Characterising Encapsulated Nuclear Waste Using Cosmic-ray Muon Tomography (MT)

A prototype scintillating-fibre detector system has been developed at the University of Glasgow in collaboration with the UK National Nuclear Laboratory (NNL) for the non-destructive assay of UK legacy nuclear waste containers. This system consists of four tracking modules, two above and two below the container under interrogation. Each module consists of two orthogonal planes of 2 mm-pitch fibres yielding one space point. Per plane, 128 fibres are read out by a single Hamamatsu H8500 64-channel MAPMT with two fibres multiplexed onto each pixel. The configuration allows the reconstruction of the incoming and scattered muon trajectories, thus enabling the container content, with respect to atomic number Z, to be determined. Results are shown from experimental data collected for high-Z objects within an air matrix and within a shielded, concrete-filled container. These reconstructed images show clear discrimination between the low, medium and high-Z materials present, with dimensions and positions determined with sub-centimetre precision

Technical Design Report for PANDA Electromagnetic Calorimeter (EMC)

This document presents the technical layout and the envisaged performance of the Electromagnetic Calorimeter (EMC) for the PANDA target spectrometer. The EMC has been designed to meet the physics goals of the PANDA experiment, which is being developed for the Facility for Antiproton and Ion Research (FAIR) at Darmstadt, Germany. The performance figures are based on extensive prototype tests and radiation hardness studies. The document shows that the EMC is ready for construction up to the front-end electronics interface

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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