The omega rho pi coupling in the VMD model revisited

We determine the value of the \omega -\rho- \pi mesons coupling (g_{\omega\rho\pi}), in the context of the vector meson dominance model, from radiative decays, the \omega \rightarrow 3\pi decay width and the e^+e^- \rightarrow 3\pi cross section. For the last two observables we consider the effect of either a heavier resonance (\rho'(1450)) or a contact term. A weighted average of the results from the set of observables yields g_{\omega\rho\pi} =14.7 \pm 0.1 GeV^{-1} in absence of those contributions, and g_{\omega\rho\pi} =11.9 \pm 0.2 GeV^{-1} or g_{\omega\rho\pi} =11.7 \pm 0.1 GeV^{-1} when including the \rho' or contact term respectively. The inclusion of these additional terms makes the estimates from the different observables to lay in a more reduced range. Improved measurements of these observables and the \rho'(1450) meson parameters are needed to give a definite answer on the pertinence of the inclusion of this last one in the considered processes.Comment: 14 pages, 5 figures. Extended analysis including SND and CMD2 data. References added. Matches published versio

Form Factors in the radiative pion decay

We perform an analysis of the form factors that rule the structure-dependent amplitude in the radiative pion decay. The resonance contributions to pion -> e nu_e gamma decays are computed through the proper construction of the vector and axial-vector form factors by setting the QCD driven asymptotic properties of the three-point Green functions VVP and VAP, and by demanding the smoothing of the form factors at high transfer of momentum. A comparison between theoretical and experimental determinations of the form factors is also carried out. We also consider and evaluate the role played by a non-standard tensor form factor. We conclude that, at present and due to the hadronic incertitudes, the search for New Physics in this process is not feasible.Comment: 14 pages, no figures. Typos corrected. Accepted for publication in The European Physical Journal

The European Solar Telescope

The European Solar Telescope (EST) is a project aimed at studying the magnetic connectivity of the solar atmosphere, from the deep photosphere to the upper chromosphere. Its design combines the knowledge and expertise gathered by the European solar physics community during the construction and operation of state-of-the-art solar telescopes operating in visible and near-infrared wavelengths: the Swedish 1m Solar Telescope, the German Vacuum Tower Telescope and GREGOR, the French Télescope Héliographique pour l'Étude du Magnétisme et des Instabilités Solaires, and the Dutch Open Telescope. With its 4.2 m primary mirror and an open configuration, EST will become the most powerful European ground-based facility to study the Sun in the coming decades in the visible and near-infrared bands. EST uses the most innovative technological advances: the first adaptive secondary mirror ever used in a solar telescope, a complex multi-conjugate adaptive optics with deformable mirrors that form part of the optical design in a natural way, a polarimetrically compensated telescope design that eliminates the complex temporal variation and wavelength dependence of the telescope Mueller matrix, and an instrument suite containing several (etalon-based) tunable imaging spectropolarimeters and several integral field unit spectropolarimeters. This publication summarises some fundamental science questions that can be addressed with the telescope, together with a complete description of its major subsystems

The European Solar Telescope

The European Solar Telescope (EST) is a project aimed at studying the magnetic connectivity of the solar atmosphere, from the deep photosphere to the upper chromosphere. Its design combines the knowledge and expertise gathered by the European solar physics community during the construction and operation of state-of-the-art solar telescopes operating in visible and near-infrared wavelengths: the Swedish 1m Solar Telescope, the German Vacuum Tower Telescope and GREGOR, the French Télescope Héliographique pour l’Étude du Magnétisme et des Instabilités Solaires, and the Dutch Open Telescope. With its 4.2 m primary mirror and an open configuration, EST will become the most powerful European ground-based facility to study the Sun in the coming decades in the visible and near-infrared bands. EST uses the most innovative technological advances: the first adaptive secondary mirror ever used in a solar telescope, a complex multi-conjugate adaptive optics with deformable mirrors that form part of the optical design in a natural way, a polarimetrically compensated telescope design that eliminates the complex temporal variation and wavelength dependence of the telescope Mueller matrix, and an instrument suite containing several (etalon-based) tunable imaging spectropolarimeters and several integral field unit spectropolarimeters. This publication summarises some fundamental science questions that can be addressed with the telescope, together with a complete description of its major subsystems

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

A first update on mapping the human genetic architecture of COVID-19

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