Transcultural satire in German fiction of Turkish migration: Self-deprecation, ethnic impersonation, intertexuality

My dissertation presents a study of satire in contemporary German Fiction of Turkish migration. Engaging with a body of works hitherto neglected in scholarship, I examine how satirical texts, films, and plays intervene critically in discourses on post-unification German national identity. Drawing on the seminal work of scholars such as Leslie Adelson, Tom Cheesman, B. Venkat Mani, Petra Fachinger, and Deniz Göktürk, my dissertation expands the scholarship of Turkish German Studies by linking a discussion of satire as a critical rhetoric to the question of how we talk about what it means to be German.

Chapter one offers a novel framework of the satirical vis-à-vis standard conceptions of satire and deconstructionist theories of reading. I understand satire as a form of rhetoric that creates moments of ambiguity by bringing together intersectional categories like gender, ethnicity, race, religion, in order to challenge the audience’s practices of interpreting cultural otherness. Chapter two examines the use of ethnic self-deprecation as one such strategy in Osman Engin’s short stories and his first novel, Kanaken-Ghandi through the lens of Bakhtinian polyphony and Judith Butler’s work on hate speech. Engin, I argue, employs ethnic selfdeprecation as a narrative strategy to straddle the line between deconstructing and re-affirming cultural stereotypes. Investigating the role of ethnic impersonation in Hussi Kutlucan’s film Ich Chef, Du Turnshuh, the third chapter turns to the question of ethnicity as a visual signifier for the negotiation of cultural inclusion and exclusion in post-1990 film. In dialogue with Katrin Sieg’s work on ethnic drag and Amy Robinson’s theory of passing, I show how the film challenges ethnically-coded narratives of Germanness. In the final chapter on Nurkan Erpulat and Jens Hillje’s play Verrücktes Blut, I discuss how intertextuality and adaptation (Hutcheon, Genette) of different story and character worlds are used to create moments of ambiguity and overdeterminacy in the play, in order to challenge the audience’s perception of what an inclusive German society might look like.

Socialization of Early Prosocial Behavior: Parents' Talk about Emotions is Associated with Sharing and Helping in Toddlers.

What role does socialization play in the origins of prosocial behavior? We examined one potential socialization mechanism, parents' discourse about others' emotions with very young children in whom prosocial behavior is still nascent. Two studies are reported, one of sharing in 18- and 24-month-olds (n = 29), and one of instrumental and empathy-based helping in 18- and 30-month-olds (n = 62). In both studies, parents read age-appropriate picture books to their children and the content and structure of their emotion-related and internal state discourse were coded. Results showed that children who helped and shared more quickly and more often, especially in tasks that required more complex emotion understanding, had parents who more often asked them to label and explain the emotions depicted in the books. Moreover, it was parents' elicitation of children's talk about emotions rather than parents' own production of emotion labels and explanations that explained children's prosocial behavior, even after controlling for age. Thus, it is the quality, not the quantity, of parents' talk about emotions with their toddlers that matters for early prosocial behavior.

UVB radiation generates sunburn pain and affects skin by activating epidermal TRPV4 ion channels and triggering endothelin-1 signaling.

At our body surface, the epidermis absorbs UV radiation. UV overexposure leads to sunburn with tissue injury and pain. To understand how, we focus on TRPV4, a nonselective cation channel highly expressed in epithelial skin cells and known to function in sensory transduction, a property shared with other transient receptor potential channels. We show that following UVB exposure mice with induced Trpv4 deletions, specifically in keratinocytes, are less sensitive to noxious thermal and mechanical stimuli than control animals. Exploring the mechanism, we find that epidermal TRPV4 orchestrates UVB-evoked skin tissue damage and increased expression of the proalgesic/algogenic mediator endothelin-1. In culture, UVB causes a direct, TRPV4-dependent Ca(2+) response in keratinocytes. In mice, topical treatment with a TRPV4-selective inhibitor decreases UVB-evoked pain behavior, epidermal tissue damage, and endothelin-1 expression. In humans, sunburn enhances epidermal expression of TRPV4 and endothelin-1, underscoring the potential of keratinocyte-derived TRPV4 as a therapeutic target for UVB-induced sunburn, in particular pain.