical problem. In this paper, we present a shape optimization formulation for elastoplastic materials with a constitutive model for anisotropic additive elastoplasticity in the logarithmic strain space. A discrete sensitivity analysis is performed and gives the analytical gradient of the objective function needed in the optimization algorithm. We found that the use of the coordinates of the functional component as design variables led to mesh distortions. Without a split of the total force applied on the component and an update of the undeformed configuration between two steps the optimization algorithm is not able to find an appropriate minimum. Three numerical examples in isotropic and anisotropic elastoplasticity illustrate the structure of such a recursive algorithm for avoiding mesh distortions