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cs.AI, q-bio.NC updates on arXiv.org
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EchoDistill:Alignment Noisy-to-Clean Self-Distillation for Robust Audio LLMs
arXiv:2605.23954v1 Announce Type: cross Abstract: Audio Large Language Models (ALLMs) are highly vulnerable to real-world noise, which often induces severe semantic drift and hallucinations. Existing robustness methods primarily rely on waveform-level acoustic enhancement, answer-level supervision, or the internal suppression of noise representations. To address these issues, we propose echodistill, an alignment-based noisy-to-clean self-distillation framework. Echodistill leverages a frozen cl
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cs.AI, q-bio.NC updates on arXiv.org
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PathMem: Toward Cognition-Aligned Memory Transformation for Pathology MLLMs
arXiv:2603.09943v2 Announce Type: replace Abstract: Computational pathology demands both visual pattern recognition and dynamic integration of structured domain knowledge, including taxonomy, grading criteria, and clinical evidence. In practice, diagnostic reasoning requires linking morphological evidence with formal diagnostic and grading criteria. Although multimodal large language models (MLLMs) demonstrate strong vision language reasoning capabilities, they lack explicit mechanisms for stru
PathMem: Toward Cognition-Aligned Memory Transformation for Pathology MLLMs
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cs.AI, q-bio.NC updates on arXiv.org
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Krause Synchronization Transformers
arXiv:2602.11534v4 Announce Type: replace-cross Abstract: Self-attention in Transformers relies on globally normalized softmax weights, causing all tokens to compete for influence at every layer. When composed across depth, this interaction pattern induces strong synchronization dynamics that favor convergence toward a dominant mode, a behavior associated with representation collapse and attention sink phenomena. We introduce Krause Attention, a principled attention mechanism inspired by bounde
Krause Synchronization Transformers
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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