Representing Autistic Masculinity: Hegemonic Gender Performances in Contemporary Autism Films

While longstanding notions of autism have conceptualized it as medicalized disability, recent scholarship has advanced theories of autism as cultural production; in other words, autism may be better understood as a synthesis of medical science, media portrayals, and societal attitudes rather than the product of any of these arenas individually. Academic inquiry into the intersection of autism and gender, though, remains largely underdeveloped. Work has been done theorizing how autistic people understand their gender but little exists regarding how cultural apparatuses actually produce it. My study, then, addresses this gap through examining media representations of autism, specifically autistic masculinity in contemporary popular film. I utilize R.W. Connell’s theory of hegemonic masculinity and Stuart Hall’s encoding/decoding model of communication to interrogate filmic representations of young adult autistic male characters in Mozart and the Whale (2005), Adam (2009), and My Name is Khan (2010), specifically noting the ways that their masculinity is represented. I expand on Conn and Bhugra’s (2012) examination of tropes used in “autism films” to discuss how these representations of autistic men also align with hegemonic gender norms. From this, I examine how the aforementioned films work to produce autism as a gendered identity. Additionally, I unearth how representations of autism are bound to dominant understandings of gender, and that media portrayals of autistic men are problematic beyond stereotyping disability. Implications on the future of studying depictions of autism in media will be discussed, as well as how such scholarship may be useful for actual autistic men to more effectively navigate the culture

A Rapid Method for Sequencing Double-Stranded RNAs Purified from Yeasts and the Identification of a Potent K1 Killer Toxin Isolated from Saccharomyces cerevisiae

Mycoviruses infect a large number of diverse fungal species, but considering their prevalence, relatively few high-quality genome sequences have been determined. Many mycoviruses have linear double-stranded RNA genomes, which makes it technically challenging to ascertain their nucleotide sequence using conventional sequencing methods. Different specialist methodologies have been developed for the extraction of double-stranded RNAs from fungi and the subsequent synthesis of cDNAs for cloning and sequencing. However, these methods are often labor-intensive, time-consuming, and can require several days to produce cDNAs from double-stranded RNAs. Here, we describe a comprehensive method for the rapid extraction and sequencing of dsRNAs derived from yeasts, using short-read next generation sequencing. This method optimizes the extraction of high-quality double-stranded RNAs from yeasts and 3′ polyadenylation for the initiation of cDNA synthesis for next-generation sequencing. We have used this method to determine the sequence of two mycoviruses and a double-stranded RNA satellite present within a single strain of the model yeast Saccharomyces cerevisiae. The quality and depth of coverage was sufficient to detect fixed and polymorphic mutations within viral populations extracted from a clonal yeast population. This method was also able to identify two fixed mutations within the alpha-domain of a variant K1 killer toxin encoded on a satellite double-stranded RNA. Relative to the canonical K1 toxin, these newly reported mutations increased the cytotoxicity of the K1 toxin against a specific species of yeast

Genome-wide association study meta-analysis provides insights into the etiology of heart failure and its subtypes

Heart failure (HF) is a major contributor to global morbidity and mortality. While distinct clinical subtypes, defined by etiology and left ventricular ejection fraction, are well recognized, their genetic determinants remain inadequately understood. In this study, we report a genome-wide association study of HF and its subtypes in a sample of 1.9 million individuals. A total of 153,174 individuals had HF, of whom 44,012 had a nonischemic etiology (ni-HF). A subset of patients with ni-HF were stratified based on left ventricular systolic function, where data were available, identifying 5,406 individuals with reduced ejection fraction and 3,841 with preserved ejection fraction. We identify 66 genetic loci associated with HF and its subtypes, 37 of which have not previously been reported. Using functionally informed gene prioritization methods, we predict effector genes for each identified locus, and map these to etiologic disease clusters through phenome-wide association analysis, network analysis and colocalization. Through heritability enrichment analysis, we highlight the role of extracardiac tissues in disease etiology. We then examine the differential associations of upstream risk factors with HF subtypes using Mendelian randomization. These findings extend our understanding of the mechanisms underlying HF etiology and may inform future approaches to prevention and treatment.</p