Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Can AI Agents Detect and Repair Artifact Drift in Network Experiments?
arXiv:2609.09849v1 Announce Type: cross Abstract: In recent years, AI agents have evolved into capable assistants that carry out multi-step tasks in digital environments. The network systems community is beginning to explore these capabilities in operational and experimental settings. However, an agent operating in network systems should not be judged solely by whether it completes the immediate task. The experiment record it modifies must also remain trustworthy. We call this property artifact
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cs.AI, q-bio.NC updates on arXiv.org
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Can AI Agents Deliver Verifiable Network-Wide Outcomes Across Authority Boundaries?
arXiv:2609.10181v1 Announce Type: cross Abstract: AI agents are increasingly involved in network automation, where they can initiate configuration changes through mediated operational interfaces and assess the resulting state. Nonetheless, operational networks usually span many devices and administrative domains. Realizing an operator's intent requires coordinating agents with distinct authority scopes that define the resources they can access, the operations they can invoke, and the network st
Can AI Agents Deliver Verifiable Network-Wide Outcomes Across Authority Boundaries?
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Cell
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A bivalent molecular glue linking lysine acetyltransferases to oncogene-induced cell death
Chemically induced proximity of lysine acetyltransferases (KATs) with BCL6 reprograms epigenetic signaling to eliminate lymphoma tumors. Structural and mechanistic studies demonstrate that fortuitous protein-protein contacts convert proximity induction into targeted changes in chromatin, revealing a key mechanism by which small molecules can co-opt oncogenic transcriptional regulators to elicit malignant cell death.
A bivalent molecular glue linking lysine acetyltransferases to oncogene-induced cell death
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(Multiomics OR Omics) AND (Pancreatic)
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High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications
Chin Med J (Engl). 2026 May 19. doi: 10.1097/CM9.0000000000004098. Online ahead of print.ABSTRACTHigh-salt diet (HSD) has emerged as a prevalent environmental factor that exacerbates chronic inflammation and insulin resistance in obesity-associated type 2 diabetes (T2D) by modulating macrophage polarization, metabolic reprogramming, and epigenetic imprinting. Current evidence demonstrates that HSD activates p38/mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), and NOD-like
High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications
Chin Med J (Engl). 2026 May 19. doi: 10.1097/CM9.0000000000004098. Online ahead of print.
ABSTRACT
High-salt diet (HSD) has emerged as a prevalent environmental factor that exacerbates chronic inflammation and insulin resistance in obesity-associated type 2 diabetes (T2D) by modulating macrophage polarization, metabolic reprogramming, and epigenetic imprinting. Current evidence demonstrates that HSD activates p38/mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathways, by which it drives macrophage polarization toward a proinflammatory M1 phenotype while inducing a glycolysis-dominant metabolic shift, thereby establishing a persistent "metabolic memory". Moreover, HSD orchestrates metabolic memory in macrophages through coordinated epigenetic machinery, including histone modifications (Trimethylation of histone H3 at lysine 4 [H3K4me3] and Acetylation of histone H3 at lysine 27 [H3K27ac]), DNA methylation, and noncoding RNAs (e.g., long non-coding RNA MALAT1 and miR-155), leading to sustained inflammatory phenotypes. In multiple metabolic organs (e.g., adipose tissue, liver, pancreas, and gut), the HSD-macrophage axis aggravates systemic insulin resistance through shared proinflammatory signaling and other tissue-specific mechanisms. Most importantly, therapeutic strategies targeting the NLRP3 inflammasome, metabolic pathways, and epigenetic alterations offer novel approaches for managing metabolic inflammation. Future investigations are encouraged to leverage lineage tracing, single-cell sequencing, and spatial multi-omics technologies to advance the development of precision medicine for macrophage-associated metabolic disorders.
PMID:42156155 | DOI:10.1097/CM9.0000000000004098
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Omics In Lung
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Pulmonary-Intestinal Axis: Shared Genetic Basis and Mediating Factors Identified Through Multi-Omics Analysis
Int J Chron Obstruct Pulmon Dis. 2026 Apr 7;21:561645. doi: 10.2147/COPD.S561645. eCollection 2026.ABSTRACTBACKGROUND: Chronic obstructive pulmonary disease (COPD) is a systemic condition with comorbidities beyond the lung (eg, cardiovascular and metabolic disorders), and gastrointestinal (GI) disorders are also common. The shared genetic basis of COPD-GI comorbidity and its mediating factors remain unclear. We hypothesized that COPD and GI diseases share pleiotropic genetic architecture implica
Pulmonary-Intestinal Axis: Shared Genetic Basis and Mediating Factors Identified Through Multi-Omics Analysis
Int J Chron Obstruct Pulmon Dis. 2026 Apr 7;21:561645. doi: 10.2147/COPD.S561645. eCollection 2026.
