860 research outputs found

    Spin-Flip Noise in a Multi-Terminal Spin-Valve

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    We study shot noise and cross correlations in a four terminal spin-valve geometry using a Boltzmann-Langevin approach. The Fano factor (shot noise to current ratio) depends on the magnetic configuration of the leads and the spin-flip processes in the normal metal. In a four-terminal geometry, spin-flip processes are particular prominent in the cross correlations between terminals with opposite magnetization.Comment: 4 pages, 3 figure

    Orientational ordering of commensurate Fe(CO)5 monolayers on graphite

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    URL:http://link.aps.org/doi/10.1103/PhysRevB.27.5864 DOI:10.1103/PhysRevB.27.5864Elastic neutron diffraction and Mössbauer spectroscopy have been used to study the structure, orientational-disordering (OD) transition, and melting of an Fe(CO)5 submonolayer adsorbed on Grafoil. The OD transition occurs between 150 and 167 K from a two-sublattice (√7×√21) structure to a nearly (√7×√7) phase in which the molecules are believed to rotate about the surface normal. Mössbauer spectra exhibit a more abrupt variation with temperature near melting at 170 K than through the OD transition.This work was supported by NSF under Grants No. DMR-7905958 and No. INT-8012228, Israel-U.S. Binational Science Foundation Grant No. 2687, and the Danish Research Counci

    Dilepton production in proton-proton collisions at BEVALAC energies

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    The dilepton production in elementary ppe+eX{pp\to e^{+}e^{-}X} reactions at BEVALAC energies Tlab=1÷5T_{lab}=1\div 5 GeV is investigated. The calculations include direct e+e{e^{+}e^{-}} decays of the vector mesons ρ0\rho ^{0}, ω\omega , and ϕ\phi , Dalitz decays of the π0\pi ^{0}-, η\eta -, % \rho -, ω\omega -, and ϕ\phi -mesons, and of the baryon resonances % \Delta (1232),N(1520), ...... . The subthreshold vector meson production cross sections in pppp collisions are treated in a way sufficient to avoid double counting with the inclusive vector meson production. The vector meson dominance model for the transition form factors of the resonance Dalitz decays Re+eNR\to e^{+}e^{-}N is used in an extended form to ensure correct asymptotics which are in agreement with the quark counting rules. Such a modification gives an unified and consistent description of both RNγR\to N\gamma radiative decays and RNρ(ω)R\to N\rho (\omega) meson decays. The effect of multiple pion production on the experimental efficiency for the detection of the dilepton pairs is studied. We find the dilepton yield in reasonable agreement with the experimental data for the set of intermediate energies whereas at the highest energy Tlab=4.88T_{lab}=4.88 GeV the number of dilepton pairs is likely to be overestimated experimentally in the mass range M=300÷700M=300\div 700 MeV.Comment: 25 pages (IOP style), 5 figures, revised manuscript accepted for publication in JP

    Novel role for the innate immune receptor toll-like receptor 4 (TLR4) in the regulation of the wnt signaling pathway and photoreceptor apoptosis

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    Recent evidence has implicated innate immunity in regulating neuronal survival in the brain during stroke and other neurodegenerations. Photoreceptors are specialized light-detecting neurons in the retina that are essential for vision. In this study, we investigated the role of the innate immunity receptor TLR4 in photoreceptors. TLR4 activation by lipopolysaccharide (LPS) significantly reduced the survival of cultured mouse photoreceptors exposed to oxidative stress. With respect to mechanism, TLR4 suppressed Wnt signaling, decreased phosphorylation and activation of the Wnt receptor LRP6, and blocked the protective effect of the Wnt3a ligand. Paradoxically, TLR4 activation prior to oxidative injury protected photoreceptors, in a phenomenon known as preconditioning. Expression of TNFα and its receptors TNFR1 and TNFR2 decreased during preconditioning, and preconditioning was mimicked by TNFα antagonists, but was independent of Wnt signaling. Therefore, TLR4 is a novel regulator of photoreceptor survival that acts through the Wnt and TNFα pathways. © 2012 Yi et al

    Plx1 is required for chromosomal DNA replication under stressful conditions

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    Polo-like kinase (Plk)1 is required for mitosis progression. However, although Plk1 is expressed throughout the cell cycle, its function during S-phase is unknown. Using Xenopus laevis egg extracts, we demonstrate that Plx1, the Xenopus orthologue of Plk1, is required for DNA replication in the presence of stalled replication forks induced by aphidicolin, etoposide or reduced levels of DNA-bound Mcm complexes. Plx1 binds to chromatin and suppresses the ATM/ATR-dependent intra-S-phase checkpoint that inhibits origin firing. This allows Cdc45 loading and derepression of DNA replication initiation. Checkpoint activation increases Plx1 binding to the Mcm complex through its Polo box domain. Plx1 recruitment to chromatin is independent of checkpoint mediators Tipin and Claspin. Instead, ATR-dependent phosphorylation of serine 92 of Mcm2 is required for the recruitment of Plx1 to chromatin and for the recovery of DNA replication under stress. Depletion of Plx1 leads to accumulation of chromosomal breakage that is prevented by the addition of recombinant Plx1. These data suggest that Plx1 promotes genome stability by regulating DNA replication under stressful conditions

