11. |
- Adare, A., et al.
(författare)
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Charged-pion cross sections and double-helicity asymmetries in polarized p plus p collisions at root s=200 GeV
- 2015
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Ingår i: Physical Review D (Particles, Fields, Gravitation and Cosmology). - 1550-2368. ; 91:3
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Tidskriftsartikel (refereegranskat)abstract
- We present midrapidity charged-pion invariant cross sections, the ratio of the pi(-) to pi(+) cross sections and the charge-separated double-spin asymmetries in polarized p + p collisions at root s = p + 200 GeV. While the cross section measurements are consistent within the errors of next-to-leading-order (NLO) perturbative quantum chromodynamics predictions (pQCD), the same calculations overestimate the ratio of the charged-pion cross sections. This discrepancy arises from the cancellation of the substantial systematic errors associated with the NLO-pQCD predictions in the ratio and highlights the constraints these data will place on flavor-dependent pion fragmentation functions. The charge-separated pion asymmetries presented here sample an x range of similar to 0.03-0.16 and provide unique information on the sign of the gluon-helicity distribution.
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12. |
- Adare, A., et al.
(författare)
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Cross section for b(b)over-bar production via dielectrons in d plus Au collisions at root s(NN)=200 GeV
- 2015
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Ingår i: Physical Review C (Nuclear Physics). - 0556-2813. ; 91:1
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Tidskriftsartikel (refereegranskat)abstract
- We report a measurement of e(+)e(-) pairs from semileptonic heavy-flavor decays in d + Au collisions at root s(NN) = 200 GeV. By exploring the mass and transverse-momentum dependence of the yield, the bottom decay contribution can be isolated from charm, and quantified by comparison to PYTHIA and MC@NLO simulations. The resulting b (b) over bar -production cross section is sigma(dAu)(b (b) over bar) = 1.37 +/- 0.28 (stat) +/- 0.46 (syst) mb, which is equivalent to a nucleon-nucleon cross section of sigma(NN)(b (b) over bar) = 3.4 +/- 0.8 (stat) +/- 1.1 ( syst) mu b.
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13. |
- Adare, A., et al.
(författare)
-
Heavy-quark production and elliptic flow in Au plus Au collisions at root(NN)-N-S=62.4 GeV
- 2015
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Ingår i: Physical Review C (Nuclear Physics). - 0556-2813. ; 91:4
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Tidskriftsartikel (refereegranskat)abstract
- We present measurements of electrons and positrons from the semileptonic decays of heavy-flavor hadrons at midrapidity (vertical bar gamma vertical bar < 0.35) in Au + Au collisions at root(NN)-N-S = 62.4 GeV. The data were collected in 2010 by the PHENIX experiment that included the new hadron-blind detector. The invariant yield of electrons from heavy-flavor decays is measured as a function of transverse momentum in the range 1 < p(T)(e) < 5 GeV/c. The invariant yield per binary collision is slightly enhanced above the p + p reference in Au + Au 0%-20%, 20%-40%, and 40%-60% centralities at a comparable level. At this low beam energy this may be a result of the interplay between initial-state Cronin effects, final-state flow, and energy loss in medium. The v(2) of electrons from heavy-flavor decays is nonzero when averaged between 1.3 < p(T)(e) < 2.5 GeV/c for 0%-40% centrality collisions at root(NN)-N-S = 62.4 GeV. For 20%-40% centrality collisions, the v(2) at root(NN)-N-S = 62.4 GeV is smaller than that for heavy-flavor decays at root(NN)-N-S = 200 GeV. The v2 of the electrons from heavy-flavor decay at the lower beam energy is also smaller than v(2) for pions. Both results indicate that the heavy quarks interact with the medium formed in these collisions, but they may not be at the same level of thermalization with the medium as observed at root(NN)-N-S = 200 GeV.
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14. |
- Kraehling, J. R., et al.
(författare)
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Genome-wide RNAi screen reveals ALK1 mediates LDL uptake and transcytosis in endothelial cells
- 2016
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Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7
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Tidskriftsartikel (refereegranskat)abstract
- In humans and animals lacking functional LDL receptor (LDLR), LDL from plasma still readily traverses the endothelium. To identify the pathways of LDL uptake, a genome-wide RNAi screen was performed in endothelial cells and cross-referenced with GWAS-data sets. Here we show that the activin-like kinase 1 (ALK1) mediates LDL uptake into endothelial cells. ALK1 binds LDL with lower affinity than LDLR and saturates only at hypercholesterolemic concentrations. ALK1 mediates uptake of LDL into endothelial cells via an unusual endocytic pathway that diverts the ligand from lysosomal degradation and promotes LDL transcytosis. The endothelium-specific genetic ablation of Alk1 in Ldlr-KO animals leads to less LDL uptake into the aortic endothelium, showing its physiological role in endothelial lipoprotein metabolism. In summary, identification of pathways mediating LDLR-independent uptake of LDL may provide unique opportunities to block the initiation of LDL accumulation in the vessel wall or augment hepatic LDLR-dependent clearance of LDL. © The Author(s) 2016.
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