ABSTRACT
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a systemic condition with comorbidities beyond the lung (eg, cardiovascular and metabolic disorders), and gastrointestinal (GI) disorders are also common. The shared genetic basis of COPD-GI comorbidity and its mediating factors remain unclear. We hypothesized that COPD and GI diseases share pleiotropic genetic architecture implicating lipid-metabolic pathways, with smoking mediating part of the association.
METHODS: We analyzed publicly available European-ancestry GWAS summary statistics for COPD (Global Biobank Meta-analysis Initiative), 15 GI diseases (FinnGen), and smoking phenotypes (UK Biobank). Genetic correlation was estimated using linkage disequilibrium score regression (LDSC) and high-definition likelihood (HDL). Multi-trait analysis of GWAS (MTAG) boosted COPD discovery by leveraging genetically correlated GI traits. We integrated locus-to-gene mapping with multi-tissue expression quantitative trait loci (eQTL) and plasma protein quantitative trait loci (pQTL) evidence to prioritize shared loci, genes, and proteins. Bidirectional two-sample Mendelian randomization (MR) tested causal directions, and two-step mediation MR evaluated smoking.
RESULTS: COPD showed significant genetic correlation with nine GI diseases. We identified six comorbidity-associated loci (three with CADD > 12.37) and 13 unique candidate pleiotropic genes; APOE was supported by proteomic evidence. Enrichment analyses highlighted lipid-metabolism pathways. MR suggested COPD increases risk of gastroesophageal reflux disease (GERD), irritable bowel syndrome (IBS), acute appendicitis, and gastric ulcer, while diverticular disease showed reverse causality toward COPD. Smoking partially mediated the COPD effect on GERD, acute appendicitis, and gastric ulcer.
CONCLUSION: COPD and multiple GI disorders share a distributed pleiotropic genetic basis within the broader systemic comorbidity spectrum of COPD. Multi-omics evidence supports a genomic pulmonary-intestinal axis in which lipid metabolism and smoking-related mechanisms contribute to COPD and GI comorbidity, providing targets for risk stratification and potential intervention.
PMID:41978582 | PMC:PMC13070119 | DOI:10.2147/COPD.S561645
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cs.AI, q-bio.NC updates on arXiv.org
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WIMLE: Uncertainty-Aware World Models with IMLE for Sample-Efficient Continuous Control
arXiv:2602.14351v2 Announce Type: replace-cross Abstract: Model-based reinforcement learning promises strong sample efficiency but often underperforms in practice due to compounding model error, unimodal world models that average over multi-modal dynamics, and overconfident predictions that bias learning. We introduce WIMLE, a model-based method that extends Implicit Maximum Likelihood Estimation (IMLE) to the model-based RL framework to learn stochastic, multi-modal world models without iterat
WIMLE: Uncertainty-Aware World Models with IMLE for Sample-Efficient Continuous Control
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cs.AI, q-bio.NC updates on arXiv.org
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ReFlow: Self-correction Motion Learning for Dynamic Scene Reconstruction
arXiv:2604.01561v1 Announce Type: cross Abstract: We present ReFlow, a unified framework for monocular dynamic scene reconstruction that learns 3D motion in a novel self-correction manner from raw video. Existing methods often suffer from incomplete scene initialization for dynamic regions, leading to unstable reconstruction and motion estimation, which often resorts to external dense motion guidance such as pre-computed optical flow to further stabilize and constrain the reconstruction of dyna
ReFlow: Self-correction Motion Learning for Dynamic Scene Reconstruction
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cs.AI, q-bio.NC updates on arXiv.org
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MindCube: Spatial Mental Modeling from Limited Views
arXiv:2506.21458v2 Announce Type: replace Abstract: Can Vision-Language Models (VLMs) imagine the full scene from just a few views, like humans do? Humans form spatial mental models naturally, internal representations of unseen space, to reason about layout, perspective, and motion. Our MindCube benchmark with 21,154 questions across 3,268 images exposes this critical gap, where existing VLMs exhibit near-random performance. Using MindCube, we systematically evaluate how well VLMs build robust
MindCube: Spatial Mental Modeling from Limited Views
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(Multiomics OR Omics) AND (Pancreatic)
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Robust transcriptomic hallmarks targeting intratumor heterogeneity in intrahepatic cholangiocarcinoma
Cell Rep Med. 2026 Mar 30:102708. doi: 10.1016/j.xcrm.2026.102708. Online ahead of print.ABSTRACTIntratumor heterogeneity (ITH) undermines transcriptome-based stratification in intrahepatic cholangiocarcinoma (iCCA). Here, we integrate multi-omics data from multi-region, single-region, and single-cell RNA sequencing cohorts to systematically characterize gene expression ITH. We uncover that immune and stromal heterogeneity are primary drivers of ITH, leading to misclassification of a median 27.8
Robust transcriptomic hallmarks targeting intratumor heterogeneity in intrahepatic cholangiocarcinoma
Cell Rep Med. 2026 Mar 30:102708. doi: 10.1016/j.xcrm.2026.102708. Online ahead of print.
