4,860 research outputs found

    Classical communication and non-classical fidelity of quantum teleportation

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    In quantum teleportation, the role of entanglement has been much discussed. It is known that entanglement is necessary for achieving non-classical teleportation fidelity. Here we focus on the amount of classical communication that is necessary to obtain non-classical fidelity in teleportation. We quantify the amount of classical communication that is sufficient for achieving non-classical fidelity for two independent 1-bit and single 2-bits noisy classical channels. It is shown that on average 0.208 bits of classical communication is sufficient to get non-classical fidelity. We also find the necessary amount of classical communication in case of isotropic transformation. Finally we study how the amount of sufficient classical communication increases with weakening of entanglement used in the teleportation process.Comment: Accepted in Quantum Info. Proces

    Convection and the Extracellular Matrix Dictate Inter- and Intra-Biofilm Quorum Sensing Communication in Environmental Systems.

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    The mechanisms and impact of bacterial quorum sensing (QS) for the coordination of population-level behaviors are well studied under laboratory conditions. However, it is unclear how, in otherwise open environmental systems, QS signals accumulate to sufficient concentration to induce QS phenotypes, especially when quorum quenching (QQ) organisms are also present. We explore the impact of QQ activity on QS signaling in spatially organized biofilms in scenarios that mimic open systems of natural and engineered environments. Using a functionally differentiated biofilm system, we show that the extracellular matrix, local flow, and QQ interact to modulate communication. In still aqueous environments, convection facilitates signal dispersal while the matrix absorbs and relays signals to the cells. This process facilitates inter-biofilm communication even at low extracellular signal concentrations. Within the biofilm, the matrix further regulates the transport of the competing QS and QQ molecules, leading to heterogenous QS behavior. Importantly, only extracellular QQ enzymes can effectively control QS signaling, suggesting that the intracellular QQ enzymes may not have evolved to degrade environmental QS signals for competition

    Resolving the M2-brane

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    We construct deformed, T^2 wrapped, rotating M2-branes on a resolved cone over Q^{1,1,1} and Q^{1,1,1}/Z_2, as well as on a product of two Eguchi-Hanson instantons. All worldvolume directions of these supersymmetric and regular solutions are fibred over the transverse space. These constitute gravity duals of D=3, N=2 gauge theories. In particular, the deformed M2-brane on a resolved cone over Q^{1,1,1} and the S^1 wrapped M2-brane on a resolved cone over Q^{1,1,1}/Z_2 provide explicit realizations of holographic renormalization group flows in M-theory for which both conformal and Lorentz symmetries are broken in the IR region and restored in the UV limit. These solutions can be dualized to supersymmetric type IIB pp-waves, which are rendered non-singular either by additional flux or a twisted time-like direction.Comment: Latex, 23 pages, references adde

    Quantification of the Frequency and Multiplicity of Infection of Respiratory- and Lymph Node–Resident Dendritic Cells During Influenza Virus Infection

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    Background: Previous studies have demonstrated that DC differentially regulate influenza A virus (IAV)–specific CD8 T cell responses in vivo during high and low dose IAV infections. Furthermore, in vitro infection of DC with IAV at low versus high multiplicities of infection (MOI) results in altered cytokine production and a reduced ability to prime naïve CD8 T cell responses. Flow cytometric detection of IAV proteins within DC, a commonly used method for detection of cellular IAV infection, does not distinguish between the direct infection of these cells or their uptake of viral proteins from dying epithelial cells. Methods/Principal Findings: We have developed a novel, sensitive, single-cell RT-PCR–based approach to assess the infection of respiratory DC (rDC) and lymph node (LN)-resident DC (LNDC) following high and low dose IAV infections. Our results show that, while a fraction of both rDC and LNDC contain viral mRNA following IAV infection, there is little correlation between the percentage of rDC containing viral mRNA and the initial IAV inoculum dose. Instead, increasing IAV inoculums correlate with augmented rDC MOI. Conclusion/Significance: Together, our results demonstrate a novel and sensitive method for the detection of direct IAV infection at the single-cell level and suggest that the previously described ability of DC to differentially regulate IAV-specific T cell responses during high and low dose IAV infections could relate to the MOI of rDC within the LN rather than th

