John Piper's Modernist Scenography

The file attached to this record is the author's final peer reviewed version. The Publisher's final version can be found by following the DOI link.As one of the pre-eminent British painters of the twentieth century, John Piper secured his legacy with his depictions of swirling seas, grand country houses, and secluded churches. However his contribution to the theatre is less well known. This paper aims to address this lacuna, focusing on his scenographic contribution to two modernist performances: Stephen Spender’s Trial of a Judge (1938) and Edith Sitwell’s Façade (1942). I aim to present Piper as a vital force in a British avant-garde theatre scene and to reimagine his canon of work as inherently theatrical. This theatrical element unites his diverse oeuvre, from his most abstract geometric collages to his most quintessentially English landscapes. This paper resurrects two often overlooked performances, and sheds new light on the cross-disciplinary nature of British modernist art and the importance of theatrical motifs for a thorough understanding of Piper’s work

“A Glimpse of ‘Another Russia’”: Elisaveta Fen's Chekhov translations

“A Glimpse of ‘Another Russia’”: Elisaveta Fen's Chekhov translation

“Just Look At His Vascularity:” The Dangerous Theatricality of the World Bodybuilding Federation

“Just look at his vascularity:” the dangerous theatricality of the World Bodybuilding Federatio

When was the Last Time that You Heard of Ian McKellen Blowing out His Knee? The Performance and Practice of Risk in British Professional Wrestling

Professional wrestling has a poor record of caring for athlete-artists’ health and wellbeing. The data gathered through the Health and Wellbeing in Professional Wrestling project aims to confront this issue. During the data collection process, we noted that interviewees’ reflections shifted the meaning of terms and ideas associated with wrestling but, until now, not fully understood. One such concept is risk. Wrestling has been criticised for being too risky by parents’ groups and teachers, and not risky enough by those who dismiss it as fake and phony. This article recognises that such miscomprehensions of wrestling risk have broader implications: an absence of suitable medical support, a lack of appreciation for its artistry, performing dangerous moves without professional training, and more. In order to comprehend wrestling risk in this deeper sense, this article reads it through the notion of edgework. Wrestling enables a reimagining of edgework more generally through the real-not-real spectrum, and as collaborative rather than competitive endeavor. There are broader implications here, then: a study of wrestling provides a model for comprehending the health and wellbeing benefits and challenges of contemporary risk. Finally, the article asks what difference this more nuanced and multifaceted version of risk makes to future innovations in wrestling health and wellbeing

Scholarly grappling:Collaborative 'work' in the study of professional wrestling

In 2016 Benjamin Litherland, Tom Phillips, and Claire Warden began a research collaboration centered on a shared interest in professional wrestling. All three of us have made contributions to the burgeoning field of professional wrestling studies, and we approach wrestling from different but intersecting disciplinary backgrounds—cultural studies, media studies, and performance studies, respectively. Through our collaboration, we have found new ways of crossing disciplinary borders and new lexicons with which to discuss this hybrid “sporting entertainment.

ABCA7 p.G215S as potential protective factor for Alzheimer’s disease

Genome-wide association studies (GWASs) have been effective approaches to dissect common genetic variability underlying complex diseases in a systematic and unbiased way. Recently, GWASs have led to the discovery of over 20 susceptibility loci for Alzheimer’s disease (AD). Despite the evidence showing the contribution of these loci to AD pathogenesis, their genetic architecture has not been extensively investigated, leaving the possibility that low frequency and rare coding variants may also occur and contribute to the risk of disease. We have used exome and genome sequencing data to analyse the single independent and joint effect of rare and low frequency protein coding variants in 9 AD GWAS loci with the strongest effect sizes after APOE (BIN1, CLU, CR1, PICALM, MS4A6A, ABCA7, EPHA1, CD33, CD2AP) in a cohort of 332 sporadic AD cases and 676 elderly controls of British and North American ancestry. We identified coding variability in ABCA7 as contributing to AD risk. This locus harbors a low frequency coding variant (p.G215S, rs72973581, MAF=4.3%) conferring a modest but statistically significant protection against AD (p-value= 6x10-4, OR=0.57, 95% CI 0.41-0.80). Notably, our results are not driven by an enrichment of loss of function variants in ABCA7, recently reported as main pathogenic factor underlying AD risk at this locus. In summary, our study confirms the role of ABCA7 in AD and provide new insights that should address functional studies

Mendelian adult-onset leukodystrophy genes in Alzheimer's disease:critical influence of CSF1R and NOTCH3

Mendelian adult-onset leukodystrophies are a spectrum of rare inherited progressive neurodegenerative disorders affecting the white matter of the central nervous system. Among these, cerebral autosomal dominant and recessive arteriopathy with subcortical infarcts and leukoencephalopathy, cerebroretinal vasculopathy, metachromatic leukodystrophy, hereditary diffuse leukoencephalopathy with spheroids, and vanishing white matter disease present with rapidly progressive dementia as dominant feature and are caused by mutations in NOTCH3, HTRA1, TREX1, ARSA, CSF1R, EIF2B1, EIF2B2, EIF2B3, EIF2B4, and EIF2B5, respectively. Given the rare incidence of these disorders and the lack of unequivocally diagnostic features, leukodystrophies are frequently misdiagnosed with common sporadic dementing diseases such as Alzheimer's disease (AD), raising the question of whether these overlapping phenotypes may be explained by shared genetic risk factors. To investigate this intriguing hypothesis, we have combined gene expression analysis (1) in 6 different AD mouse strains (APPPS1, HOTASTPM, HETASTPM, TPM, TAS10, and TAU) at 5 different developmental stages (embryo [E15], 2, 4, 8, and 18 months), (2) in APPPS1 primary cortical neurons under stress conditions (oxygen-glucose deprivation) and single-variant–based and single-gene–based (c-alpha test and sequence kernel association test (SKAT)) genetic screening in a cohort composed of 332 Caucasian late-onset AD patients and 676 Caucasian elderly controls. Csf1r was significantly overexpressed (log2FC &gt; 1, adj. p-value &lt; 0.05) in the cortex and hippocampus of aged HOTASTPM mice with extensive Aβ dense-core plaque pathology. We identified 3 likely pathogenic mutations in CSF1R TK domain (p.L868R, p.Q691H, and p.H703Y) in our discovery and validation cohort, composed of 465 AD and mild cognitive impairment (MCI) Caucasian patients from the United Kingdom. Moreover, NOTCH3 was a significant hit in the c-alpha test (adj p-value = 0.01). Adult-onset Mendelian leukodystrophy genes are not common factors implicated in AD. Nevertheless, our study suggests a potential pathogenic link between NOTCH3, CSF1R, and sporadic late-onset AD, which warrants further investigation.</p