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Sökning: WFRF:(Ivarsson Sten)

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1.
  • Nilsson, Anna-Lena, et al. (författare)
  • Relationship between Ljungan virus antibodies, HLA-DQ8, and insulin autoantibodies in newly diagnosed type 1 diabetes children
  • 2013
  • Ingår i: Viral immunology. - : Mary Ann Liebert, Inc.. - 0882-8245 .- 1557-8976. ; 26:3, s. 207-215
  • Tidskriftsartikel (refereegranskat)abstract
    • Environmental factors, including viral infections, may explain an increasing and fluctuating incidence of childhood type 1 diabetes (T1D). Ljungan virus (LV) isolated from bank voles have been implicated, but it is unclear whether LV contributes to islet autoimmunity, progression to clinical onset, or both, of T1D. The aim was to test whether LV antibodies (LVAb) were related to HLA-DQ and islet autoantibodies in newly diagnosed T1D patients (n = 676) and controls (n = 309). Patients, 0-18 years of age, diagnosed with T1D in 1996-2005 were analyzed for LVAb, HLA-DQ genotypes, and all seven known islet autoantibodies (GADA, IA-2A, IAA, ICA, ZnT8RA, ZnT8WA, and ZnT8QA). LVAb at 75th percentile, defined as cut off, was 90 (range 6-3936) U/mL and 4th quartile LVAb were found in 25% (170/676) of which 64% were < 10 (n = 108, p < 0.0001), and 27% were < 5 (n = 45; p < 0.0001) years old. The 4th quartile LVAb in children < 10 years of age correlated to HLA DQ2/8, 8/8, and 8/X (p < 0.0001). Furthermore, in the group with 4th quartile LVAb, 55% were IAA positive (p = 0.01) and correlation was found between 4th quartile LVAb and IAA in children < 10 years of age (p = 0.035). It is concluded that 1) LVAb were common among the young T1D patients and LVAb levels were higher in the younger age groups; 2) 4th quartile LVAb correlated with IAA; and 3) there was a correlation between 4th quartile LVAb and HLA-DQ8, particularly in the young patients. The presence of LVAb supports the notion that prior exposure to LV may be associated with T1D.
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  • Andersson, C, et al. (författare)
  • The three ZNT8 autoantibody variants together improve the diagnostic sensitivity of childhood and adolescent type 1 diabetes
  • 2011
  • Ingår i: Autoimmunity. - : Taylor & Francis. - 0891-6934 .- 1607-842X. ; 44:5, s. 394-405
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: We tested whether autoantibodies to all three ZnT8RWQ variants, GAD65, insulinoma-associated protein 2 (IA-2), insulin and autoantibodies to islet cell cytoplasm (ICA) in combination with human leukocyte antigen (HLA) would improve the diagnostic sensitivity of childhood type 1 diabetes by detecting the children who otherwise would have been autoantibody-negative.Methods: A total of 686 patients diagnosed in 1996–2005 in Skåne were analyzed for all the seven autoantibodies [arginin 325 zinc transporter 8 autoantibody (ZnT8RA), tryptophan 325 zinc transporter 8 autoantibody (ZnT8WA), glutamine 325 Zinc transporter 8 autoantibody (ZnT8QA), autoantibodies to glutamic acid decarboxylase (GADA), Autoantibodies to islet-antigen-2 (IA-2A), insulin autoantibodies (IAA) and ICA] in addition to HLA-DQ genotypes.Results: Zinc transporter 8 autoantibody to either one or all three amino acid variants at position 325 (ZnT8RWQA) was found in 65% (449/686) of the patients. The frequency was independent of age at diagnosis. The ZnT8RWQA reduced the frequency of autoantibody-negative patients from 7.5 to 5.4%—a reduction by 28%. Only 2 of 108 (2%) patients who are below 5 years of age had no autoantibody at diagnosis. Diagnosis without any islet autoantibody increased with increasing age at onset. DQA1-B1*X-0604 was associated with both ZnT8RA (p = 0.002) and ZnT8WA (p = 0.01) but not with ZnT8QA (p = 0.07). Kappa agreement analysis showed moderate (>0.40) to fair (>0.20) agreement between pairs of autoantibodies for all combinations of GADA, IA-2A, ZnT8RWQA and ICA but only slight ( < 0.19) agreement for any combination with IAA.Conclusions: This study revealed that (1) the ZnT8RWQA was common, independent of age; (2) multiple autoantibodies were common among the young; (3) DQA1-B1*X-0604 increased the risk for ZnT8RA and ZnT8WA; (4) agreement between autoantibody pairs was common for all combinations except IAA. These results suggest that ZnT8RWQA is a necessary complement to the classification and prediction of childhood type 1 diabetes as well as to randomize the subjects in the prevention and intervention of clinical trials.
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4.
