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Rape Culture is complicated; it’s about as much as what is not said and imagined as it is about what is said. It thrives in the silence–the silence of survivors, the silence of people denying its existence, and the silence of people who don’t know how to handle this sensitive topic. It is imagined in what is said; the pervasive behavior of victim blaming, slut-shaming, sexual objectification, or trivializing rape. Each engagement continues to normalize our societal attitudes about gender and sexuality, and Art History is complicit in that normalization. We continue to reproduce rape images through movements like the Renaissance, Rococo, Baroque, Modern, and Contemporary art, which in turns pushes survivors into isolation or risk silencing them forever. This thesis will navigate three women artists, Diane Arbus, Adrian Piper, and Ana Mendieta, to analyze how rape has affected the work of each of these artists. Most importantly, to demonstrate how engrained rape culture is in our society, and how representing images of rape accurately can start a necessary dialogue to combatting rape culture. Diane Arbus was sexually assaulted from the time she was a young child until a few weeks before she committed suicide, Adrian Piper’s work deals with the objectification of violence against White women, and Ana Mendieta depicts explicitly violent rape images. Each artist was silenced in their own way, and I hope to alleviate that silence through this paper; to undermine Art History’s contribution to rape culture and think critically of the depiction of rape. I will argue that images of rape deserve a place in Art History, considering that Art should reflect the world, but it must be done sensitively and accurately. No more objectification or trivializing rape through images–rather, holding Art History accountable for our current state of rape culture, and how we should rectify the wrongdoings of the past.

Equine Cushing's Disease (Pituitary pars intermedia dysfunction (PPID)) is a common condition of older horses but its pathophysiology is complex and poorly understood. In contrast to pituitary-dependent hyperadrenocorticism in other species, PPID is characterised by elevated plasma ACTH but not elevated plasma cortisol. In this study, we address this paradox and the hypothesis that PPID is a syndrome of ACTH excess in which there is dysregulation of peripheral glucocorticoid metabolism and binding. In 14 PPID horses compared with 15 healthy controls, we show that: in plasma, cortisol levels and cortisol binding to CBG were not different; in urine, glucocorticoid and androgen metabolites were increased up to four-fold; in liver, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) expression was reduced; in peri-renal adipose tissue 11β-HSD1 and carbonyl reductase 1 expression was increased; and tissue cortisol levels were not measurably different. The combination of normal plasma cortisol with markedly enhanced urinary cortisol metabolite excretion and dysregulated tissue-specific steroid-metabolising enzymes suggests that cortisol clearance is increased in PPID horses. We infer that the ACTH excess may be compensatory and pituitary pathology and autonomous secretion may be a secondary rather than primary pathology. It is possible, that successful therapy in PPID may be targeted either at lowering ACTH or, paradoxically, at reducing cortisol clearance.