Production of cold fragments in nucleus-nucleus collisions in the Fermi-energy domain

The reaction mechanism of nucleus-nucleus collisions at projectile energies around the Fermi energy is investigated with emphasis on the production of fragmentation-like residues. The results of simulations are compared to experimental mass distributions of elements with Z = 21 - 29 observed in the reactions 86Kr+124,112Sn at 25 AMeV. The model of incomplete fusion is modified and a component of excitation energy of the cold fragment dependent on isospin asymmetry is introduced. The modifications in the model of incomplete fusion appear consistent with both overall model framework and available experimental data. A prediction is provided for the production of very neutron-rich nuclei using a secondary beam of 132Sn where e.g. the reaction 132Sn+238U at 28 AMeV appears as a possible alternative to the use of fragmentation reactions at higher energies.Comment: LaTeX, 15 pages, 5 figures, minor modifications, accepted for publication in Nuclear Physics

Measuring the Temperature of Hot Nuclear Fragments

A new thermometer based on fragment momentum fluctuations is presented. This thermometer exhibited residual contamination from the collective motion of the fragments along the beam axis. For this reason, the transverse direction has been explored. Additionally, a mass dependence was observed for this thermometer. This mass dependence may be the result of the Fermi momentum of nucleons or the different properties of the fragments (binding energy, spin etc..) which might be more sensitive to different densities and temperatures of the exploding fragments. We expect some of these aspects to be smaller for protons (and/or neutrons); consequently, the proton transverse momentum fluctuations were used to investigate the temperature dependence of the source

Observation of exclusive DVCS in polarized electron beam asymmetry measurements

We report the first results of the beam spin asymmetry measured in the reaction e + p -> e + p + gamma at a beam energy of 4.25 GeV. A large asymmetry with a sin(phi) modulation is observed, as predicted for the interference term of Deeply Virtual Compton Scattering and the Bethe-Heitler process. The amplitude of this modulation is alpha = 0.202 +/- 0.028. In leading-order and leading-twist pQCD, the alpha is directly proportional to the imaginary part of the DVCS amplitude.Comment: 6 pages, 5 figure

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

Structural Evolution of Solid Phenanthrene at High Pressures

The effect of hydrostatic pressure on the structure of solid phenanthrene (C₁₄H₁₀) was investigated up to 25.7 GPa through synchrotron X-ray powder diffraction and an evolutionary algorithm for crystal structure prediction based on van der Waals density functional calculations. We observed the onset of a phase transition around 8 GPa from the monoclinic <i>P</i>2₁ low-pressure phase with two molecules per unit cell arranged in a herringbone fashion to a new high-pressure phase. The best candidate structure for this phase exhibits three molecules in a <i>P</i>1 triclinic unit cell in a parallel arrangement, stabilized by dominant π–π intermolecular interactions. The <i>P</i>2₁ and <i>P</i>1 phases coexist in the pressure range from 8 to 13 GPa, whereas above 13 GPa only the <i>P</i>1 high-pressure phase is present. At higher pressures (<i>P</i> > 20 GPa), experiments and first-principles calculations suggest a tendency toward amorphization