Role of dynamical particle-vibration coupling in reconciliation of the d3/2d_{3/2} puzzle for spherical proton emitters

It has been observed that decay rate for proton emission from $d_{3/2}$ single particle state is systematically quenched compared with the prediction of a one dimensional potential model although the same model successfully accounts for measured decay rates from $s_{1/2}$ and $h_{11/2}$ states. We reconcile this discrepancy by solving coupled-channels equations, taking into account couplings between the proton motion and vibrational excitations of a daughter nucleus. We apply the formalism to proton emitting nuclei $^{160,161}$Re to show that there is a certain range of parameter set of the excitation energy and the dynamical deformation parameter for the quadrupole phonon excitation which reproduces simultaneously the experimental decay rates from the 2$d_{3/2}$, 3$s_{1/2}$ and 1$h_{11/2}$ states in these nuclei.Comment: RevTex, 12 pages, 4 eps figure

Tides in colliding galaxies

Long tails and streams of stars are the most noticeable upshots of galaxy collisions. Their origin as gravitational, tidal, disturbances has however been recognized only less than fifty years ago and more than ten years after their first observations. This Review describes how the idea of galactic tides emerged, in particular thanks to the advances in numerical simulations, from the first ones that included tens of particles to the most sophisticated ones with tens of millions of them and state-of-the-art hydrodynamical prescriptions. Theoretical aspects pertaining to the formation of tidal tails are then presented. The third part of the review turns to observations and underlines the need for collecting deep multi-wavelength data to tackle the variety of physical processes exhibited by collisional debris. Tidal tails are not just stellar structures, but turn out to contain all the components usually found in galactic disks, in particular atomic / molecular gas and dust. They host star-forming complexes and are able to form star-clusters or even second-generation dwarf galaxies. The final part of the review discusses what tidal tails can tell us (or not) about the structure and content of present-day galaxies, including their dark components, and explains how tidal tails may be used to probe the past evolution of galaxies and their mass assembly history. On-going deep wide-field surveys disclose many new low-surface brightness structures in the nearby Universe, offering great opportunities for attempting galactic archeology with tidal tails.Comment: 46 pages, 13 figures, Review to be published in "Tidal effects in Astronomy and Astrophysics", Lecture Notes in Physics. Comments are most welcom

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

Transforming growth factor-β impairs glucocorticoid activity in the A549 lung adenocarcinoma cell line

Background and purpose.  The lung adenocarcinoma cell line, A549, undergoes epithelial mesenchymal cell transition (EMT) in response to transforming growth factor-β (TGF-β). Glucocorticoids did not prevent the EMT response, but TGF-β induced resistance to the cytokine-regulatory action of glucocorticoids. We sought to characterise the impairment of glucocorticoid response in A549 cells. Experimental approach.  A549 cells were exposed to TGF-β for up to 96 h before glucocorticoid treatment and challenge with IL-1α to ascertain the extent of glucocorticoid regulation of interleukin-6 (IL-6) and CXCL8 production. Nuclear localisation of glucocorticoid receptor (GR) α was ascertained by immunofluorescence and Western blotting. Glucocorticoid-response element (GRE) transactivation was measured with a transfected GRE-SEAP reporter. Key Results.  TGF-β (40-400 pM) reduced the maximum inhibitory effect of dexamethasone on IL-1α-induced IL-6 and CXCL8 production. The impaired glucocorticoid response was detected with 4 h of TGF-β (40 pM) exposure (and 4 h IL-1α to induce CXCL8 expression) and therefore was not secondary to EMT, a process that requires longer incubation periods and higher concentrations of TGF-β. TGF-β also impaired dexamethasone regulation of granulocyte-macrophage colony-stimulating factor in thrombin-stimulated BEAS-2B epithelial cells. Impaired regulation of CXCL8 was associated with markedly reduced GRE transactivation and reduced induction of IκBα mRNA, glucocorticoid-inducible leucine zipper (GILZ) and the epithelial sodium channel (SCNN1A). The expression, cellular levels and nuclear localisation of glucocorticoid receptor α were reduced by TGF-β. Conclusions and Implications.  We have identified that TGF-β impairs glucocorticoid responses in the A549 and BEAS-2B cell lines. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society

Pre-mitotic genome re-organisation bookends the B cell differentiation process

During cellular differentiation chromosome conformation is intricately remodelled to support the lineage-specific transcriptional programs required for initiating and maintaining lineage identity. When these changes occur in relation to cell cycle, division and time in response to cellular activation and differentiation signals has yet to be explored, although it has been proposed to occur during DNA synthesis or after mitosis. Here, we elucidate the chromosome conformational changes in B lymphocytes as they differentiate and expand from a naive, quiescent state into antibody secreting plasma cells. We find gene-regulatory chromosome reorganization in late G1 phase before the first division, and that this configuration is remarkably stable as the cells massively and rapidly clonally expand. A second wave of conformational change occurs as cells terminally differentiate into plasma cells, coincident with increased time in G1 phase. These results provide further explanation for how lymphocyte fate is imprinted prior to the first division. They also suggest that chromosome reconfiguration occurs prior to DNA replication and mitosis, and is linked to a gene expression program that controls the differentiation process required for the generation of immunity.Wing Fuk Chan, Hannah D. Coughlan, Jie H. S. Zhou, Christine R. Keenan, Naiara G. Bediaga, Philip D. Hodgkin, Gordon K. Smyth, Timothy M. Johanson, Rhys S. Alla