Popular imperialism, Scottish identity, and William Wallace in an Australian colonial city

The narrative of William Wallace holds a prominent position in the current conception of England as a negative referent for Scotland’s national identity—its binary “Other”, against which Wallace valiantly fought. This article considers a contrasting understanding of Scottish national identity from the late-nineteenth century, and explores the events surrounding the unveiling of a statue of William Wallace in Australia during the year of 1889. It illuminates how settlers interpreted this national hero in such a way that demonstrated loyalty to the Union and Empire, and accommodated a convergence of English, Scottish, Irish, and Welsh migrants in a British colonial city. The article highlights how statues, the ceremonies surrounding them, and their public reception help us to investigate the symbolic, ritualistic, and performative dimensions of identity formulation. It considers how public monuments, providing a sense of authority to particular groups, can marginalise others by acting to settle cultural competition, and will reflect on competing interpretations of the statue at its unveiling.

DNA methylation and the social gradient of osteoporotic fracture: a conceptual model

INTRODUCTION: Although there is a documented social gradient for osteoporosis, the underlying mechanism(s) for that gradient remain unknown. We propose a conceptual model based upon the allostatic load theory, to suggest how DNA methylation (DNAm) might underpin the social gradient in osteoporosis and fracture. We hypothesise that social disadvantage is associated with priming of inflammatory pathways mediated by epigenetic modification that leads to an enhanced state of inflammatory reactivity and oxidative stress, and thus places socially disadvantaged individuals at greater risk of osteoporotic fracture. METHODS/RESULTS: Based on a review of the literature, we present a conceptual model in which social disadvantage increases stress throughout the lifespan, and engenders a proinflammatory epigenetic signature, leading to a heightened inflammatory state that increases risk for osteoporotic fracture in disadvantaged groups that are chronically stressed. CONCLUSIONS: Our model proposes that, in addition to the direct biological effects exerted on bone by factors such as physical activity and nutrition, the recognised socially patterned risk factors for osteoporosis also act via epigenetic-mediated dysregulation of inflammation. DNAm is a dynamic modulator of gene expression with considerable relevance to the field of osteoporosis. Elucidating the extent to which this epigenetic mechanism transduces the psycho-social environment to increase the risk of osteoporotic fracture may yield novel entry points for intervention that can be used to reduce individual and population-wide risks for osteoporotic fracture. Specifically, an epigenetic evidence-base may strengthen the importance of lifestyle modification and stress reduction programs, and help to reduce health inequities across social groups. MINI ABSTRACT: Our conceptual model proposes how DNA methylation might underpin the social gradient in osteoporotic fracture. We suggest that social disadvantage is associated with priming of inflammatory signalling pathways, which is mediated by epigenetic modifications, leading to a chronically heightened inflammatory state that places disadvantaged individuals at greater risk of osteoporosis.