1,158 research outputs found

    Using ontologies to map between research data and policymakers’ presumptions: the experience of the KNOWMAK project

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    Understanding knowledge co-creation in key emerging areas of European research is critical for policy makers wishing to analyze impact and make strategic decisions. However, purely data-driven methods for characterising policy topics have limitations relating to the broad nature of such topics and the differences in language and topic structure between the political language and scientific and technological outputs. In this paper, we discuss the use of ontologies and semantic technologies as a means to bridge the linguistic and conceptual gap between policy questions and data sources for characterising European knowledge production. Our experience suggests that the integration between advanced techniques for language processing and expert assessment at critical junctures in the process is key for the success of this endeavour

    A Study of Time-Dependent CP-Violating Asymmetries and Flavor Oscillations in Neutral B Decays at the Upsilon(4S)

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    We present a measurement of time-dependent CP-violating asymmetries in neutral B meson decays collected with the BABAR detector at the PEP-II asymmetric-energy B Factory at the Stanford Linear Accelerator Center. The data sample consists of 29.7 fb1{\rm fb}^{-1} recorded at the Υ(4S)\Upsilon(4S) resonance and 3.9 fb1{\rm fb}^{-1} off-resonance. One of the neutral B mesons, which are produced in pairs at the Υ(4S)\Upsilon(4S), is fully reconstructed in the CP decay modes J/ψKS0J/\psi K^0_S, ψ(2S)KS0\psi(2S) K^0_S, χc1KS0\chi_{c1} K^0_S, J/ψK0J/\psi K^{*0} (K0KS0π0K^{*0}\to K^0_S\pi^0) and J/ψKL0J/\psi K^0_L, or in flavor-eigenstate modes involving D()π/ρ/a1D^{(*)}\pi/\rho/a_1 and J/ψK0J/\psi K^{*0} (K0K+πK^{*0}\to K^+\pi^-). The flavor of the other neutral B meson is tagged at the time of its decay, mainly with the charge of identified leptons and kaons. The proper time elapsed between the decays is determined by measuring the distance between the decay vertices. A maximum-likelihood fit to this flavor eigenstate sample finds Δmd=0.516±0.016(stat)±0.010(syst)ps1\Delta m_d = 0.516\pm 0.016 {\rm (stat)} \pm 0.010 {\rm (syst)} {\rm ps}^{-1}. The value of the asymmetry amplitude sin2β\sin2\beta is determined from a simultaneous maximum-likelihood fit to the time-difference distribution of the flavor-eigenstate sample and about 642 tagged B0B^0 decays in the CP-eigenstate modes. We find sin2β=0.59±0.14(stat)±0.05(syst)\sin2\beta=0.59\pm 0.14 {\rm (stat)} \pm 0.05 {\rm (syst)}, demonstrating that CP violation exists in the neutral B meson system. (abridged)Comment: 58 pages, 35 figures, submitted to Physical Review

    Prion Protein Modulates Cellular Iron Uptake: A Novel Function with Implications for Prion Disease Pathogenesis

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    Converging evidence leaves little doubt that a change in the conformation of prion protein (PrPC) from a mainly α-helical to a β-sheet rich PrP-scrapie (PrPSc) form is the main event responsible for prion disease associated neurotoxicity. However, neither the mechanism of toxicity by PrPSc, nor the normal function of PrPC is entirely clear. Recent reports suggest that imbalance of iron homeostasis is a common feature of prion infected cells and mouse models, implicating redox-iron in prion disease pathogenesis. In this report, we provide evidence that PrPC mediates cellular iron uptake and transport, and mutant PrP forms alter cellular iron levels differentially. Using human neuroblastoma cells as models, we demonstrate that over-expression of PrPC increases intra-cellular iron relative to non-transfected controls as indicated by an increase in total cellular iron, the cellular labile iron pool (LIP), and iron content of ferritin. As a result, the levels of iron uptake proteins transferrin (Tf) and transferrin receptor (TfR) are decreased, and expression of iron storage protein ferritin is increased. The positive effect of PrPC on ferritin iron content is enhanced by stimulating PrPC endocytosis, and reversed by cross-linking PrPC on the plasma membrane. Expression of mutant PrP forms lacking the octapeptide-repeats, the membrane anchor, or carrying the pathogenic mutation PrP102L decreases ferritin iron content significantly relative to PrPC expressing cells, but the effect on cellular LIP and levels of Tf, TfR, and ferritin is complex, varying with the mutation. Neither PrPC nor the mutant PrP forms influence the rate or amount of iron released into the medium, suggesting a functional role for PrPC in cellular iron uptake and transport to ferritin, and dysfunction of PrPC as a significant contributing factor of brain iron imbalance in prion disorders

    Measurement of the Branching Fraction for B- --> D0 K*-

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    We present a measurement of the branching fraction for the decay B- --> D0 K*- using a sample of approximately 86 million BBbar pairs collected by the BaBar detector from e+e- collisions near the Y(4S) resonance. The D0 is detected through its decays to K- pi+, K- pi+ pi0 and K- pi+ pi- pi+, and the K*- through its decay to K0S pi-. We measure the branching fraction to be B.F.(B- --> D0 K*-)= (6.3 +/- 0.7(stat.) +/- 0.5(syst.)) x 10^{-4}.Comment: 7 pages, 1 postscript figure, submitted to Phys. Rev. D (Rapid Communications

