19 research outputs found

    Search for pair-produced long-lived neutral particles decaying to jets in the ATLAS hadronic calorimeter in ppcollisions at √s=8TeV

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    The ATLAS detector at the Large Hadron Collider at CERN is used to search for the decay of a scalar boson to a pair of long-lived particles, neutral under the Standard Model gauge group, in 20.3fb−1of data collected in proton–proton collisions at √s=8TeV. This search is sensitive to long-lived particles that decay to Standard Model particles producing jets at the outer edge of the ATLAS electromagnetic calorimeter or inside the hadronic calorimeter. No significant excess of events is observed. Limits are reported on the product of the scalar boson production cross section times branching ratio into long-lived neutral particles as a function of the proper lifetime of the particles. Limits are reported for boson masses from 100 GeVto 900 GeV, and a long-lived neutral particle mass from 10 GeVto 150 GeV

    死体肺移植におけるrecombinant tissue-field name="type" plasminogen activator(rt-PA)の効果について

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    [[sponsorship]]物理研究所[[note]]已出版;[SCI];有審查制度;具代表性[[note]]http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Drexel&SrcApp=hagerty_opac&KeyRecord=1434-6044&DestApp=JCR&RQ=IF_CAT_BOXPLO

    Erratum to: Measurement of the W boson polarisation in tt^{¯} events from pp collisions at √s = 8 TeV in the lepton + jets channel with Atlas

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    1 Erratum to: Eur. Phys. J. C (2017) 77:264 [https://doi.org/10.1140/epjc/s10052-017-4819-4]. The original article can be found online at [https://doi.org/10.1140/epjc/s10052-017-4819-4]

    Measurement of the inclusive isolated prompt photon cross section in pp collisions at root s=8 TeV with the ATLAS detector

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    A measurement of the cross section for the inclusive production of isolated prompt photons in proton-proton collisions at a centre-of-mass energy of √ s = 8 TeV is presented. The measurement covers the pseudorapidity ranges |η γ | < 1.37 and 1.56 ≤ |η γ | < 2.37 in the transverse energy range 25 < Eγ T < 1500 GeV. The results are based on an integrated luminosity of 20.2 fb−1 , recorded by the ATLAS detector at the LHC. Photon candidates are identified by combining information from the calorimeters and the inner tracker. The background is subtracted using a data-driven technique, based on the observed calorimeter shower-shape variables and the deposition of hadronic energy in a narrow cone around the photon candidate. The measured cross sections are compared with leading-order and next-to-leading order perturbative QCD calculations and are found to be in a good agreement over ten orders of magnitude

    Identification and energy calibration of hadronically decaying tau leptons with the ATLAS experiment in pp collisions at root s=8 TeV

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    This paper describes the trigger and offline reconstruction, identification and energy calibration algorithms for hadronic decays of tau leptons employed for the data collected from pp collisions in 2012 with the ATLAS detector at the LHC center-of-mass energy root s = 8 TeV. The performance of these algorithms is measured in most cases with Z decays to tau leptons using the full 2012 dataset, corresponding to an integrated luminosity of 20.3 fb(-1). An uncertainty on the offline reconstructed tau energy scale of 2-4%, depending on transverse energy and pseudorapidity, is achieved using two independent methods. The offline tau identification efficiency is measured with a precision of 2.5% for hadronically decaying tau leptons with one associated track, and of 4% for the case of three associated tracks, inclusive in pseudorapidity and for a visible transverse energy greater than 20 GeV. For hadronic tau lepton decays selected by offline algorithms, the tau trigger identification efficiency is measured with a precision of 2-8%, depending on the transverse energy. The performance of the tau algorithms, both offline and at the trigger level, is found to be stable with respect to the number of concurrent proton-proton interactions and has supported a variety of physics results using hadronically decaying tau leptons at ATLAS

    Calcium Signaling: From Normal B Cell Development to Tolerance Breakdown and Autoimmunity.

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    International audienceMaintenance of self-tolerance of auto-reactive lymphocytes is a fundamental mechanism to prevent the onset of autoimmune diseases. Deciphering the mechanisms involved in the deregulations leading to tolerance disruption and autoimmunity is still a major area of interest to identify new therapeutic targets and options. Ca(2+) signaling plays a major role in B cell normal development and is therefore finely tuned by B cell receptor (BCR)-dependent and independent pathways. Developmental changes in the characteristics of BCR-dependent Ca(2+) signals as well as the modulation of basal intracellular concentration ([Ca(2+)]i) contribute strongly to self-tolerance maintaining mechanisms responsible for the physical or functional elimination of autoreactive B cells such as clonal deletion, receptor editing, and anergy. Implication of Ca(2+) signals in B tolerance mechanisms mainly occurs through the specific activation of transcriptional programs depending on the amplitude, shape, and duration of Ca(2+) signals. A large number of studies reported Ca(2+) signaling defects in autoimmune pathology such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and primary Sjӧgren's syndrome (pSS). However, the precise nature of the molecular events responsible for these deregulations is not fully understood. Moreover, the demonstration of a direct correlation between Ca(2+) signaling defects and tolerance disruption is still lacking. The recent identification of proteins involved in B cell Ca(2+) signals such as ORAI, stromal interaction molecule and transient receptor potential is opening new horizons for understanding Ca(2+) signaling defects observed in autoimmune diseases and for proposing potentially new therapeutic solutions. This review aims to present an overview of the developmental evolution of BCR dependent Ca(2+) signaling and to place this signaling pathway in the context of mechanisms involved in tolerance maintenance and breakdown
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