Single Spin Asymmetry ANA_N in Polarized Proton-Proton Elastic Scattering at s=200\sqrt{s}=200 GeV

We report a high precision measurement of the transverse single spin asymmetry $A_N$ at the center of mass energy $\sqrt{s}=200$ GeV in elastic proton-proton scattering by the STAR experiment at RHIC. The $A_N$ was measured in the four-momentum transfer squared $t$ range $0.003 \leqslant |t| \leqslant 0.035$ \GeVcSq, the region of a significant interference between the electromagnetic and hadronic scattering amplitudes. The measured values of $A_N$ and its $t$-dependence are consistent with a vanishing hadronic spin-flip amplitude, thus providing strong constraints on the ratio of the single spin-flip to the non-flip amplitudes. Since the hadronic amplitude is dominated by the Pomeron amplitude at this $\sqrt{s}$, we conclude that this measurement addresses the question about the presence of a hadronic spin flip due to the Pomeron exchange in polarized proton-proton elastic scattering.Comment: 12 pages, 6 figure

Measurement of the xx- and Q2Q^2-Dependence of the Asymmetry A1A_1 on the Nucleon

We report results for the virtual photon asymmetry $A_1$ on the nucleon from new Jefferson Lab measurements. The experiment, which used the CEBAF Large Acceptance Spectrometer and longitudinally polarized proton ($^{15}$NH$_3$) and deuteron ($^{15}$ND$_3$) targets, collected data with a longitudinally polarized electron beam at energies between 1.6 GeV and 5.7 GeV. In the present paper, we concentrate on our results for $A_1(x,Q^2)$ and the related ratio $g_1/F_1(x,Q^2)$ in the resonance and the deep inelastic regions for our lowest and highest beam energies, covering a range in momentum transfer $Q^2$ from 0.05 to 5.0 GeV$^2$ and in final-state invariant mass $W$ up to about 3 GeV. Our data show detailed structure in the resonance region, which leads to a strong $Q^2$--dependence of $A_1(x,Q^2)$ for $W$ below 2 GeV. At higher $W$, a smooth approach to the scaling limit, established by earlier experiments, can be seen, but $A_1(x,Q^2)$ is not strictly $Q^2$--independent. We add significantly to the world data set at high $x$, up to $x = 0.6$. Our data exceed the SU(6)-symmetric quark model expectation for both the proton and the deuteron while being consistent with a negative $d$-quark polarization up to our highest $x$. This data setshould improve next-to-leading order (NLO) pQCD fits of the parton polarization distributions.Comment: 7 pages LaTeX, 5 figure

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

Historical Roots of the Dutch Sustainability Challenge

Database on materials flows in the Dutch economy: 1850-1910-1970-200