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How Do Companies Manage the Environmental Sustainability of AI? An Interview Study About Green AI Efforts and Regulations
scGALA advances graph link prediction-based cell alignment for comprehensive data integration and harmonization
Nat Commun. 2025 Nov 26. doi: 10.1038/s41467-025-66644-5. Online ahead of print.
ABSTRACT
Single-cell technologies have transformed our understanding of cellular heterogeneity through multimodal data acquisition. However, robust cell alignment remains a major challenge for data integration and harmonization, including batch correction, label transfer, and multi-omics integration. Many existing methods constrain alignment based on rigid feature-wise distance metrics, limiting their ability to capture accurate cell correspondence across diverse cell populations and conditions. We introduce scGALA, a graph-based learning framework that redefines cell alignment by combining graph attention networks with a score-driven, task-independent optimization strategy. scGALA constructs enriched graphs of cell-cell relationships by integrating gene expression profiles with auxiliary information, such as spatial coordinates, and iteratively refines alignment via self-supervised graph link prediction, where a deep neural network is trained to identify and reinforce high-confidence correspondences across datasets. In extensive benchmarks, scGALA identifies over 25 percent more high-confidence alignments without compromising accuracy. By improving the core step of cell alignment, scGALA serves as a versatile enhancer for a wide range of single-cell data integration tasks.
PMID:41298467 | DOI:10.1038/s41467-025-66644-5
Clinician-Directed Large Language Model Software Generation for Therapeutic Interventions in Physical Rehabilitation
AI-Assisted Cardiovascular Risk Assessment by General Practitioners in Resource-Constrained Indonesian Settings Using a Conceptual Prototype: Randomized Controlled Study
The missing value of medical artificial intelligence
Nature Medicine, Published online: 25 November 2025; doi:10.1038/s41591-025-04050-6
The missing value of medical artificial intelligenceDecoding the cholesterol-apoptosis axis in HCC: a machine learning-based multi-omics integration and single-cell transcriptomic analysis
Discov Oncol. 2025 Nov 25;16(1):2162. doi: 10.1007/s12672-025-04010-z.
ABSTRACT
Liver hepatocellular carcinoma (LIHC), a predominant form of primary hepatic malignancy, demonstrates a progressively escalating global incidence, imposing substantial health and economic burdens on patients and society. Early diagnosis remains challenging, often resulting in late-stage detection, which limits the efficacy of current therapeutic strategies. This study systematically examines the transcriptional signatures of apoptosis-associated and cholesterol metabolic pathways in LIHC, providing insights into its underlying mechanisms and identifying potential prognostic markers. We employed multi-omics and machine learning to evaluate gene expression variations and construct a prognostic risk scoring model. This study identified apoptosis- and cholesterol metabolism-related differentially expressed genes (ACMRDEGs). Importantly, LASSO regression analysis identified six hub genes (EPHX2, FABP5, SQLE, ADH4, HMGCS2, and CYP7A1) as critical prognostic biomarkers, demonstrating significant correlation with overall survival (OS). Furthermore, immune cell infiltration analysis indicated significant differences in 12 immune cell types within LIHC microenvironment, underscoring the immune system's involvement in disease progression. cholesterol and alcohol metabolism pathways were significantly enriched among hub gene modules, as quantified by multiple gene enrichment analyses. Single-cell analysis identified six major cell types, providing a deeper understanding of the cellular heterogeneity within LIHC. In summarize, this study presents the first integrated apoptosis-cholesterol metabolic pathway-based six-gene prognostic model for LIHC, validated for robustness across multiple cohorts, which may facilitate personalized therapeutic strategies and refined risk assessment in clinical practice.
PMID:41288805 | PMC:PMC12647489 | DOI:10.1007/s12672-025-04010-z
Decoding the cholesterol-apoptosis axis in HCC: a machine learning-based multi-omics integration and single-cell transcriptomic analysis
Discov Oncol. 2025 Nov 25;16(1):2162. doi: 10.1007/s12672-025-04010-z.
