| 1. |
- Aggarwal, M. M., et al.
(författare)
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Photon and eta production in p plus Pb and p plus C collisions at root(NN)-N-S=17.4 GeV
- 2013
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Ingår i: Nuclear Physics, Section A. - : Elsevier BV. - 0375-9474. ; 898, s. 14-23
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Tidskriftsartikel (refereegranskat)abstract
- Measurements of direct photon production in p + Pb and p + C collisions at root(NN)-N-s = 17.4 GeV are presented. Upper limits on the direct photon yield as a function of p(T) are derived and compared to the results for Pb + Pb collisions at root(NN)-N-s = 17.3 GeV. The production of the eta meson, which is an important input to the direct photon signal extraction, has been determined in the eta -> 2 gamma channel for p + C collisions at root(NN)-N-s = 17.4 GeV. (c) 2012 Elsevier B.V. All rights reserved.
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| 2. |
- Aggarwal, M. M., et al.
(författare)
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Event-by-event charged-neutral fluctuations in Pb plus Pb collisions at 158 A GeV
- 2011
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Ingår i: Physics Letters. Section B: Nuclear, Elementary Particle and High-Energy Physics. - : Elsevier BV. - 0370-2693. ; 701:3, s. 300-305
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Tidskriftsartikel (refereegranskat)abstract
- Charged particles and photons have been measured in central Pb + Pb collisions at 158 A GeV in a common (eta-phi)-phase space region in the WA98 experiment at the CERN SPS. The measured distributions have been analyzed to quantify the frequency with which phase space regions of varying sizes have either small or large neutral pion fraction. The measured results are compared with VENUS model simulated events and with mixed events. Events with both large and small charged-neutral fluctuations are observed to occur more frequently than expected statistically, as deduced from mixed events, or as predicted by model simulations, with the difference becoming more prominent with decreasing size of the A Delta eta-Delta phi region. (C) 2011 Elsevier B.V. All rights reserved.
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| 3. |
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| 4. |
- Pinto, Dalila, et al.
(författare)
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Convergence of Genes and Cellular Pathways Dysregulated in Autism Spectrum Disorders.
- 2014
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Ingår i: American journal of human genetics. - : Elsevier BV. - 1537-6605 .- 0002-9297. ; 94:5, s. 677-694
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Tidskriftsartikel (refereegranskat)abstract
- Rare copy-number variation (CNV) is an important source of risk for autism spectrum disorders (ASDs). We analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0× 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability (odds ratio = 12.62, p = 2.7× 10(-15), ∼3% of ASD subjects). Pathogenic CNVs, often showing variable expressivity, included rare de novo and inherited events at 36 loci, implicating ASD-associated genes (CHD2, HDAC4, and GDI1) previously linked to other neurodevelopmental disorders, as well as other genes such as SETD5, MIR137, and HDAC9. Consistent with hypothesized gender-specific modulators, females with ASD were more likely to have highly penetrant CNVs (p = 0.017) and were also overrepresented among subjects with fragile X syndrome protein targets (p = 0.02). Genes affected by de novo CNVs and/or loss-of-function single-nucleotide variants converged on networks related to neuronal signaling and development, synapse function, and chromatin regulation.
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