Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Towards trustworthy agentic AI: a comprehensive survey of safety, robustness, privacy, and system security
arXiv:2605.23989v1 Announce Type: new Abstract: Agentic AI systems -- Large Language Models (LLMs) augmented with planning, tool use, memory, and long-horizon interactions -- can execute complex tasks autonomously, but their multi-step trajectories introduce new failure modes that challenge trustworthiness. This survey provides a focused examination of trustworthy agentic AI through two core dimensions that are critical for high-risk deployments: Safety and Robustness, and Privacy and System Se
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cs.AI, q-bio.NC updates on arXiv.org
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GlobalDentBench: A Multinational Benchmark for Evaluating LLM Clinical Reasoning in Dentistry with Expert Calibration
arXiv:2605.24636v2 Announce Type: new Abstract: While large language models (LLMs) hold transformative potential for medicine, their reasoning robustness and safety in real-world clinical scenarios remain critically underexplored, particularly in dentistry. Here we introduce GlobalDentBench, the first multinational dental benchmark, featuring a taxonomy that encompasses 14 dental specialties across 88 countries and regions spanning six continents. The benchmark comprises 8,978 expert-validated
GlobalDentBench: A Multinational Benchmark for Evaluating LLM Clinical Reasoning in Dentistry with Expert Calibration
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cs.AI, q-bio.NC updates on arXiv.org
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HoloFair: Unified T2I Fairness Evaluation and Fair-GRPO Debiasing
arXiv:2605.24687v1 Announce Type: cross Abstract: Text-to-Image (T2I) models have made significant strides in visual realism and semantic consistency, yet they often perpetuate and amplify societal biases. Existing evaluation methods typically address only single-dimensional biases, lacking perspectives to uncover model biases at social-related deeper semantic levels. We introduce HoloFair, a comprehensive benchmark framework for multidimensional demographic bias analysis. Built upon our large-
HoloFair: Unified T2I Fairness Evaluation and Fair-GRPO Debiasing
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Cell Death Discovery nature.com science feeds
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Cuproptosis causes meiotic metaphase I arrest by disrupting mitochondrial functions in oocytes
Cell Death Discovery, Published online: 23 May 2026; doi:10.1038/s41420-026-03168-xCuproptosis causes meiotic metaphase I arrest by disrupting mitochondrial functions in oocytes
Cuproptosis causes meiotic metaphase I arrest by disrupting mitochondrial functions in oocytes
Cell Death Discovery, Published online: 23 May 2026; doi:10.1038/s41420-026-03168-x
Cuproptosis causes meiotic metaphase I arrest by disrupting mitochondrial functions in oocytes-
Omics in Gastric
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Integrative multi-omics analysis identifies stromal-immune crosstalk as a determinant of immunotherapy efficacy and establishes a prognostic signature in gastric cancer
Comput Biol Chem. 2026 Apr 23;124(Pt 1):109095. doi: 10.1016/j.compbiolchem.2026.109095. Online ahead of print.ABSTRACTImmune checkpoint inhibitors like pembrolizumab exhibit variable efficacy in metastatic gastric cancer (GC). This study aimed to identify molecular drivers of pembrolizumab response, explore mechanisms of immune checkpoint inhibitors (ICIs) efficacy, and develop a prognostic signature. Transcriptomic analysis of pembrolizumab-treated GC (TIGER database) identified 165 response-a
Integrative multi-omics analysis identifies stromal-immune crosstalk as a determinant of immunotherapy efficacy and establishes a prognostic signature in gastric cancer
Comput Biol Chem. 2026 Apr 23;124(Pt 1):109095. doi: 10.1016/j.compbiolchem.2026.109095. Online ahead of print.
ABSTRACT
Immune checkpoint inhibitors like pembrolizumab exhibit variable efficacy in metastatic gastric cancer (GC). This study aimed to identify molecular drivers of pembrolizumab response, explore mechanisms of immune checkpoint inhibitors (ICIs) efficacy, and develop a prognostic signature. Transcriptomic analysis of pembrolizumab-treated GC (TIGER database) identified 165 response-associated differentially expressed genes (DEGs). Functional annotation and single-cell RNA sequencing (scRNA-seq) data from the Gene Expression Omnibus (GEO) revealed that responder-upregulated genes (R-DEGs) were enriched in immune activation pathways and mainly localized to CD8 + T/NK cells. In contrast, non-responder-upregulated genes (D-DEGs) were linked to extracellular matrix (ECM) remodeling and mainly expressed in fibroblasts/endothelial cells. CellChat analysis demonstrated that key DEGs mediate immune-stromal crosstalk via MHC-I and collagen/laminin signaling. A prognostic signature (Lasso-StepCox[forward] Riskscore; LSR: APOD, APOH, BATF2, GJA1, MAGED1, SLC5A1, SLCO2A1, VWF, VCAN) was derived and validated in four independent GC cohorts from the GEO and Cancer Genome Atlas (TCGA) database. Multi-omics analyses showed that LSR-high tumors exhibited aggressive clinicopathological features, increased stromal components, reduced cytotoxic immune infiltration, diminished tumor mutational burden (TMB), and poorer prognosis. Immunohistochemistry (IHC) and spatial transcriptomics in GC showed that stromal VWF/VCAN expression correlates with reduced CD8⁺ T cell granzyme B expression, suggesting T cell dysfunction. High VWF expression in GC predicted poor survival, and a combined VWF/VCAN score showed enhanced prognostic stratification. This study highlights stromal-immune crosstalk as a driver of pembrolizumab resistance and provides a signature as a clinical tool for prognosis and personalized therapy in metastatic GC.
PMID:42068630 | DOI:10.1016/j.compbiolchem.2026.109095
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Omics In Lung
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Integrin β3 deficiency unleashes spontaneous pulmonary inflammation by promoting B cell hyperactivation via the CD40-CD40L axis
Front Immunol. 2026 Mar 24;17:1796926. doi: 10.3389/fimmu.2026.1796926. eCollection 2026.ABSTRACTBACKGROUND: Pulmonary immune homeostasis requires tight control of adaptive responses. Integrin β3 is a well-known mediator of cell adhesion and platelet function. However, its role in adaptive immunity, especially in B cell responses, remains unclear.METHODS: We defined the pulmonary phenotype of constitutive β3-deficient (β3-/-) mice by histopathology. We performed integrated transcriptomic and pro
Integrin β3 deficiency unleashes spontaneous pulmonary inflammation by promoting B cell hyperactivation via the CD40-CD40L axis
Front Immunol. 2026 Mar 24;17:1796926. doi: 10.3389/fimmu.2026.1796926. eCollection 2026.
ABSTRACT
BACKGROUND: Pulmonary immune homeostasis requires tight control of adaptive responses. Integrin β3 is a well-known mediator of cell adhesion and platelet function. However, its role in adaptive immunity, especially in B cell responses, remains unclear.
METHODS: We defined the pulmonary phenotype of constitutive β3-deficient (β3-/-) mice by histopathology. We performed integrated transcriptomic and proteomic profiling of lung tissue to map the molecular signature of spontaneous pulmonary inflammation. We further probed the underlying mechanisms with additional histology and functional assays and tested for biological significance using transcriptomics data from auto-immune disease patients.
RESULTS: β3-/- mice developed spontaneous pulmonary inflammation marked by B cell activation and in situ immune-complex deposition within alveoli. Multi-omics integration implicated the CD40-CD40 Ligand (CD40L) axis as a central driver of this pathology. Mechanistically, loss of β3 enhanced CD40L-CD40 engagement on B cells, resulting in NF-κB pathway hyperactivation. Consistent with our murine data, reduced ITGB3 expression in patients with autoimmune disease correlated with transcriptional signatures of B cell activation and inflammation.
CONCLUSIONS: These results reframe integrin β3 as a threshold regulator of B cell activation. The β3-CD40L-CD40 axis therefore represents a potential therapeutic target for B cell-mediated autoimmune diseases.
