Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Reason--Imagine--Act: Closed-Loop LLM Decision Making with World Models for Autonomous Driving
arXiv:2605.24004v1 Announce Type: new Abstract: Large language models (LLMs) are promising for autonomous driving, but semantics-only decision policies can yield physically unsafe behavior in dynamic traffic. Existing methods either perform online language reasoning without explicit dynamics verification or use world models mainly in offline pipelines, leaving a gap between semantic intent and physical feasibility at decision time. We propose Reason--Imagine--Act (RIA), a closed-loop framework
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cs.AI, q-bio.NC updates on arXiv.org
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Search, Do not Guess: Teaching Small Language Models to Be Effective Search Agents
arXiv:2604.04651v1 Announce Type: new Abstract: Agents equipped with search tools have emerged as effective solutions for knowledge-intensive tasks. While Large Language Models (LLMs) exhibit strong reasoning capabilities, their high computational cost limits practical deployment for search agents. Consequently, recent work has focused on distilling agentic behaviors from LLMs into Small Language Models (SLMs). Through comprehensive evaluation on complex multi-hop reasoning tasks, we find that
Search, Do not Guess: Teaching Small Language Models to Be Effective Search Agents
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cs.AI, q-bio.NC updates on arXiv.org
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ESG-Bench: Benchmarking Long-Context ESG Reports for Hallucination Mitigation
arXiv:2603.13154v1 Announce Type: cross Abstract: As corporate responsibility increasingly incorporates environmental, social, and governance (ESG) criteria, ESG reporting is becoming a legal requirement in many regions and a key channel for documenting sustainability practices and assessing firms' long-term and ethical performance. However, the length and complexity of ESG disclosures make them difficult to interpret and automate the analysis reliably. To support scalable and trustworthy analy
ESG-Bench: Benchmarking Long-Context ESG Reports for Hallucination Mitigation
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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CircRNA-encoded RIPK1-98 protein drives lung adenocarcinoma progression
Dev Cell. 2026 Mar 12:S1534-5807(26)00079-1. doi: 10.1016/j.devcel.2026.02.014. Online ahead of print.ABSTRACTUnexplored biological matter-including uncharacterized genetic elements, molecular entities, and microbial components-remains poorly understood. Here, we use integrated multi-omics approaches to identify and characterize previously unrecognized protein products encoded by circular RNAs (circRNAs) in human tissue specimens and to delineate their roles in the progression of lung adenocarci
CircRNA-encoded RIPK1-98 protein drives lung adenocarcinoma progression
Dev Cell. 2026 Mar 12:S1534-5807(26)00079-1. doi: 10.1016/j.devcel.2026.02.014. Online ahead of print.
ABSTRACT
Unexplored biological matter-including uncharacterized genetic elements, molecular entities, and microbial components-remains poorly understood. Here, we use integrated multi-omics approaches to identify and characterize previously unrecognized protein products encoded by circular RNAs (circRNAs) in human tissue specimens and to delineate their roles in the progression of lung adenocarcinoma (LUAD). The transcription of precursor mRNA by RNA polymerase Ⅱ subunit A (RPB1) is crucial for the biogenesis of these potential circRNA-encoded proteins. Functional and translational analyses link their expression to distinct pathological stages of LUAD in patients. The protein RIPK1-98, encoded by circRIPK1, was identified as functionally distinct from its parental gene product, receptor-interacting serine/threonine kinase 1 (RIPK1). RIPK1-98 modulates cyclin-dependent kinase 2 (CDK2)-dependent cell-cycle regulation, thereby facilitating tumor proliferation in cellular and animal models. Together, these findings suggest that RIPK1-98 serves as a biomarker for cell-cycle progression in LUAD and highlight its potential as a therapeutic target to counteract resistance to first-line treatments, such as osimertinib.
PMID:41825439 | DOI:10.1016/j.devcel.2026.02.014
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Omics In Lung
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CircRNA-encoded RIPK1-98 protein drives lung adenocarcinoma progression
Dev Cell. 2026 Mar 12:S1534-5807(26)00079-1. doi: 10.1016/j.devcel.2026.02.014. Online ahead of print.ABSTRACTUnexplored biological matter-including uncharacterized genetic elements, molecular entities, and microbial components-remains poorly understood. Here, we use integrated multi-omics approaches to identify and characterize previously unrecognized protein products encoded by circular RNAs (circRNAs) in human tissue specimens and to delineate their roles in the progression of lung adenocarci
CircRNA-encoded RIPK1-98 protein drives lung adenocarcinoma progression
Dev Cell. 2026 Mar 12:S1534-5807(26)00079-1. doi: 10.1016/j.devcel.2026.02.014. Online ahead of print.
ABSTRACT
Unexplored biological matter-including uncharacterized genetic elements, molecular entities, and microbial components-remains poorly understood. Here, we use integrated multi-omics approaches to identify and characterize previously unrecognized protein products encoded by circular RNAs (circRNAs) in human tissue specimens and to delineate their roles in the progression of lung adenocarcinoma (LUAD). The transcription of precursor mRNA by RNA polymerase Ⅱ subunit A (RPB1) is crucial for the biogenesis of these potential circRNA-encoded proteins. Functional and translational analyses link their expression to distinct pathological stages of LUAD in patients. The protein RIPK1-98, encoded by circRIPK1, was identified as functionally distinct from its parental gene product, receptor-interacting serine/threonine kinase 1 (RIPK1). RIPK1-98 modulates cyclin-dependent kinase 2 (CDK2)-dependent cell-cycle regulation, thereby facilitating tumor proliferation in cellular and animal models. Together, these findings suggest that RIPK1-98 serves as a biomarker for cell-cycle progression in LUAD and highlight its potential as a therapeutic target to counteract resistance to first-line treatments, such as osimertinib.
PMID:41825439 | DOI:10.1016/j.devcel.2026.02.014
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cs.AI, q-bio.NC updates on arXiv.org
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HarmonyCell: Automating Single-Cell Perturbation Modeling under Semantic and Distribution Shifts
arXiv:2603.01396v2 Announce Type: replace Abstract: Single-cell perturbation studies face dual heterogeneity bottlenecks: (i) semantic heterogeneity--identical biological concepts encoded under incompatible metadata schemas across datasets; and (ii) statistical heterogeneity--distribution shifts from biological variation demanding dataset-specific inductive biases. We propose HarmonyCell, an end-to-end agent framework resolving each challenge through a dedicated mechanism: an LLM-driven Semanti