Leadership and the media: Gendered framings of Julia Gillard's ‘sexism and misogyny’ speech

This article analyses Australian media portrayals of former Australian Prime Minister Julia Gillard's ‘sexism and misogyny’ speech to parliament in October 2012. Our analysis reveals that coverage of the speech comprised three principal gendered framings: strategic attack, uncontrolled emotional outpouring and hypocrisy. We argue that these framings demonstrate the role the media plays as a gendered mediator, perpetuating the gender double bind that constrains female political leaders, as they negotiate the demand to demonstrate masculine leadership attributes without tarnishing the feminine qualities expected of them. In this instance, gendered media framings limited the saliency of Gillard's speech, curtailed calls for wider introspection on Australian political culture and further disassociated women from political leadership

Does European Union Studies have a Gender Problem? Experiences from Researching Brexit

On International Women’s Day 2017, EU Vice-President Frans Timmermans and High Representative Federica Mogherini claimed, “the European Union stands by women in Europe and around the globe today, as it did at the time of its foundation.” Indeed, (gender) equality has long been used as a foundational narrative of the EU (MacRae 2010). If we take these claims seriously, then gender-sensitive analysis should have a central place within EU studies. So, why do (gender) equality and the insights of feminist scholarship remain largely marginal to the EU studies canon? And how has the United Kingdom’s decision to exit the EU (Brexit) amplified this marginalization? By drawing on our experiences of researching and writing about the gendered impact of Brexit, we draw attention to significant blind spots at the heart of our discipline. This analysis ultimately highlights disparities in focus that reproduce disciplinary hierarchie

Equalities in Freefall? Ontological Insecurity and the long-term Impact of COVID-19 in the Academy

This intervention focuses on the impact of the global crisis resulting from the COVID‐19 pandemic on existing racialized and gendered inequalities within the academy and in particular our discipline of Politics and International Relations. We argue that responses to recent crises within the academy have exacerbated ontological insecurity among minoritized groups, including women. When coupled with increased caring responsibilities the current crises call into question who can be creative and innovative, necessary conditions for knowledge production. While University managers seek to reassure University staff of the temporary nature of COVID‐19 interventions, we argue that the possibilities for progressive leaps at a later state of institutional regeneration is unlikely when efforts to address structural inequalities are sidelined and crisis responses are undertaken which run counter to such work

Transforming CSDP? Feminist Triangles and Gender Regimes

Despite equality being considered one of the key normative foundations of the EU, gender has not yet been mainstreamed within the Common Security and Defence Policy (CSDP). This article investigates the impact of institutional structures on the inclusion of a gender dimension in this policy area. The article adopts Woodward’s (2003) model of feminist triangles to unpack the role of actors and processes; specifically, highlighting key innovations and missed opportunities to integrate gender into CSDP. Focusing in particular on femocrats, the article argues that for gender mainstreaming to take place, the office of the Gender Advisor needs to bridge the division between the military and civilian dimension of CSDP. It concludes that CSDP remains largely gender blind in spite of the EU’s adoption of an action plan for the implementation of UN Security Council Resolution 1325 on Women, Peace and Security

Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes

OBJECTIVE - Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired b-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS - We have conducted a meta-analysis of genome-wide association tests of ;2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS - Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10-8). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/ C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 3 10-4), improved b-cell function (P = 1.1 × 10-5), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10-6). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS - We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis

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