The polaroid image as photo-object

This article is part of a larger project on the cultural history of Polaroid photography and draws on research done at the Polaroid Corporate archive at Harvard and at the Polaroid company itself. It identifies two cultural practices engendered by Polaroid photography, which, at the point of its extinction, has briefly flared into visibility again. It argues that these practices are mistaken as novel but are in fact rediscoveries of practices that stretch back as many as five decades. The first section identifies Polaroid image-making as a photographic equivalent of what Tom Gunning calls the ‘cinema of attractions’. That is, the emphasis in its use is on the display of photographic technologies rather than the resultant image. Equally, the common practice, in both fine art and vernacular circles, of making composite pictures with Polaroid prints, draws attention from image content and redirects it to the photo as object

Ignore This Title and HackAPrompt: Exposing Systemic Vulnerabilities of LLMs through a Global Scale Prompt Hacking Competition

Large Language Models (LLMs) are deployed in interactive contexts with direct user engagement, such as chatbots and writing assistants. These deployments are vulnerable to prompt injection and jailbreaking (collectively, prompt hacking), in which models are manipulated to ignore their original instructions and follow potentially malicious ones. Although widely acknowledged as a significant security threat, there is a dearth of large-scale resources and quantitative studies on prompt hacking. To address this lacuna, we launch a global prompt hacking competition, which allows for free-form human input attacks. We elicit 600K+ adversarial prompts against three state-of-the-art LLMs. We describe the dataset, which empirically verifies that current LLMs can indeed be manipulated via prompt hacking. We also present a comprehensive taxonomical ontology of the types of adversarial prompts.Comment: 34 pages, 8 figures Codebase: https://github.com/PromptLabs/hackaprompt Dataset: https://huggingface.co/datasets/hackaprompt/hackaprompt-dataset/blob/main/README.md Playground: https://huggingface.co/spaces/hackaprompt/playgroun

Enhanced sensitivity to acute angiotensin II is testosterone dependent in adult male growth-restricted offspring

Placental insufficiency results in intrauterine growth restriction (IUGR) and hypertension in adult male growth-restricted rats. Although renal ANG II and plasma renin activity do not differ between growth-restricted and control rats, blockade of the renin-angiotensin system (RAS) abolishes hypertension in growth-restricted rats, suggesting that the RAS contributes to IUGR-induced hypertension. Moreover, castration abolishes hypertension in growth-restricted rats, indicating an important role for testosterone. Therefore, we hypothesized that enhanced responsiveness to ANG II contributes to hypertension in this model of IUGR and that androgens may play a pivotal role in this enhanced response. Physiological parameters were determined at 16 wk of age in male rats pretreated with enalapril (40 mg·kg−1·day−1) for 1 wk. Baseline blood pressures were similar between growth-restricted (112 ± 3 mmHg) and control (110 ± 2 mmHg) rats; however, an enhanced pressor response to acute ANG II (100 ng·kg−1·min−1 for 30 min) was observed in growth-restricted (160 ± 2 mmHg) vs. control (136 ± 2 mmHg; P < 0.05) rats. Castration abolished the enhanced pressor response to acute ANG II in growth-restricted (130 ± 2 mmHg) rats with no significant effect on blood pressure in controls (130 ± 2 mmHg). Blood pressure was increased to a similar extent above baseline in response to acute phenylephrine (100 μg/min) in control (184 ± 5 mmHg) and growth-restricted (184 ± 8 mmHg) rats, suggesting the enhanced pressor response in growth-restricted rats is ANG II specific. Thus, these results suggest that growth-restricted rats exhibit an enhanced responsiveness to ANG II that is testosterone dependent and indicate that the RAS may serve as an underlying mechanism in mediating hypertension programmed in response to IUGR