1,721,914 research outputs found

    Barycentered NICER event list from ObsID 1200120106, used in Stingray tutorial

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    <p>This is a NASA NICER observation of the accreting black hole MAXI 1820+070 during its 2018 outburst</p> <p>The raw X-ray event data in FITS format were obtained from the NICER archive at HEASARC:</p> <p>https://heasarc.gsfc.nasa.gov/cgi-bin/W3Browse/w3hdprods.pl?files=Preview&Coordinates=Equatorial&Equinox=2000&CheckSize=1&showgifs=1&Target=heasarc%5Fnicermastr%7C%7C%7C%5F%5Frow%3D30877%7C%7C&popupFrom=&querytime=1708425079</p> <p>Processing:  <br>We ran the barycorr FTOOL, using the JPL DE 430 ephemeris (all details of processing can be found in the header of the FITS file). </p> <p>We distribute it to be used as practice data for Spectral Timing tutorials. Scientific use might require better processing, involving a re-run of the Level-2 data pipeline.</p&gt

    No time for dead time: timing analysis of bright black hole binaries with NuSTAR

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    Timing of high-count-rate sources with the NuSTAR Small Explorer Mission requires specialized analysis techniques. NuSTAR was primarily designed for spectroscopic observations of sources with relatively low count rates rather than for timing analysis of bright objects. The instrumental dead time per event is relatively long (~2.5 msec) and varies event-to-event by a few percent. The most obvious effect is a distortion of the white noise level in the power density spectrum (PDS) that cannot be easily modeled with standard techniques due to the variable nature of the dead time. In this paper, we show that it is possible to exploit the presence of two completely independent focal planes and use the cospectrum, the real part of the cross PDS, to obtain a good proxy of the white-noise-subtracted PDS. Thereafter, one can use a Monte Carlo approach to estimate the remaining effects of dead time, namely, a frequency-dependent modulation of the variance and a frequency-independent drop of the sensitivity to variability. In this way, most of the standard timing analysis can be performed, albeit with a sacrifice in signal-to-noise ratio relative to what would be achieved using more standard techniques. We apply this technique to NuSTAR observations of the black hole binaries GX 339–4, Cyg X-1, and GRS 1915+10

    Adsorción del herbicida atrazina y bioaumento con Arthrobacter sp. AAC22 en suelo agrícola de la localidad de Villa María, Córdoba

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    Fil: Morgante, Carolina. Universidad Nacional de Villa María; Argentina.Fil: Morgante, Verónica. Universidad Nacional de Villa María; Argentina.Fil: Miloc, Evangelina. Universidad Nacional de Villa María; Argentina.Fil: Bachetti, Romina. Universidad Nacional de Villa María; Argentina.Fil: Urseler, Noelia. Universidad Nacional de Villa María; Argentina

    Tumor necrosis factor receptor-associated periodic syndrome as a model linking autophagy and inflammation in protein aggregation diseases

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    Autophagy prevents cellular damage by eliminating insoluble aggregates of mutant misfolded proteins, which accumulate under different pathological conditions. Downregulation of autophagy enhances the inflammatory response and thus represents a possible common pathogenic event underlying a number of autoinflammatory syndromes, such as tumor necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS). The pathogenesis of other monogenic or complex disorders that display symptoms of excessive inflammation also involve the autophagy pathway. Studies have shown that TRAPS-associated TNFRSF1A mutations induce cytoplasmic retention of the TNFR1 receptor, defective TNF-induced apoptosis, and production of reactive oxygen species (ROS). Furthermore, autophagy impairment may account for the pathogenic effects of TNFRSF1A mutations, thus inducing inflammation in TRAPS. In this review, we summarize the molecular interactions and functional links between autophagy with regard to nuclear factor-kappa B activation, ROS production, and apoptosis. Furthermore, we propose a complex interplay of these pathways as a model to explain the relationship between mutant protein misfolding and inflammation in genetically determined and aggregation-prone diseases. Accordingly, autophagy function should be investigated in all diseases showing an inflammatory component, and for which the molecular pathogenesis is still unclear. © 2014 Springer-Verlag Berlin Heidelberg

    Causative and common PHOX2B variants define a broad phenotypic spectrum

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    Paired Like homeobox 2B (PHOX2B) is a gene crucial for the differentiation of the neural lineages of the autonomic nervous system (ANS), whose coding mutations cause congenital central hypoventilation syndrome (CCHS). The vast majority of PHOX2B mutations in CCHS is represented by expansions of a polyalanine region in exon 3, collectively defined PARMs (PolyAlanine Repeat Mutations), the minority being frameshift, missense and nonsense mutations, defined as NPARMs (Non‐PARMs). While PARMs are nearly exclusively associated with isolated CCHS, most of NPARMs is detected in syndromic CCHS, presenting with neuroblastoma and/or Hirschsprung disease. More recently, evidence of a complex role of PHOX2B in the pathogenesis of a wider spectrum of ANS disorders has emerged. Indeed, common and hypomorphic PHOX2B variants, including synonymous, polyalanine‐contractions, gene deletions may influence the occurrence of either apparent life‐threatening event (ALTE), Sudden Infant Death Syndrome (SIDS), neuroblastoma, or isolated HSCR, likely through small effects on PHOX2B expression levels. After an introduction to the role of PHOX2B in the ANS development, causative mutations, common variants, and gene expression deregulation of the PHOX2B gene are discussed, though the involvement of synonymous variants and contractions requires further confirmations with respect to ANS disorders and molecular mechanisms underlying the PHOX2B phenotypic heterogeneity

    OSM/OSMR and Interleukin 6 Family Cytokines in Physiological and Pathological Condition

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    Oncostatin M (OSM) is a member of the interleukin-6 (IL-6) family of cytokines and can bind two different receptors, Leukemia inhibitory factor receptor (LIFR) and Oncostatin M receptor (OSMR), through a complex containing the common glycoprotein 130 (gp130) subunit [...

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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