ABSTRACT
Intratumor heterogeneity (ITH) undermines transcriptome-based stratification in intrahepatic cholangiocarcinoma (iCCA). Here, we integrate multi-omics data from multi-region, single-region, and single-cell RNA sequencing cohorts to systematically characterize gene expression ITH. We uncover that immune and stromal heterogeneity are primary drivers of ITH, leading to misclassification of a median 27.8% of tumors by existing subtyping systems. To overcome this, we identify a low-intratumor-heterogeneity/high-intertumor-variability (LIHV) gene set and develop an ITH-insensitive classification system defining five subgroups: inflammatory (SI), metabolic (SII), atypical (SIII-1), immune-silent (SIII-2), and neurodegenerative (SIII-3). These subgroups exhibit distinct clinical outcomes, molecular features, immune landscapes, and therapeutic vulnerabilities. GPRC5A and VTCN1 serve as robust immunohistochemical biomarkers for SI and SIII tumors, while serum CEA and CA19-9 identify inflammatory iCCA. Therapeutically, HSP90 inhibition synergizes with anti-PD1 in inflammatory iCCA, whereas combined anti-PD1 and anti-TIM3 suppresses neurodegenerative iCCA. Collectively, our study provides a robust molecular framework and actionable therapeutic strategies for iCCA.
PMID:41916296 | DOI:10.1016/j.xcrm.2026.102708
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Omics In Lung
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Single-cell multiomics uncovers an endothelial mechanosensitive PIEZO1-IL-33 axis driving pulmonary fibrosis
Nat Commun. 2026 Mar 20;17(1):2655. doi: 10.1038/s41467-026-70193-w.ABSTRACTPulmonary fibrosis represents a progressive interstitial lung disease marked by excessive extracellular matrix deposition and architectural distortion. Vascular endothelial cells critically contribute to fibrogenesis through paracrine secretion of pro-fibrotic mediators, yet their mechanobiological regulation remains elusive. Using integrated single-cell multi-omics profiling of human pulmonary fibrosis specimens and exp
Single-cell multiomics uncovers an endothelial mechanosensitive PIEZO1-IL-33 axis driving pulmonary fibrosis
Nat Commun. 2026 Mar 20;17(1):2655. doi: 10.1038/s41467-026-70193-w.
ABSTRACT
Pulmonary fibrosis represents a progressive interstitial lung disease marked by excessive extracellular matrix deposition and architectural distortion. Vascular endothelial cells critically contribute to fibrogenesis through paracrine secretion of pro-fibrotic mediators, yet their mechanobiological regulation remains elusive. Using integrated single-cell multi-omics profiling of human pulmonary fibrosis specimens and experimental fibrosis models induced by bleomycin or silica, we identify mechanosensitive Piezo1 upregulation in Endothelial cells as a hallmark of fibrotic progression. Endothelial-specific Piezo1 knockout significantly attenuates Bleomycin-induced fibrotic remodeling in male mice, establishing its pathogenic necessity. Mechanistically, PIEZO1 activation promotes pulmonary fibrosis development via CAPN2-mediated STAT3 phosphorylation, which may regulate the secretion of the pro-fibrotic molecule interleukin-33. These findings suggest that the endothelial PIEZO1-CAPN2-STAT3-IL33 axis is a potential therapeutic target for PF intervention.
