Table of Contents and Prologue

Editorial board, Table of contents, and Prologue, an introduction to volume 1

Tim Gales Senior Cello Recital

https://dc.ewu.edu/music_performances/1695/thumbnail.jp

Microstructural and mechanical characterisation of post-tentioning strands following elevated temperature exposure

Prestressing strands lose strength and become more susceptible to creep deformation when they are heated during a fire. The consequent loss in prestressing force could under certain conditions result in structural collapse, potentially outwith the heated region of the structure. This paper describes a test programme characterising the changes in microstructure of steel prestressing tendons exposed to elevated temperatures. The residual strength tests, hardness testing, and elevated temperature mechanical test were performed to demonstrate how recovery and recrystallisation of the initially work-hardened steel produce changes in its mechanical properties at elevated temperatures. The research results of this paper are beneficial not only in the fire design of post-tensioned structures using modern prestressing steel, but also in the assessment of the tendons’ residual strength after being affected by fire

Chamber Ensemble

https://dc.ewu.edu/music_performances/1681/thumbnail.jp

CELLObration

https://dc.ewu.edu/music_performances/1683/thumbnail.jp

EWURA Annual Concert

https://dc.ewu.edu/music_performances/1682/thumbnail.jp

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