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Enhancing behavioral nudges with large language model-based iterative personalization: A field experiment on electricity and hot-water conservation

arXiv:2604.03881v1 Announce Type: cross Abstract: Nudging is widely used to promote behavioral change, but its effectiveness is often limited when recipients must repeatedly translate feedback into workable next steps under changing circumstances. Large language models (LLMs) may help reduce part of this cognitive work by generating personalized guidance and updating it iteratively across intervention rounds. We developed an LLM agent for iterative personalization and tested it in a three-arm randomized experiment among 233 university residents in China, using daily electricity and shower hot-water conservation as objectively measured cases differing in friction. LLM-personalized nudges (T2) produced the largest conservation effects, while image-enhanced conventional nudges (T1) and text-based conventional nudges (C) showed similar outcomes (omnibus p = 0.009). Relative to C, T2 reduced electricity consumption by 0.56 kWh per room-day (p = 0.014), corresponding to an 18.3 percentage-point higher adjusted saving rate. This advantage emerged within the first two intervention rounds, alongside iterative updating of personalized guidance, and persisted thereafter. Hot-water outcomes followed the same direction but were smaller, less precisely estimated, and attenuated over time, consistent with stronger friction in this domain. LLM-personalized nudges emphasized prospective and context-specific guidance and were associated with higher participant engagement. This study provides field evidence that LLM-based iterative personalization can enhance behavioral nudging, with behavioral friction as a potential boundary condition. Larger trials and extension to more behaviors are warranted.
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Protective Effects of the Ethyl Acetate Fraction from Madeng'ai on Lipopolysaccharide-Induced Acute Lung Injury in Mice: Insights from Integrated Multi-Omics Analysis

J Ethnopharmacol. 2026 Apr 4:121650. doi: 10.1016/j.jep.2026.121650. Online ahead of print.

ABSTRACT

ETHNOPHARMACOLOGICAL RELEVANCE: Madeng'ai (MDA) is a traditional medicinal plant of the Dong ethnic group. Its roots have been widely used in folk medicine for clearing heat and removing toxins, alleviating swelling and relieving pain, dispersing blood stasis and arresting bleeding, as well as promoting wound healing. It is taxonomically classified as a variety of Potentilla freyniana Bornm.

AIM OF THE STUDY: Acute lung injury (ALI) is a life-threatening pulmonary disorder associated with high mortality, underscoring the urgent need to explore novel therapeutic strategies. This study aimed to evaluate the protective effects of the ethyl acetate fraction of MDA (MEA) against LPS-induced ALI in mice and to investigate its underlying mechanisms.

MATERIALS AND METHODS: LC-MS/MS was employed to tentatively identify the bioactive components of MEA. A mouse model of ALI was established by LPS induction. The protective effects of MEA were evaluated through assessments of lung histopathology, inflammatory cytokine levels, and oxidative stress markers. The underlying mechanisms were systematically investigated by integrating transcriptomics, metabolomics, network pharmacology, molecular docking, and Western blotting.

RESULTS: MEA significantly attenuated LPS-induced pulmonary pathological lesions, pulmonary edema, and excessive inflammatory responses in ALI mice. Comprehensive bioinformatics analyses predicted potential mechanisms involving oxidative stress and the regulation of metabolic pathways. Experimental validation via Western blotting confirmed that MEA inhibited TLR4-mediated inflammatory signaling and modulated the PI3K/AKT pathway, thereby exerting multi-pathway protective effects against ALI.

CONCLUSIONS: Collectively, this study confirms that MEA, as a traditional herbal extract, holds potential as an adjuvant therapeutic agent for ALI, providing experimental evidence for the modernization and development of ethnic medicines.

PMID:41941987 | DOI:10.1016/j.jep.2026.121650

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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

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Protective Effects of the Ethyl Acetate Fraction from Madeng'ai on Lipopolysaccharide-Induced Acute Lung Injury in Mice: Insights from Integrated Multi-Omics Analysis

J Ethnopharmacol. 2026 Apr 4:121650. doi: 10.1016/j.jep.2026.121650. Online ahead of print.

ABSTRACT

ETHNOPHARMACOLOGICAL RELEVANCE: Madeng'ai (MDA) is a traditional medicinal plant of the Dong ethnic group. Its roots have been widely used in folk medicine for clearing heat and removing toxins, alleviating swelling and relieving pain, dispersing blood stasis and arresting bleeding, as well as promoting wound healing. It is taxonomically classified as a variety of Potentilla freyniana Bornm.

AIM OF THE STUDY: Acute lung injury (ALI) is a life-threatening pulmonary disorder associated with high mortality, underscoring the urgent need to explore novel therapeutic strategies. This study aimed to evaluate the protective effects of the ethyl acetate fraction of MDA (MEA) against LPS-induced ALI in mice and to investigate its underlying mechanisms.

