❌

Reading view

How AI Aggregation Affects Knowledge

arXiv:2604.04906v1 Announce Type: cross Abstract: Artificial intelligence (AI) changes social learning when aggregated outputs become training data for future predictions. To study this, we extend the DeGroot model by introducing an AI aggregator that trains on population beliefs and feeds synthesized signals back to agents. We define the learning gap as the deviation of long-run beliefs from the efficient benchmark, allowing us to capture how AI aggregation affects learning. Our main result identifies a threshold in the speed of updating: when the aggregator updates too quickly, there is no positive-measure set of training weights that robustly improves learning across a broad class of environments, whereas such weights exist when updating is sufficiently slow. We then compare global and local architectures. Local aggregators trained on proximate or topic-specific data robustly improve learning in all environments. Consequently, replacing specialized local aggregators with a single global aggregator worsens learning in at least one dimension of the state.
  •  

C-TRAIL: A Commonsense World Framework for Trajectory Planning in Autonomous Driving

arXiv:2603.29908v1 Announce Type: new Abstract: Trajectory planning for autonomous driving increasingly leverages large language models (LLMs) for commonsense reasoning, yet LLM outputs are inherently unreliable, posing risks in safety-critical applications. We propose C-TRAIL, a framework built on a Commonsense World that couples LLM-derived commonsense with a trust mechanism to guide trajectory planning. C-TRAIL operates through a closed-loop Recall, Plan, and Update cycle: the Recall module queries an LLM for semantic relations and quantifies their reliability via a dual-trust mechanism; the Plan module injects trust-weighted commonsense into Monte Carlo Tree Search (MCTS) through a Dirichlet trust policy; and the Update module adaptively refines trust scores and policy parameters from environmental feedback. Experiments on four simulated scenarios in Highway-env and two real-world levelXData datasets (highD, rounD) show that C-TRAIL consistently outperforms state-of-the-art baselines, reducing ADE by 40.2%, FDE by 51.7%, and improving SR by 16.9 percentage points on average. The source code is available at https://github.com/ZhihongCui/CTRAIL.
  •  

Profiling of the mycobiome and metabolome: a comparative study of benign pulmonary nodules and lung adenocarcinoma

Front Cell Infect Microbiol. 2026 Feb 23;16:1732958. doi: 10.3389/fcimb.2026.1732958. eCollection 2026.

ABSTRACT

INTRODUCTION: Lung adenocarcinoma (LUAD), the most common subtype of non-small cell lung cancer, is a form of malignant pulmonary nodule that requires clinical differentiation from benign pulmonary nodules (BPN). The mechanisms underlying the development of LUAD are complex, and effective non-invasive methods for differentiating BPN from LUAD are lacking. This study aimed not only to distinguish BPN from LUAD using gut fungi and serum metabolites, but also to establish an integrated network of gut fungi-metabolite-cytokine interactions.

METHODS: Fecal and serum samples from individuals with BPN and patients with LUAD were subjected to internal transcribed spacer sequencing, ultra-performance liquid chromatography-tandem mass spectrometry, and multiplex Luminex assays to quantify gut fungi, metabolites, and cytokines, respectively.

RESULTS: A significant difference in gut fungal communities was observed between the BPN and LUAD groups. Multiple genera and species were more abundant in LUAD than in BPN. Docosapentaenoic acid n-6 (DPAn-6), indole-3-propionic acid (IPA), and interferon-Ξ³-induced protein 10 (IP-10) were significantly elevated in the LUAD group. The integrated model established using a combination of gut fungi and metabolites demonstrated excellent performance in distinguishing BPN from LUAD. A network of interactions was established among differentially abundant gut fungi, serum metabolites, and cytokines.

CONCLUSION: Our study identifies a novel panel of fungal and metabolite biomarkers for differentiating between BPN and LUAD, and constructs a multi-omics network that provides new insights into investigating the mechanistic role of gut mycobiota dysbiosis in LUAD.

PMID:41809995 | PMC:PMC12968269 | DOI:10.3389/fcimb.2026.1732958

  •  
❌