Comparative Efficacy of Different AI Systems for Polyp Detection by Size During Colonoscopy: Systematic Review and Network Meta-Analysis

By: Ling Ba · Yaxin Qi · Xinrui Lv · Sipu Wang · Lu Yang · Yufeng Wang · Bangmao Wang · Hailong Cao · Xin Xu

9 September 2026 at 19:00

Background: Colorectal cancer remains a leading cause of death despite being largely preventable through polypectomy. AI systems designed to enhance polyp detection during colonoscopy have shown promise, but the extent to which they improve detection of different-sized polyps remains unclear. Objective: This study compared the size-stratified efficacy of AI-assisted colonoscopy vs standard colonoscopy using the Hartung-Knapp-Sidik-Jonkman (HKSJ) method, and generated exploratory rankings while acknowledging all cross-platform comparisons are indirect. Methods: This systematic review and network meta-analysis (NMA) searched PubMed, Embase, Cochrane CENTRAL, and Web of Science from inception to July 25, 2026, supplemented by citation searching. We included randomized controlled trials (RCTs) comparing AI-assisted vs standard colonoscopy in adults (≥18 years of age), reporting mean polyp detection counts stratified by size (≤5 mm, 6-9 mm, and ≥10 mm). Two reviewers screened studies, extracted data, and assessed risk of bias using the Cochrane Risk of Bias 2.0. We conducted frequentist NMA using the HKSJ method with restricted maximum likelihood estimation, calculated 95% prediction intervals (PIs), and assessed heterogeneity using I² and τ². Certainty of evidence was rated using the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) framework. Results: A total of 13 RCTs (4156 participants) compared 8 AI systems to standard colonoscopy, forming a network without direct AI comparisons. For diminutive polyps (≤5 mm), AI showed a modest advantage (standardized mean difference [SMD] 0.21, 95% CI 0.07 to 0.35, 95% PI –1.12 to 1.54), but substantial heterogeneity (I²=86.6%) and wide PI crossing the null indicated high uncertainty. EndoScreener showed the most consistent evidence (SMD 0.36, 95% CI 0.18-0.54). For small and large polyps, effects were minimal (SMD 0.02, 95% CI –0.02 to 0.06, 95% PI –0.03 to 0.07; SMD 0.01, 95% CI 0.00-0.02, 95% PI –0.01 to 0.03). GRADE certainty was very low for diminutive polyps and low for small and large polyps. Sensitivity analysis excluding Tianjin YuJin did not materially change findings. Conclusions: AI may modestly enhance diminutive polyp detection, but effects on small and large polyps are minimal, with no platform superiority. Given very low to low certainty, findings are hypothesis-generating. This exploratory NMA provides size-stratified comparisons that can inform future head-to-head trial design. Unlike prior reviews aggregating all polyp sizes, we show the overall AI benefit is driven by diminutive polyp detection, providing a framework for targeted deployment—prioritizing AI for diminutive polyp screening, with limited value for larger lesions. Head-to-head trials are urgently needed. Trial Registration: PROSPERO International Prospective Register of Systematic Reviews CRD420251266932; https://www.crd.york.ac.uk/PROSPERO/view/CRD420251266932

Fine-Tuning Language Models to Know What They Know

cs.AI, q-bio.NC updates on arXiv.org

By: Sangjun Park · Elliot Meyerson · Xin Qiu · Risto Miikkulainen

26 May 2026 at 12:00

arXiv:2602.02605v2 Announce Type: replace-cross Abstract: Evaluating true metacognition in Large Language Models (LLMs) is difficult due to biases and heuristics. This paper presents a framework to measure and enhance LLM metacognition while controlling for these biases. A measurement method using the $d'_{\rm type2}$ metric is established to isolate metacognitive ability. The Evolution Strategy for Metacognitive Alignment (ESMA) is proposed, demonstrating robust generalization across unseen datasets, languages, and newly acquired knowledge. Finally, parameter analysis reveals that these improvements are driven by a sparse set of parameters, offering new pathways for targeted metacognitive optimization.

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

(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)

By: Zhengyu Hu · Jiaqi Wang · Jialin Yu · Zheqing Hu · Jing Xue · Zhanbing Ma · Miaomiao Nian · Ruixin Qi · Tingting Zhao · Xia Cao · Hongxia Xin · Xiuyan Wang · Guilan Yang · Zhenzhen Gui · Xiaoming Liu · Juan Chen

6 April 2026 at 18:00

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

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

Omics In Lung

By: Zhengyu Hu · Jiaqi Wang · Jialin Yu · Zheqing Hu · Jing Xue · Zhanbing Ma · Miaomiao Nian · Ruixin Qi · Tingting Zhao · Xia Cao · Hongxia Xin · Xiuyan Wang · Guilan Yang · Zhenzhen Gui · Xiaoming Liu · Juan Chen

6 April 2026 at 18:00

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

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