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# Observation of a new χ(b) state in radiative transitions to Υ(1S) and Υ(2S) at ATLAS.

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Fakultät für Mathematik und Physik, Albert-Ludwigs-Universität, Freiburg i.Br., Germany.
(Impact Factor: 7.51). 04/2012; 108(15):152001.
Source: PubMed

ABSTRACT

The χ(b)(nP) quarkonium states are produced in proton-proton collisions at the Large Hadron Collider at sqrt[s] = 7  TeV and recorded by the ATLAS detector. Using a data sample corresponding to an integrated luminosity of 4.4  fb(-1), these states are reconstructed through their radiative decays to Υ(1S,2S) with Υ → μ+ μ-. In addition to the mass peaks corresponding to the decay modes χ(b)(1P,2P) → Υ(1S)γ, a new structure centered at a mass of 10.530 ± 0.005(stat) ± 0.009(syst)  GeV is also observed, in both the Υ(1S)γ and Υ(2S)γ decay modes. This structure is interpreted as the χ(b)(3P) system.

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Available from: Andres Pacheco Pages, Jul 24, 2015
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##### Article: Measurement of the fraction of ϒ (1S) originating from χb(1P) decays in pp collisions at √s = 7TeV
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ABSTRACT: The production of χb(1P ) mesons in pp collisions at a centre-of-mass energy of 7 TeV is studied using 32 pb−1 of data collected with the LHCb detector. The χb(1P ) mesons are reconstructed in the decay mode χb (1P ) → Υ (1S)γ → μ +μ −γ. The fraction of Υ (1S) originating from χb(1P ) decays in the Υ (1S) transverse momentum range 6 < pTΥ (1S) < 15 GeV/c and rapidity range 2.0 < y Υ (1S)< 4.5 is measured to be $\left( {20.7\pm 5.7\pm 2.1_{-5.4}^{+2.7 }} \right)\%$ , where the first uncertainty is statistical, the second is systematic and the last gives the range of the result due to the unknown Υ (1S) and χb(1P) polarizations.
Full-text · Article · Nov 2012 · Journal of High Energy Physics
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##### Article: Measurement of ϒ production in pp collisions at √s =7 TeV
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ABSTRACT: The production of Upsilon(1S), Upsilon(2S) and Upsilon(3S) mesons in proton-proton collisions at the centre-of-mass energy of sqrt(s)=7 TeV is studied with the LHCb detector. The analysis is based on a data sample of 25 pb-1 collected at the Large Hadron Collider. The Upsilon mesons are reconstructed in the decay mode Upsilon -> mu+ mu- and the signal yields are extracted from a fit to the mu+ mu- invariant mass distributions. The differential production cross-sections times dimuon branching fractions are measured as a function of the Upsilon transverse momentum pT and rapidity y, over the range pT < 15 GeV/c and 2.0 < y < 4.5. The cross-sections times branching fractions, integrated over these kinematic ranges, are measured to be sigma(pp -> Upsilon(1S) X) x B(Upsilon(1S)->mu+ mu-) = 2.29 {\pm} 0.01 {\pm} 0.10 -0.37 +0.19 nb, sigma(pp -> Upsilon(2S) X) x B(Upsilon(2S)->mu+ mu-) = 0.562 {\pm} 0.007 {\pm} 0.023 -0.092 +0.048 nb, sigma(pp -> Upsilon(3S) X) x B(Upsilon(3S)->mu+ mu-) = 0.283 {\pm} 0.005 {\pm} 0.012 -0.048 +0.025 nb, where the first uncertainty is statistical, the second systematic and the third is due to the unknown polarisation of the three Upsilon states.
Full-text · Article · Feb 2012 · European Physical Journal C
• ##### Article: Exome sequencing identifies de novo gain of function missense mutation in KCND2 in identical twins with autism and seizures that slows potassium channel inactivation
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ABSTRACT: Numerous studies and case reports show co-morbidity of autism and epilepsy, suggesting some common molecular underpinnings of the two phenotypes. However, the relationship between the two on the molecular level remains unclear. Here, whole exome sequencing was performed on a family with identical twins affected with autism and severe, intractable seizures. A de novo variant was identified in the KCND2 gene, which encodes the Kv4.2 potassium channel. Kv4.2 is a major pore-forming subunit in somatodendritic subthreshold A-type potassium current (ISA) channels. The de novo mutation p.Val404Met is novel and occurs at a highly conserved residue within the C-terminal end of the transmembrane helix S6 region of the ion permeation pathway. Functional analysis revealed the likely pathogenicity of the variant in that the p.Val404Met mutant construct showed significantly slowed inactivation, either by itself or after equimolar co-expression with the wild-type Kv4.2 channel construct consistent with a dominant effect. Further, the effect of the mutation on closed-state inactivation was evident in the presence of auxiliary subunits that associate with Kv4 subunits to form ISAchannels in vivo. Discovery of a functionally relevant novel de novo variant, coupled with physiological evidence that the mutant protein disrupts potassium current inactivation, strongly supports KCND2 as the causal gene for epilepsy in this family. Interaction of KCND2 with other genes implicated in autism, and the role of KCND2 in synaptic plasticity provide suggestive evidence of an etiological role in autism.
No preview · Article · Feb 2014 · Human Molecular Genetics