Book review: Welfare, inequality and social citizenship: deprivation and affluence in austerity Britain by Daniel Edmiston

In Welfare, Inequality and Social Citizenship: Deprivation and Affluence in Austerity Britain, Daniel Edmiston offers insight into how austerity and inequality impact upon citizen identities, showing that low-income individuals are excluded from dominant narratives of citizenship. Heather Mew recommends this structural account for evidencing how austerity in the UK is intensifying the gulf between social and welfare rights available to low- and high-income citizens

Book review: hunger pains: life inside foodbank Britain by Kayleigh Garthwaite

In Hunger Pains: Life Inside Foodbank Britain, Kayleigh Garthwaite draws upon eighteen months spent volunteering as a foodbank worker in Stockton-on-Tees to take readers through the workings of a foodbank and to reflect on the experiences of those who use them including discussion of shame and stigma. This is a revealing, impassioned and self-reflective book on the taboo subject of food poverty in a rich country, drawing timely and vital attention to the injustice of food hunger in Britain today, writes Heather Mew

Book review: student lives in crisis: deepening inequality in times of austerity by Lorenza Antonucci

In Student Lives in Crisis: Deepening Inequality in Times of Austerity, Lorenza Antonucci examines the material inequalities that shape young people’s experiences of Higher Education by examining welfare provision in three European countries – England, Italy and Sweden. Heather Mew welcomes this book as an eye-opening account that shows how austerity policies are leading universities to reinforce rather than remedy social inequalities

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

Governing inclusive finance workshop: towards a manifesto for change

The Governing Inclusive Finance Workshop was designed to foster new conversations between academics and multiple stakeholder groups in response to problems of financial exclusion, and possibilities for fostering progressive change. On Wednesday 27 June 2018, a diverse group of credit unions, community banks, alternative lenders, local-, county- and regional- government officials, advisory organizations and academic researchers – each involved or interested in financial provision for historically excluded people, families and communities – joined one another in conversation around three core themes: Making visible the lived realities of financial exclusion in the UK; Alleviating financial hardship: organizational successes and ongoing governance challenges; and Developing a manifesto for financial justice. By coming together as a group around these themes – discussing them freely and sharing experiences, challenges and ideas – our overarching aim was to begin an ongoing conversation around financial inclusion in the UK with a view to imagining more socially just forms of financial inclusion: i.e. forms of finance that have 'inclusiveness' at their heart. The day was arranged around three sessions in which a panel of experts each spoke for ten minutes about their experiences and ideas. The goal was to keep the format as relaxed as possible (no power point presentations!) – just the participants sharing themselves, their organizations and the people they deal with day-to-day. An academic Chair kept the sessions moving and on time, firing animating questions at the panel members, then guiding all participants through the various breakout discussions and plenary conversations. All in all, the day was filled with lively conversation and mutual engagement as a sense of purpose and potential filled the air

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