MATERIALS AND METHODS: LC-MS/MS was employed to tentatively identify the bioactive components of MEA. A mouse model of ALI was established by LPS induction. The protective effects of MEA were evaluated through assessments of lung histopathology, inflammatory cytokine levels, and oxidative stress markers. The underlying mechanisms were systematically investigated by integrating transcriptomics, metabolomics, network pharmacology, molecular docking, and Western blotting.

RESULTS: MEA significantly attenuated LPS-induced pulmonary pathological lesions, pulmonary edema, and excessive inflammatory responses in ALI mice. Comprehensive bioinformatics analyses predicted potential mechanisms involving oxidative stress and the regulation of metabolic pathways. Experimental validation via Western blotting confirmed that MEA inhibited TLR4-mediated inflammatory signaling and modulated the PI3K/AKT pathway, thereby exerting multi-pathway protective effects against ALI.

CONCLUSIONS: Collectively, this study confirms that MEA, as a traditional herbal extract, holds potential as an adjuvant therapeutic agent for ALI, providing experimental evidence for the modernization and development of ethnic medicines.

PMID:41941987 | DOI:10.1016/j.jep.2026.121650

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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

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A Multi-Agent Human-LLM Collaborative Framework for Closed-Loop Scientific Literature Summarization

arXiv:2604.01452v1 Announce Type: new Abstract: Scientific discovery is slowed by fragmented literature that requires excessive human effort to gather, analyze, and understand. AI tools, including autonomous summarization and question answering, have been developed to aid in understanding scientific literature. However, these tools lack the structured, multi-step approach necessary for extracting deep insights from scientific literature. Large Language Models (LLMs) offer new possibilities for literature analysis, but remain unreliable due to hallucinations and incomplete extraction. We introduce Elhuyar, a multi-agent, human-in-the-loop system that integrates LLMs, structured AI, and human scientists to extract, analyze, and iteratively refine insights from scientific literature. The framework distributes tasks among specialized agents for filtering papers, extracting data, fitting models, and summarizing findings, with human oversight ensuring reliability. The system generates structured reports with extracted data, visualizations, model equations, and text summaries, enabling deeper inquiry through iterative refinement. Deployed in materials science, it analyzed literature on tungsten under helium-ion irradiation, showing experimentally correlated exponential helium bubble growth with irradiation dose and temperature, offering insight for plasma-facing materials (PFMs) in fusion reactors. This demonstrates how AI-assisted literature review can uncover scientific patterns and accelerate discovery.
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Reducing Hallucinations in LLM-based Scientific Literature Analysis Using Peer Context Outlier Detection

arXiv:2604.01461v1 Announce Type: new Abstract: Reducing hallucinations in Large Language Models (LLMs) is essential for improving the accuracy of data extraction from large text corpora. Current methods, like prompt engineering and chain-of-thought prompting, focus on individual documents but fail to consider relationships across a corpus. This paper introduces Peer Context Outlier Detection (P-COD), a novel approach that uses the relationships between documents to improve extraction accuracy. Our application domain is in scientific literature summarization, where papers with similar experiment settings should draw similar conclusions. By comparing extracted data to validated peer information within the corpus, we adjust confidence scores and flag low-confidence results for expert review. High-confidence results, supported by peer validation, are considered reliable. Our experiments demonstrate up to 98% precision in outlier detection across 6 domains of science, demonstrating that our design reduces hallucinations, enhances trust in automated systems, and allows researchers to focus on ambiguous cases, streamlining the data extraction workflows.
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Lifting Unlabeled Internet-level Data for 3D Scene Understanding

arXiv:2604.01907v1 Announce Type: cross Abstract: Annotated 3D scene data is scarce and expensive to acquire, while abundant unlabeled videos are readily available on the internet. In this paper, we demonstrate that carefully designed data engines can leverage web-curated, unlabeled videos to automatically generate training data, to facilitate end-to-end models in 3D scene understanding alongside human-annotated datasets. We identify and analyze bottlenecks in automated data generation, revealing critical factors that determine the efficiency and effectiveness of learning from unlabeled data. To validate our approach across different perception granularities, we evaluate on three tasks spanning low-level perception, i.e., 3D object detection and instance segmentation, to high-evel reasoning, i.e., 3D spatial Visual Question Answering (VQA) and Vision-Lanugage Navigation (VLN). Models trained on our generated data demonstrate strong zero-shot performance and show further improvement after finetuning. This demonstrates the viability of leveraging readily available web data as a path toward more capable scene understanding systems.
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Ferritin aggregation cell engager for CAR T avidity engineering against refractory leukemias

