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SortedRL: Accelerating RL Training for LLMs through Online Length-Aware Scheduling
Cerebra: A Multidisciplinary AI Board for Multimodal Dementia Characterization and Risk Assessment
Dataset Distillation-based Hybrid Federated Learning on Non-IID Data
Graph Structure Learning with Privacy Guarantees for Open Graph Data
Do Vision-Language Models Measure Up? Benchmarking Visual Measurement Reading with MeasureBench
Think Before You Drive: World Model-Inspired Multimodal Grounding for Autonomous Vehicles
Performance of DeepSeek in the generation of in-training examination questions in radiology resident education
npj Digital Medicine, Published online: 24 March 2026; doi:10.1038/s41746-026-02568-8
Performance of DeepSeek in the generation of in-training examination questions in radiology resident educationNon-classic deubiquitinase USP13 inhibits bladder cancer metastasis through destabilizing cytoplasmic KDM3A
Oncogene, Published online: 24 March 2026; doi:10.1038/s41388-026-03730-y
Non-classic deubiquitinase USP13 inhibits bladder cancer metastasis through destabilizing cytoplasmic KDM3ASpatial Omics in Gastrointestinal Oncology: Recent Advances, Therapeutic Insights, and Clinical Translation
J Cancer. 2026 Jan 30;17(3):515-523. doi: 10.7150/jca.127381. eCollection 2026.
ABSTRACT
Gastrointestinal (GI) cancers remain a leading cause of cancer-related morbidity and mortality worldwide, largely due to their molecular heterogeneity, complex tumor microenvironment (TME), and variable treatment responses. In recent years, the emergence of spatially resolved omics technologies-encompassing spatial transcriptomics, proteomics, metabolomics, and epigenomics-has revolutionized the ability to interrogate tumor architecture with unprecedented resolution. These methods enable precise mapping of cellular and molecular interactions within intact tissue contexts, thereby uncovering spatially defined niches that influence tumor progression, immune evasion, and therapeutic resistance. In GI malignancies such as colorectal, gastric, and esophageal cancers, spatial omics have provided critical insights into cancer-stromal-immune crosstalk, identified predictive biomarkers for immunotherapy and targeted agents, and guided the development of novel therapeutic strategies. This review synthesizes the latest advances in spatial omics applied to GI oncology over the past five years, with an emphasis on their integration into early diagnosis, treatment stratification, and real-time monitoring of therapeutic efficacy. We also discuss current challenges, including standardization, data integration, and clinical validation, as well as future directions for incorporating spatial profiling into routine oncology practice. By bridging the gap between bench discoveries and bedside applications, spatial omics hold transformative potential for achieving truly personalized treatment in gastrointestinal cancers.
PMID:41869445 | PMC:PMC13003551 | DOI:10.7150/jca.127381
Integrated Machine Learning and Multi-Omics Identifies a Novel Molecular Signature for Improving the Prognosis of Hepatocellular Carcinoma
J Hepatocell Carcinoma. 2026 Mar 11;13:574690. doi: 10.2147/JHC.S574690. eCollection 2026.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) exhibits significant molecular heterogeneity and complex immune microenvironment, which to some extent limits the accuracy of prognosis assessment and the formulation of individualized treatment strategies. This study aims to identify immune-derived molecular signatures based on multi-omics data and machine learning methods for the prognosis prediction and risk stratification of HCC.
METHODS: Based on weighted gene co-expression network analysis(WGCNA) and differential gene analysis,immune-derived molecular signature (IDMS) were screened in both single-cell and bulk transcriptomes. Prognostic model was constructed by multi-machine learning approachs. Subsequently, we investigated the differences in mutations, biological functions, and immune cell infiltration within the tumor microenvironment between the high- and low-risk groups.In addition, we comprehensively analyzed the drug sensitivity of IDMS and predicted potential drugs.
RESULTS: We identified seven hub genes at the single-cell and bulk transcriptome levels. Based on multiple machine learning, we constructed a prognostic model that demonstrated excellent performance in predicting overall survival for patients with HCC. IDMS -integrated normograms provide a promising and quantitative tool for clinical risk management.Notably, a significant difference in microsatellite instability (MSI) was observed between the high- and low-risk groups. This indicates that patients in the high-risk group might have a better response to immunotherapy. Additionally, we predicted potential drugs targeting to these risk subgroups.
CONCLUSION: Our research developed an IDMS that could serve as an effective tool for patient stratification management and prognosis prediction. This signature could provide a reference for immunotherapy for patients with HCC and improve their prognosis.
