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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: 7.73). 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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##### Article: Measurement of the fraction of Υ (1S) originating from χb(1P) decays in pp collisions at \sqrt{s}=7\,TeV
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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.
Journal of High Energy Physics 2012(11). DOI:10.1007/JHEP11(2012)031 · 6.22 Impact Factor
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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.
Human Molecular Genetics 02/2014; DOI:10.1093/hmg/ddu056 · 6.68 Impact Factor