Longitudinal double-spin asymmetry and cross section for inclusive neutral pion production at midrapidity in polarized proton collisions at sqrt(s) = 200 GeV

We report a measurement of the longitudinal double-spin asymmetry A_LL and the differential cross section for inclusive Pi0 production at midrapidity in polarized proton collisions at sqrt(s) = 200 GeV. The cross section was measured over a transverse momentum range of 1 < p_T < 17 GeV/c and found to be in good agreement with a next-to-leading order perturbative QCD calculation. The longitudinal double-spin asymmetry was measured in the range of 3.7 < p_T < 11 GeV/c and excludes a maximal positive gluon polarization in the proton. The mean transverse momentum fraction of Pi0's in their parent jets was found to be around 0.7 for electromagnetically triggered events.Comment: 6 pages, 3 figures, submitted to Phys. Rev. D (RC

Event-plane-dependent Dihadron Correlations With Harmonic Vn Subtraction In Au + Au Collisions At S Nn =200 Gev

STAR measurements of dihadron azimuthal correlations (Δφ) are reported in midcentral (20-60%) Au+Au collisions at sNN=200 GeV as a function of the trigger particle's azimuthal angle relative to the event plane, φs=|φt-ψEP|. The elliptic (v2), triangular (v3), and quadratic (v4) flow harmonic backgrounds are subtracted using the zero yield at minimum (ZYAM) method. The results are compared to minimum-bias d+Au collisions. It is found that a finite near-side (|Δφ|π/2) correlation shows a modification from d+Au data, varying with φs. The modification may be a consequence of path-length-dependent jet quenching and may lead to a better understanding of high-density QCD. © 2014 American Physical Society.894DOE; U.S. Department of EnergyArsene, I., (2005) Nucl. Phys. A, 757, p. 1. , (BRAHMS Collaboration), () NUPABL 0375-9474 10.1016/j.nuclphysa.2005.02. 130;Back, B.B., (2005) Nucl. Phys. 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NUPABL 0375-9474 10.1016/S0375-9474(99)85117-3Adams, J., (2004) Phys. Rev. Lett., 92, p. 112301. , (STAR Collaboration),. PRLTAO 0031-9007 10.1103/PhysRevLett.92.112301Borghini, N., Dinh, P.M., Ollitrault, J.Y., (2000) Phys. Rev. C, 62, p. 034902. , PRVCAN 0556-2813 10.1103/PhysRevC.62.034902Adams, J., (2005) Phys. Rev. C, 72, p. 014904. , (STAR Collaboration),. PRVCAN 0556-2813 10.1103/PhysRevC.72.014904Abelev, B.I., (2009) Phys. Rev. C, 79, p. 034909. , (STAR Collaboration),. PRVCAN 0556-2813 10.1103/PhysRevC.79.034909Bielcikova, J., (2004) Phys. Rev C, 69, p. 021901. , (R) () PRVCAN 0556-2813 10.1103/PhysRevC.69.021901;Konzer, J., Wang, F., (2009) Nucl. Instrum. Meth., A606, p. 713. , NIMAER 0168-9002 10.1016/j.nima.2009.05.011Mishra, A.P., (2008) Phys. Rev. C, 77, p. 064902. , PRVCAN 0556-2813 10.1103/PhysRevC.77.064902;Alver, B., Roland, G., (2010) Phys. Rev. C, 81, p. 054905. , PRVCAN 0556-2813 10.1103/PhysRevC.81.054905Alver, B., Roland, G., (2010) Phys. Rev. C, 82, p. 039903. , 0556-2813 10.1103/PhysRevC.82.039903Xu, J., Ko, C.M., (2011) Phys. Rev. C, 84, p. 014903. , PRVCAN 0556-2813 10.1103/PhysRevC.84.014903Petersen, H., (2010) Phys. Rev. C, 82, p. 041901. , PRVCAN 0556-2813 10.1103/PhysRevC.82.041901Takahashi, J., (2009) Phys. Rev. Lett., 103, p. 242301. , PRLTAO 0031-9007 10.1103/PhysRevLett.103.242301;Andrade, R.P.G., (2012) Phys. Lett. B, 712, p. 226. , PYLBAJ 0370-2693 10.1016/j.physletb.2012.04.044;Qian, W.L., (2013) Phys. Rev. C, 87, p. 014904. , PRVCAN 0556-2813 10.1103/PhysRevC.87.014904Schenke, B., Jeon, S., Gale, C., (2011) Phys. Rev. Lett., 106, p. 042301. , PRLTAO 0031-9007 10.1103/PhysRevLett.106.042301;Qiu, Z., Heinz, U.W., (2011) Phys. Rev. C, 84, p. 024911. , PRVCAN 0556-2813 10.1103/PhysRevC.84.024911;Song, H., (2011) Phys. Rev. Lett., 106, p. 192301. , PRLTAO 0031-9007 10.1103/PhysRevLett.106.192301;Schenke, B., Jeon, S., Gale, C., (2012) Phys. Rev. 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Fluctuations Of Charge Separation Perpendicular To The Event Plane And Local Parity Violation In S Nn = 200 Gev Au + Au Collisions At The Bnl Relativistic Heavy Ion Collider

Previous experimental results based on data (∼15×106 events) collected by the STAR detector at the BNL Relativistic Heavy Ion Collider suggest event-by-event charge-separation fluctuations perpendicular to the event plane in noncentral heavy-ion collisions. Here we present the correlator previously used split into its two component parts to reveal correlations parallel and perpendicular to the event plane. The results are from a high-statistics 200-GeV Au + Au collisions data set (57×106 events) collected by the STAR experiment. We explicitly count units of charge separation from which we find clear evidence for more charge-separation fluctuations perpendicular than parallel to the event plane. We also employ a modified correlator to study the possible P-even background in same- and opposite-charge correlations, and find that the P-even background may largely be explained by momentum conservation and collective motion. © 2013 American Physical Society.886NRF-2012004024; National Research FoundationLee, T.D., Yang, C.N., (1956) Phys. Rev., 104. , 1, 254. 0031-899X PHRVAO 10.1103/PhysRev.104.254Vafa, C., Witten, E., (1984) Phys. Rev. Lett., 53. , 2, 535. 0031-9007 PRLTAO 10.1103/PhysRevLett.53.535Lee, T.D., (1973) Phys. Rev. D, 8. , 3, 1226. 0556-2821 10.1103/PhysRevD.8.1226Lee, T.D., Wick, G.C., (1974) Phys. Rev. D, 9. , 4, 2291. 0556-2821 10.1103/PhysRevD.9.2291Kharzeev, D., Parity violation in hot QCD: Why it can happen, and how to look for it (2006) Physics Letters, Section B: Nuclear, Elementary Particle and High-Energy Physics, 633 (2-3), pp. 260-264. , DOI 10.1016/j.physletb.2005.11.075, PII S0370269305017430Kharzeev, D., Zhitnitsky, A., (2007) Nucl. Phys. 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Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease