Scaling of the specific heat in superfluid films

We study the specific heat of the $x-y$ model on lattices $L \times L \times H$ with $L \gg H$ (i.e. on lattices representing a film geometry) using the Cluster Monte--Carlo method. In the $H$--direction we apply Dirichlet boundary conditions so that the order parameter in the top and bottom layers is zero. We find that our results for the specific heat of various thickness size $H$ collapse on the same universal scaling function. The extracted scaling function of the specific heat is in good agreement with the experimentally determined universal scaling function using no free parameters.Comment: 4 pages, uuencoded compressed PostScrip

The specific heat of thin films near the lambda-transition: A Monte Carlo study of an improved three-dimensional lattice model

We study the finite size scaling behaviour of the specific heat of thin films in the neighbourhood of the lambda-transition. To this end we have simulated the improved two-component phi^4 model on the simple cubic lattice. We employ free boundary conditions in the short direction to mimic the vanishing order parameter at the boundaries of a 4He film. Most of our simulations are performed for the thicknesses L_0=8,16 and 32 of the film. It turns out that one has to take into account corrections proportional 1/L_0 to obtain a good collapse of the finite size scaling functions obtained from different L_0. Our results are compared with those obtained from experiments on thin films of 4He near the lambda-transition, from field theory and from previous Monte Carlo simulations.Comment: 46 pages, 15 figure

Li14Ln5[Si11N19O5]O2F2 with Ln = Ce, Nd-Representatives of a Family of Potential Lithium Ion Conductors

The isotypic layered oxonitridosilicates Li14Ln5[Si11N19O5]O2F2 (Ln = Ce, Nd) have been synthesized using Li as fluxing agent and crystallize in the orthorhombic space group Pmmn (Z = 2, Li14Ce5[Si11N19O5]O2F2: a = 17.178(3), b = 7.6500(15), c = 10.116(2) Å, R1 = 0.0409, wR2 = 0.0896; Li14Nd5 Si11N19O5]O2F2: a = 17.126(2), b = 7.6155 15), c = 10.123(2) Å, R1 = 0.0419, wR2 = 0.0929). The silicate layers consist of dreier and sechser rings interconnected via common corners, yielding an unprecedented silicate substructure. A topostructural analysis indicates possible 1D ion migration pathways between five crystallographic independent Li positions. The specific Li-ionic conductivity and its temperature dependence were determined by impedance spectroscopy as well as DC polarization/depolarization measurements. The ionic conductivity is on the order of 5 × 10−5 S/cm at 300°C, while the activation energy is 0.69 eV. Further adjustments of the defect chemistry (e.g., through doping)can make these compounds interesting candidates for novel oxonitridosilicate based ion conductors

Advanced backcross QTL mapping of resistance to Fusarium head blight and plant morphological traits in a Triticum macha × T. aestivum population

While many reports on genetic analysis of Fusarium head blight (FHB) resistance in bread wheat have been published during the past decade, only limited information is available on FHB resistance derived from wheat relatives. In this contribution, we report on the genetic analysis of FHB resistance derived from Triticum macha (Georgian spelt wheat). As the origin of T. macha is in the Caucasian region, it is supposed that its FHB resistance differs from other well-investigated resistance sources. To introduce valuable alleles from the landrace T. macha into a modern genetic background, we adopted an advanced backcross QTL mapping scheme. A backcross-derived recombinant-inbred line population of 321 BC2F3 lines was developed from a cross of T. macha with the Austrian winter wheat cultivar Furore. The population was evaluated for Fusarium resistance in seven field experiments during four seasons using artificial inoculations. A total of 300 lines of the population were genetically fingerprinted using SSR and AFLP markers. The resulting linkage map covered 33 linkage groups with 560 markers. Five novel FHB-resistance QTL, all descending from T. macha, were found on four chromosomes (2A, 2B, 5A, 5B). Several QTL for morphological and developmental traits were mapped in the same population, which partly overlapped with FHB-resistance QTL. Only the 2BL FHB-resistance QTL co-located with a plant height QTL. The largest-effect FHB-resistance QTL in this population mapped at the spelt-type locus on chromosome 5A and was associated with the wild-type allele q, but it is unclear whether q has a pleiotropic effect on FHB resistance or is closely linked to a nearby resistance QTL

