Sex Segregation and Salary Structure in Academia

This article reports a study of aggregate unit salary levels, within a major research university. We analyze these salary levels, as they are influenced by unit sex composition, and modified by unit attainment levels—where unit refers to the departments, colleges and schools, and other academic divisions of the university. We investigate three central issues of sex and salary, previously overlooked in salary studies of academic employees: Do high proportions of women depress men's unit salary levels ("competition" hypothesis)? Are women's salary levels higher in male-dominated, and lower in female-dominated, units ("concentration" hypothesis)? Are men salary-compensated for working with women ("compensation" hypothesis)? The findings support none of these hypotheses. Rather, the relationship between unit sex composition and salary rests upon the connection between units' composition and attainment levels.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/69126/2/10.1177_073088848100800103.pd

Transnational academic mobility and gender

This is an Accepted Manuscript of an article published by Taylor & Francis in Globalisation, Societies and Education on 24 June 2011, available online: http://wwww.tandfonline.com/10.1080/14767724.2011.577199This paper examines to what extent the participation of researchers in transnational academic mobility, their experiences and perceived outcomes vary by gender. Based on longitudinal statistics, original survey data and semi-structured interviews with former visiting researchers in Germany, the paper shows that the academic world of female researchers tends to be less international than that of their male colleagues, particularly in the natural sciences. This situation has improved since the 1980s but significant variations remain by source country, subject, career stage and length of stay. The paper argues that the underlying reasons go far beyond direct gender relationships and suggests that conceptualising transnational academic mobility as an integral part of mobilisation processes in Latourian 'centres of calculation' underlines the need for making this experience accessible to the widest possible range of researchers. © 2011 Taylor & Francis

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 hospitalization2,3,4 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