PMID:41862476 | PMC:PMC13004862 | DOI:10.1038/s41467-026-70193-w
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cs.AI, q-bio.NC updates on arXiv.org
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Phys4D: Fine-Grained Physics-Consistent 4D Modeling from Video Diffusion
arXiv:2603.03485v1 Announce Type: cross Abstract: Recent video diffusion models have achieved impressive capabilities as large-scale generative world models. However, these models often struggle with fine-grained physical consistency, exhibiting physically implausible dynamics over time. In this work, we present \textbf{Phys4D}, a pipeline for learning physics-consistent 4D world representations from video diffusion models. Phys4D adopts \textbf{a three-stage training paradigm} that progressive
Phys4D: Fine-Grained Physics-Consistent 4D Modeling from Video Diffusion
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cs.AI, q-bio.NC updates on arXiv.org
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Learning to Generate and Extract: A Multi-Agent Collaboration Framework For Zero-shot Document-level Event Arguments Extraction
arXiv:2603.02909v2 Announce Type: replace-cross Abstract: Document-level event argument extraction (DEAE) is essential for knowledge acquisition, aiming to extract participants of events from documents . In the zero-shot setting, existing methods employ LLMs to generate synthetic data to address the challenge posed by the scarcity of annotated data. However, relying solely on Event-type-only prompts makes it difficult for the generated content to accurately capture the contextual and structural
Learning to Generate and Extract: A Multi-Agent Collaboration Framework For Zero-shot Document-level Event Arguments Extraction
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cs.AI, q-bio.NC updates on arXiv.org
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Learning to Generate and Extract: A Multi-Agent Collaboration Framework For Zero-shot Document-level Event Arguments Extraction
arXiv:2603.02909v1 Announce Type: cross Abstract: Document-level event argument extraction (DEAE) is essential for knowledge acquisition, aiming to extract participants of events from documents.In the zero-shot setting, existing methods employ LLMs to generate synthetic data to address the challenge posed by the scarcity of annotated data. However, relying solely on Event-type-only prompts makes it difficult for the generated content to accurately capture the contextual and structural relations
Learning to Generate and Extract: A Multi-Agent Collaboration Framework For Zero-shot Document-level Event Arguments Extraction
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cs.AI, q-bio.NC updates on arXiv.org
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MedLA: A Logic-Driven Multi-Agent Framework for Complex Medical Reasoning with Large Language Models
arXiv:2509.23725v3 Announce Type: replace Abstract: Answering complex medical questions requires not only domain expertise and patient-specific information, but also structured and multi-perspective reasoning. Existing multi-agent approaches often rely on fixed roles or shallow interaction prompts, limiting their ability to detect and resolve fine-grained logical inconsistencies. To address this, we propose \textsc{MedLA}, a logic-driven multi-agent framework built on large language models. Eac
MedLA: A Logic-Driven Multi-Agent Framework for Complex Medical Reasoning with Large Language Models
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cs.AI, q-bio.NC updates on arXiv.org
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EBPO: Empirical Bayes Shrinkage for Stabilizing Group-Relative Policy Optimization
arXiv:2602.05165v3 Announce Type: replace-cross Abstract: Reinforcement Learning with Verifiable Rewards (RLVR) has proven effective for enhancing the reasoning capabilities of Large Language Models (LLMs). However, dominant approaches like Group Relative Policy Optimization (GRPO) face critical stability challenges: they suffer from high estimator variance under computational constraints (small group sizes) and vanishing gradient signals in saturated failure regimes where all responses yield i
EBPO: Empirical Bayes Shrinkage for Stabilizing Group-Relative Policy Optimization
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cs.AI, q-bio.NC updates on arXiv.org
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WIMLE: Uncertainty-Aware World Models with IMLE for Sample-Efficient Continuous Control
arXiv:2602.14351v1 Announce Type: cross Abstract: Model-based reinforcement learning promises strong sample efficiency but often underperforms in practice due to compounding model error, unimodal world models that average over multi-modal dynamics, and overconfident predictions that bias learning. We introduce WIMLE, a model-based method that extends Implicit Maximum Likelihood Estimation (IMLE) to the model-based RL framework to learn stochastic, multi-modal world models without iterative samp