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Träfflista för sökning "WFRF:(Smolek Tomas) srt2:(2016)"

Sökning: WFRF:(Smolek Tomas) > (2016)

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1.
  • Abulaiti, Yiming, et al. (författare)
  • Search for the Standard Model Higgs boson produced by vector-boson fusion and decaying to bottom quarks in root s=8TeV pp collisions with the ATLAS detector
  • 2016
  • Ingår i: Journal of High Energy Physics (JHEP). - : Springer. - 1126-6708 .- 1029-8479. ; :11
  • Tidskriftsartikel (refereegranskat)abstract
    • A search with the ATLAS detector is presented for the Standard Model Higgs boson produced by vector-boson fusion and decaying to a pair of bottom quarks, using 20.2 fb(-1) of LHC proton-proton collision data at root s - 8 TeV. The signal is searched for as a resonance in the invariant mass distribution of a pair of jets containing b-hadrons in vector-boson-fusion candidate events. The yield is measured to be -0.8 +/- 2.3 times the Standard Model cross-section for a Higgs boson mass of 125 GeV. The upper limit on the cross-section times the branching ratio is found to be 4.4 times the Standard Model cross-section at the 95% confidence level, consistent with the expected limit value of 5.4 (5.7) in the background-only (Standard Model production) hypothesis.
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2.
  • Sutovsky, Stanislav, et al. (författare)
  • Atypical Huntington's disease with the clinical presentation of behavioural variant of frontotemporal dementia
  • 2016
  • Ingår i: Journal of neural transmission. - : Springer Science and Business Media LLC. - 0300-9564 .- 1435-1463. ; 123:12, s. 1423-1433
  • Tidskriftsartikel (refereegranskat)abstract
    • Huntington's disease is an incurable, adult-onset, autosomal dominant inherited disorder caused by an expanded trinucleotide repeat (CAG). In this study, we describe a Huntington's disease patient displaying clinical symptoms of the behavioural variant of frontotemporal dementia in the absence of tremor and ataxia. The clinical onset was at the age of 36 years and the disease progressed slowly (18 years). Genetic testing revealed expanded trinucleotide CAG repeats in the Huntingtin gene, together with a Glu318Gly polymorphism in presenilin 1. Neuropathological assessment revealed extensive amyloid beta (A beta) aggregates in all cortical regions. No inclusions displaying hyperphosphorylated tau or phosphorylated transactive response DNA-binding protein 43 (TDP43) were found. A high number of p62 (sequestosome 1) immunopositive intranuclear inclusions were seen mainly in the cortex, while subcortical areas were affected to a lesser extent. Confocal microscopy revealed that the majority of p62 intranuclear lesions co-localised with the fused-in-sarcoma protein (FUS) immunostaining. The morphology of the inclusions resembled intranuclear aggregates in Huntington's disease. The presented proband suffered from Huntington's disease showed atypical distribution of FUS positive intranuclear aggregates in the cortical areas with concomitant Alzheimer's disease pathology.
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