458 research outputs found

    Primitive divisors on twists of the Fermat cubic

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    We show that for an elliptic divisibility sequence on a twist of the Fermat cubic, u3+v3=m, with m cube-free, all the terms beyond the first have a primive divisor

    Mortality associated with avian reovirus infection in a free-living magpie (Pica pica) in Great Britain

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    Avian reoviruses (ARVs) cause a range of disease presentations in domestic, captive and free-living bird species. ARVs have been reported as a cause of significant disease and mortality in free-living corvid species in North America and continental Europe. Until this report, there have been no confirmed cases of ARV-associated disease in British wild birds

    Images of dissipation layers to quantify mixing within a turbulent jet

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/77254/1/AIAA-13435-811.pd

    Euclidean Mahler measure and twisted links

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    If the twist numbers of a collection of oriented alternating link diagrams are bounded, then the Alexander polynomials of the corresponding links have bounded euclidean Mahler measure (see Definition 1.2). The converse assertion does not hold. Similarly, if a collection of oriented link diagrams, not necessarily alternating, have bounded twist numbers, then both the Jones polynomials and a parametrization of the 2-variable Homflypt polynomials of the corresponding links have bounded Mahler measure.Comment: This is the version published by Algebraic & Geometric Topology on 7 April 200

    The elliptic curve discrete logarithm problem and equivalent hard problems for elliptic divisibility sequences

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    We define three hard problems in the theory of elliptic divisibility sequences (EDS Association, EDS Residue and EDS Discrete Log), each of which is solvable in sub-exponential time if and only if the elliptic curve discrete logarithm problem is solvable in sub-exponential time. We also relate the problem of EDS Association to the Tate pairing and the MOV, Frey-R\"{u}ck and Shipsey EDS attacks on the elliptic curve discrete logarithm problem in the cases where these apply.Comment: 18 pages; revised version includes some small mathematical corrections, reformatte

    On the Isomorphic Description of Chiral Symmetry Breaking by Non-Unitary Lie Groups

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    It is well-known that chiral symmetry breaking (χ\chiSB) in QCD with Nf=2N_{f}=2 light quark flavours can be described by orthogonal groups as O(4)→O(3)O(4) \to O(3), due to local isomorphisms. Here we discuss the question how specific this property is. We consider generalised forms of χ\chiSB involving an arbitrary number of light flavours of continuum or lattice fermions, in various representations. We search systematically for isomorphic descriptions by non-unitary, compact Lie groups. It turns out that there are a few alternative options in terms of orthogonal groups, while we did not find any description entirely based on symplectic or exceptional Lie groups. If we adapt such an alternative as the symmetry breaking pattern for a generalised Higgs mechanism, we may consider a Higgs particle composed of bound fermions and trace back the mass generation to χ\chiSB. In fact, some of the patterns that we encounter appear in technicolour models. In particular if one observes a Higgs mechanism that can be expressed in terms of orthogonal groups, we specify in which cases it could also represent some kind of χ\chiSB of techniquarks.Comment: 18 pages, to appear in Int. J. Mod. Phys.

    CRF Mediates Stress-Induced Pathophysiological High-Frequency Oscillations in Traumatic Brain Injury

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    Copyright © 2019 Narla et al. It is not known why there is increased risk to have seizures with increased anxiety and stress after traumatic brain injury (TBI). Stressors cause the release of corticotropin-releasing factor (CRF) both from the hypothalamic pituitary adrenal (HPA) axis and from CNS neurons located in the central amygdala and GABAergic interneurons. We have previously shown that CRF signaling is plastic, becoming excitatory instead of inhibitory after the kindling model of epilepsy. Here, using Sprague Dawley rats we have found that CRF signaling increased excitability after TBI. Following TBI, CRF type 1 receptor (CRFR1)-mediated activity caused abnormally large electrical responses in the amygdala, including fast ripples, which are considered to be epileptogenic. After TBI, we also found the ripple (120-250 Hz) and fast ripple activity (\u3e250 Hz) was cross-frequency coupled with θ (3-8 Hz) oscillations. CRFR1 antagonists reduced the incidence of phase coupling between ripples and fast ripples. Our observations indicate that pathophysiological signaling of the CRFR1 increases the incidence of epileptiform activity after TBI. The use for CRFR1 antagonist may be useful to reduce the severity and frequency of TBI associated epileptic seizures
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