  • Kanatsuna, N, et al. (författare)
  • Doubly reactive INS-IGF2 autoantibodies in children with newly diagnosed autoimmune (type 1) diabetes
  • 2015
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley-Blackwell. - 0300-9475 .- 1365-3083. ; 82:4, s. 361-369
  • Tidskriftsartikel (refereegranskat)abstract
    • The splice variant INS-IGF2 entails the preproinsulin signal peptide, the insulin B-chain, eight amino acids of the C-peptide and 138 unique amino acids from an ORF in the IGF2 gene. The aim of this study was to determine whether levels of specific INS-IGF2 autoantibodies (INS-IGF2A) were related to age at diagnosis, islet autoantibodies, HLA-DQ or both, in patients and controls with newly diagnosed type 1 diabetes. Patients (n = 676), 0-18 years of age, diagnosed with type 1 diabetes in 1996-2005 and controls (n = 363) were analysed for specific INS-IGF2A after displacement with both cold insulin and INS-IGF2 to correct for non-specific binding and identify double reactive sera. GADA, IA-2A, IAA, ICA, ZnT8RA, ZnT8WA, ZnT8QA and HLA-DQ genotypes were also determined. The median level of specific INS-IGF2A was higher in patients than in controls (P < 0.001). Irrespective of age at diagnosis, 19% (126/676) of the patients had INS-IGF2A when the cut-off was the 95th percentile of the controls (P < 0.001). The risk of INS-IGF2A was increased among HLA-DQ2/8 (OR = 1.509; 95th CI 1.011, 2.252; P = 0.045) but not in 2/2, 2/X, 8/8, 8/X or X/X (X is neither 2 nor 8) patients. The association with HLA-DQ2/8 suggests that this autoantigen may be presented on HLA-DQ trans-heterodimers, rather than cis-heterodimers. Autoantibodies reactive with both insulin and INS-IGF2A at diagnosis support the notion that INS-IGF2 autoimmunity contributes to type 1 diabetes.
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5.
  • Aad, G, et al. (författare)
  • Beam-induced and cosmic-ray backgrounds observed in the ATLAS detector during the LHC 2012 proton-proton running period
  • 2016
  • Ingår i: Journal of Instrumentation. - : IOP PUBLISHING LTD. - 1748-0221. ; 11:5
  • Tidskriftsartikel (refereegranskat)abstract
    • This paper discusses various observations on beam-induced and cosmic-ray backgrounds in the ATLAS detector during the LHC 2012 proton-proton run. Building on published results based on 2011 data, the correlations between background and residual pressure of the beam vacuum are revisited. Ghost charge evolution over 2012 and its role for backgrounds are evaluated. New methods to monitor ghost charge with beam-gas rates are presented and observations of LHC abort gap population by ghost charge are discussed in detail. Fake jets from colliding bunches and from ghost charge are analysed with improved methods, showing that ghost charge in individual radio-frequency buckets of the LHC can be resolved. Some results of two short periods of dedicated cosmic-ray background data-taking are shown; in particular cosmic-ray muon induced fake jet rates are compared to Monte Carlo simulations and to the fake jet rates from beam background. A thorough analysis of a particular LHC fill, where abnormally high background was observed, is presented. Correlations between backgrounds and beam intensity losses in special fills with very high β∗ are studied. © 2016 CERN for the benefit of the ATLAS collaboration.
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8.
  • Aad, G., et al. (författare)
  • Identification and energy calibration of hadronically decaying tau leptons with the ATLAS experiment in pp collisions at root s=8 TeV
  • 2015
  • Ingår i: European Physical Journal C. Particles and Fields. - : Springer Science and Business Media LLC. - 1434-6044 .- 1434-6052. ; 75:7
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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9.
  • Aad, G., et al. (författare)
  • Measurement of exclusive gamma gamma -> l(+)l(-) production in proton-proton collisions at root s=7 TeV with the ATLAS detector
  • 2015
  • Ingår i: Physics Letters. Section B: Nuclear, Elementary Particle and High-Energy Physics. - : Elsevier BV. - 0370-2693 .- 1873-2445. ; 749, s. 242-261
  • Tidskriftsartikel (refereegranskat)abstract
    • This Letter reports a measurement of the exclusive gamma gamma -> l(+)l(-) (l = e, mu) cross-section in proton-proton collisions at a centre-of-mass energy of 7 TeV by the ATLAS experiment at the LHC, based on an integrated luminosity of 4.6 fb(-1). For the electron or muon pairs satisfying exclusive selection criteria, a fit to the dilepton acoplanarity distribution is used to extract the fiducial cross-sections. The cross-section in the electron channel is determined to be sigma(excl)(gamma gamma -> e+e-) = 0.428 +/- 0.035 (stat.) +/- 0.018 (syst.) pbfor a phase-space region with invariant mass of the electron pairs greater than 24GeV, in which both electrons have transverse momentum p(T) > 12 GeV and pseudorapidity vertical bar eta vertical bar < 2.4. For muon pairs with invariant mass greater than 20GeV, muon transverse momentum pT> 10 GeV and pseudorapidity vertical bar eta vertical bar < 2.4, the cross-section is determined to be sigma(excl)(gamma gamma -> mu+mu-) = 0.628 +/- 0.032(stat.) +/- 0.021 (syst.) pb. When proton absorptive effects due to the finite size of the proton are taken into account in the theory calculation, the measured cross-sections are found to be consistent with the theory prediction. (C) 2015 CERN for the benefit of the ATLAS Collaboration. Published by Elsevier B.V.
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10.
  • Aad, G, et al. (författare)
  • Measurement of the ZZ production cross section in pp collisions at √s = 13 TeV with the ATLAS detector
  • 2016
  • Ingår i: Physical Review Letters. - : American Physical Society. - 1079-7114 .- 0031-9007. ; 116:10
  • Tidskriftsartikel (refereegranskat)abstract
    • The ZZ production cross section in proton-proton collisions at 13 TeV center-of-mass energy is measured using 3.2 fb-1 of data recorded with the ATLAS detector at the Large Hadron Collider. The considered Z boson candidates decay to an electron or muon pair of mass 66-116 GeV. The cross section is measured in a fiducial phase space reflecting the detector acceptance. It is also extrapolated to a total phase space for Z bosons in the same mass range and of all decay modes, giving 16.7-2.0+2.2(stat)+0.9-0.7(syst)+1.0-0.7(lumi) pb. The results agree with standard model predictions. © 2016 CERN. Published by the American Physical Society under the terms of the "http://creativecommons.org/licenses/by/3.0/" Creative Commons Attribution 3.0 License. Further distribution of this work must maintain attribution to the author(s) and the published article's title, journal citation, and DOI.
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