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cs.AI, q-bio.NC updates on arXiv.org
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SCQ: Stabilizing Conservative Q-Learning with Sigmoid-Bounded Entropy
arXiv:2609.12749v1 Announce Type: new Abstract: Offline-to-online reinforcement learning reduces interaction cost for real-world robot learning but suffers from persistent value estimation instability. Existing methods address this through pessimistic regularization, lower-bound calibration, and architectural normalization, but an overlooked source of instability lies in the entropy formulation: the standard log-entropy term can become negative, destabilizing policy updates. We introduce SCQ (S
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cs.AI, q-bio.NC updates on arXiv.org
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Recommendation Retrievers Need Verifiers: Universal Generative Reranking for Sequential Recommendations
arXiv:2609.12270v1 Announce Type: cross Abstract: First-stage recommenders in multi-stage systems produce a ranked candidate list from which a limited prefix is forwarded to downstream rankers. Because each forwarded item must be processed by more expensive ranking stages, this shortlist cannot be arbitrarily large. The first-stage objective is therefore high coverage of relevant items within the forwarded prefix, commonly measured by Recall@$k$. A relevant item may be available deeper in the r
Recommendation Retrievers Need Verifiers: Universal Generative Reranking for Sequential Recommendations
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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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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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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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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