3,124 research outputs found

    Tuning Monte Carlo Generators: The Perugia Tunes

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    We present 9 new tunes of the pT-ordered shower and underlying-event model in PYTHIA 6.4. These "Perugia" tunes update and supersede the older "S0" family. The data sets used to constrain the models include hadronic Z0 decays at LEP, Tevatron minimum-bias data at 630, 1800, and 1960 GeV, Tevatron Drell-Yan data at 1800 and 1960 GeV, and SPS min-bias data at 200, 546, and 900 GeV. In addition to the central parameter set, called "Perugia 0", we introduce a set of 8 related "Perugia Variations" that attempt to systematically explore soft, hard, parton density, and colour structure variations in the theoretical parameters. Based on these variations, a best-guess prediction of the charged track multiplicity in inelastic, nondiffractive minimum-bias events at the LHC is made. Note that these tunes can only be used with PYTHIA 6, not with PYTHIA 8. Note: this report was updated in March 2011 with a new set of variations, collectively labeled "Perugia 2011", that are optimized for matching applications and which also take into account some lessons from the early LHC data. In order not to break the original text, these are described separately in Appendix B. Note 2: a subsequent "Perugia 2012" update is described in Appendix C.Comment: 46 page

    t' at the LHC: the physics of discovery

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    A search for a fourth family at the LHC is presently a low priority, but we argue that an effective search can be conducted early with only a few inverse femtobarns of data. We discuss a method based on invariant masses of single jets for identifying the WW's originating from heavy quark decays. This can significantly increase signal to background in the reconstruction of the t′t' mass. We also study the various types of physics that can impact the background estimate, most notably higher order effects, initial state radiation, and models of the underlying event.Comment: 16 pages, 12 figures, small improvements, version to appear in JHE

    Functional and genetic characterization of the non-lysosomal glucosylceramidase 2 as a modifier for Gaucher disease

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    Background: Gaucher disease (GD) is the most common inherited lysosomal storage disorder in humans, caused by mutations in the gene encoding the lysosomal enzyme glucocerebrosidase (GBA1). GD is clinically heterogeneous and although the type of GBA1 mutation plays a role in determining the type of GD, it does not explain the clinical variability seen among patients. Cumulative evidence from recent studies suggests that GBA2 could play a role in the pathogenesis of GD and potentially interacts with GBA1. Methods: We used a framework of functional and genetic approaches in order to further characterize a potential role of GBA2 in GD. Glucosylceramide (GlcCer) levels in spleen, liver and brain of GBA2-deficient mice and mRNA and protein expression of GBA2 in GBA1-deficient murine fibroblasts were analyzed. Furthermore we crossed GBA2-deficient mice with conditional Gba1 knockout mice in order to quantify the interaction between GBA1 and GBA2. Finally, a genetic approach was used to test whether genetic variation in GBA2 is associated with GD and/or acts as a modifier in Gaucher patients. We tested 22 SNPs in the GBA2 and GBA1 genes in 98 type 1 and 60 type 2/3 Gaucher patients for single-and multi-marker association with GD. Results: We found a significant accumulation of GlcCer compared to wild-type controls in all three organs studied. In addition, a significant increase of Gba2-protein and Gba2-mRNA levels in GBA1-deficient murine fibroblasts was observed. GlcCer levels in the spleen from Gba1/Gba2 knockout mice were much higher than the sum of the single knockouts, indicating a cross-talk between the two glucosylceramidases and suggesting a partially compensation of the loss of one enzyme by the other. In the genetic approach, no significant association with severity of GD was found for SNPs at the GBA2 locus. However, in the multi-marker analyses a significant result was detected for p.L444P (GBA1) and rs4878628 (GBA2), using a model that does not take marginal effects into account. Conclusions: All together our observations make GBA2 a likely candidate to be involved in GD etiology. Furthermore, they point to GBA2 as a plausible modifier for GBA1 in patients with GD

    Sphingolipid Activator Proteins Are Required for Epidermal Permeability Barrier Formation

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    The epidermal permeability barrier is maintained by extracellular lipid membranes within the interstices of the stratum corneum. Ceramides, the major components of these multilayered membranes, derive in large part from hydrolysis of glucosylceramides mediated by stratum corneum beta-glucocerebrosidase (beta-GlcCerase). Prosaposin (pSAP) is a large precursor protein that is proteolytically cleaved to form four distinct sphingolipid activator proteins, which stimulate enzymatic hydrolysis of sphingolipids, including glucosylceramide. Recently, pSAP has been eliminated in a mouse model using targeted deletion and homologous recombination. In addition to the extracutaneous findings noted previously, our present data indicate that pSAP deficiency in the epidermis has significant consequences including: 1) an accumulation of epidermal glucosylceramides together with below normal levels of ceramides; 2) alterations in lipids that are bound by ester linkages to proteins of the cornified cell envelope; 3) a thickened stratum lucidum with evidence of scaling; and 4) a striking abnormality in lamellar membrane maturation within the interstices of the stratum corneum. Together, these results demonstrate that the production of pSAP, and presumably mature sphingolipid activator protein generation, is required for normal epidermal barrier formation and function. Moreover, detection of significant amounts of covalently bound omega-OH-GlcCer in pSAP-deficient epidermis suggests that deglucosylation to omega-OH-Cer is not a requisite step prior to covalent attachment of lipid to cornified envelope proteins

    Single hadron response measurement and calorimeter jet energy scale uncertainty with the ATLAS detector at the LHC

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    The uncertainty on the calorimeter energy response to jets of particles is derived for the ATLAS experiment at the Large Hadron Collider (LHC). First, the calorimeter response to single isolated charged hadrons is measured and compared to the Monte Carlo simulation using proton-proton collisions at centre-of-mass energies of sqrt(s) = 900 GeV and 7 TeV collected during 2009 and 2010. Then, using the decay of K_s and Lambda particles, the calorimeter response to specific types of particles (positively and negatively charged pions, protons, and anti-protons) is measured and compared to the Monte Carlo predictions. Finally, the jet energy scale uncertainty is determined by propagating the response uncertainty for single charged and neutral particles to jets. The response uncertainty is 2-5% for central isolated hadrons and 1-3% for the final calorimeter jet energy scale.Comment: 24 pages plus author list (36 pages total), 23 figures, 1 table, submitted to European Physical Journal

    Measurement of the cross-section and charge asymmetry of WW bosons produced in proton-proton collisions at s=8\sqrt{s}=8 TeV with the ATLAS detector