So, where is queer? A critical geography of queer exhibitions in Australia

This paper interrogates the geography of queer exhibitions in museums and galleries in Australia. The analysis draws on data from Museums Australia\u27s database of queer exhibitions (1982-2005), which are cross-tabulated with geographical variables such as location, scale and state/territory population. The findings show an uneven geographical distribution of exhibitions, how geography also frames the themes of queer exhibitions, and an imbalanced geography, in which regional histories are few, national and state scale histories are prevalent, and minimal exhibitions occur outside metropolitan areas. This is problematic because queer identities, communities and histories vary across scales and between places. Appreciation of geography is thus useful for developing policies and practices that ensure the diversity of queer communities and histories is represented and communicated in exhibitions

Rural Cultural Studies: Introduction

This themed section of Australian Humanities Review seeks to establish the emerging field of \u27rural cultural studies\u27 firmly on the agenda of the contemporary humanities and social sciences. This is a timely intervention as rural Australia has featured increasingly over the last decade and especially over the last few years as a topic of national policy attention, public commentary and social analysis. If the notion of a crisis in rural Australia has become something of a one-sided cliché, the changes being faced in non-urban-rural, remote and regional-Australia are nonetheless significant, complex and widespread. For example, one of the topics for the federal 2020 Summit, \u27Rural Australia\u27, addressed future policy directions for rural industries and populations. In this wider context, the purpose of the present collection of papers is to argue for the significance of the cultural dimension-and the multiple dimensions of the cultural-in understanding the key issues of demographic change, economic productivity, environmental and climatic crisis, Indigenous/non-indigenous relations and land ownership, and the role of \u27cultural\u27 factors in the renewal, or potential renewal, of country towns and communities

Mapping same-sex couple family households in Australia

The map (1:1,218,987) accompanying this report is the first to depict the distribution of same-sex couple family households across Australia. The map and the report contribute to emerging scholarship combining critical geographies of sexualities with quantitative techniques and GIS in order to advance the political claims of sexual minorities. The data were collected through the 2006 Census and obtained via consultation with the Australian Bureau of Statistics. These data included the number of same-sex couple family households for all Statistical Divisions across Australia and for Statistical Sub-Divisions within metropolitan capital cities. Geographical concentrations of same-sex couple family households were determined by calculating the proportion of couple family households that were same-sex in each Statistical Division and Statistical Sub-Division, since the Census defines same-sex couples as a subset of couple family households. To visualise where the proportions fell above and below the national average, and thus where concentrations were found, these ratios were converted to location quotients using the Australian average as the denominator. The map combines different scales – Statistical Divisions and Statistical Sub-Divisions – to illustrate distributional patterns between inner-city and suburban areas, as well as between urban and regional localities, across Australia. While high concentrations are found in inner-cities, there are also significant suburban and regional concentrations, thus contesting assumptions about same-sex couples’ inner-city residential choices. Moreover, since same-sex couples were found in most Statistical Divisions, those areas below the national average cannot be considered devoid of these families, with implications for the effective operationalisation of equal rights legislation

Mapping same-sex couple family households in Australia

The map (1:1,218,987) accompanying this report is the first to depict the distribution of same-sex couple family households across Australia. The map and the report contribute to emerging scholarship combining critical geographies of sexualities with quantitative techniques and GIS in order to advance the political claims of sexual minorities. The data were collected through the 2006 Census and obtained via consultation with the Australian Bureau of Statistics. These data included the number of same-sex couple family households for all Statistical Divisions across Australia and for Statistical Sub-Divisions within metropolitan capital cities. Geographical concentrations of same-sex couple family households were determined by calculating the proportion of couple family households that were same-sex in each Statistical Division and Statistical Sub-Division, since the Census defines same-sex couples as a subset of couple family households. To visualise where the proportions fell above and below the national average, and thus where concentrations were found, these ratios were converted to location quotients using the Australian average as the denominator. The map combines different scales – Statistical Divisions and Statistical Sub-Divisions – to illustrate distributional patterns between inner-city and suburban areas, as well as between urban and regional localities, across Australia. While high concentrations are found in inner-cities, there are also significant suburban and regional concentrations, thus contesting assumptions about same-sex couples’ inner-city residential choices. Moreover, since same-sex couples were found in most Statistical Divisions, those areas below the national average cannot be considered devoid of these families, with implications for the effective operationalisation of equal rights legislation

A recurrent mitochondrial p.Trp22Arg NDUFB3 variant causes a distinctive facial appearance, short stature and a mild biochemical and clinical phenotype

Background Isolated Complex I deficiency is the most common paediatric mitochondrial disease presentation, associated with poor prognosis and high mortality. Complex I comprises 44 structural subunits with at least 10 ancillary proteins; mutations in 29 of these have so far been associated with mitochondrial disease but there are limited genotype-phenotype correlations to guide clinicians to the correct genetic diagnosis. Methods Patients were analysed by whole-exome sequencing, targeted capture or candidate gene sequencing. Clinical phenotyping of affected individuals was performed. Results We identified a cohort of 10 patients from 8 families (7 families are of unrelated Irish ancestry) all of whom have short stature (C, p.Trp22Arg NDUFB3 variant. Two sibs presented with primary short stature without obvious metabolic dysfunction. Analysis of skeletal muscle from three patients confirmed a defect in Complex I assembly. Conclusions Our report highlights that the long-term prognosis related to the p.Trp22Arg NDUFB3 mutation can be good, even for some patients presenting in acute metabolic crisis with evidence of an isolated Complex I deficiency in muscle. Recognition of the distinctive facial features—particularly when associated with markers of mitochondrial dysfunction and/or Irish ancestry—should suggest screening for the p.Trp22Arg NDUFB3 mutation to establish a genetic diagnosis, circumventing the requirement of muscle biopsy to direct genetic investigations

Introduction: Toward an Engaged Feminist Heritage Praxis

We advocate a feminist approach to archaeological heritage work in order to transform heritage practice and the production of archaeological knowledge. We use an engaged feminist standpoint and situate intersubjectivity and intersectionality as critical components of this practice. An engaged feminist approach to heritage work allows the discipline to consider women’s, men’s, and gender non-conforming persons’ positions in the field, to reveal their contributions, to develop critical pedagogical approaches, and to rethink forms of representation. Throughout, we emphasize the intellectual labor of women of color, queer and gender non-conforming persons, and early white feminists in archaeology

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.

Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice