Coronal Diagnostics from Narrowband Images around 30.4 nm

Images taken in the band centered at 30.4 nm are routinely used to map the radiance of the He II Ly alpha line on the solar disk. That line is one of the strongest, if not the strongest, line in the EUV observed in the solar spectrum, and one of the few lines in that wavelength range providing information on the upper chromosphere or lower transition region. However, when observing the off-limb corona the contribution from the nearby Si XI 30.3 nm line can become significant. In this work we aim at estimating the relative contribution of those two lines in the solar corona around the minimum of solar activity. We combine measurements from CDS taken in August 2008 with temperature and density profiles from semiempirical models of the corona to compute the radiances of the two lines, and of other representative coronal lines (e.g., Mg X 62.5 nm, Si XII 52.1 nm). Considering both diagnosed quantities from line ratios (temperatures and densities) and line radiances in absolute units, we obtain a good overall match between observations and models. We find that the Si XI line dominates the He II line from just above the limb up to ~2 R_Sun in streamers, while its contribution to narrowband imaging in the 30.4 nm band is expected to become smaller, even negligible in the corona beyond ~2 - 3 R_Sun, the precise value being strongly dependent on the coronal temperature profile.Comment: 26 pages, 11 figures; to be published in: Solar Physic

Theoretical and technological building blocks for an innovation accelerator

The scientific system that we use today was devised centuries ago and is inadequate for our current ICT-based society: the peer review system encourages conservatism, journal publications are monolithic and slow, data is often not available to other scientists, and the independent validation of results is limited. Building on the Innovation Accelerator paper by Helbing and Balietti (2011) this paper takes the initial global vision and reviews the theoretical and technological building blocks that can be used for implementing an innovation (in first place: science) accelerator platform driven by re-imagining the science system. The envisioned platform would rest on four pillars: (i) Redesign the incentive scheme to reduce behavior such as conservatism, herding and hyping; (ii) Advance scientific publications by breaking up the monolithic paper unit and introducing other building blocks such as data, tools, experiment workflows, resources; (iii) Use machine readable semantics for publications, debate structures, provenance etc. in order to include the computer as a partner in the scientific process, and (iv) Build an online platform for collaboration, including a network of trust and reputation among the different types of stakeholders in the scientific system: scientists, educators, funding agencies, policy makers, students and industrial innovators among others. Any such improvements to the scientific system must support the entire scientific process (unlike current tools that chop up the scientific process into disconnected pieces), must facilitate and encourage collaboration and interdisciplinarity (again unlike current tools), must facilitate the inclusion of intelligent computing in the scientific process, must facilitate not only the core scientific process, but also accommodate other stakeholders such science policy makers, industrial innovators, and the general public

Observation of Events with an Energetic Forward Neutron in Deep Inelastic Scattering at HERA

In deep inelastic neutral current scattering of positrons and protons at the center of mass energy of 300 GeV, we observe, with the ZEUS detector, events with a high energy neutron produced at very small scattering angles with respect to the proton direction. The events constitute a fixed fraction of the deep inelastic, neutral current event sample independent of Bjorken x and Q2 in the range 3 · 10-4 \u3c xBJ \u3c 6 · 10-3 and 10 \u3c Q2 \u3c 100 GeV2

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