253 research outputs found

    Weak randomness completely trounces the security of QKD

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    In usual security proofs of quantum protocols the adversary (Eve) is expected to have full control over any quantum communication between any communicating parties (Alice and Bob). Eve is also expected to have full access to an authenticated classical channel between Alice and Bob. Unconditional security against any attack by Eve can be proved even in the realistic setting of device and channel imperfection. In this Letter we show that the security of QKD protocols is ruined if one allows Eve to possess a very limited access to the random sources used by Alice. Such knowledge should always be expected in realistic experimental conditions via different side channels

    Relational interpretation of the wave function and a possible way around Bell's theorem

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    The famous ``spooky action at a distance'' in the EPR-szenario is shown to be a local interaction, once entanglement is interpreted as a kind of ``nearest neighbor'' relation among quantum systems. Furthermore, the wave function itself is interpreted as encoding the ``nearest neighbor'' relations between a quantum system and spatial points. This interpretation becomes natural, if we view space and distance in terms of relations among spatial points. Therefore, ``position'' becomes a purely relational concept. This relational picture leads to a new perspective onto the quantum mechanical formalism, where many of the ``weird'' aspects, like the particle-wave duality, the non-locality of entanglement, or the ``mystery'' of the double-slit experiment, disappear. Furthermore, this picture cirumvents the restrictions set by Bell's inequalities, i.e., a possible (realistic) hidden variable theory based on these concepts can be local and at the same time reproduce the results of quantum mechanics.Comment: Accepted for publication in "International Journal of Theoretical Physics

    High-fidelity state detection and tomography of a single ion Zeeman qubit

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    We demonstrate high-fidelity Zeeman qubit state detection in a single trapped 88 Sr+ ion. Qubit readout is performed by shelving one of the qubit states to a metastable level using a narrow linewidth diode laser at 674 nm followed by state-selective fluorescence detection. The average fidelity reached for the readout of the qubit state is 0.9989(1). We then measure the fidelity of state tomography, averaged over all possible single-qubit states, which is 0.9979(2). We also fully characterize the detection process using quantum process tomography. This readout fidelity is compatible with recent estimates of the detection error-threshold required for fault-tolerant computation, whereas high-fidelity state tomography opens the way for high-precision quantum process tomography

    On Multiparticle Entanglement via Resonant Interaction between Light and atomic Ensembles

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    Multiparticle entangled states generated via interaction between narrow-band light and an ensemble of identical two-level atoms are considered. Depending on the initial photon statistics, correlation between atoms and photons can give rise to entangled states of these systems. It is found that the state of any pair of atoms interacting with weak single-mode squeezed light is inseparable and robust against decay. Optical schemes for preparing entangled states of atomic ensembles by projective measurement are described.Comment: 11 pages, 1 figure, revtex

    The writing on the wall: the concealed communities of the East Yorkshire horselads

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    This paper examines the graffiti found within late nineteenth and early-twentieth century farm buildings in the Wolds of East Yorkshire. It suggests that the graffiti were created by a group of young men at the bottom of the social hierarchy - the horselads – and was one of the ways in which they constructed a distinctive sense of communal identity, at a particular stage in their lives. Whilst it tells us much about changing agricultural regimes and social structures, it also informs us about experiences and attitudes often hidden from official histories and biographies. In this way, the graffiti are argued to inform our understanding, not only of a concealed community, but also about their hidden histor

    Acquisition of Ca2+ and HCO3−/CO32− for shell formation in embryos of the common pond snail Lymnaea stagnalis

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    Embryos of the freshwater common pond snail Lymnaea stagnalis develop to hatch within 10 days under control conditions (22°C, Miami-Dade tap water) and this development is impaired by removal of ambient calcium. In contrast, embryos did not exhibit dependence upon an ambient HCO3−/CO32− source, developing and hatching in HCO3−/CO32−-free water at rates comparable to controls. Post-metamorphic, shell-laying embryos exhibited a significant saturation-type calcium uptake as a function of increasing ambient calcium concentration. However, changes in ambient bicarbonate concentration did not influence calcium or apparent titratable alkalinity uptake. There was a distinct shift from no significant flux in pre-metamorphic embryos to net uptake of calcium in post-metamorphic stages as indicated by an increased uptake from the micro-environment surrounding the egg mass and increased net uptake in 24-h, whole egg mass flux measurements. Furthermore, HCO3−/CO32− acquisition as measured by titratable alkalinity flux is at least partially attributable to an endogenous carbonate source that is associated with acid extrusion. Thus, calcium requirements for embryonic shell formation are met via uptake but HCO3−/CO32−, which is also necessary for shell formation is acquired in part from endogenous sources with no detectable correlation to ambient HCO3−/CO32− availability

    Phenotypic alterations in type II alveolar epithelial cells in CD4+ T cell mediated lung inflammation

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    <p>Abstract</p> <p>Background</p> <p>Although the contribution of alveolar type II epithelial cell (AEC II) activities in various aspects of respiratory immune regulation has become increasingly appreciated, our understanding of the contribution of AEC II transcriptosome in immunopathologic lung injury remains poorly understood. We have previously established a mouse model for chronic T cell-mediated pulmonary inflammation in which influenza hemagglutinin (HA) is expressed as a transgene in AEC II, in mice expressing a transgenic T cell receptor specific for a class II-restricted epitope of HA. Pulmonary inflammation in these mice occurs as a result of CD4<sup>+ </sup>T cell recognition of alveolar antigen. This model was utilized to assess the profile of inflammatory mediators expressed by alveolar epithelial target cells triggered by antigen-specific recognition in CD4<sup>+ </sup>T cell-mediated lung inflammation.</p> <p>Methods</p> <p>We established a method that allows the flow cytometric negative selection and isolation of primary AEC II of high viability and purity. Genome wide transcriptional profiling was performed on mRNA isolated from AEC II isolated from healthy mice and from mice with acute and chronic CD4<sup>+ </sup>T cell-mediated pulmonary inflammation.</p> <p>Results</p> <p>T cell-mediated inflammation was associated with expression of a broad array of cytokine and chemokine genes by AEC II cell, indicating a potential contribution of epithelial-derived chemoattractants to the inflammatory cell parenchymal infiltration. Morphologically, there was an increase in the size of activated epithelial cells, and on the molecular level, comparative transcriptome analyses of AEC II from inflamed versus normal lungs provide a detailed characterization of the specific inflammatory genes expressed in AEC II induced in the context of CD4<sup>+ </sup>T cell-mediated pneumonitis.</p> <p>Conclusion</p> <p>An important contribution of AEC II gene expression to the orchestration and regulation of interstitial pneumonitis is suggested by the panoply of inflammatory genes expressed by this cell population, and this may provide insight into the molecular pathogenesis of pulmonary inflammatory states. CD4<sup>+ </sup>T cell recognition of antigen presented by AEC II cells appears to be a potent trigger for activation of the alveolar cell inflammatory transcriptosome.</p
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