Λ and K0^0S_S production in Pb-Pb and pp collisions with ALICE at the LHC

In this work, the transverse momentum spectra of Λ and K$^0$$_S$ measured with the ALICE experiment at the LHC are discussed. Measurements are presented for colliding systems of protons, at centre of mass energies 2.76 TeV and 7 TeV, and for lead ions at a centre of mass energy of 2.76 TeV per nucleon. The spectra are discussed within a theoretical framework of a thermally equilibrated, hydrodynamically evolving system, which serves to explain the shape of the spectra for p$_T$ 6 GeV/c jet quenching is evident, but no evidence of particle species dependance in jet quenching is observed. The Λ/K$^0$$_S$ ratio shows an enhancement for 2 < p$_T$ < 6 GeV/c, peaking at 1.5 for the 5% most central Pb–Pb collisions compared to 0.6 for pp. This is discussed in terms of a coalescence model. It cannot be explained purely by enhanced baryon production, but must also involve a redistribution of particles within p$_T$. This supports the hydrodynamical picture of hadron production. A brief comparison to the results presently available in p–Pb collisions at the LHC is also given

Where Brain, Body and World Collide

The production cross section of electrons from semileptonic decays of beauty hadrons was measured at mid-rapidity (|y| &lt; 0.8) in the transverse momentum range 1 &lt; pt &lt; 8 Gev/c with the ALICE experiment at the CERN LHC in pp collisions at a center of mass energy sqrt{s} = 7 TeV using an integrated luminosity of 2.2 nb^{-1}. Electrons from beauty hadron decays were selected based on the displacement of the decay vertex from the collision vertex. A perturbative QCD calculation agrees with the measurement within uncertainties. The data were extrapolated to the full phase space to determine the total cross section for the production of beauty quark-antiquark pairs

Stratified analyses refine association between TLR7 rare variants and severe COVID-19

Summary: Despite extensive global research into genetic predisposition for severe COVID-19, knowledge on the role of rare host genetic variants and their relation to other risk factors remains limited. Here, 52 genes with prior etiological evidence were sequenced in 1,772 severe COVID-19 cases and 5,347 population-based controls from Spain/Italy. Rare deleterious TLR7 variants were present in 2.4% of young (<60 years) cases with no reported clinical risk factors (n = 378), compared to 0.24% of controls (odds ratio [OR] = 12.3, p = 1.27 × 10−10). Incorporation of the results of either functional assays or protein modeling led to a pronounced increase in effect size (ORmax = 46.5, p = 1.74 × 10−15). Association signals for the X-chromosomal gene TLR7 were also detected in the female-only subgroup, suggesting the existence of additional mechanisms beyond X-linked recessive inheritance in males. Additionally, supporting evidence was generated for a contribution to severe COVID-19 of the previously implicated genes IFNAR2, IFIH1, and TBK1. Our results refine the genetic contribution of rare TLR7 variants to severe COVID-19 and strengthen evidence for the etiological relevance of genes in the interferon signaling pathway