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cs.AI, q-bio.NC updates on arXiv.org
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CODESKILL: Learning Self-Evolving Skills for Coding Agents
arXiv:2605.25430v1 Announce Type: new Abstract: Coding agents produce rich trajectories while solving software-engineering tasks. To enable agent self-evolution, these trajectories can be distilled into reusable procedural skills that compactly encode experience to guide future behavior. However, existing skill construction and maintenance methods often rely on fixed prompts and heuristic update rules, leaving it unclear how knowledge should be selected, abstracted, and maintained to best serve
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cs.AI, q-bio.NC updates on arXiv.org
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Weakly Supervised Camouflaged Object Detection Based on the SAM Model and Mask Guidance
arXiv:2605.25385v1 Announce Type: cross Abstract: Camouflaged object detection (COD) from a single image is a challenging task due to the high similarity between objects and their surroundings. Existing fully supervised methods require labor-intensive pixel-level annotations, making weakly supervised methods a viable compromise that balances accuracy and annotation efficiency. However, weakly supervised methods often experience performance degradation due to the use of coarse annotations. In th
Weakly Supervised Camouflaged Object Detection Based on the SAM Model and Mask Guidance
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Omics In Lung
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ANP32E drives lung adenocarcinoma progression via GSK3beta-mediated glycolytic reprogramming
Cell Death Dis. 2026 Apr 14. doi: 10.1038/s41419-026-08712-2. Online ahead of print.ABSTRACTLung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and atte
ANP32E drives lung adenocarcinoma progression via GSK3beta-mediated glycolytic reprogramming
Cell Death Dis. 2026 Apr 14. doi: 10.1038/s41419-026-08712-2. Online ahead of print.
ABSTRACT
Lung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and attenuated xenograft growth, while overexpression promoted tumorigenesis. Mechanistically, ANP32E transcriptionally upregulates histone demethylase KDM3B, reducing repressive H3K9me2 marks at the EGFR promoter to enhance EGFR transcription. This activates PI3K/AKT signaling, inducing inhibitory GSK3β phosphorylation. Combined with ANP32E-mediated GSK3β suppression, this dual inactivation liberates oncogenic glycolysis. Crucially, KDM3B silencing or EGFR inhibition (Cetuximab) abrogated ANP32E-driven phenotypes. High-throughput screening identified Penta-O-galloyl-β-D-glucose (PGG) as an ANP32E-targeting compound, with molecular dynamics confirming binding. PGG dose-dependently inhibited the ANP32E/KDM3B/EGFR axis in vitro and suppressed tumor growth in vivo. Thus, ANP32E drives LUAD progression via KDM3B/EGFR-mediated GSK3β inactivation, representing a prognostic biomarker and therapeutic target validated by PGG.
PMID:41980942 | DOI:10.1038/s41419-026-08712-2
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(Multiomics OR Omics) AND (Pancreatic)
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FCGR2B (+) Macrophages as a Critical Node Linking Ferroptosis and Immunosuppression: A Multiomics Framework for Prognosis and Therapy in High-Grade Serous Ovarian Cancer
Hum Mutat. 2026 Apr 6;2026:8027584. doi: 10.1155/humu/8027584. eCollection 2026.ABSTRACTBACKGROUND: High-grade serous ovarian cancer (HGSOC) is characterized by a complex tumor microenvironment and poor prognosis, yet the roles of specific tumor-associated macrophages (TAMs) subpopulations in driving disease progression remain elusive.METHODS: This study evaluated the prognostic relevance of FCGR2B in HGSOC. Single-cell RNA sequencing identified FCGR2B + TAMs as a distinct macrophage subpopulati
FCGR2B (+) Macrophages as a Critical Node Linking Ferroptosis and Immunosuppression: A Multiomics Framework for Prognosis and Therapy in High-Grade Serous Ovarian Cancer
Hum Mutat. 2026 Apr 6;2026:8027584. doi: 10.1155/humu/8027584. eCollection 2026.