    Study of e+e- --> pi+ pi- pi0 process using initial state radiation with BABAR

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    The process e+e- --> pi+ pi- pi0 gamma has been studied at a center-of-mass energy near the Y(4S) resonance using a 89.3 fb-1 data sample collected with the BaBar detector at the PEP-II collider. From the measured 3pi mass spectrum we have obtained the products of branching fractions for the omega and phi mesons, B(omega --> e+e-)B(omega --> 3pi)=(6.70 +/- 0.06 +/- 0.27)10-5 and B(phi --> e+e-)B(phi --> 3pi)=(4.30 +/- 0.08 +/- 0.21)10-5, and evaluated the e+e- --> pi+ pi- pi0 cross section for the e+e- center-of-mass energy range 1.05 to 3.00 GeV. About 900 e+e- --> J/psi gamma --> pi+ pi- pi0 gamma events have been selected and the branching fraction B(J/psi --> pi+ pi- pi0)=(2.18 +/- 0.19)% has been measured.Comment: 21 pages, 37 postscript figues, submitted to Phys. Rev.

    Pleosporales

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    One hundred and five generic types of Pleosporales are described and illustrated. A brief introduction and detailed history with short notes on morphology, molecular phylogeny as well as a general conclusion of each genus are provided. For those genera where the type or a representative specimen is unavailable, a brief note is given. Altogether 174 genera of Pleosporales are treated. Phaeotrichaceae as well as Kriegeriella, Zeuctomorpha and Muroia are excluded from Pleosporales. Based on the multigene phylogenetic analysis, the suborder Massarineae is emended to accommodate five families, viz. Lentitheciaceae, Massarinaceae, Montagnulaceae, Morosphaeriaceae and Trematosphaeriaceae

    Evidence for the Rare Decay B -> K*ll and Measurement of the B -> Kll Branching Fraction

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    We present evidence for the flavor-changing neutral current decay BK+B\to K^*\ell^+\ell^- and a measurement of the branching fraction for the related process BK+B\to K\ell^+\ell^-, where +\ell^+\ell^- is either an e+ee^+e^- or μ+μ\mu^+\mu^- pair. These decays are highly suppressed in the Standard Model, and they are sensitive to contributions from new particles in the intermediate state. The data sample comprises 123×106123\times 10^6 Υ(4S)BBˉ\Upsilon(4S)\to B\bar{B} decays collected with the Babar detector at the PEP-II e+ee^+e^- storage ring. Averaging over K()K^{(*)} isospin and lepton flavor, we obtain the branching fractions B(BK+)=(0.650.13+0.14±0.04)×106{\mathcal B}(B\to K\ell^+\ell^-)=(0.65^{+0.14}_{-0.13}\pm 0.04)\times 10^{-6} and B(BK+)=(0.880.29+0.33±0.10)×106{\mathcal B}(B\to K^*\ell^+\ell^-)=(0.88^{+0.33}_{-0.29}\pm 0.10)\times 10^{-6}, where the uncertainties are statistical and systematic, respectively. The significance of the BK+B\to K\ell^+\ell^- signal is over 8σ8\sigma, while for BK+B\to K^*\ell^+\ell^- it is 3.3σ3.3\sigma.Comment: 7 pages, 2 postscript figues, submitted to Phys. Rev. Let

    Cognitive behavioural therapy in elderly type 2 diabetes patients with minor depression or mild major depression: study protocol of a randomized controlled trial (MIND-DIA)

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    <p>Abstract</p> <p>Background</p> <p>The global prevalence of diabetes among adults will be 6.4% in 2010 and will increase to 7.7% by 2030. Diabetes doubles the odds of depression, and 9% of patients with diabetes are affected by depressive disorders. When subclinical depression is included, the proportion of patients who have clinically relevant depressive symptoms increases to 26%. In patients aged over 65 years, the interaction of diabetes and depression has predicted increased mortality, complications, disability, and earlier occurrence of all of these adverse outcomes. These deleterious effects were observed even in minor depression, where the risk of mortality within 7 years was 4.9 times higher compared with diabetes patients who did not have depressive symptoms. In this paper we describe the design and methods of the Minor Depression and Diabetes trial, a clinical trial within the 'Competence Network for Diabetes mellitus', which is funded by the German Federal Ministry of Education and Research.</p> <p>Methods/Design</p> <p>Patients' inclusion criteria are: Type 2 diabetes mellitus, 65 to 85 years of age, 3 to 6 depressive symptoms (minor depression or mild major depression). Our aim is to compare the efficacy of diabetes-specific cognitive behavioural therapy adapted for the elderly vs. intensified treatment as usual vs. a guided self-help intervention regarding improvement of health related quality of life as the primary outcome. The trial will be conducted as a multicentre, open, observer-blinded, parallel group (3 groups) randomized controlled trial. Patients will be randomized to one of the three treatment conditions. After 12 weeks of open-label therapy in all treatment conditions, both group interventions will be reduced to one session per month during the one-year long-term phase of the trial. At the one-year follow-up, all groups will be re-examined regarding the primary and secondary parameters, for example reduction of depressive symptoms, prevention of moderate/severe major depression, improvement of glycaemic control, mortality, and cost effectiveness. Depending on additional funding, the sample will be continuously observed as a prospective cohort; the primary outcome will be changed to mortality for all subsequent follow-up measurements.</p> <p>Trial registration</p> <p>Current Controlled Trials Register (ISRCTN58007098).</p
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