Non-traditional students as field outsiders: a case study of the institutional sub-field of an ‘elite’ university and its role in social reproduction

This thesis explores the perceptions and experiences of non-traditional students at a high-tariff, prestigious and so-called ‘elite’ university in the UK. The premise of this research is that universities that sit at the top of UK league tables constitute a distinct segment of the higher education field, characterised by a homogenous demographic intake of middle- class and advantaged students and the relative security it provides its graduates in accessing professional employment. Existing research indicates that there is a significant pool of qualified non-traditional students who opt to study elsewhere (Sutton Trust and HEFCE, 2004; Boliver, 2013), and government and institutional interventions primarily aim to change this through raising the aspirations of these students (Byrom, 2009). In response to these findings, this PhD research contributes to updating the evidence base through three novel approaches. Firstly, it moves beyond deficit approaches to the changes that universities themselves can make to become inclusive environments. To do so, it adopts a qualitative case study of one ‘elite’ HEI - Durham University - to explore the culture of a university holistically and the processes and practices that underpin it. Secondly, it employs an immersive research design - including a longitudinal interviews - with first year students who self-define as coming from a background where going to university was not common. This produces detailed insight into their prior perceptions of the university and their social experiences whilst at it – in relation to the institutional culture - at a level of detail unmatched by other studies. Thirdly, the research conceptualises the university as a “social field” (Bourdieu, 1966). My Bourdieusian analysis of data shows how students who may be seen to have “won” the “game” of the UK Higher Education field by entering an ‘elite’ institution, and who take up objectively similar positions to each other in the HE field once they do so, actually face very different experiences, opportunities and likely outcomes due to their social background, associated habitus and levels of capital. I find that the University draws on its historical position as a “field outsider” to position itself as “distinct” (Bourdieu, 1984) in today’s marketized HE field. Internally, the institutional field of the collegiate university is still structured around the habitus of the elite and “invented traditions” (Hosbawm and Ranger, 1983) are used to claim the legitimacy of this field structure. Initially, participants were attracted to these practices and saw them as markers of the institution’s high quality, which they sought in order to gain the symbolic capital of a Durham degree to become upwardly socially mobile. In reality, however, the internal social structure of the collegiate system requires a fitting habitus and extremely high levels of economic capital for participation, excluding those without. It is on these grounds that I make recommendations for change to make the social and cultural environment of this ‘elite’ university a more inclusive space

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