ABSTRACT
BACKGROUND: High-grade serous ovarian cancer (HGSOC) is characterized by a complex tumor microenvironment and poor prognosis, yet the roles of specific tumor-associated macrophages (TAMs) subpopulations in driving disease progression remain elusive.
METHODS: This study evaluated the prognostic relevance of FCGR2B in HGSOC. Single-cell RNA sequencing identified FCGR2B + TAMs as a distinct macrophage subpopulation with unique transcriptional features. Integrative analyses combining single-cell and bulk differentially expressed genes, macrophage-associated modules, and ferroptosis-related gene sets identified 26 candidate prognostic genes, from which a four-gene signature (CRYAB, PLAUR, EREG, and C5AR1) was derived to construct the prognostic risk model. The model was validated in an independent cohort. Immune infiltration, single-cell trajectory, copy number variation, and drug-gene associations were analyzed to explore the molecular and therapeutic implications of risk stratification.
RESULTS: HGSOC patients classified as high risk exhibited poorer survival outcomes, increased infiltration of M2-like macrophages, elevated expression of immune checkpoints, and enrichment of immune- and ferroptosis-related pathways. Trajectory and copy number variation analyses revealed stage-specific gene expression patterns and amplification-associated regulation. Drug-gene association analyses further suggested that high-risk patients may be more responsive to targeted therapies and proteasome inhibitors, whereas low-risk patients may benefit from conventional chemotherapy.
CONCLUSION: FCGR2B + TAMs are closely linked to HGSOC progression, and the proposed prognostic model based on FCGR2B + TAMs provides predictive value and potential therapeutic insights for patient stratification.
PMID:41953398 | PMC:PMC13054137 | DOI:10.1155/humu/8027584
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Cell Death Discovery nature.com science feeds
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Programmed cell death in cancer: targeting necroptosis to kill tumor cell
Cell Death Discovery, Published online: 06 April 2026; doi:10.1038/s41420-026-03002-4Programmed cell death in cancer: targeting necroptosis to kill tumor cell
Programmed cell death in cancer: targeting necroptosis to kill tumor cell
Cell Death Discovery, Published online: 06 April 2026; doi:10.1038/s41420-026-03002-4
Programmed cell death in cancer: targeting necroptosis to kill tumor cell-
(Multiomics OR Omics) AND (Pancreatic)
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Unmasking FCGR2B as a high-grade serous ovarian cancer specific marker of immune suppression and tumor progression through multi-omics mining
Transl Oncol. 2026 Apr 3;67:102748. doi: 10.1016/j.tranon.2026.102748. Online ahead of print.ABSTRACTBACKGROUND: Epithelial ovarian cancer (EOC) encompasses five major histological subtypes with marked genetic, immunological, and clinical heterogeneity. While genome-wide association studies (GWAS) have identified subtype-specific risk loci, a critical gap remains in understanding how plasma proteins influence immune-cell traits and contribute to EOC pathogenesis.METHODS: We integrated subtype-st
Unmasking FCGR2B as a high-grade serous ovarian cancer specific marker of immune suppression and tumor progression through multi-omics mining
Transl Oncol. 2026 Apr 3;67:102748. doi: 10.1016/j.tranon.2026.102748. Online ahead of print.
ABSTRACT
BACKGROUND: Epithelial ovarian cancer (EOC) encompasses five major histological subtypes with marked genetic, immunological, and clinical heterogeneity. While genome-wide association studies (GWAS) have identified subtype-specific risk loci, a critical gap remains in understanding how plasma proteins influence immune-cell traits and contribute to EOC pathogenesis.
METHODS: We integrated subtype-stratified GWAS data from two EOC cohorts with plasma proteomics and immune-cell traits to construct protein-immune-EOC regulatory landscapes using a three-stage Mendelian randomization framework. Single-cell RNA-seq and multiplex immunofluorescence were employed to delineate the cellular distribution and spatial context of causal proteins. Subsequent analyses characterized immune infiltration, macrophage polarization, and clinicopathological associations. Drug-gene correlations were used to identify potential therapeutic targets, and transcriptomic analyses were applied to delineate the underlying transcriptional landscape.