ABSTRACT
Liver hepatocellular carcinoma (LIHC), a predominant form of primary hepatic malignancy, demonstrates a progressively escalating global incidence, imposing substantial health and economic burdens on patients and society. Early diagnosis remains challenging, often resulting in late-stage detection, which limits the efficacy of current therapeutic strategies. This study systematically examines the transcriptional signatures of apoptosis-associated and cholesterol metabolic pathways in LIHC, providing insights into its underlying mechanisms and identifying potential prognostic markers. We employed multi-omics and machine learning to evaluate gene expression variations and construct a prognostic risk scoring model. This study identified apoptosis- and cholesterol metabolism-related differentially expressed genes (ACMRDEGs). Importantly, LASSO regression analysis identified six hub genes (EPHX2, FABP5, SQLE, ADH4, HMGCS2, and CYP7A1) as critical prognostic biomarkers, demonstrating significant correlation with overall survival (OS). Furthermore, immune cell infiltration analysis indicated significant differences in 12 immune cell types within LIHC microenvironment, underscoring the immune system's involvement in disease progression. cholesterol and alcohol metabolism pathways were significantly enriched among hub gene modules, as quantified by multiple gene enrichment analyses. Single-cell analysis identified six major cell types, providing a deeper understanding of the cellular heterogeneity within LIHC. In summarize, this study presents the first integrated apoptosis-cholesterol metabolic pathway-based six-gene prognostic model for LIHC, validated for robustness across multiple cohorts, which may facilitate personalized therapeutic strategies and refined risk assessment in clinical practice.
PMID:41288805 | DOI:10.1007/s12672-025-04010-z
When Alignment Fails: Multimodal Adversarial Attacks on Vision-Language-Action Models
ConCISE: A Reference-Free Conciseness Evaluation Metric for LLM-Generated Answers
SMILE: A Composite Lexical-Semantic Metric for Question-Answering Evaluation
Artificial Intelligence Index Report 2025
Multimodal analysis of whole slide images in colorectal cancer
npj Digital Medicine, Published online: 24 November 2025; doi:10.1038/s41746-025-02095-y
Multimodal analysis of whole slide images in colorectal cancerTen years of oncogene editorship: a decade of transformation
Oncogene, Published online: 24 November 2025; doi:10.1038/s41388-025-03648-x
Ten years of oncogene editorship: a decade of transformationHealth care Experiences of Educated Young Adults With Blindness in the Digital Age: Qualitative Study
A Biopsy-Free Future: Science Fiction or Science Reality?
JACC Heart Fail. 2025 Nov 21:102782. doi: 10.1016/j.jchf.2025.102782. Online ahead of print.
NO ABSTRACT
PMID:41273317 | DOI:10.1016/j.jchf.2025.102782
Benchmark on Drug Target Interaction Modeling from a Drug Structure Perspective
Reply to: Utilizing foundation models for developing clinical tools
npj Digital Medicine, Published online: 18 November 2025; doi:10.1038/s41746-025-02066-3
Reply to: Utilizing foundation models for developing clinical toolsA Workflow for Full Traceability of AI Decisions
The dual immunomodulatory role of B cells in tumorigenesis: mechanisms, microenvironment crosstalk, and therapeutic implications
Front Immunol. 2025 Oct 30;16:1649812. doi: 10.3389/fimmu.2025.1649812. eCollection 2025.
ABSTRACT
B lymphocytes exhibit a multifaceted and context-dependent role in tumor biology, acting as both promoters and suppressors of malignancy through dynamic interactions within the tumor microenvironment (TME). This review synthesizes current evidence on the dual functions of B cells in tumor immunity, highlighting their capacity to orchestrate antitumor responses via antigen presentation, antibody-dependent cytotoxicity, and tertiary lymphoid structure (TLS)-mediated T cell activation, while paradoxically driving immunosuppression through regulatory B cells (Bregs), pro-angiogenic signaling, and immune checkpoint modulation. Key mechanisms include TLS formation, which enhances cytotoxic T cell priming and correlates with improved immunotherapy outcomes, and Breg-mediated secretion of IL-10/TGF-β, which fosters T cell exhaustion and myeloid-derived suppressor cell recruitment. Tumor-type specificity is evident: TLS-rich malignancies like melanoma and Non-Small Cell Lung Cancer (NSCLC) show B cell-driven immune activation, whereas pancreatic and hepatocellular carcinomas demonstrate B cell functional plasticity influenced by metabolic and epigenetic reprogramming. Therapeutically, B cell-targeted strategies-including CD20 antibodies, CAR-T cells, and B cell epitope vaccines-demonstrate efficacy in hematologic and solid tumors, yet face challenges due to subset heterogeneity and sex-specific response disparities. Emerging approaches combine immune checkpoint inhibitors (ICBs) with TLS-inducing agents or exploit B cell-derived biomarkers for personalized therapy. Future directions emphasize deciphering B cell metabolic-niche crosstalk, optimizing combinatorial regimens, and leveraging spatial multiomics to resolve functional heterogeneity. By bridging mechanistic insights with clinical translation, this work underscores B cells as pivotal regulators of tumor immunity and advocates for precision strategies to harness their antitumor potential while mitigating pro-tumor plasticity.
PMID:41246318 | PMC:PMC12611826 | DOI:10.3389/fimmu.2025.1649812