Normal view
-
cs.AI, q-bio.NC updates on arXiv.org
-
Schema-Aware Planning and Hybrid Knowledge Toolset for Reliable Knowledge Graph Triple Verification
arXiv:2604.04190v1 Announce Type: new Abstract: Knowledge Graphs (KGs) serve as a critical foundation for AI systems, yet their automated construction inevitably introduces noise, compromising data trustworthiness. Existing triple verification methods, based on graph embeddings or language models, often suffer from single-source bias by relying on either internal structural constraints or external semantic evidence, and usually follow a static inference paradigm. As a result, they struggle with
-
cs.AI, q-bio.NC updates on arXiv.org
-
Determined by User Needs: A Salient Object Detection Rationale Beyond Conventional Visual Stimuli
arXiv:2604.03526v1 Announce Type: cross Abstract: Existing \textbf{s}alient \textbf{o}bject \textbf{d}etection (SOD) methods adopt a \textbf{passive} visual stimulus-based rationale--objects with the strongest visual stimuli are perceived as the user's primary focus (i.e., salient objects). They ignore the decisive role of users' \textbf{proactive needs} in segmenting salient objects--if a user has a need before seeing an image, the user's salient objects align with their needs, e.g., if a user
Determined by User Needs: A Salient Object Detection Rationale Beyond Conventional Visual Stimuli
-
cs.AI, q-bio.NC updates on arXiv.org
-
Explainable Token-level Noise Filtering for LLM Fine-tuning Datasets
arXiv:2602.14536v3 Announce Type: replace-cross Abstract: Large Language Models (LLMs) have seen remarkable advancements, achieving state-of-the-art results in diverse applications. Fine-tuning, an important step for adapting LLMs to specific downstream tasks, typically involves further training on corresponding datasets. However, a fundamental discrepancy exists between current fine-tuning datasets and the token-level optimization mechanism of LLMs: most datasets are designed at the sentence-l
Explainable Token-level Noise Filtering for LLM Fine-tuning Datasets
-
(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
-
Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.ABSTRACTBACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-
Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.
ABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.
METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-cell and spatial transcriptomics, as well as peripheral blood multi-omics data to uncover key molecular signatures in IPF. Furthermore, machine learning techniques were utilized to identify core genes, whereas functional analyses and Mendelian randomization were conducted to evaluate the causal relationships among gut microbiota, immune cells, and IPF. Additionally, experimental validation using qPCR and ELISA assays was conducted in vitro, in vivo, and in patient plasma to confirm the expression patterns of key genes.
RESULTS: Across integrated public bulk, single-cell, spatial, and blood multi-omics, CXCL13, IL33, TLR4, and IGF1 were identified as core IPF genes consistently linked to immune infiltration and fibrotic remodeling. Deconvolution, scRNA-seq, and spatial mapping localized their dysregulation to fibroblasts and immune compartments (notably B-cell, macrophage, and mast-cell axes), highlighting fibroblast-immune crosstalk in fibrotic foci. A four-gene model robustly distinguished IPF from controls across cohorts. Mendelian randomization supported a gut-immune-lung axis, indicating causal effects of specific gut taxa on IPF risk via immune phenotypes. qPCR/ELISA in TGF-β1-stimulated fibroblasts, bleomycin mouse lungs, and patient plasma corroborated upregulation of IL33, CXCL13, IGF1 and downregulation of TLR4. Drug-signature reversal nominated cucurbitacin I and temsirolimus; molecular docking was performed as a preliminary in silico, computer-simulation-based assessment of potential ligand-protein interactions between these compounds and the four core targets.
CONCLUSION: This study provides new insights into the importance of gut-immune-lung axis in IPF and identifies CXCL13, IL33, TLR4, and IGF1 as diagnostic signatures and therapeutic targets. By integrating public multi-omics resources with experimental validation, our findings offer a foundation for future diagnostic and treatment strategies aimed at modulating the gut microbiota and immune system in IPF.
PMID:41939867 | PMC:PMC13043422 | DOI:10.3389/fimmu.2026.1730289
-
Omics In Lung
-
Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.ABSTRACTBACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-
Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation
Front Immunol. 2026 Mar 19;17:1730289. doi: 10.3389/fimmu.2026.1730289. eCollection 2026.
ABSTRACT
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options and a poor prognosis. Recent studies suggest a critical role for the gut-immune-lung axis in IPF, yet the underlying molecular mechanisms remain unclear.
METHODS: The current study performed in silico multi-omics integration of publicly available datasets, including bulk RNA-seq, single-cell and spatial transcriptomics, as well as peripheral blood multi-omics data to uncover key molecular signatures in IPF. Furthermore, machine learning techniques were utilized to identify core genes, whereas functional analyses and Mendelian randomization were conducted to evaluate the causal relationships among gut microbiota, immune cells, and IPF. Additionally, experimental validation using qPCR and ELISA assays was conducted in vitro, in vivo, and in patient plasma to confirm the expression patterns of key genes.
RESULTS: Across integrated public bulk, single-cell, spatial, and blood multi-omics, CXCL13, IL33, TLR4, and IGF1 were identified as core IPF genes consistently linked to immune infiltration and fibrotic remodeling. Deconvolution, scRNA-seq, and spatial mapping localized their dysregulation to fibroblasts and immune compartments (notably B-cell, macrophage, and mast-cell axes), highlighting fibroblast-immune crosstalk in fibrotic foci. A four-gene model robustly distinguished IPF from controls across cohorts. Mendelian randomization supported a gut-immune-lung axis, indicating causal effects of specific gut taxa on IPF risk via immune phenotypes. qPCR/ELISA in TGF-β1-stimulated fibroblasts, bleomycin mouse lungs, and patient plasma corroborated upregulation of IL33, CXCL13, IGF1 and downregulation of TLR4. Drug-signature reversal nominated cucurbitacin I and temsirolimus; molecular docking was performed as a preliminary in silico, computer-simulation-based assessment of potential ligand-protein interactions between these compounds and the four core targets.
CONCLUSION: This study provides new insights into the importance of gut-immune-lung axis in IPF and identifies CXCL13, IL33, TLR4, and IGF1 as diagnostic signatures and therapeutic targets. By integrating public multi-omics resources with experimental validation, our findings offer a foundation for future diagnostic and treatment strategies aimed at modulating the gut microbiota and immune system in IPF.
PMID:41939867 | PMC:PMC13043422 | DOI:10.3389/fimmu.2026.1730289
-
Oncogene - Issue - nature.com science feeds
-
SRSF10 promotes cisplatin resistance in bladder cancer via BIN1 Exon 12 retention and ANXA1 activation
Oncogene, Published online: 06 April 2026; doi:10.1038/s41388-026-03735-7SRSF10 promotes cisplatin resistance in bladder cancer via BIN1 Exon 12 retention and ANXA1 activation
SRSF10 promotes cisplatin resistance in bladder cancer via BIN1 Exon 12 retention and ANXA1 activation
Oncogene, Published online: 06 April 2026; doi:10.1038/s41388-026-03735-7
SRSF10 promotes cisplatin resistance in bladder cancer via BIN1 Exon 12 retention and ANXA1 activation