RESULTS: We identified 20 subtype-specific protein-immune-EOC regulatory axes, with FCGR2B emerging as a causal plasma protein in immune regulation and high-grade serous ovarian cancer (HGSOC) progression. FCGR2B was highly expressed in tumor-associated macrophages and was associated with an M2-like polarization phenotype. Functional characterization revealed that FCGR2B was associated with shorter progression-free survival and an immunosuppressive tumor microenvironment. Transcriptomic analyses revealed altered NF-κB signaling upon FCGR2B knockdown, and drug-response data suggested a potential association between high FCGR2B expression and sensitivity to NF-κB inhibitors.
CONCLUSIONS: These findings delineate subtype-specific genetically informed protein-immune regulatory landscapes in EOC and identify FCGR2B as a key immunoregulatory and prognostic biomarker in HGSOC, suggesting FCGR2B as a potential therapeutic vulnerability that warrants further investigation.
PMID:41934917 | DOI:10.1016/j.tranon.2026.102748
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Omics in Hepatocellular
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Elevation of Liver Elastic Value Following Radiofrequency Ablation Reflected Neutrophils Mediated Abscopal Effect in Liver Cancer
JHEP Rep. 2026 Mar 23:101824. doi: 10.1016/j.jhepr.2026.101824. Online ahead of print.ABSTRACTBACKGROUND & AIMS: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality globally. Radiofrequency ablation (RFA) is a widely used treatment for HCC, but its efficacy is often limited by tumor relapse. Neutrophils, serve as a double-edged sword in tumor immunology, have recently been implicated in anti-tumor immunity post-RFA. Shear wave elastography (SWE) is a non-invasive ex
Elevation of Liver Elastic Value Following Radiofrequency Ablation Reflected Neutrophils Mediated Abscopal Effect in Liver Cancer
JHEP Rep. 2026 Mar 23:101824. doi: 10.1016/j.jhepr.2026.101824. Online ahead of print.
ABSTRACT
BACKGROUND & AIMS: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality globally. Radiofrequency ablation (RFA) is a widely used treatment for HCC, but its efficacy is often limited by tumor relapse. Neutrophils, serve as a double-edged sword in tumor immunology, have recently been implicated in anti-tumor immunity post-RFA. Shear wave elastography (SWE) is a non-invasive examination for liver tissue, and associated with immune response. This study investigates the correlation between dynamic change of SWE values and neutrophils response following RFA, and explores potential adjuvant strategies for RFA.
METHODS: We conducted a comprehensive analysis using both clinical data from patients undergoing RFA (n=102) and experimental studies in mouse models (n=4-6 per group). Single-cell RNA sequencing (scRNA-seq) and multi-omics analyses including multiplex immunofluorescence staining and flow cytometric analysis were performed to identify neutrophil subsets. To assess the therapeutic potential of neutrophils-activating therapy for enhancing anti-tumor immunity post-RFA, we tested CD40 agonist in combination with RFA in preclinical models.
RESULTS: We noticed that rising liver SWE values following RFA were significantly associated with reduce relapse (n=102, p<0.001), and demonstrated that this phenomenon was linked to the inflammatory environment induced by the infiltration of neutrophils (2.5-fold increase, p<0.001). scRNA-seq analysis identified neutrophil subsets characterized by high expression of interferon-stimulated genes, which exhibited potent anti-tumor activity via nitric oxide. Importantly, treatment with CD40 agonist significantly augmented this immune response, leading to reduced tumor growth in mice (149.6±38.12 mm3 vs 23.92±4.43 mm3, p=0.008).
CONCLUSIONS: We linked clinical features to neutrophil-mediated immunity post-RFA. Neutrophil-activating therapy like CD40 agonists may prevent HCC relapse after RFA.
