48 research outputs found

    Two decades of pulsar timing of Vela

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    Pulsar timing at the Mt Pleasant observatory has focused on Vela, which can be tracked for 18 hours of the day. These nearly continuous timing records extend over 24 years allowing a greater insight into details of timing noise, micro glitches and other more exotic effects. In particular we report the glitch parameters of the 2004 event, along with the reconfirmation that the spin up for the Vela pulsar occurs instantaneously to the accuracy of the data. This places a lower limit of about 30 seconds for the acceleration of the pulsar to the new rotational frequency. We also confirm of the low braking index for Vela, and the continued fall in the DM for this pulsar.Comment: Isolated Neutron Stars conference, London, April 24-28 200

    Recent glitches detected in the Crab pulsar

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    From 2000 to 2010, monitoring of radio emission from the Crab pulsar at Xinjiang Observatory detected a total of nine glitches. The occurrence of glitches appears to be a random process as described by previous researches. A persistent change in pulse frequency and pulse frequency derivative after each glitch was found. There is no obvious correlation between glitch sizes and the time since last glitch. For these glitches Δνp\Delta\nu_{p} and Δν˙p\Delta\dot{\nu}_{p} span two orders of magnitude. The pulsar suffered the largest frequency jump ever seen on MJD 53067.1. The size of the glitch is \sim 6.8 ×106\times 10^{-6} Hz, \sim 3.5 times that of the glitch occured in 1989 glitch, with a very large permanent changes in frequency and pulse frequency derivative and followed by a decay with time constant \sim 21 days. The braking index presents significant changes. We attribute this variation to a varying particle wind strength which may be caused by glitch activities. We discuss the properties of detected glitches in Crab pulsar and compare them with glitches in the Vela pulsar.Comment: Accepted for publication in Astrophysics & Space Scienc

    Loop-Generated Bounds on Changes to the Graviton Dispersion Relation

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    We identify the effective theory appropriate to the propagation of massless bulk fields in brane-world scenarios, to show that the dominant low-energy effect of asymmetric warping in the bulk is to modify the dispersion relation of the effective 4-dimensional modes. We show how such changes to the graviton dispersion relation may be bounded through the effects they imply, through loops, for the propagation of standard model particles. We compute these bounds and show that they provide, in some cases, the strongest constraints on nonstandard gravitational dispersions. The bounds obtained in this way are the strongest for the fewest extra dimensions and when the extra-dimensional Planck mass is the smallest. Although the best bounds come for warped 5-D scenarios, for which the 5D Planck Mass is O(TeV), even in 4 dimensions the graviton loop can lead to a bound on the graviton speed which is comparable with other constraints.Comment: 18 pages, LaTeX, 4 figures, uses revte

    The structure of PGC Morale Scale in American and Japanese aged: A further note

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    This study involves a further replication of cross-cultural comparison of the structure of the Philadelphia Geriatric Center Morale Scale (PGCMS). Using Japanese and American data sets, the present research replicates and extends the findings reported by Liang et al. (1987). In particular, the earlier findings that four PGCMS items behave differently in two cultures are replicated. The present study yields two additional observations. First, the invariance in the PGCMS can now be extended beyond the urban elderly residents studied by Liang et al. (1987) to the entire aged population in the U.S. and Japan. Second, this comparability is robust despite the elimination of correlated measurement errors from the earlier specifications and when several exogenous variables are controlled. Further, the impact of selected demographic variables on the PGCMS was evaluated. In addition, qualitative data from in-depth interviews provide further insights concerning the cultural differences in the expression of well-being.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42991/1/10823_2004_Article_BF00116576.pd

    Random effects diagonal metric multidimensional scaling models

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    By assuming a distribution for the subject weights in a diagonal metric (INDSCAL) multidimensional scaling model, the subject weights become random effects. Including random effects in multidimensional scaling models offers several advantages over traditional diagonal metric models such as those fitted by the INDSCAL, ALSCAL, and other multidimensional scaling programs. Unlike traditional models, the number of parameters does not increase with the number of subjects, and, because the distribution of the subject weights is modeled, the construction of linear models of the subject weights and the testing of those models is immediate. Here we define a random effects diagonal metric multidimensional scaling model, give computational algorithms, describe our experiences with these algorithms, and provide an example illustrating the use of the model and algorithms.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/45758/1/11336_2005_Article_BF02295730.pd

    Novel Loci for Adiponectin Levels and Their Influence on Type 2 Diabetes and Metabolic Traits : A Multi-Ethnic Meta-Analysis of 45,891 Individuals

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    J. Kaprio, S. Ripatti ja M.-L. Lokki työryhmien jäseniä.Peer reviewe

    Measurement of the lifetime of the Bc+B_c^+ meson using the Bc+J/ψπ+B_c^+\rightarrow J/\psi\pi^+ decay mode

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    The difference in total widths between the Bc+B_c^+ and B+B^+ mesons is measured using 3.0fb1^{-1} of data collected by the LHCb experiment in 7 and 8 TeV centre-of-mass energy proton-proton collisions at the LHC. Through the study of the time evolution of Bc+J/ψπ+B_c^+ \rightarrow J/\psi \pi^+ and B+J/ψK+B^+\rightarrow J/\psi K^+ decays, the width difference is measured to be ΔΓΓBc+ΓB+=4.46±0.14±0.07mm1c, \Delta\Gamma \equiv \Gamma_{B_c^+} - \Gamma_{B^+} = 4.46 \pm 0.14 \pm 0.07mm^{-1}c, where the first uncertainty is statistical and the second systematic. The known lifetime of the B+B^+ meson is used to convert this to a precise measurement of the Bc+B_c^+ lifetime, τBc+=513.4±11.0±5.7fs,\tau_{B_c^+} = 513.4 \pm 11.0 \pm 5.7fs, where the first uncertainty is statistical and the second systematic.Comment: 19 pagers, 3 figure

    The Physics of the B Factories

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    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
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