PMID:41953039 | PMC:PMC13055533 | DOI:10.3389/fimmu.2026.1796926
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Integrin β3 deficiency unleashes spontaneous pulmonary inflammation by promoting B cell hyperactivation via the CD40-CD40L axis
Front Immunol. 2026 Mar 24;17:1796926. doi: 10.3389/fimmu.2026.1796926. eCollection 2026.ABSTRACTBACKGROUND: Pulmonary immune homeostasis requires tight control of adaptive responses. Integrin β3 is a well-known mediator of cell adhesion and platelet function. However, its role in adaptive immunity, especially in B cell responses, remains unclear.METHODS: We defined the pulmonary phenotype of constitutive β3-deficient (β3-/-) mice by histopathology. We performed integrated transcriptomic and pro
Integrin β3 deficiency unleashes spontaneous pulmonary inflammation by promoting B cell hyperactivation via the CD40-CD40L axis
Front Immunol. 2026 Mar 24;17:1796926. doi: 10.3389/fimmu.2026.1796926. eCollection 2026.
ABSTRACT
BACKGROUND: Pulmonary immune homeostasis requires tight control of adaptive responses. Integrin β3 is a well-known mediator of cell adhesion and platelet function. However, its role in adaptive immunity, especially in B cell responses, remains unclear.
METHODS: We defined the pulmonary phenotype of constitutive β3-deficient (β3-/-) mice by histopathology. We performed integrated transcriptomic and proteomic profiling of lung tissue to map the molecular signature of spontaneous pulmonary inflammation. We further probed the underlying mechanisms with additional histology and functional assays and tested for biological significance using transcriptomics data from auto-immune disease patients.
RESULTS: β3-/- mice developed spontaneous pulmonary inflammation marked by B cell activation and in situ immune-complex deposition within alveoli. Multi-omics integration implicated the CD40-CD40 Ligand (CD40L) axis as a central driver of this pathology. Mechanistically, loss of β3 enhanced CD40L-CD40 engagement on B cells, resulting in NF-κB pathway hyperactivation. Consistent with our murine data, reduced ITGB3 expression in patients with autoimmune disease correlated with transcriptional signatures of B cell activation and inflammation.
CONCLUSIONS: These results reframe integrin β3 as a threshold regulator of B cell activation. The β3-CD40L-CD40 axis therefore represents a potential therapeutic target for B cell-mediated autoimmune diseases.
PMID:41953039 | PMC:PMC13055533 | DOI:10.3389/fimmu.2026.1796926
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npj Digital Medicine
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A neural-symbolic AI agent system for biomedical concept mapping
npj Digital Medicine, Published online: 04 April 2026; doi:10.1038/s41746-026-02594-6A neural-symbolic AI agent system for biomedical concept mapping
A neural-symbolic AI agent system for biomedical concept mapping
npj Digital Medicine, Published online: 04 April 2026; doi:10.1038/s41746-026-02594-6
A neural-symbolic AI agent system for biomedical concept mapping-
npj Digital Medicine
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HoloTrauma 3X Triadic AI Co reasoning for robot assisted emergency maxillofacial reconstruction
npj Digital Medicine, Published online: 04 April 2026; doi:10.1038/s41746-026-02573-xHoloTrauma 3X Triadic AI Co reasoning for robot assisted emergency maxillofacial reconstruction
HoloTrauma 3X Triadic AI Co reasoning for robot assisted emergency maxillofacial reconstruction
npj Digital Medicine, Published online: 04 April 2026; doi:10.1038/s41746-026-02573-x
HoloTrauma 3X Triadic AI Co reasoning for robot assisted emergency maxillofacial reconstruction-
cs.AI, q-bio.NC updates on arXiv.org
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Countering Catastrophic Forgetting of Large Language Models for Better Instruction Following via Weight-Space Model Merging
arXiv:2604.01538v1 Announce Type: cross Abstract: Large language models have been adopted in the medical domain for clinical documentation to reduce clinician burden. However, studies have reported that LLMs often "forget" a significant amount of instruction-following ability when fine-tuned using a task-specific medical dataset, a critical challenge in adopting general-purpose LLMs for clinical applications. This study presents a model merging framework to efficiently adapt general-purpose LLM
Countering Catastrophic Forgetting of Large Language Models for Better Instruction Following via Weight-Space Model Merging
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cs.AI, q-bio.NC updates on arXiv.org
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Bridging Large-Model Reasoning and Real-Time Control via Agentic Fast-Slow Planning
arXiv:2604.01681v1 Announce Type: cross Abstract: Large foundation models enable powerful reasoning for autonomous systems, but mapping semantic intent to reliable real-time control remains challenging. Existing approaches either (i) let Large Language Models (LLMs) generate trajectories directly - brittle, hard to verify, and latency-prone - or (ii) adjust Model Predictive Control (MPC) objectives online - mixing slow deliberation with fast control and blurring interfaces. We propose Agentic F
Bridging Large-Model Reasoning and Real-Time Control via Agentic Fast-Slow Planning
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cs.AI, q-bio.NC updates on arXiv.org
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DIAL: Decoupling Intent and Action via Latent World Modeling for End-to-End VLA
arXiv:2603.29844v1 Announce Type: cross Abstract: The development of Vision-Language-Action (VLA) models has been significantly accelerated by pre-trained Vision-Language Models (VLMs). However, most existing end-to-end VLAs treat the VLM primarily as a multimodal encoder, directly mapping vision-language features to low-level actions. This paradigm underutilizes the VLM's potential in high-level decision making and introduces training instability, frequently degrading its rich semantic represe
DIAL: Decoupling Intent and Action via Latent World Modeling for End-to-End VLA
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Omics in Hepatocellular
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Hepatotoxicity Prediction and Multi-omics Reveal Mitochondrial and Lipid Metabolic Dysregulation in PM<sub>2.5</sub>-Induced Liver Fibrosis
Environ Health (Wash). 2025 Nov 14;4(3):513-521. doi: 10.1021/envhealth.5c00401. eCollection 2026 Mar 20.ABSTRACTProlonged exposure to fine particulate matter (PM2.5) has been linked to chronic liver injury and cancer. However, an alternative risk assessment method to prospective longitudinal studies of exposome-metabolome interactions for liver inflammation-associated hepatocellular carcinoma (HCC) is lacking. This study investigates the risk of long-term real-world PM2.5 exposure in hepatocarc
Hepatotoxicity Prediction and Multi-omics Reveal Mitochondrial and Lipid Metabolic Dysregulation in PM<sub>2.5</sub>-Induced Liver Fibrosis
Environ Health (Wash). 2025 Nov 14;4(3):513-521. doi: 10.1021/envhealth.5c00401. eCollection 2026 Mar 20.
ABSTRACT
Prolonged exposure to fine particulate matter (PM2.5) has been linked to chronic liver injury and cancer. However, an alternative risk assessment method to prospective longitudinal studies of exposome-metabolome interactions for liver inflammation-associated hepatocellular carcinoma (HCC) is lacking. This study investigates the risk of long-term real-world PM2.5 exposure in hepatocarcinogenesis through machine learning techniques. Shotgun mass spectrometry (MS) imaging data were acquired from mouse models across a continuum of fibrosis, cirrhosis, and HCC for training a multiclass classification model to identify "No Risk", "Cancer Risk", and "Cancer". Direct infusion-MS data from PM2.5-exposed mouse livers were analyzed to classify risk. By integrating data-driven and knowledge-based approaches, 14 disease progression biomarkers were identified for modeling. Our results suggest that chronic real-world PM2.5 exposure can induce liver fibrosis, presenting cancer risk. Incorporating metabolomics, lipidomics, and transcriptomics, we propose PM2.5 exposure induces mitochondrial dysfunction, activates AMPK signaling, and increases ceramide accumulation, potentially mediating insulin resistance that contributes to nonalcoholic fatty liver disease and HCC progression. This work represents a significant advancement in assessing hepatotoxicity of environmental toxicants by reducing reliance on traditional animal testing methods. It also underscores the potential of emerging technologies in transforming our understanding of PM2.5 exposure, paving the way for targeted interventions.
PMID:41883379 | PMC:PMC13010293 | DOI:10.1021/envhealth.5c00401
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Nature - Issue - nature.com science feeds
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Author Correction: 7-Dehydrocholesterol is an endogenous suppressor of ferroptosis
Nature, Published online: 24 March 2026; doi:10.1038/s41586-026-10403-zAuthor Correction: 7-Dehydrocholesterol is an endogenous suppressor of ferroptosis
Author Correction: 7-Dehydrocholesterol is an endogenous suppressor of ferroptosis
Nature, Published online: 24 March 2026; doi:10.1038/s41586-026-10403-z
Author Correction: 7-Dehydrocholesterol is an endogenous suppressor of ferroptosis-
cs.AI, q-bio.NC updates on arXiv.org
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AOI: Turning Failed Trajectories into Training Signals for Autonomous Cloud Diagnosis
arXiv:2603.03378v1 Announce Type: cross Abstract: Large language model (LLM) agents offer a promising data-driven approach to automating Site Reliability Engineering (SRE), yet their enterprise deployment is constrained by three challenges: restricted access to proprietary data, unsafe action execution under permission-governed environments, and the inability of closed systems to improve from failures. We present AOI (Autonomous Operations Intelligence), a trainable multi-agent framework formul
AOI: Turning Failed Trajectories into Training Signals for Autonomous Cloud Diagnosis
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cs.AI, q-bio.NC updates on arXiv.org
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Chat-Based Support Alone May Not Be Enough: Comparing Conversational and Embedded LLM Feedback for Mathematical Proof Learning
arXiv:2602.18807v1 Announce Type: cross Abstract: We evaluate GPTutor, an LLM-powered tutoring system for an undergraduate discrete mathematics course. It integrates two LLM-supported tools: a structured proof-review tool that provides embedded feedback on students' written proof attempts, and a chatbot for math questions. In a staggered-access study with 148 students, earlier access was associated with higher homework performance during the interval when only the experimental group could use t
Chat-Based Support Alone May Not Be Enough: Comparing Conversational and Embedded LLM Feedback for Mathematical Proof Learning
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cs.AI, q-bio.NC updates on arXiv.org
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To Reason or Not to: Selective Chain-of-Thought in Medical Question Answering
arXiv:2602.20130v1 Announce Type: cross Abstract: Objective: To improve the efficiency of medical question answering (MedQA) with large language models (LLMs) by avoiding unnecessary reasoning while maintaining accuracy. Methods: We propose Selective Chain-of-Thought (Selective CoT), an inference-time strategy that first predicts whether a question requires reasoning and generates a rationale only when needed. Two open-source LLMs (Llama-3.1-8B and Qwen-2.5-7B) were evaluated on four biomedic
To Reason or Not to: Selective Chain-of-Thought in Medical Question Answering
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cs.AI, q-bio.NC updates on arXiv.org
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Emotion-LLaMAv2 and MMEVerse: A New Framework and Benchmark for Multimodal Emotion Understanding
arXiv:2601.16449v2 Announce Type: replace-cross Abstract: Understanding human emotions from multimodal signals poses a significant challenge in affective computing and human-robot interaction. While multimodal large language models (MLLMs) have excelled in general vision-language tasks, their capabilities in emotional reasoning remain limited. The field currently suffers from a scarcity of large-scale datasets with high-quality, descriptive emotion annotations and lacks standardized benchmarks
Emotion-LLaMAv2 and MMEVerse: A New Framework and Benchmark for Multimodal Emotion Understanding
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cs.AI, q-bio.NC updates on arXiv.org
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ALOE: Action-Level Off-Policy Evaluation for Vision-Language-Action Model Post-Training
arXiv:2602.12691v2 Announce Type: replace-cross Abstract: We study how to improve large foundation vision-language-action (VLA) systems through online reinforcement learning (RL) in real-world settings. Central to this process is the value function, which provides learning signals to guide VLA learning from experience. In practice, the value function is estimated from trajectory fragments collected from different data sources, including historical policies and intermittent human interventions.