ORCID Profile
0000-0002-4956-5235
Current Organisation
University of Melbourne
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Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Oxford University Press
Date: 13-06-2019
DOI: 10.1093/OXFORDHB/9780199860067.013.41
Abstract: This chapter examines the state of the field of Charles Brockden Brown studies since 2000. Taking a thematic approach, I discuss four dominant strands in twenty-first-century criticism: geographies, medical humanities, economies, and aesthetics. These sections cover the scholarly debate over a transnational, imperial, or postcolonial Brown consider the new ways in which early national medicine intersects with his fiction chart the rise of market and class-based criticism and discuss a return to formal concerns in light of the aesthetic or postcritique turn. The final section of this chapter looks ahead to emergent trends in future Brown scholarship in response to the previous decade’s work.
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Project MUSE
Date: 2017
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Wiley
Date: 12-08-2022
Publisher: Oxford University Press (OUP)
Date: 12-2022
Abstract: This article argues for implementing a Critical Whiteness studies approach to canonical White literature. After providing an overview of Critical Whiteness studies, I discuss ex les from teaching nineteenth-century American literature where Critical Whiteness approaches are fruitful. Alongside widening the selection of what we teach in English departments, incorporating Critical Whiteness studies as part of decolonizing the curriculum reorients how we teach canonical White literature that remains on our syllabi and supports students to recognize continuing discourses of White supremacy today.
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 31-12-2022
Publisher: Cambridge University Press (CUP)
Date: 18-09-2020
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Cambridge University Press (CUP)
Date: 29-10-2015
Publisher: The Pennsylvania State University Press
Date: 05-2022
DOI: 10.5325/NATHHAWTREVI.48.1.0050
Abstract: This article considers the authority and social currency given to rumor and viral news in Hawthorne’s “Mr Higginbotham’s Catastrophe.” As previous critics have noted, Hawthorne ridicules the sensational antebellum press that peddles fabricated racial conspiracy for profit. Telling and retelling Higginbotham’s sensational “murder” at the hands of an Irishman and an “Ethiopian,” peddler Dominicus Pike’s oral tale exploits racial and class stereotype to garner attention and sales. I argue that Pike’s identity depends on the ongoing transmission of his “respectable narrative.” The creation and control of a narrative is central to Pike’s idea of a respectable self and desires for cultural capital and social mobility that depend on his story of race and class upheaval being believed, even in the face of compelling competing testimony. Mutating from gossip, to oral story, to print media, Pike’s viral load increases at each occasion until his sense of identity and self-making hinges on Higginbotham’s unmaking, the specter of which haunts him as texts progresses. Hawthorne’s comic short story is a potent reminder of how the in idual’s identity is bolstered by—yet also dependent on—the satisfying narratives of rumor and conspiracy.
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Project MUSE
Date: 09-2021
Publisher: Cambridge University Press (CUP)
Date: 12-07-2017
Publisher: Oxford University Press (OUP)
Date: 13-06-2022
Abstract: Brain voltage-gated sodium channel NaV1.1 (SCN1A) loss-of-function variants cause the severe epilepsy Dravet syndrome, as well as milder phenotypes associated with genetic epilepsy with febrile seizures plus. Gain of function SCN1A variants are associated with familial hemiplegic migraine type 3. Novel SCN1A-related phenotypes have been described including early infantile developmental and epileptic encephalopathy with movement disorder, and more recently neonatal presentations with arthrogryposis. Here we describe the clinical, genetic and functional evaluation of affected in iduals. Thirty-five patients were ascertained via an international collaborative network using a structured clinical questionnaire and from the literature. We performed whole-cell voltage-cl electrophysiological recordings comparing sodium channels containing wild-type versus variant NaV1.1 subunits. Findings were related to Dravet syndrome and familial hemiplegic migraine type 3 variants. We identified three distinct clinical presentations differing by age at onset and presence of arthrogryposis and/or movement disorder. The most severely affected infants (n = 13) presented with congenital arthrogryposis, neonatal onset epilepsy in the first 3 days of life, tonic seizures and apnoeas, accompanied by a significant movement disorder and profound intellectual disability. Twenty-one patients presented later, between 2 weeks and 3 months of age, with a severe early infantile developmental and epileptic encephalopathy and a movement disorder. One patient presented after 3 months with developmental and epileptic encephalopathy only. Associated SCN1A variants cluster in regions of channel inactivation associated with gain of function, different to Dravet syndrome variants (odds ratio = 17.8 confidence interval = 5.4–69.3 P = 1.3 × 10−7). Functional studies of both epilepsy and familial hemiplegic migraine type 3 variants reveal alterations of gating properties in keeping with neuronal hyperexcitability. While epilepsy variants result in a moderate increase in action current litude consistent with mild gain of function, familial hemiplegic migraine type 3 variants induce a larger effect on gating properties, in particular the increase of persistent current, resulting in a large increase of action current litude, consistent with stronger gain of function. Clinically, 13 out of 16 (81%) gain of function variants were associated with a reduction in seizures in response to sodium channel blocker treatment (carbamazepine, oxcarbazepine, phenytoin, lamotrigine or lacosamide) without evidence of symptom exacerbation. Our study expands the spectrum of gain of function SCN1A-related epilepsy phenotypes, defines key clinical features, provides novel insights into the underlying disease mechanisms between SCN1A-related epilepsy and familial hemiplegic migraine type 3, and identifies sodium channel blockers as potentially efficacious therapies. Gain of function disease should be considered in early onset epilepsies with a pathogenic SCN1A variant and non-Dravet syndrome phenotype.
Publisher: Edinburgh University Press
Date: 21-05-2021
Publisher: Edinburgh University Press
Date: 21-05-2021
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Hannah Lauren Murray.