Neutron-Unbound Excited States of 23N

Neutron unbound states in 23N were populated via proton knockout from an 83.4 MeV/nucleon 24O beam on a liquid deuterium target. The two-body decay energy displays two peaks at E1∼100keV and E2∼1MeV with respect to the neutron separation energy. The data are consistent with shell model calculations predicting resonances at excitation energies of ∼3.6MeV and ∼4.5MeV. The selectivity of the reaction implies that these states correspond to the first and second 3/2− states. The energy of the first state is about 1.3 MeV lower than the first excited 2+ in 24O. This decrease is largely due to coupling with the πp−13/2 hole along with a small reduction of the N=16 shell gap in 23N

Increasing Access to Electricity: An Assessment of the Energy and Power Generation Potential from Biomass Waste Residues in Tanzania

Tanzania has a high rural population, of which many rely on off-grid diesel generators to produce electricity. The focus of this paper is to assess if the waste biomass residues in Tanzania have sufficient energy potential to produce renewable electrical energy for small-scale electricity generation using off-grid diesel generators coupled with anaerobic digestion (AD) and/or gasification. The gaseous fuel produced can then be used to substitute diesel fuel used in small-scale dual fuel diesel gen-sets; thus, providing more affordable electricity whilst reducing dependency on fossil fuels. The biomass waste streams estimated are those arising from agriculture, forestry, livestock, and urban human waste. To answer this question, the energy potentials of each of these biomass waste streams are quantified, followed by further calculations to determine the electricity generation capacity per stream based on overall efficiencies of 10 and 25%. The results show that combined these waste streams have an energy potential of 385 PJ (for the base year of 2018) generated from 26,924 kilotonnes (kt). Collectively, these residues can produce at least 1.2 times the electricity generated nationally in 2018 using AD and gasification coupled with a diesel gen-set engine

Reduced quasifission competition in fusion reactions forming neutron-rich heavy elements

Measurements of mass-angle distributions (MADs) for Cr + W reactions, providing a wide range in the neutron-to-proton ratio of the compound system, (N/Z)CN, have allowed for the dependence of quasifission on the (N/Z)CN to be determined in a model-independent way. Previous experimental and theoretical studies had produced conflicting conclusions. The experimental MADs reveal an increase in contact time and mass evolution of the quasifission fragments with increasing (N/Z)CN, which is indicative of an increase in the fusion probability. The experimental results are in agreement with microscopic time-dependent Hartree-Fock calculations of the quasifission process. The experimental and theoretical results favor the use of the most neutron-rich projectiles and targets for the production of heavy and superheavy nuclei.Comment: Accepted to PRC as a Rapid Communicatio

Two-Neutron Sequential Decay of 24^{24}O

A two-neutron unbound excited state of $^{24}$O was populated through a (d,d') reaction at 83.4 MeV/nucleon. A state at $E = 715 \pm 110$ (stat) $\pm 45$ (sys) keV with a width of $\Gamma < 2$ MeV was observed above the two-neutron separation energy placing it at 7.65 $\pm$ 0.2 MeV with respect to the ground state. Three-body correlations for the decay of $^{24}$O $\rightarrow$ $^{22}$O + $2n$ show clear evidence for a sequential decay through an intermediate state in $^{23}$O. Neither a di-neutron nor phase-space model for the three-body breakup were able to describe these correlations

Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity

The combined impact of common and rare exonic variants in COVID-19 host genetics is currently insufficiently understood. Here, common and rare variants from whole-exome sequencing data of about 4000 SARS-CoV-2-positive individuals were used to define an interpretable machine-learning model for predicting COVID-19 severity. First, variants were converted into separate sets of Boolean features, depending on the absence or the presence of variants in each gene. An ensemble of LASSO logistic regression models was used to identify the most informative Boolean features with respect to the genetic bases of severity. The Boolean features selected by these logistic models were combined into an Integrated PolyGenic Score that offers a synthetic and interpretable index for describing the contribution of host genetics in COVID-19 severity, as demonstrated through testing in several independent cohorts. Selected features belong to ultra-rare, rare, low-frequency, and common variants, including those in linkage disequilibrium with known GWAS loci. Noteworthily, around one quarter of the selected genes are sex-specific. Pathway analysis of the selected genes associated with COVID-19 severity reflected the multi-organ nature of the disease. The proposed model might provide useful information for developing diagnostics and therapeutics, while also being able to guide bedside disease management. © 2021, The Author(s)

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

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 hospitalization2–4 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