Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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JT-SAFE-V2: Safety-by-Design Foundation Model with World-Context Data
arXiv:2605.24414v1 Announce Type: new Abstract: We introduce JT-Safe-V2, a large language model designed to advance the safety and trustworthiness of foundation models, extending our previous JT-Safe model toward a more comprehensive safety-by-design paradigm. JT-Safe-V2 emphasizes the joint optimization of general intelligence and safety-by-design through several key innovations: enriching pre-training data with contextual world knowledge, high-certainty pre-training procedures, and safety str
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cs.AI, q-bio.NC updates on arXiv.org
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Parameter Efficient Multi-Class Intelligent Scheduling for Multimodal Online Distributed Industrial Anomaly Detection
arXiv:2605.23984v1 Announce Type: cross Abstract: Industrial anomaly detection has attracted significant attention as a fundamental challenge in industrial systems. The rapid advancement of heterogeneous industrial sensors has driven industrial anomaly detection from unimodal to multimodal paradigms. However, existing methods are primarily designed for centralized and offline settings, overlooking the distributed and continuously generated data characteristic of real-world industrial environmen
Parameter Efficient Multi-Class Intelligent Scheduling for Multimodal Online Distributed Industrial Anomaly Detection
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cs.AI, q-bio.NC updates on arXiv.org
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NSR-Boost: A Neuro-Symbolic Residual Boosting Framework for Industrial Legacy Models
arXiv:2601.10457v3 Announce Type: replace Abstract: Although the Gradient Boosted Decision Trees (GBDTs) dominate industrial tabular applications, upgrading legacy models in high-concurrency production environments still faces prohibitive retraining costs and systemic risks. To address this problem, we present NSR-Boost, a neuro-symbolic residual boosting framework designed specifically for industrial scenarios. Its core advantage lies in being ``non-intrusive''. It treats the legacy model as a
NSR-Boost: A Neuro-Symbolic Residual Boosting Framework for Industrial Legacy Models
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cs.AI, q-bio.NC updates on arXiv.org
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SkillOpt: Executive Strategy for Self-Evolving Agent Skills
arXiv:2605.23904v2 Announce Type: replace Abstract: Agent skills today are hand-crafted, generated one-shot, or evolved through loosely controlled self-revision, none of which behaves like a deep-learning optimizer for the skill, and none of which reliably improves over its starting point under feedback. We argue the skill should instead be trained as the external state of a frozen agent, with the same discipline that makes weight-space optimization reproducible. SkillOpt is, to our knowledge,
SkillOpt: Executive Strategy for Self-Evolving Agent Skills
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cs.AI, q-bio.NC updates on arXiv.org
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VILAS: A VLA-Integrated Low-cost Architecture with Soft Grasping for Robotic Manipulation
arXiv:2605.02037v2 Announce Type: replace-cross Abstract: We present VILAS, a fully low-cost, modular robotic manipulation platform designed to support end-to-end vision-language-action (VLA) policy learning and deployment on accessible hardware. The system integrates a Fairino FR5 collaborative arm, a Jodell RG52-50 electric gripper, and a dual-camera perception module, unified through a ZMQ-based communication architecture that seamlessly coordinates teleoperation, data collection, and policy
VILAS: A VLA-Integrated Low-cost Architecture with Soft Grasping for Robotic Manipulation
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cs.AI, q-bio.NC updates on arXiv.org
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Break the Brake, Not the Wheel: Untargeted Jailbreak via Entropy Maximization
arXiv:2605.10764v2 Announce Type: replace-cross Abstract: Recent studies show that gradient-based universal image jailbreaks on vision-language models (VLMs) exhibit little or no cross-model transferability, casting doubt on the feasibility of transferable multimodal jailbreaks. We revisit this conclusion under a strictly untargeted threat model without enforcing a fixed prefix or response pattern. Our preliminary experiment reveals that refusal behavior concentrates at high-entropy tokens duri
Break the Brake, Not the Wheel: Untargeted Jailbreak via Entropy Maximization
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cs.AI, q-bio.NC updates on arXiv.org
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BacktestBench: Benchmarking Large Language Models for Automated Quantitative Strategy Backtesting
arXiv:2605.17937v2 Announce Type: replace-cross Abstract: Quantitative backtesting is essential for evaluating trading strategies but remains hampered by high technical barriers and limited scalability. While Large Language Models (LLMs) offer a transformative path to automate this complex, interdisciplinary workflow through advanced code generation, tool usage, and agentic planning, the practical realization is significantly challenged by the current lack of a large-scale benchmark dedicated t
BacktestBench: Benchmarking Large Language Models for Automated Quantitative Strategy Backtesting
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cs.AI, q-bio.NC updates on arXiv.org
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Simply Stabilizing the Loop via Fully Looped Transformer
arXiv:2605.18797v2 Announce Type: replace-cross Abstract: Scaling model performance typically requires increasing model size. Looped Transformer offers a compelling alternative by iteratively reusing the same Transformer blocks, trading additional computation for improved performance without increasing parameter count or context length. Because the number of loop iterations can be adjusted at inference, it also provides a natural mechanism for balancing performance and test-time compute. Howeve
Simply Stabilizing the Loop via Fully Looped Transformer
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Omics in Hepatocellular
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Unlocking the Future of Hepatocellular Carcinoma Early Diagnosis: The Promise of Extracellular Vesicle Biomarkers
J Clin Transl Hepatol. 2026 Apr 28;14(4):462-477. doi: 10.14218/JCTH.2025.00589. Epub 2026 Apr 8.ABSTRACTHepatocellular carcinoma (HCC) is one of the most prevalent and aggressive malignant tumors globally, with a notably low five-year survival rate. Its high mortality is largely attributed to challenges in early detection. Extracellular vesicles (EVs) are naturally occurring nanoparticles secreted by nearly all cell types and carry a diverse array of bioactive molecules, including proteins, nuc
Unlocking the Future of Hepatocellular Carcinoma Early Diagnosis: The Promise of Extracellular Vesicle Biomarkers
J Clin Transl Hepatol. 2026 Apr 28;14(4):462-477. doi: 10.14218/JCTH.2025.00589. Epub 2026 Apr 8.
ABSTRACT
Hepatocellular carcinoma (HCC) is one of the most prevalent and aggressive malignant tumors globally, with a notably low five-year survival rate. Its high mortality is largely attributed to challenges in early detection. Extracellular vesicles (EVs) are naturally occurring nanoparticles secreted by nearly all cell types and carry a diverse array of bioactive molecules, including proteins, nucleic acids (particularly non-coding RNAs), and lipids. EVs play pivotal roles in remodeling the tumor microenvironment and driving cancer progression through intercellular communication. Accumulating evidence has established that EVs are critically involved in the pathogenesis of HCC and are emerging as promising biomarkers for its early detection. With advances in EV isolation technologies, these vesicles have garnered considerable attention in the field of liquid biopsy for HCC. This review provides a comprehensive overview of the diagnostic potential of EV-derived biomarkers in HCC, including DNA, RNA, proteins, and lipids. Additionally, it discusses the advantages of integrating multi-omics approaches for HCC diagnosis. Furthermore, the review highlights the technical challenges in EV isolation and characterization, as well as the crucial role of reference genes in the standardization of EV data. These insights underscore the potential of EVs as novel, minimally invasive liquid biopsy biomarkers for the early diagnosis of HCC.
PMID:42181837 | PMC:PMC13195390 | DOI:10.14218/JCTH.2025.00589
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Omics in Hepatocellular
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Multi-omics integration identifies ribosome biogenesis-active macrophage subpopulation and its key gene GNL2 in driving liver hepatocellular carcinoma progression and mechanisms
Cancer Cell Int. 2026 May 14. doi: 10.1186/s12935-026-04330-2. Online ahead of print.ABSTRACTBACKGROUND: Liver hepatocellular carcinoma (LIHC) is a common malignancy, yet the core genes driving its progression and potential therapeutic targets remain insufficiently explored. Ribosome biogenesis (RB) is a critical biological process linked to various cancers; however, its systematic role in LIHC remains unclear.METHODS: This study integrated LIHC single-cell RNA-Seq, bulk RNA-Seq, and spatial tra
Multi-omics integration identifies ribosome biogenesis-active macrophage subpopulation and its key gene GNL2 in driving liver hepatocellular carcinoma progression and mechanisms
Cancer Cell Int. 2026 May 14. doi: 10.1186/s12935-026-04330-2. Online ahead of print.
ABSTRACT
BACKGROUND: Liver hepatocellular carcinoma (LIHC) is a common malignancy, yet the core genes driving its progression and potential therapeutic targets remain insufficiently explored. Ribosome biogenesis (RB) is a critical biological process linked to various cancers; however, its systematic role in LIHC remains unclear.
METHODS: This study integrated LIHC single-cell RNA-Seq, bulk RNA-Seq, and spatial transcriptomic data with ribosome biogenesis-related gene sets to construct a single-cell atlas of LIHC. Weighted Gene Co-expression Network Analysis (WGCNA) was employed to characterize myeloid cell subsets. Furthermore, an LIHC prognostic risk model based on RB-related genes was developed using 117 machine-learning algorithm combinations. Key findings were subsequently corroborated through experimental validation and clinical sample analysis.
RESULTS: We identified a distinct macrophage subpopulation with high ribosome biogenesis activity, termed ribosome biogenesis-active macrophages (RAMs). These cells exhibited strong communication with inflammatory macrophages, potentially mediated by MIF-related receptor-ligand interactions. We further constructed an 8-gene prognostic model (PA2G4, GNL2, PWP1, DDX49, NOC4L, GDI2, CST7, and RCL1), which showed good predictive performance. Drug sensitivity analysis suggested that the high-risk group may be more responsive to several agents, including docetaxel. Among these genes, GNL2 was selected for further investigation. Elevated GNL2 expression was associated with increased stemness features in myeloid cells. Molecular docking analysis identified several candidate compounds with potential binding affinity to GNL2. Functionally, GNL2 knockdown in macrophages reduced TGF-β and TNF-α expression and was associated with decreased proliferation, migration, and invasion of LIHC cells.
CONCLUSION: We identified a highly active ribosome biogenesis-macrophage subpopulation (RAM), and constructed a robust risk model to aid in the diagnosis, prognosis, and treatment of LIHC. GNL2 is associated with increased expression of TGF-β and TNF-α and may contribute to LIHC progression.
PMID:42135716 | DOI:10.1186/s12935-026-04330-2
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Oncogene - Issue - nature.com science feeds
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Sirt1 sustains Sonic hedgehog signaling to promote medulloblastoma progression through regulating Gli3 processing
Oncogene, Published online: 18 April 2026; doi:10.1038/s41388-026-03781-1Sirt1 sustains Sonic hedgehog signaling to promote medulloblastoma progression through regulating Gli3 processing
Sirt1 sustains Sonic hedgehog signaling to promote medulloblastoma progression through regulating Gli3 processing
Oncogene, Published online: 18 April 2026; doi:10.1038/s41388-026-03781-1
Sirt1 sustains Sonic hedgehog signaling to promote medulloblastoma progression through regulating Gli3 processing-
Omics In Lung
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Integrative fragmentomic and mutational signature profile of plasma cfDNA for early lung cancer detection
NPJ Precis Oncol. 2026 Apr 15. doi: 10.1038/s41698-026-01416-y. Online ahead of print.ABSTRACTDetecting lung cancer effectively in the general population is essential for optimizing treatment outcomes and improving the 5-year survival rate. While low-dose computed tomography (LDCT) is the current standard, it has limitations in broader populations. We developed a blood-based multi-omics model using whole-genome cell-free DNA (cfDNA) features to distinguish lung cancer from non-cancer individuals
Integrative fragmentomic and mutational signature profile of plasma cfDNA for early lung cancer detection
NPJ Precis Oncol. 2026 Apr 15. doi: 10.1038/s41698-026-01416-y. Online ahead of print.
ABSTRACT
Detecting lung cancer effectively in the general population is essential for optimizing treatment outcomes and improving the 5-year survival rate. While low-dose computed tomography (LDCT) is the current standard, it has limitations in broader populations. We developed a blood-based multi-omics model using whole-genome cell-free DNA (cfDNA) features to distinguish lung cancer from non-cancer individuals. This study included 1600 patients and an equal number of non-cancer controls, divided into training and validation cohorts. The model achieved an area under the curve (AUC) of 95.59% for the training cohort and 95.74% for the validation cohort. The model consistently performed well across various cancer stages and histological subtypes. To further validate the performance of the model, an external validation cohort was utilized. Notably, it also effectively differentiated non-cancer samples from cancer samples in the external validation cohort, with 85.9% sensitivity and 94.78% specificity. Importantly, in simulated population screenings, our ctDNA assay outperformed both LDCT and a previously established method. This suggests its potential utility in wider lung cancer screening programs, possibly complementing the LDCT approach. In conclusion, our ctDNA assay emerges as a promising and highly sensitive tool for the early detection and categorization of lung cancer.
PMID:41986614 | DOI:10.1038/s41698-026-01416-y
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Oncogene - Issue - nature.com science feeds
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Correction: Steroid receptor coactivator-1 facilitates METTL3-mediated m6A modification by coactivating NF-κB and promotes the malignant progression of glioblastoma
Oncogene, Published online: 15 April 2026; doi:10.1038/s41388-026-03788-8Correction: Steroid receptor coactivator-1 facilitates METTL3-mediated m6A modification by coactivating NF-κB and promotes the malignant progression of glioblastoma
Correction: Steroid receptor coactivator-1 facilitates METTL3-mediated m6A modification by coactivating NF-κB and promotes the malignant progression of glioblastoma
Oncogene, Published online: 15 April 2026; doi:10.1038/s41388-026-03788-8
Correction: Steroid receptor coactivator-1 facilitates METTL3-mediated m6A modification by coactivating NF-κB and promotes the malignant progression of glioblastoma-
cs.AI, q-bio.NC updates on arXiv.org
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AdaptFuse: Training-Free Sequential Preference Learning via Externalized Bayesian Inference
arXiv:2604.03925v1 Announce Type: cross Abstract: Large language models struggle to accumulate evidence across multiple rounds of user interaction, failing to update their beliefs in a manner consistent with Bayesian inference. Existing solutions require fine-tuning on sensitive user interaction data, limiting their applicability in privacy-conscious settings. We propose AdaptFuse, a training-free framework that externalizes probabilistic computation entirely from the LLM: a symbolic module mai
AdaptFuse: Training-Free Sequential Preference Learning via Externalized Bayesian Inference
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cs.AI, q-bio.NC updates on arXiv.org
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Preserving Forgery Artifacts: AI-Generated Video Detection at Native Scale
arXiv:2604.04634v1 Announce Type: cross Abstract: The rapid advancement of video generation models has enabled the creation of highly realistic synthetic media, raising significant societal concerns regarding the spread of misinformation. However, current detection methods suffer from critical limitations. They rely on preprocessing operations like fixed-resolution resizing and cropping. These operations not only discard subtle, high-frequency forgery traces but also cause spatial distortion an
Preserving Forgery Artifacts: AI-Generated Video Detection at Native Scale
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cs.AI, q-bio.NC updates on arXiv.org
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Discovering Failure Modes in Vision-Language Models using RL
arXiv:2604.04733v1 Announce Type: cross Abstract: Vision-language Models (VLMs), despite achieving strong performance on multimodal benchmarks, often misinterpret straightforward visual concepts that humans identify effortlessly, such as counting, spatial reasoning, and viewpoint understanding. Previous studies manually identified these weaknesses and found that they often stem from deficits in specific skills. However, such manual efforts are costly, unscalable, and subject to human bias, whic
Discovering Failure Modes in Vision-Language Models using RL
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cs.AI, q-bio.NC updates on arXiv.org
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ContextDrag: Precise Drag-Based Image Editing via Context-Preserving Token Injection and Position-Aligned Attention
arXiv:2512.08477v2 Announce Type: replace-cross Abstract: Drag-based image editing enables intuitive visual manipulation through point-based drag operations. Existing methods mainly rely on diffusion inversion or pixel-space warping with inpainting. However, inversion inherently introduces approximation errors that degrade texture fidelity, whereas rigid pixel-space operations discard semantic context and produce unnatural deformations. To address these issues, we introduce ContextDrag, to our
ContextDrag: Precise Drag-Based Image Editing via Context-Preserving Token Injection and Position-Aligned Attention
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cs.AI, q-bio.NC updates on arXiv.org
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GPA: Learning GUI Process Automation from Demonstrations
arXiv:2604.01676v2 Announce Type: replace-cross Abstract: GUI Process Automation (GPA) is a lightweight but general vision-based Robotic Process Automation (RPA), which enables fast and stable process replay with only a single demo. Addressing the fragility of traditional RPA and the non-deterministic risks of current vision language model-based GUI agents, GPA introduces three core benefits: (1) Robustness via Sequential Monte Carlo-based localization to handle rescaling and detection uncertai
GPA: Learning GUI Process Automation from Demonstrations
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.ABSTRACTBACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-
Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.
ABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.
METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-cell and spatial transcriptomics, as well as peripheral blood multi-omics data to uncover key molecular signatures in IPF. Furthermore, machine learning techniques were utilized to identify core genes, whereas functional analyses and Mendelian randomization were conducted to evaluate the causal relationships among gut microbiota, immune cells, and IPF. Additionally, experimental validation using qPCR and ELISA assays was conducted in vitro, in vivo, and in patient plasma to confirm the expression patterns of key genes.
RESULTS: Across integrated public bulk, single-cell, spatial, and blood multi-omics, CXCL13, IL33, TLR4, and IGF1 were identified as core IPF genes consistently linked to immune infiltration and fibrotic remodeling. Deconvolution, scRNA-seq, and spatial mapping localized their dysregulation to fibroblasts and immune compartments (notably B-cell, macrophage, and mast-cell axes), highlighting fibroblast-immune crosstalk in fibrotic foci. A four-gene model robustly distinguished IPF from controls across cohorts. Mendelian randomization supported a gut-immune-lung axis, indicating causal effects of specific gut taxa on IPF risk via immune phenotypes. qPCR/ELISA in TGF-β1-stimulated fibroblasts, bleomycin mouse lungs, and patient plasma corroborated upregulation of IL33, CXCL13, IGF1 and downregulation of TLR4. Drug-signature reversal nominated cucurbitacin I and temsirolimus; molecular docking was performed as a preliminary in silico, computer-simulation-based assessment of potential ligand-protein interactions between these compounds and the four core targets.
CONCLUSION: This study provides new insights into the importance of gut-immune-lung axis in IPF and identifies CXCL13, IL33, TLR4, and IGF1 as diagnostic signatures and therapeutic targets. By integrating public multi-omics resources with experimental validation, our findings offer a foundation for future diagnostic and treatment strategies aimed at modulating the gut microbiota and immune system in IPF.
PMID:41939867 | PMC:PMC13043422 | DOI:10.3389/fimmu.2026.1730289
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Omics In Lung
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Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.ABSTRACTBACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-
Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.
ABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.
METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-cell and spatial transcriptomics, as well as peripheral blood multi-omics data to uncover key molecular signatures in IPF. Furthermore, machine learning techniques were utilized to identify core genes, whereas functional analyses and Mendelian randomization were conducted to evaluate the causal relationships among gut microbiota, immune cells, and IPF. Additionally, experimental validation using qPCR and ELISA assays was conducted in vitro, in vivo, and in patient plasma to confirm the expression patterns of key genes.
RESULTS: Across integrated public bulk, single-cell, spatial, and blood multi-omics, CXCL13, IL33, TLR4, and IGF1 were identified as core IPF genes consistently linked to immune infiltration and fibrotic remodeling. Deconvolution, scRNA-seq, and spatial mapping localized their dysregulation to fibroblasts and immune compartments (notably B-cell, macrophage, and mast-cell axes), highlighting fibroblast-immune crosstalk in fibrotic foci. A four-gene model robustly distinguished IPF from controls across cohorts. Mendelian randomization supported a gut-immune-lung axis, indicating causal effects of specific gut taxa on IPF risk via immune phenotypes. qPCR/ELISA in TGF-β1-stimulated fibroblasts, bleomycin mouse lungs, and patient plasma corroborated upregulation of IL33, CXCL13, IGF1 and downregulation of TLR4. Drug-signature reversal nominated cucurbitacin I and temsirolimus; molecular docking was performed as a preliminary in silico, computer-simulation-based assessment of potential ligand-protein interactions between these compounds and the four core targets.
CONCLUSION: This study provides new insights into the importance of gut-immune-lung axis in IPF and identifies CXCL13, IL33, TLR4, and IGF1 as diagnostic signatures and therapeutic targets. By integrating public multi-omics resources with experimental validation, our findings offer a foundation for future diagnostic and treatment strategies aimed at modulating the gut microbiota and immune system in IPF.
PMID:41939867 | PMC:PMC13043422 | DOI:10.3389/fimmu.2026.1730289