A critical ethnographic study of discriminatory social practice during clinical practice in emergency medical care

Background: Post-apartheid, South Africa adopted an inclusive education system that was intended to be free of unfair discrimination. This qualitative study examines the experiences and perceptions of racial discrimination between Emergency Medical Care (EMC) students, clinical mentors, and patients within an Emergency Medical Service (EMS) during clinical practice. Understanding the nature of such discrimination is critical for redress. Methods: Within the conceptual framework of Critical Race Theory, critical ethnographic methodology explored how discriminatory social practice manifests during clinical practice. Semi-structured interviews enabled thematic analysis. We purposively sampled 13 undergraduate EMC students and 5 Emergency Care (EC) providers. Results: EMC student participants reported experiences of racial and gender discrimination during work-integrated learning (WIL) as they were treated differently on the basis of race and gender. Language was used as an intentional barrier to isolate students from the patients during WIL because EC providers would intentionally speak in a language not understood by the student and failed to translate vital medical information about the case. This conduct prevented some students from engaging in clinical decision-making. Conclusions: Unfair discrimination within the pre-hospital setting have an impact on the learning opportunities of EMC students. Such practice violates basic human rights and has the potential to negatively affect the clinical management of patients, thus it has the potential to violate patient’s rights. This study confirms the existence of discriminatory practices during WIL which is usually unreported. The lack of a structured approach to redress the discrimination causes a lack of inclusivity and unequal access to clinical education in a public clinical platform

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