PMID:41847219 | PMC:PMC12991065 | DOI:10.2147/JHC.S574690
Multi-Agent Guided Policy Optimization
Guided Policy Optimization under Partial Observability
SvfEye: A Semantic-Visual Fusion Framework with Multi-Scale Visual Context for Multimodal Reasoning
Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats
Int J Mol Sci. 2026 Feb 25;27(5):2170. doi: 10.3390/ijms27052170.
ABSTRACT
Carbosulfan is a widely used carbamate insecticide, yet its mechanisms of respiratory toxicity remain poorly understood. This study integrated network toxicology, untargeted metabolomics, and molecular docking to systematically investigate the potential mechanisms of carbosulfan-induced respiratory toxicity in male Sprague Dawley rats. Rats were administered a single oral dose of carbosulfan (125 or 250 mg/kg) and assessed after 12 h. Exposure resulted in significant pathological lung damage, characterized by disrupted alveolar architecture, inflammatory cell infiltration, and increased serum levels of the pro-inflammatory cytokines IL-6, IL-1β, and TNF-α. Network toxicology analysis identified 51 potential targets associated with respiratory toxicity, with core targets including SRC, EGFR, PTGS2, CXCL8, CYP3A4, and NR3C1. Enriched pathways were primarily related to neuroactive ligand-receptor interaction, VEGF signaling, and arachidonic acid metabolism. Untargeted metabolomics revealed significant metabolic perturbations in pathways central to antioxidant defense and energy homeostasis, including glutathione metabolism, the tricarboxylic acid cycle, and arginine biosynthesis. Molecular docking confirmed stable in silico binding affinities between carbosulfan and the predicted core targets. Integrative analysis suggests that carbosulfan exposure is associated with respiratory damage, potentially through interconnected mechanisms involving oxidative stress, inflammation, and disruption of cell signaling and metabolic enzyme systems. However, given the acute high-dose nature of the model and the interpretative integration of multi-omics data, these findings should be considered hypothesis-generating. This study provides a novel system-level perspective on carbosulfan-induced respiratory toxicity and highlights key pathways and targets for future validation in chronic exposure models.
PMID:41828400 | PMC:PMC12984169 | DOI:10.3390/ijms27052170
Integrated Network Toxicology and Metabolomics Elucidate Mechanisms of Carbosulfan-Induced Respiratory Toxicity in Rats
Int J Mol Sci. 2026 Feb 25;27(5):2170. doi: 10.3390/ijms27052170.
ABSTRACT
Carbosulfan is a widely used carbamate insecticide, yet its mechanisms of respiratory toxicity remain poorly understood. This study integrated network toxicology, untargeted metabolomics, and molecular docking to systematically investigate the potential mechanisms of carbosulfan-induced respiratory toxicity in male Sprague Dawley rats. Rats were administered a single oral dose of carbosulfan (125 or 250 mg/kg) and assessed after 12 h. Exposure resulted in significant pathological lung damage, characterized by disrupted alveolar architecture, inflammatory cell infiltration, and increased serum levels of the pro-inflammatory cytokines IL-6, IL-1β, and TNF-α. Network toxicology analysis identified 51 potential targets associated with respiratory toxicity, with core targets including SRC, EGFR, PTGS2, CXCL8, CYP3A4, and NR3C1. Enriched pathways were primarily related to neuroactive ligand-receptor interaction, VEGF signaling, and arachidonic acid metabolism. Untargeted metabolomics revealed significant metabolic perturbations in pathways central to antioxidant defense and energy homeostasis, including glutathione metabolism, the tricarboxylic acid cycle, and arginine biosynthesis. Molecular docking confirmed stable in silico binding affinities between carbosulfan and the predicted core targets. Integrative analysis suggests that carbosulfan exposure is associated with respiratory damage, potentially through interconnected mechanisms involving oxidative stress, inflammation, and disruption of cell signaling and metabolic enzyme systems. However, given the acute high-dose nature of the model and the interpretative integration of multi-omics data, these findings should be considered hypothesis-generating. This study provides a novel system-level perspective on carbosulfan-induced respiratory toxicity and highlights key pathways and targets for future validation in chronic exposure models.
PMID:41828400 | PMC:PMC12984169 | DOI:10.3390/ijms27052170
MAPK14/SLC7A11/GPX4 axis dysregulation drives podocyte ferroptosis via mediating glycerophospholipid metabolism
Cell Death Discovery, Published online: 11 March 2026; doi:10.1038/s41420-026-02990-7
MAPK14/SLC7A11/GPX4 axis dysregulation drives podocyte ferroptosis via mediating glycerophospholipid metabolism