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Prompting LLMs for complex tasks (e.g., building a trip advisor chatbot) needs humans to clearly articulate customized requirements (e.g., “start the response with a tl;dr”). However, existing prompt engineering instructions often lack focused training on requirement articulation and instead tend to emphasize increasingly automatable strategies (e.g., tricks like adding role-plays and “think step-by-step”). To address the gap, we introduce Requirement-Oriented Prompt Engineering (ROPE), a paradigm that focuses human attention on generating clear, complete requirements during prompting. We implement ROPE through an assessment and training suite that provides deliberate practice with LLM-generated feedback. In a randomized controlled experiment with 30 novices, ROPE significantly outperforms conventional prompt engineering training (20% vs. 1% gains), a gap that automatic prompt optimization cannot close. Furthermore, we demonstrate a direct correlation between the quality of input requirements and LLM outputs. Our work paves the way to empower more end-users to build complex LLM applications. 

Large Language Models (LLMs) now excel at generative skills and can create content at impeccable speeds. However, they are imperfect and still make various mistakes. In a Computer Science education context, as these models are widely recognized as “AI pair programmers,” it becomes increasingly important to train students on evaluating and debugging the LLM-generated code. In this work, we introduce HypoCompass, a novel system to facilitate deliberate practice on debugging, where human novices play the role of Teaching Assistants and help LLM-powered teachable agents debug code. We enable effective task delegation between students and LLMs in this learning-by-teaching environment: students focus on hypothesizing the cause of code errors, while adjacent skills like code completion are offloaded to LLM-agents. Our evaluations demonstrate that HypoCompass generates high-quality training materials (e.g., bugs and fixes), outperforming human counterparts fourfold in efficiency, and significantly improves student performance on debugging by 12% in the pre-to-post test. 

The in-context learning capabilities of LLMs like GPT-3 allow annotators to customize an LLM to their specific tasks with a small number of examples. However, users tend to include only the most obvious patterns when crafting examples, resulting in underspecified in-context functions that fall short on unseen cases. Further, it is hard to know when “enough” examples have been included even for known patterns. In this work, we present ScatterShot, an interactive system for building high-quality demonstration sets for in-context learning. ScatterShot iteratively slices unlabeled data into task-specific patterns, samples informative inputs from underexplored or not-yet-saturated slices in an active learning manner, and helps users label more efficiently with the help of an LLM and the current example set. In simulation studies on two text perturbation scenarios, ScatterShot sampling improves the resulting few-shot functions by 4-5 percentage points over random sampling, with less variance as more examples are added. In a user study, ScatterShot greatly helps users in covering different patterns in the input space and labeling in-context examples more efficiently, resulting in better in-context learning and less user effort. 

Despite their tremendous success in a range of domains, deep learning systems are inherently susceptible to two types of manipulations: adversarial inputs -- maliciously crafted samples that deceive target deep neural network (DNN) models, and poisoned models -- adversely forged DNNs that misbehave on pre-defined inputs. While prior work has intensively studied the two attack vectors in parallel, there is still a lack of understanding about their fundamental connections: what are the dynamic interactions between the two attack vectors? what are the implications of such interactions for optimizing existing attacks? what are the potential countermeasures against the enhanced attacks? Answering these key questions is crucial for assessing and mitigating the holistic vulnerabilities of DNNs deployed in realistic settings. Here we take a solid step towards this goal by conducting the first systematic study of the two attack vectors within a unified framework. Specifically, (i) we develop a new attack model that jointly optimizes adversarial inputs and poisoned models; (ii) with both analytical and empirical evidence, we reveal that there exist intriguing "mutual reinforcement" effects between the two attack vectors -- leveraging one vector significantly amplifies the effectiveness of the other; (iii) we demonstrate that such effects enable a large design spectrum for the adversary to enhance the existing attacks that exploit both vectors (e.g., backdoor attacks), such as maximizing the attack evasiveness with respect to various detection methods; (iv) finally, we discuss potential countermeasures against such optimized attacks and their technical challenges, pointing to several promising research directions. 

Injury to the newborn mouse heart is efficiently regenerated, but this capacity is lost by one week after birth. We found that IGF2, an important mitogen in heart development, is required for neonatal heart regeneration. IGF2 originates from the endocardium/endothelium and is transduced in cardiomyocytes by the insulin receptor. Following injury on postnatal day 1, absence of IGF2 abolished injury-induced cell cycle entry during the early part of the first postnatal week. Consequently, regeneration failed despite the later presence of additional cell cycle-inducing activities 7 days following injury. Most cardiomyocytes transition from mononuclear diploid to polyploid during the first postnatal week. Regeneration was rescued in Igf2-deficient neonates in three different contexts that elevate the percentage of mononuclear diploid cardiomyocytes beyond postnatal day 7. Thus, IGF2 is a paracrine-acting mitogen for heart regeneration during the early postnatal period, and IGF2-deficiency unmasks the dependence of this process on proliferation-competent mononuclear diploid cardiomyocytes.