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Sökning: WFRF:(Ross O A) > (2015-2019) > (2017)

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1.
  • 2017
  • swepub:Mat__t
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2.
  • Abazov, V. M., et al. (författare)
  • Combination of D0 measurements of the top quark mass
  • 2017
  • Ingår i: Physical Review D. - : AMER PHYSICAL SOC. - 2470-0010 .- 2470-0029. ; 95:11
  • Tidskriftsartikel (refereegranskat)abstract
    • We present a combination of measurements of the top quark mass by the D0 experiment in the lepton + jets and dilepton channels. We use all the data collected in Run I (1992-1996) at root s = 1.8 TeV and Run II (2001-2011) at root s = 1.96 TeV of the Tevatron p (p) over bar collider, corresponding to integrated luminosities of 0.1 fb(-1) and 9.7 fb(-1), respectively. The combined result is: m(t) = 174.95 +/- 0.40(stat)+/- 0.64(syst) GeV = 174.95 +/- 0.75 GeV.
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3.
  • Abazov, V. M., et al. (författare)
  • Measurement of the direct CP violating charge asymmetry in B-+/- -> mu(+/-)nu D-mu(0) decays
  • 2017
  • Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 95:3
  • Tidskriftsartikel (refereegranskat)abstract
    • We present the first measurement of the CP violating charge asymmetry in B-+/- -> mu(+/-)nu D-mu(0) decays using the full Run II integrated luminosity of 10.4 fb(-1) in proton-antiproton collisions collected with the D0 detector at the Fermilab Tevatron Collider. We measure a difference in the yield of B- and B+ mesons in these decays by fitting the reconstructed invariant mass distributions. This results in an asymmetry of A(mu D0) = [-0.14 +/- 0.20] %, which is consistent with standard model predictions.
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4.
  • Abazov, V. M., et al. (författare)
  • Measurement of top quark polarization in t(t)over-bar lepton+jets final states
  • 2017
  • Ingår i: PHYSICAL REVIEW D. - 2470-0010. ; 95:1
  • Tidskriftsartikel (refereegranskat)abstract
    • We present a measurement of top quark polarization in t (t) over bar pair production in p (p) over bar collisions at root s = 1.96 TeV using data corresponding to 9.7 fb(-1) of integrated luminosity recorded with the D0 detector at the Fermilab Tevatron Collider. We consider final states containing a lepton and at least three jets. The polarization is measured through the distribution of lepton angles along three axes: the beam axis, the helicity axis, and the transverse axis normal to the t (t) over bar production plane. This is the first measurement of top quark polarization at the Tevatron using lepton + jet final states and the first measurement of the transverse polarization in t (t) over bar production. The observed distributions are consistent with standard model predictions of nearly no polarization.
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5.
  • Willems, S. M., et al. (författare)
  • Large-scale GWAS identifies multiple loci for hand grip strength providing biological insights into muscular fitness
  • 2017
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 8
  • Tidskriftsartikel (refereegranskat)abstract
    • Hand grip strength is a widely used proxy of muscular fitness, a marker of frailty, and predictor of a range of morbidities and all-cause mortality. To investigate the genetic determinants of variation in grip strength, we perform a large-scale genetic discovery analysis in a combined sample of 195,180 individuals and identify 16 loci associated with grip strength (P<5 × 10-8) in combined analyses. A number of these loci contain genes implicated in structure and function of skeletal muscle fibres (ACTG1), neuronal maintenance and signal transduction (PEX14, TGFA, SYT1), or monogenic syndromes with involvement of psychomotor impairment (PEX14, LRPPRC and KANSL1). Mendelian randomization analyses are consistent with a causal effect of higher genetically predicted grip strength on lower fracture risk. In conclusion, our findings provide new biological insight into the mechanistic underpinnings of grip strength and the causal role of muscular strength in age-related morbidities and mortality. © The Author(s) 2017.
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8.
  • Puschmann, Andreas, et al. (författare)
  • Heterozygous PINK1 p.G411S increases risk of Parkinson's disease via a dominant-negative mechanism
  • 2017
  • Ingår i: Brain. - : Oxford University Press (OUP). - 1460-2156 .- 0006-8950. ; 140:1, s. 98-117
  • Tidskriftsartikel (refereegranskat)abstract
    • SEE GANDHI AND PLUN-FAVREAU DOI101093/AWW320 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: It has been postulated that heterozygous mutations in recessive Parkinson's genes may increase the risk of developing the disease. In particular, the PTEN-induced putative kinase 1 (PINK1) p.G411S (c.1231G>A, rs45478900) mutation has been reported in families with dominant inheritance patterns of Parkinson's disease, suggesting that it might confer a sizeable disease risk when present on only one allele. We examined families with PINK1 p.G411S and conducted a genetic association study with 2560 patients with Parkinson's disease and 2145 control subjects. Heterozygous PINK1 p.G411S mutations markedly increased Parkinson's disease risk (odds ratio = 2.92, P = 0.032); significance remained when supplementing with results from previous studies on 4437 additional subjects (odds ratio = 2.89, P = 0.027). We analysed primary human skin fibroblasts and induced neurons from heterozygous PINK1 p.G411S carriers compared to PINK1 p.Q456X heterozygotes and PINK1 wild-type controls under endogenous conditions. While cells from PINK1 p.Q456X heterozygotes showed reduced levels of PINK1 protein and decreased initial kinase activity upon mitochondrial damage, stress-response was largely unaffected over time, as expected for a recessive loss-of-function mutation. By contrast, PINK1 p.G411S heterozygotes showed no decrease of PINK1 protein levels but a sustained, significant reduction in kinase activity. Molecular modelling and dynamics simulations as well as multiple functional assays revealed that the p.G411S mutation interferes with ubiquitin phosphorylation by wild-type PINK1 in a heterodimeric complex. This impairs the protective functions of the PINK1/parkin-mediated mitochondrial quality control. Based on genetic and clinical evaluation as well as functional and structural characterization, we established p.G411S as a rare genetic risk factor with a relatively large effect size conferred by a partial dominant-negative function phenotype.
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