The specific heat of superfluids near the transition temperature

The specific heat of the $x-y$ model is studied on cubic lattices of sizes $L \times L \times L$ and on lattices $L \times L \times H$ with $L \gg H$ (i.e. on lattices representing a film geometry) using the Cluster Monte Carlo method. Periodic boundary conditions were applied in all directions. In the cubic case we obtained the ratio of the critical exponents $\alpha/\nu$ from the size dependence of the energy density at the critical temperature $T_{\lambda}$. Using finite--size scaling theory, we find that while for both geometries our results scale to universal functions, these functions differ for the different geometries. We compare our findings to experimental results and results of renormalization group calculations.Comment: self-unpacking uuencoded PostScript file (for instructions see the beginning of the file), 18 pages

Networked T Cell Death following Macrophage Infection by Mycobacterium tuberculosis

<div><h3>Background</h3><p>Depletion of T cells following infection by <em>Mycobacterium tuberculosis</em> (Mtb) impairs disease resolution, and interferes with clinical test performance that relies on cell-mediated immunity. A number of mechanisms contribute to this T cell suppression, such as activation-induced death and trafficking of T cells out of the peripheral circulation and into the diseased lungs. The extent to which Mtb infection of human macrophages affects T cell viability however, is not well characterised.</p> <h3>Methodology/Principal Findings</h3><p>We found that lymphopenia (<1.5×10⁹ cells/l) was prevalent among culture-positive tuberculosis patients, and lymphocyte counts significantly improved post-therapy. We previously reported that Mtb-infected human macrophages resulted in death of infected and uninfected bystander macrophages. In the current study, we sought to examine the influence of infected human alveolar macrophages on T cells. We infected primary human alveolar macrophages (the primary host cell for Mtb) or PMA-differentiated THP-1 cells with Mtb H37Ra, then prepared cell-free supernatants. The supernatants of Mtb-infected macrophages caused dose-dependent, caspase-dependent, T cell apoptosis. This toxic effect of infected macrophage secreted factors did not require TNF-α or Fas. The supernatant cytotoxic signal(s) were heat-labile and greater than 50 kDa in molecular size. Although ESAT-6 was toxic to T cells, other Mtb-secreted factors tested did not influence T cell viability; nor did macrophage-free Mtb bacilli or broth from Mtb cultures. Furthermore, supernatants from <em>Mycobacterium bovis</em> Bacille de Calmette et Guerin (BCG)- infected macrophages also elicited T cell death suggesting that ESAT-6 itself, although cytotoxic, was not the principal mediator of T cell death in our system.</p> <h3>Conclusions</h3><p>Mtb-Infected macrophages secrete heat-labile factors that are toxic to T cells, and may contribute to the immunosuppression seen in tuberculosis as well as interfere with microbial eradication in the granuloma.</p> </div

Influenza A Virus Inhibits Type I IFN Signaling via NF-κB-Dependent Induction of SOCS-3 Expression

The type I interferon (IFN) system is a first line of defense against viral infections. Viruses have developed various mechanisms to counteract this response. So far, the interferon antagonistic activity of influenza A viruses was mainly observed on the level of IFNβ gene induction via action of the viral non-structural protein 1 (NS1). Here we present data indicating that influenza A viruses not only suppress IFNβ gene induction but also inhibit type I IFN signaling through a mechanism involving induction of the suppressor of cytokine signaling-3 (SOCS-3) protein. Our study was based on the observation that in cells that were infected with influenza A virus and subsequently stimulated with IFNα/β, phosphorylation of the signal transducer and activator of transcription protein 1 (STAT1) was strongly reduced. This impaired STAT1 activation was not due to the action of viral proteins but rather appeared to be induced by accumulation of viral 5′ triphosphate RNA in the cell. SOCS proteins are potent endogenous inhibitors of Janus kinase (JAK)/STAT signaling. Closer examination revealed that SOCS-3 but not SOCS-1 mRNA levels increase in an RNA- and nuclear factor kappa B (NF-κB)-dependent but type I IFN-independent manner early in the viral replication cycle. This direct viral induction of SOCS-3 mRNA and protein expression appears to be relevant for suppression of the antiviral response since in SOCS-3 deficient cells a sustained phosphorylation of STAT1 correlated with elevated expression of type I IFN-dependent genes. As a consequence, progeny virus titers were reduced in SOCS-3 deficient cells or in cells were SOCS-3 expression was knocked-down by siRNA. These data provide the first evidence that influenza A viruses suppress type I IFN signaling on the level of JAK/STAT activation. The inhibitory effect is at least in part due to the induction of SOCS-3 gene expression, which results in an impaired antiviral response