AI 中文总结
DoAtlas-2是一个自进化因果生物医学发现基础模型，整合多源数据与证据网络，自主提出并验证因果问题，实现机制发现、群体检验和可解释预测的统一闭环。
AI 中文摘要
我们推出DoAtlas-2，一个用于自进化因果生物医学发现的基础模型，它围绕因果机制组织知识，并通过来自人类群体的外部证据不断推进。DoAtlas-2整合了771项研究资源，覆盖48个国家超过72万名参与者，涵盖从纵向临床表型、医学影像和连续生理信号到八个分子层的数据，同时构建了一个包含约470万条文献衍生记录的证据网络，涉及93,566个概念和149,383条候选因果关系。DoAtlas-2能够自主地从证据空白和未解决的机制中提出研究问题，预先指定其因果设计，并生成经过验证的分析。支持性、挑战性和未解决的结果持续修正机制解释、因果证据状态和发现前沿，从而使DoAtlas-2在假设生成、实证检验和更新发现的闭环中自我进化。DoAtlas-2已系统评估了2,031个研究问题。在人类表型项目（HPP）中，它提出了涵盖血管、早期血糖和肝脏代谢系统的4,014个候选通路问题，对前1,079个问题的筛选中有756个获得了统计支持。代表性研究确定血压是连接肥胖、肝脏和脂质表型与血管结局的汇聚节点，并表明肥胖-炎症-血压通路在很大程度上通过联合调整体质指数（BMI）和吸烟因素而被削弱。所发现的血管网络构成了一个完全可解释的预测基础，允许对每个预测进行精确归因，并提供闭式中介效应。因此，DoAtlas-2将因果机制发现、群体证据检验和可解释预测统一在一个持续进化的基础模型之中。
英文摘要
We introduce DoAtlas-2, a foundation for self-evolving causal biomedical discovery that organizes knowledge around causal mechanisms and advances through external evidence from human populations. DoAtlas-2 integrates 771 research resources covering more than 720,000 participants in 48 countries, from longitudinal clinical phenotypes, medical imaging, and continuous physiological signals to eight molecular layers, together with an evidence network of approximately 4.7 million literature-derived records over 93,566 concepts and 149,383 candidate causal relations. DoAtlas-2 autonomously formulates research questions from evidence gaps and unresolved mechanisms, prespecifies their causal designs, and generates validated analyses. Supporting, challenging, and unresolved results continuously revise mechanistic interpretations, the causal evidence state, and the discovery frontier, so that DoAtlas-2 self-evolves within a closed loop of hypothesis generation, empirical testing, and renewed discovery. DoAtlas-2 has systematically evaluated 2,031 research questions. In the Human Phenotype Project (HPP), it formulated 4,014 candidate pathway questions across vascular, early-glycemic, and hepatic-metabolic systems, and screening of the first 1,079 yielded statistical support for 756. Representative studies identify blood pressure as a convergence node linking adiposity, hepatic, and lipid phenotypes to vascular outcomes, and show that an adiposity-inflammation-blood-pressure pathway is largely attenuated by joint adjustment for body mass index (BMI) and smoking. The discovered vascular network constitutes a completely interpretable predictive foundation, admitting exact attribution of every prediction and closed-form mediation effects. DoAtlas-2 thereby unifies causal mechanism discovery, population-evidence testing, and interpretable prediction within one continuously evolving foundation.
CommentsTechnical report. 185 pages, 5 figures. Yulong Li, Rong Xia and Yuxuan Zhang contributed equally. Corresponding authors: Eran Segal, Imran Razzak
