46 research outputs found
Extreme Ultra-Violet Spectroscopy of the Lower Solar Atmosphere During Solar Flares
The extreme ultraviolet portion of the solar spectrum contains a wealth of
diagnostic tools for probing the lower solar atmosphere in response to an
injection of energy, particularly during the impulsive phase of solar flares.
These include temperature and density sensitive line ratios, Doppler shifted
emission lines and nonthermal broadening, abundance measurements, differential
emission measure profiles, and continuum temperatures and energetics, among
others. In this paper I shall review some of the advances made in recent years
using these techniques, focusing primarily on studies that have utilized data
from Hinode/EIS and SDO/EVE, while also providing some historical background
and a summary of future spectroscopic instrumentation.Comment: 34 pages, 8 figures. Submitted to Solar Physics as part of the
Topical Issue on Solar and Stellar Flare
Solar parameters for modeling interplanetary background
The goal of the Fully Online Datacenter of Ultraviolet Emissions (FONDUE)
Working Team of the International Space Science Institute in Bern, Switzerland,
was to establish a common calibration of various UV and EUV heliospheric
observations, both spectroscopic and photometric. Realization of this goal
required an up-to-date model of spatial distribution of neutral interstellar
hydrogen in the heliosphere, and to that end, a credible model of the radiation
pressure and ionization processes was needed. This chapter describes the solar
factors shaping the distribution of neutral interstellar H in the heliosphere.
Presented are the solar Lyman-alpha flux and the solar Lyman-alpha resonant
radiation pressure force acting on neutral H atoms in the heliosphere, solar
EUV radiation and the photoionization of heliospheric hydrogen, and their
evolution in time and the still hypothetical variation with heliolatitude.
Further, solar wind and its evolution with solar activity is presented in the
context of the charge exchange ionization of heliospheric hydrogen, and in the
context of dynamic pressure variations. Also the electron ionization and its
variation with time, heliolatitude, and solar distance is presented. After a
review of all of those topics, we present an interim model of solar wind and
the other solar factors based on up-to-date in situ and remote sensing
observations of solar wind. Results of this effort will further be utilised to
improve on the model of solar wind evolution, which will be an invaluable asset
in all heliospheric measurements, including, among others, the observations of
Energetic Neutral Atoms by the Interstellar Boundary Explorer (IBEX).Comment: Chapter 2 in the planned "Cross-Calibration of Past and Present Far
UV Spectra of Solar System Objects and the Heliosphere", ISSI Scientific
Report No 12, ed. R.M. Bonnet, E. Quemerais, M. Snow, Springe
Improved upper limits on the flavor-changing neutral current decays B→Kℓ+ℓ- and B→K*(892)ℓ+ℓ-
We have searched a sample of 9.6×106 B¯B events for the flavor-changing neutral current decays B→Kℓ+ℓ- and B→K*(892)ℓ+ℓ-. We subject the latter decay to the requirement that the dilepton mass mℓℓ exceed 0.5 GeV. There is no indication of a signal. We obtain the 90% confidence level upper limits B(B→Kℓ+ℓ-) 0.5Gev0.5Gev < 1.5×10-6. The weighted-average limit is only 50% above the standard model prediction
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