10 research outputs found

    Highly symmetric POVMs and their informational power

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    We discuss the dependence of the Shannon entropy of normalized finite rank-1 POVMs on the choice of the input state, looking for the states that minimize this quantity. To distinguish the class of measurements where the problem can be solved analytically, we introduce the notion of highly symmetric POVMs and classify them in dimension two (for qubits). In this case we prove that the entropy is minimal, and hence the relative entropy (informational power) is maximal, if and only if the input state is orthogonal to one of the states constituting a POVM. The method used in the proof, employing the Michel theory of critical points for group action, the Hermite interpolation and the structure of invariant polynomials for unitary-antiunitary groups, can also be applied in higher dimensions and for other entropy-like functions. The links between entropy minimization and entropic uncertainty relations, the Wehrl entropy and the quantum dynamical entropy are described.Comment: 40 pages, 3 figure

    Proper-motion age dating of the progeny of Nova Scorpii AD 1437.

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    'Cataclysmic variables' are binary star systems in which one star of the pair is a white dwarf, and which often generate bright and energetic stellar outbursts. Classical novae are one type of outburst: when the white dwarf accretes enough matter from its companion, the resulting hydrogen-rich atmospheric envelope can host a runaway thermonuclear reaction that generates a rapid brightening. Achieving peak luminosities of up to one million times that of the Sun, all classical novae are recurrent, on timescales of months to millennia. During the century before and after an eruption, the 'novalike' binary systems that give rise to classical novae exhibit high rates of mass transfer to their white dwarfs. Another type of outburst is the dwarf nova: these occur in binaries that have stellar masses and periods indistinguishable from those of novalikes but much lower mass-transfer rates, when accretion-disk instabilities drop matter onto the white dwarfs. The co-existence at the same orbital period of novalike binaries and dwarf novae-which are identical but for their widely varying accretion rates-has been a longstanding puzzle. Here we report the recovery of the binary star underlying the classical nova eruption of 11 March AD 1437 (refs 12, 13), and independently confirm its age by proper-motion dating. We show that, almost 500 years after a classical-nova event, the system exhibited dwarf-nova eruptions. The three other oldest recovered classical novae display nova shells, but lack firm post-eruption ages, and are also dwarf novae at present. We conclude that many old novae become dwarf novae for part of the millennia between successive nova eruptions

    Defects in mitochondrial clearance predispose human monocytes to interleukin-1β hypersecretion

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    Most hereditary periodic fever syndromes are mediated by deregulated IL-1β secretion. The generation of mature IL-1β requires two signals: one that induces synthesis of inflammasome components and substrates and a second that activates inflammasomes. The mechanisms that mediate autoinflammation in mevalonate kinase deficiency, a periodic fever disease characterized by a block in isoprenoid biosynthesis, are poorly understood. In studying the effects of isoprenoid shortage on IL-1 β generation, we identified a new inflammasome activation signal that originates from defects in autophagy. We find that hypersecretion of IL-1β and IL-18 requires reactive oxygen species and is associated with an oxidized redox status of monocytes but not lymphocytes. IL-1β hypersecretion by monocytes involves decreased mitochondrial stability, release of mitochondrial content into the cytosol and attenuated autophagosomal degradation. Defective autophagy, as established by ATG7 knockdown, results in prolonged cytosolic retention of damaged mitochondria and increased IL-1β secretion. Finally, activation of autophagy in healthy but not mevalonate kinase deficiency patient cells reduces IL-1β secretion. Together, these results indicate that defective autophagy can prime monocytes for mitochondria-mediated NLRP3 inflammasome activation, thereby contributing to hypersecretion of IL-1β in mevalonate kinase deficiency. </p

    Defects in mitochondrial clearance predispose human monocytes to interleukin-1β hypersecretion

    No full text
    Most hereditary periodic fever syndromes are mediated by deregulated IL-1β secretion. The generation of mature IL-1β requires two signals: one that induces synthesis of inflammasome components and substrates and a second that activates inflammasomes. The mechanisms that mediate autoinflammation in mevalonate kinase deficiency, a periodic fever disease characterized by a block in isoprenoid biosynthesis, are poorly understood. In studying the effects of isoprenoid shortage on IL-1 β generation, we identified a new inflammasome activation signal that originates from defects in autophagy. We find that hypersecretion of IL-1β and IL-18 requires reactive oxygen species and is associated with an oxidized redox status of monocytes but not lymphocytes. IL-1β hypersecretion by monocytes involves decreased mitochondrial stability, release of mitochondrial content into the cytosol and attenuated autophagosomal degradation. Defective autophagy, as established by ATG7 knockdown, results in prolonged cytosolic retention of damaged mitochondria and increased IL-1β secretion. Finally, activation of autophagy in healthy but not mevalonate kinase deficiency patient cells reduces IL-1β secretion. Together, these results indicate that defective autophagy can prime monocytes for mitochondria-mediated NLRP3 inflammasome activation, thereby contributing to hypersecretion of IL-1β in mevalonate kinase deficiency. </p

    Long-distance parenting: The impact of parental separation and absence due to work commitments on families

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    Dittman, CK ORCiD: 0000-0003-0203-8785This chapter reviews the theory and research related to the impact of parental separation due to work commitments on family life, with a particular focus on two categories of parental work absences: (1) long-distance commuting; and (2) military service and deployment. There is significant diversity both between and within these categories of parental absence in terms of length and timing of separation, the context and reasons for separation, and the risks associated with the parent’s employment. However, they are characterized by challenges not generally experienced by other working families, including transitions in family routines and parenting roles and responsibilities, reliance on the functioning of the athome parent or family member, and ongoing disruptions to parent–child relationships. The impact of these transitions and disruptions is only beginning to be understood. This chapter reviews the research on the effects of parental absence due to work on parenting, family relationships, and child adjustment, and aims to identify factors that influence outcomes for families. Note that in the vast majority of the literature, the absent parent is the father, and the at-home parent is the mother; exceptions to this are noted throughout the review. The chapter also highlights areas for further research, and concludes with evidence based recommendations for policy and practice
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