    K^0 pi^0 Sigma^+ and K^*0 Sigma^+ photoproduction off the proton

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    The exclusive reactions Îłp→K∗0ÎŁ+(1189)\gamma p \to K^{*0} \Sigma^+(1189) and Îłp→K0π0ÎŁ+(1189)\gamma p \to K^{0} \pi^{0}\Sigma^+(1189), leading to the p 4π0\pi^{0} final state, have been measured with a tagged photon beam for incident energies from threshold up to 2.5 GeV. The experiment has been performed at the tagged photon facility of the ELSA accelerator (Bonn). The Crystal Barrel and TAPS detectors were combined to a photon detector system of almost 4π\pi geometrical acceptance. Differential and total cross sections are reported. At energies close to the threshold, a flat angular distribution has been observed for the reaction Îłp→K0π0ÎŁ+\gamma p\to K^{0} \pi^{0}\Sigma^+ suggesting dominant s-channel production. Σ∗(1385)\Sigma^*(1385) and higher lying hyperon states have been observed. An enhancement in the forward direction in the angular distributions of the reaction Îłp→K∗0ÎŁ+\gamma p \to K^{*0}\Sigma^+ indicates a tt-channel exchange contribution to the reaction mechanism. The experimental data are in reasonable agreement with recent theoretical predictions.Comment: 11 pages, 13 figures, submitted to EPJ

    A Simple Shell Model for Quantum Dots in a Tilted Magnetic Field

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    A model for quantum dots is proposed, in which the motion of a few electrons in a three-dimensional harmonic oscillator potential under the influence of a homogeneous magnetic field of arbitrary direction is studied. The spectrum and the wave functions are obtained by solving the classical problem. The ground state of the Fermi-system is obtained by minimizing the total energy with regard to the confining frequencies. From this a dependence of the equilibrium shape of the quantum dot on the electron number, the magnetic field parameters and the slab thickness is found.Comment: 15 pages (Latex), 3 epsi figures, to appear in PhysRev B, 55 Nr. 20 (1997

    Sphingosine 1-phosphate receptor 4 promotes nonalcoholic steatohepatitis by activating NLRP3 inflammasome

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    BACKGROUND & AIMS: Sphingosine 1-phosphate receptors (S1PRs) are a group of G-protein-coupled receptors that confer a broad range of functional effects in chronic inflammatory and metabolic diseases. S1PRs also may mediate the development of nonalcoholic steatohepatitis (NASH), but the specific subtypes involved and the mechanism of action are unclear. METHODS: We investigated which type of S1PR isoforms is activated in various murine models of NASH. The mechanism of action of S1PR4 was examined in hepatic macrophages isolated from high-fat, high-cholesterol diet (HFHCD)-fed mice. We developed a selective S1PR4 functional antagonist by screening the fingolimod (2-amino-2-[2-(4- n-octylphenyl)ethyl]-1,3-propanediol hydrochloride)-like sphingolipid-focused library. RESULTS: The livers of various mouse models of NASH as well as hepatic macrophages showed high expression of S1pr4. Moreover, in a cohort of NASH patients, expression of S1PR4 was 6-fold higher than those of healthy controls. S1pr4(++/-) mice were protected from HFHCD-induced NASH and hepatic fibrosis without changes in steatosis. S1pr4 depletion in hepatic macrophages inhibited lipopolysaccharide-mediated Ca++ release and deactivated the Nod-like receptor pyrin domaincontainning protein 3 (NLRP3) inflammasome. S1P increased the expression of S1pr4 in hepatic macrophages and activated NLRP3 inflammasome through inositol trisphosphate/inositol trisphosphate-receptor-dependent [Ca++] signaling. To further clarify the biological function of S1PR4, we developed SLB736, a novel selective functional antagonist of SIPR4. Similar to S1pr4(+/-) mice, administration of SLB736 to HFHCD-fed mice prevented the development of NASH and hepatic fibrosis, but not steatosis, by deactivating the NLRP3 inflammasome. CONCLUSIONS: S1PR4 may be a new therapeutic target for NASH that mediates the activation of NLRP3 inflammasome in hepatic macrophages
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