1,464 research outputs found

    Positron-molecule interactions: resonant attachment, annihilation, and bound states

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    This article presents an overview of current understanding of the interaction of low-energy positrons with molecules with emphasis on resonances, positron attachment and annihilation. Annihilation rates measured as a function of positron energy reveal the presence of vibrational Feshbach resonances (VFR) for many polyatomic molecules. These resonances lead to strong enhancement of the annihilation rates. They also provide evidence that positrons bind to many molecular species. A quantitative theory of VFR-mediated attachment to small molecules is presented. It is tested successfully for selected molecules (e.g., methyl halides and methanol) where all modes couple to the positron continuum. Combination and overtone resonances are observed and their role is elucidated. In larger molecules, annihilation rates from VFR far exceed those explicable on the basis of single-mode resonances. These enhancements increase rapidly with the number of vibrational degrees of freedom. While the details are as yet unclear, intramolecular vibrational energy redistribution to states that do not couple directly to the positron continuum appears to be responsible for these enhanced annihilation rates. Downshifts of the VFR from the vibrational mode energies have provided binding energies for thirty species. Their dependence upon molecular parameters and their relationship to positron-atom and positron-molecule binding energy calculations are discussed. Feshbach resonances and positron binding to molecules are compared with the analogous electron-molecule (negative ion) cases. The relationship of VFR-mediated annihilation to other phenomena such as Doppler-broadening of the gamma-ray annihilation spectra, annihilation of thermalized positrons in gases, and annihilation-induced fragmentation of molecules is discussed.Comment: 50 pages, 40 figure

    Good practices for a literature survey are not followed by authors while preparing scientific manuscripts

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    The number of citations received by authors in scientific journals has become a major parameter to assess individual researchers and the journals themselves through the impact factor. A fair assessment therefore requires that the criteria for selecting references in a given manuscript should be unbiased with respect to the authors or the journals cited. In this paper, we advocate that authors should follow two mandatory principles to select papers (later reflected in the list of references) while studying the literature for a given research: i) consider similarity of content with the topics investigated, lest very related work should be reproduced or ignored; ii) perform a systematic search over the network of citations including seminal or very related papers. We use formalisms of complex networks for two datasets of papers from the arXiv repository to show that neither of these two criteria is fulfilled in practice

    Shadowing in the nuclear photoabsorption above the resonance region

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    A model based on the hadronic fluctuations of the real photon is developed to describe the total photonucleon and photonuclear cross sections in the energy region above the nucleon resonances. The hadronic spectral function of the photon is derived including the finite width of vector-meson resonances and the quark-antiquark continuum. The shadowing effect is evaluated considering the effective interaction of the hadronic component with the bound nucleons within a Glauber-Gribov multiple scattering theory. The low energy onset of the shadowing effect is interpreted as a possible signature of a modification of the hadronic spectral function in the nuclear medium. A decrease of the ρ\rho-meson mass in nuclei is suggested for a better explanation of the experimental data.Comment: 8 pages, 7 figure

    Itinerant spin excitations near the hidden order transition in URu2Si2

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    By means of neutron scattering we show that the high-temperature precursor to the hidden order state of the heavy fermion superconductor URu2_{2}Si2_{2} exhibits heavily damped incommensurate paramagnons whose strong energy dispersion is very similar to that of the long-lived longitudinal f-spin excitations that appear below T0_{0}. Since the underlying local f-exchange is preserved we expect only the f-d interactions to change across the phase transition and to cause the paramagnetic damping. The damping exhibits single-ion behavior independent of wave vector and vanishes below the hidden order transition. We suggest that this arises from a transition from valence fluctuations to a hybridized f-d state below T0_{0}. Here we present evidence that the itinerant excitations, like those in chromium, are due to Fermi surface nesting of hole and electron pockets so that the hidden order phase likely originates from a Fermi-surface instability. We identify wave vectors that span nested regions of a band calculation and that match the neutron spin crossover from incommensurate to commensurate on approach to the hidden order phase.Comment: 4 pages, 4 figures, to be submitted to PR

    Modulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming

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    Epstein-Barr virus (EBV) epigenetically reprogrammes B-lymphocytes to drive immortalization and facilitate viral persistence. Host-cell transcription is perturbed principally through the actions of EBV EBNA 2, 3A, 3B and 3C, with cellular genes deregulated by specific combinations of these EBNAs through unknown mechanisms. Comparing human genome binding by these viral transcription factors, we discovered that 25% of binding sites were shared by EBNA 2 and the EBNA 3s and were located predominantly in enhancers. Moreover, 80% of potential EBNA 3A, 3B or 3C target genes were also targeted by EBNA 2, implicating extensive interplay between EBNA 2 and 3 proteins in cellular reprogramming. Investigating shared enhancer sites neighbouring two new targets (WEE1 and CTBP2) we discovered that EBNA 3 proteins repress transcription by modulating enhancer-promoter loop formation to establish repressive chromatin hubs or prevent assembly of active hubs. Re-ChIP analysis revealed that EBNA 2 and 3 proteins do not bind simultaneously at shared sites but compete for binding thereby modulating enhancer-promoter interactions. At an EBNA 3-only intergenic enhancer site between ADAM28 and ADAMDEC1 EBNA 3C was also able to independently direct epigenetic repression of both genes through enhancer-promoter looping. Significantly, studying shared or unique EBNA 3 binding sites at WEE1, CTBP2, ITGAL (LFA-1 alpha chain), BCL2L11 (Bim) and the ADAMs, we also discovered that different sets of EBNA 3 proteins bind regulatory elements in a gene and cell-type specific manner. Binding profiles correlated with the effects of individual EBNA 3 proteins on the expression of these genes, providing a molecular basis for the targeting of different sets of cellular genes by the EBNA 3s. Our results therefore highlight the influence of the genomic and cellular context in determining the specificity of gene deregulation by EBV and provide a paradigm for host-cell reprogramming through modulation of enhancer-promoter interactions by viral transcription factors
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