20 research outputs found

    Tracing kinematical and physical asymmetries in the jet from DG Tau B

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    Stellar jets can be highly asymmetric and have multiple velocity components. To clarify the origin of jet asymmetries and constrain their launch mechanism we study the physical and kinematical structure of the flow emitted by DG Tau B. The analysis of deep spectra taken at the KECK telescope allows us to infer the physical properties (the electron and total density, ne and nh, the ionisation fraction, xe, and the temperature, te) and the spatial distribution of the velocity components in the two jet lobes. The presence of dust grains in the jet is investigated by estimating the gas-phase abundance of calcium with respect to its solar value. At the base of the jet the lines are broad (~100 km/s) and up to three velocity components are detected. At 5" from the source, however, only the denser and more excited high velocity components survive and the lines are narrower (~10-30 km/s). The jet is strongly asymmetric both in velocity and in its physical structure. The red lobe, slower (~140 km/s) and more collimated, presents low ionisation fractions (xe~0.1-0.4) and temperatures (te<5e3 K), while the total density is up to ~2.5e4 ccm. The blue lobe, faster (~-320 km/s) and less collimated, is also less dense (nh~1e4 ccm) but highly excited (te up to ~5e4 K and xe up to 0.9). The estimated mass loss rate is similar in the two lobes (~6-8e-9 Msol/yr), suggesting that the ejection power is comparable on the two sides of the system, as expected from a magneto-centrifugal ejection mechanism, and that the observed asymmetries are due to different mass load and propagation properties in an inhomogeneous environment. Calcium is strongly depleted, indicating that the jet contains dust grains and, therefore, should originate from a region of the disk extending beyond the dust sublimation radius. The depletion is lower for higher velocities, consistent with dust destruction by shocks.Comment: 14 pages, 9 figures, accepted by A&

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

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    Mapping the human genetic architecture of COVID-19

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    The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease
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