    Enamel-like apatite crown covering amorphous mineral in a crayfish mandible

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    Carbonated hydroxyapatite is the mineral found in vertebrate bones and teeth, whereas invertebrates utilize calcium carbonate in their mineralized organs. In particular, stable amorphous calcium carbonate is found in many crustaceans. Here we report on an unusual, crystalline enamel-like apatite layer found in the mandibles of the arthropod Cherax quadricarinatus (freshwater crayfish). Despite their very different thermodynamic stabilities, amorphous calcium carbonate, amorphous calcium phosphate, calcite and fluorapatite coexist in well-defined functional layers in close proximity within the mandible. The softer amorphous minerals are found primarily in the bulk of the mandible whereas apatite, the harder and less soluble mineral, forms a wear-resistant, enamel-like coating of the molar tooth. Our findings suggest a unique case of convergent evolution, where similar functional challenges of mastication led to independent developments of structurally and mechanically similar, apatite-based layers in the teeth of genetically remote phyla: vertebrates and crustaceans

    Tissue Microenvironments Define and Get Reinforced by Macrophage Phenotypes in Homeostasis or during Inflammation, Repair and Fibrosis

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    Current macrophage phenotype classifications are based on distinct in vitro culture conditions that do not adequately mirror complex tissue environments. In vivo monocyte progenitors populate all tissues for immune surveillance which supports the maintenance of homeostasis as well as regaining homeostasis after injury. Here we propose to classify macrophage phenotypes according to prototypical tissue environments, e.g. as they occur during homeostasis as well as during the different phases of (dermal) wound healing. In tissue necrosis and/or infection, damage- and/or pathogen-associated molecular patterns induce proinflammatory macrophages by Toll-like receptors or inflammasomes. Such classically activated macrophages contribute to further tissue inflammation and damage. Apoptotic cells and antiinflammatory cytokines dominate in postinflammatory tissues which induce macrophages to produce more antiinflammatory mediators. Similarly, tumor-associated macrophages also confer immunosuppression in tumor stroma. Insufficient parenchymal healing despite abundant growth factors pushes macrophages to gain a profibrotic phenotype and promote fibrocyte recruitment which both enforce tissue scarring. Ischemic scars are largely devoid of cytokines and growth factors so that fibrolytic macrophages that predominantly secrete proteases digest the excess extracellular matrix. Together, macrophages stabilize their surrounding tissue microenvironments by adapting different phenotypes as feed-forward mechanisms to maintain tissue homeostasis or regain it following injury. Furthermore, macrophage heterogeneity in healthy or injured tissues mirrors spatial and temporal differences in microenvironments during the various stages of tissue injury and repair. Copyright (C) 2012 S. Karger AG, Base

    Developmental origin and maintenance of distinct testicular macrophage populations

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    International audienceTesticular macrophages (tM phi) are the principal immune cells of the mammalian testis. Beyond classical immune functions, they have been shown to be important for organogenesis, spermatogenesis, and male hormone production. In the adult testis, two different macrophage populations have been identified based on their distinct tissue localization and morphology, but their developmental origin and mode of homeostatic maintenance are unknown. In this study, we use genetic lineage-tracing models and adoptive transfer protocols to address this question. We show that embryonic progenitors give rise to the interstitial macrophage population, whereas peritubular macrophages are exclusively seeded postnatally in the prepuberty period from bone marrow (BM)-derived progenitors. As the proliferative capacity of interstitial macrophages declines, BM progenitors also contribute to this population. Once established, both the peritubular and interstitial macrophage populations exhibit a long life span and a low turnover in the steady state. Our observations identify distinct developmental pathways for two different tM phi populations that have important implications for the further dissection of their distinct roles in organ homeostasis and testicular function

    Computational Methods to Study Kinetics of DNA Replication

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    New technologies such as DNA combing have led to the availability of large quanti-ties of data that describe the state of DNA while undergoing replication in S phase. In this chapter, we describe methods used to extract various parameters of replica-tion — fork velocity, origin initiation rate, fork density, numbers of potential and utilized origins — from such data. We first present a version of the technique that applies to “ideal ” data. We then show how to deal with a number of real-world complications, such as the asynchrony of starting times of a population of cells, the finite length of fragments used in the analysis, and the finite amount of DNA in a chromosome. Key words: DNA replication, replication fork velocity, origin initiation

    Autoimmune and autoinflammatory mechanisms in uveitis

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    The eye, as currently viewed, is neither immunologically ignorant nor sequestered from the systemic environment. The eye utilises distinct immunoregulatory mechanisms to preserve tissue and cellular function in the face of immune-mediated insult; clinically, inflammation following such an insult is termed uveitis. The intra-ocular inflammation in uveitis may be clinically obvious as a result of infection (e.g. toxoplasma, herpes), but in the main infection, if any, remains covert. We now recognise that healthy tissues including the retina have regulatory mechanisms imparted by control of myeloid cells through receptors (e.g. CD200R) and soluble inhibitory factors (e.g. alpha-MSH), regulation of the blood retinal barrier, and active immune surveillance. Once homoeostasis has been disrupted and inflammation ensues, the mechanisms to regulate inflammation, including T cell apoptosis, generation of Treg cells, and myeloid cell suppression in situ, are less successful. Why inflammation becomes persistent remains unknown, but extrapolating from animal models, possibilities include differential trafficking of T cells from the retina, residency of CD8(+) T cells, and alterations of myeloid cell phenotype and function. Translating lessons learned from animal models to humans has been helped by system biology approaches and informatics, which suggest that diseased animals and people share similar changes in T cell phenotypes and monocyte function to date. Together the data infer a possible cryptic infectious drive in uveitis that unlocks and drives persistent autoimmune responses, or promotes further innate immune responses. Thus there may be many mechanisms in common with those observed in autoinflammatory disorders
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