Standard Model baryogenesis through four-fermion operators in braneworlds

We study a new baryogenesis scenario in a class of braneworld models with low fundamental scale, which typically have difficulty with baryogenesis. The scenario is characterized by its minimal nature: the field content is that of the Standard Model and all interactions consistent with the gauge symmetry are admitted. Baryon number is violated via a dimension-6 proton decay operator, suppressed today by the mechanism of quark-lepton separation in extra dimensions; we assume that this operator was unsuppressed in the early Universe due to a time-dependent quark-lepton separation. The source of CP violation is the CKM matrix, in combination with the dimension-6 operators. We find that almost independently of cosmology, sufficient baryogenesis is nearly impossible in such a scenario if the fundamental scale is above 100 TeV, as required by an unsuppressed neutron-antineutron oscillation operator. The only exception producing sufficient baryon asymmetry is a scenario involving out-of-equilibrium c quarks interacting with equilibrium b quarks.Comment: 39 pages, 5 figures v2: typos, presentational changes, references and acknowledgments adde

Leptogenesis from a sneutrino condensate revisited

We re--examine leptogenesis from a right--handed sneutrino condensate, paying special attention to the $B-$term associated with the see--saw Majorana mass. This term generates a lepton asymmetry in the condensate whose time average vanishes. However, a net asymmetry will result if the sneutrino lifetime is not much longer than the period of oscillations. Supersymmetry breaking by thermal effects then yields a lepton asymmetry in the standard model sector after the condensate decays. We explore different possibilities by taking account of both the low--energy and Hubble $B-$terms. It will be shown that the desired baryon asymmetry of the Universe can be obtained for a wide range of Majorana mass.Comment: 17 revtex pages, 3 figures, 1 table. Slightly modified and references added. Final version accepted for publication in Phys. Rev.

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

Extracellular Calcium Modulates Chondrogenic and Osteogenic Differentiation of Human Adipose-Derived Stem Cells: A Novel Approach for Osteochondral Tissue Engineering Using a Single Stem Cell Source

We have previously shown that elevating extracellular calcium from a concentration of 1.8 to 8 mM accelerates and increases human adipose-derived stem cell (hASC) osteogenic differentiation and cell-mediated calcium accretion, even in the absence of any other soluble osteogenic factors in the culture medium. However, the effects of elevated calcium on hASC chondrogenic differentiation have not been reported. The goal of this study was to determine the effects of varied calcium concentrations on chondrogenic differentiation of hASC. We hypothesized that exposure to elevated extracellular calcium (8 mM concentration) in a chondrogenic differentiation medium (CDM) would inhibit chondrogenesis of hASC when compared to basal calcium (1.8 mM concentration) controls. We further hypothesized that a full osteochondral construct could be engineered by controlling local release of calcium to induce site-specific chondrogenesis and osteogenesis using only hASC as the cell source. Human ASC was cultured as micromass pellets in CDM containing transforming growth factor-β1 and bone morphogenetic protein 6 for 28 days at extracellular calcium concentrations of either 1.8 mM (basal) or 8 mM (elevated). Our findings indicated that elevated calcium induced osteogenesis and inhibited chondrogenesis in hASC. Based on these findings, stacked polylactic acid nanofibrous scaffolds containing either 0% or 20% tricalcium phosphate (TCP) nanoparticles were electrospun and tested for site-specific chondrogenesis and osteogenesis. Histological assays confirmed that human ASC differentiated locally to generate calcified tissue in layers containing 20% TCP, and cartilage in the layers with no TCP when cultured in CDM. This is the first study to report the effects of elevated calcium on chondrogenic differentiation of hASC, and to develop osteochondral nanofibrous scaffolds using a single cell source and controlled calcium release to induce site-specific differentiation. This approach holds great promise for osteochondral tissue engineering using a single cell source (hASC) and single scaffold

A planet in a polar orbit of 1.4 solar-mass star

Although more than a thousand transiting extrasolar planets have been discovered, only very few of them orbit stars that are more massive than the Sun. The discovery of such planets is interesting, because they have formed in disks that are more massive but had a shorter life time than those of solar-like stars. Studies of planets more massive than the Sun thus tell us how the properties of the proto-planetary disks effect the formation of planets. Another aspect that makes these planets interesting is that they have kept their original orbital inclinations. By studying them we can thus find out whether the orbital axes planets are initially aligned to the stars rotational axes, or not. Here we report on the discovery of a planet of a 1.4 solar-mass star with a period of 5.6 days in a polar orbit made by CoRoT. This new planet thus is one of the few known close-in planets orbiting a star that is substantially more massive than the Sun