PMID:41881314 | DOI:10.1016/j.jhepr.2026.101824
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cs.AI, q-bio.NC updates on arXiv.org
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Rethinking the Role of Entropy in Optimizing Tool-Use Behaviors for Large Language Model Agents
arXiv:2602.02050v3 Announce Type: replace Abstract: Tool-using agents based on Large Language Models (LLMs) excel in tasks such as mathematical reasoning and multi-hop question answering. However, in long trajectories, agents often trigger excessive and low-quality tool calls, increasing latency and degrading inference performance, making managing tool-use behavior challenging. In this work, we conduct entropy-based pilot experiments and observe a strong positive correlation between entropy red
Rethinking the Role of Entropy in Optimizing Tool-Use Behaviors for Large Language Model Agents
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cs.AI, q-bio.NC updates on arXiv.org
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LoD-Loc v3: Generalized Aerial Localization in Dense Cities using Instance Silhouette Alignment
arXiv:2603.19609v2 Announce Type: replace-cross Abstract: We present LoD-Loc v3, a novel method for generalized aerial visual localization in dense urban environments. While prior work LoD-Loc v2 achieves localization through semantic building silhouette alignment with low-detail city models, it suffers from two key limitations: poor cross-scene generalization and frequent failure in dense building scenes. Our method addresses these challenges through two key innovations. First, we develop a ne
LoD-Loc v3: Generalized Aerial Localization in Dense Cities using Instance Silhouette Alignment
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Journal of Medical Internet Research
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Effect of a Digital-Driven Physician-Pharmacist Collaborative Model for Diabetes in Primary Health Care: Cluster Randomized Trial
Background: Evidence-based physician-pharmacist collaborative clinics have demonstrated significant short-term benefits for patients with type 2 diabetes (T2D), but their long-term effectiveness remains unclear, especially in primary health care settings. Objective: This study aimed to explore the long-term effectiveness and cost-effectiveness of a novel, digital-driven, multifaceted physician-pharmacist collaborative model for managing patients with T2D in underresourced settings. Methods: We c
Effect of a Digital-Driven Physician-Pharmacist Collaborative Model for Diabetes in Primary Health Care: Cluster Randomized Trial
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Cell Death Discovery nature.com science feeds
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TRIM27-controlled endothelium-derived exosomes play a central role in podocyte injury in diabetic kidney disease
Cell Death Discovery, Published online: 07 March 2026; doi:10.1038/s41420-026-02953-yTRIM27-controlled endothelium-derived exosomes play a central role in podocyte injury in diabetic kidney disease
TRIM27-controlled endothelium-derived exosomes play a central role in podocyte injury in diabetic kidney disease
Cell Death Discovery, Published online: 07 March 2026; doi:10.1038/s41420-026-02953-y
TRIM27-controlled endothelium-derived exosomes play a central role in podocyte injury in diabetic kidney disease-
cs.AI, q-bio.NC updates on arXiv.org
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AI-driven Large-scale Electron Microscopy enables Whole-tissue Subcellular Digitization
arXiv:2511.02860v2 Announce Type: replace-cross Abstract: The distribution and interactions of cellular organelles play a critical role in mediating cellular physiology and pathology. Large-scale electron microscopy enables visualization of organelle distribution and interactions at the tissue level with nanometer resolution, but robust and efficient computational analysis tools are lacking. Here, we present a deep learning tool for universal large-scale 2D/3D electron microscopy analysis, Deep
AI-driven Large-scale Electron Microscopy enables Whole-tissue Subcellular Digitization
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cs.AI, q-bio.NC updates on arXiv.org
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PT-RAG: Structure-Fidelity Retrieval-Augmented Generation for Academic Papers
arXiv:2602.13647v1 Announce Type: cross Abstract: Retrieval-augmented generation (RAG) is increasingly applied to question-answering over long academic papers, where accurate evidence allocation under a fixed token budget is critical. Existing approaches typically flatten academic papers into unstructured chunks during preprocessing, which destroys the native hierarchical structure. This loss forces retrieval to operate in a disordered space, thereby producing fragmented contexts, misallocating