War Worlds: Violence, Sociality, and the Forms of Twentieth-Century Transatlantic Literature

“War Worlds” reads twentieth-century British and Anglophone literature to examine the social practices of marginal groups (pacifists, strangers, traitors, anticolonial rebels, queer soldiers) during the world wars. This dissertation shows that these diverse “enemies within” England and its colonies—those often deemed expendable for, but nonetheless threatening to, British state and imperial projects—provided writers with alternative visions of collective life in periods of escalated violence and social control. By focusing on the social and political activities of those who were not loyal citizens or productive laborers within the British Empire, “War Worlds” foregrounds the small group, a form of collectivity frequently portrayed in the literature of the war years but typically overlooked in literary critical studies. I argue that this shift of focus from grand politics to small groups not only illuminates surprising social fissures within England and its colonies but provides a new vantage from which to view twentieth-century experiments in literary form.

Hippocampal Transcriptomic and Proteomic Alterations in the BTBR Mouse Model of Autism Spectrum Disorder.

Autism spectrum disorders (ASD) are complex heterogeneous neurodevelopmental disorders of an unclear etiology, and no cure currently exists. Prior studies have demonstrated that the black and tan, brachyury (BTBR) T+ Itpr3tf/J mouse strain displays a behavioral phenotype with ASD-like features. BTBR T+ Itpr3tf/J mice (referred to simply as BTBR) display deficits in social functioning, lack of communication ability, and engagement in stereotyped behavior. Despite extensive behavioral phenotypic characterization, little is known about the genes and proteins responsible for the presentation of the ASD-like phenotype in the BTBR mouse model. In this study, we employed bioinformatics techniques to gain a wide-scale understanding of the transcriptomic and proteomic changes associated with the ASD-like phenotype in BTBR mice. We found a number of genes and proteins to be significantly altered in BTBR mice compared to C57BL/6J (B6) control mice controls such as BDNF, Shank3, and ERK1, which are highly relevant to prior investigations of ASD. Furthermore, we identified distinct functional pathways altered in BTBR mice compared to B6 controls that have been previously shown to be altered in both mouse models of ASD, some human clinical populations, and have been suggested as a possible etiological mechanism of ASD, including "axon guidance" and "regulation of actin cytoskeleton." In addition, our wide-scale bioinformatics approach also discovered several previously unidentified genes and proteins associated with the ASD phenotype in BTBR mice, such as Caskin1, suggesting that bioinformatics could be an avenue by which novel therapeutic targets for ASD are uncovered. As a result, we believe that informed use of synergistic bioinformatics applications represents an invaluable tool for elucidating the etiology of complex disorders like ASD.