Circles, columns and screenings: mapping the institutional, discursive, physical and gendered spaces of film criticism in 1940s London

This article revisits the period considered within ‘The Quality Film Adventure: British Critics and the Cinema 1942-1948’, mapping the professional cultures, working contexts and industry relationships that underpinned the aesthetic judgements and collective directions which John Ellis has observed within the critics published writings. Drawing on the records of the Critics’ Circle, Dilys Powell’s papers and Kinematograph Weekly, it explores the evolution of increasingly organised professional cultures of film criticism and film publicity, arguing that the material conditions imposed by war caused tensions between them to escalate. In the context of two major challenges to critical integrity and practice – the evidence given by British producer R.J. Minney in front of the 1948 Royal Commission on the Press and an ongoing libel case between a BBC critic and MGM – the different spaces of hospitality and film promotion became highly contested sites. This article focuses on the ways in which these spaces were characterised, used, and policed. It finds that the value and purpose of press screenings were hotly disputed and observes the way the advancement of women within one sector (film criticism) but not the other (film publicity) created particular difficulties, as key female critics avoided the more compromised masculine spaces of publicity, making them harder for publicists to reach and fuelling trade resentment. More broadly, the article asserts the need to consider film critics as geographically and culturally located audiences, who experience films as ‘professional’ viewers within extended and embodied cultures of habitual professional practice and physical space

Prevalence of Hepatitis E Virus Infection in Pigs at the Time of Slaughter, United Kingdom, 2013

Since 2010, reports of infection with hepatitis E virus (HEV) have increased in England and Wales. Despite mounting evidence regarding the zoonotic potential of porcine HEV, there are limited data on its prevalence in pigs in the United Kingdom. We investigated antibody prevalence, active infection, and virus variation in serum and cecal content samples from 629 pigs at slaughter. Prevalence of antibodies to HEV was 92.8% (584/629), and HEV RNA was detected in 15% of cecal contents (93/629), 3% of plasma samples (22/629), and 2% of both (14/629). However, although HEV is prevalent in pigs in the United Kingdom and viremic pigs are entering the food chain, most (22/23) viral sequences clustered separately from the dominant type seen in humans. Thus, pigs raised in the United Kingdom are unlikely to be the main source of human HEV infections in the United Kingdom. Further research is needed to identify the source of these infections

De Novo Variants in CNOT1, a Central Component of the CCR4-NOT Complex Involved in Gene Expression and RNA and Protein Stability, Cause Neurodevelopmental Delay.

CNOT1 is a member of the CCR4-NOT complex, which is a master regulator, orchestrating gene expression, RNA deadenylation, and protein ubiquitination. We report on 39 individuals with heterozygous de novo CNOT1 variants, including missense, splice site, and nonsense variants, who present with a clinical spectrum of intellectual disability, motor delay, speech delay, seizures, hypotonia, and behavioral problems. To link CNOT1 dysfunction to the neurodevelopmental phenotype observed, we generated variant-specific Drosophila models, which showed learning and memory defects upon CNOT1 knockdown. Introduction of human wild-type CNOT1 was able to rescue this phenotype, whereas mutants could not or only partially, supporting our hypothesis that CNOT1 impairment results in neurodevelopmental delay. Furthermore, the genetic interaction with autism-spectrum genes, such as ASH1L, DYRK1A, MED13, and SHANK3, was impaired in our Drosophila models. Molecular characterization of CNOT1 variants revealed normal CNOT1 expression levels, with both mutant and wild-type alleles expressed at similar levels. Analysis of protein-protein interactions with other members indicated that the CCR4-NOT complex remained intact. An integrated omics approach of patient-derived genomics and transcriptomics data suggested only minimal effects on endonucleolytic nonsense-mediated mRNA decay components, suggesting that de novo CNOT1 variants are likely haploinsufficient hypomorph or neomorph, rather than dominant negative. In summary, we provide strong evidence that de novo CNOT1 variants cause neurodevelopmental delay with a wide range of additional co-morbidities. Whereas the underlying pathophysiological mechanism warrants further analysis, our data demonstrate an essential and central role of the CCR4-NOT complex in human brain development