Li et al. developed a ferritin aggregation cell engager that helps CAR T cells better recognize and attack leukemia cells without re-engineering the CAR itself. This versatile platform overcomes antigen modulation and enables combination with chemotherapy.
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Targeting FTO shows therapeutic potential in esophageal squamous cell carcinoma by modulating microRNA biogenesis

Oncogene, Published online: 01 April 2026; doi:10.1038/s41388-026-03754-4

Targeting FTO shows therapeutic potential in esophageal squamous cell carcinoma by modulating microRNA biogenesis
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Targeting sialic acid metabolism: a therapeutic strategy against gastric cancer driven by WZ35

Cell Oncol (Dordr). 2026 Mar 23;49(2):60. doi: 10.1007/s13402-026-01194-6.

ABSTRACT

Glycolytic reprogramming is closely associated with the occurrence and progression of gastric cancer. Specifically, the energy derived from glucose metabolism and the cellular proteins by its intermediate products influence gastric cancer development. However, as an important branch of glucose metabolism, sialic acid metabolism and its mediated sialylation modifications remain insufficiently studied in gastric cancer, and their specific relationship with malignant tumor progression requires further exploration. This study employed a multi‑omics approach, integrating metabolomics, single‑cell RNA sequencing, and bulk RNA sequencing analyses, to investigate the metabolic landscape of gastric cancer and its associated alterations. The results indicated that sialic acid is a characteristic metabolite in malignant gastric cancer tissues. It modulates biological functions such as immune response, proliferative activity, and metabolic remodeling within gastric cancer tissues by influencing sialylation modifications. Furthermore, we identified the drug WZ35, which can inhibit the malignant proliferation of gastric cancer by targeting both sialic acid metabolism and sialylated protein modifications. We put forward a conjecture that the metabolism and modification of sialic acid promote the malignant development of gastric cancer, and we discovered that the drug WZ35 has an inhibitory effect on the sialic acid metabolism of gastric cancer.

GRAPHICAL ABSTRACT:

PMID:41870836 | PMC:PMC13009457 | DOI:10.1007/s13402-026-01194-6

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RFC4 drives temozolomide resistance in glioblastoma by activating STK38-BECN1-dependent autophagy

Nat Commun. 2026 Mar 23. doi: 10.1038/s41467-026-70798-1. Online ahead of print.

ABSTRACT

Glioblastoma (GBM) remains a lethal brain tumor due to therapy resistance. While autophagy contributes to temozolomide (TMZ) resistance, its regulation is incompletely understood. This study investigates the role of replication factor RFC4, which is associated with poor prognosis and TMZ resistance in GBM. Multi-omics analyses and molecular experiments reveal that TMZ-induced chromatin accessibility enables transcription factor YY1 to bind the RFC4 promoter and upregulate its expression. RFC4, in turn, stabilizes the kinase STK38, which is essential for autophagosome formation. The RFC4-STK38 interaction facilitates BECN1 recruitment, thereby activating autophagy. Phosphorylation of STK38 at T444 stabilizes this complex, whereas a phospho-deficient mutant impairs autophagy. In vivo, RFC4 overexpression confers TMZ resistance, reversible by autophagy inhibition. Thus, our findings identify the RFC4-STK38-BECN1 axis as a mechanism underlying TMZ resistance and a potential target for precision therapy in GBM.

PMID:41872171 | DOI:10.1038/s41467-026-70798-1

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<i>KRAS</i>-extrachromosomal DNA drives intratumoral heterogeneity in gastric cancer

Oncogene, Published online: 05 March 2026; doi:10.1038/s41388-026-03713-z

KRAS-extrachromosomal DNA drives intratumoral heterogeneity in gastric cancer
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PROSPECT: Unified Streaming Vision-Language Navigation via Semantic--Spatial Fusion and Latent Predictive Representation

arXiv:2603.03739v1 Announce Type: cross Abstract: Multimodal large language models (MLLMs) have advanced zero-shot end-to-end Vision-Language Navigation (VLN), yet robust navigation requires not only semantic understanding but also predictive modeling of environment dynamics and spatial structure. We propose PROSPECT, a unified streaming navigation agent that couples a streaming Vision-Language-Action (VLA) policy with latent predictive representation learning. PROSPECT uses CUT3R as a streaming 3D foundation spatial encoder to produce long-context, absolute-scale spatial features, and fuses them with SigLIP semantic features via cross-attention. During training, we introduce learnable stream query tokens that query the streaming context and predict next-step 2D and 3D latent features (rather than pixels or explicit modalities), supervised in the latent spaces of frozen SigLIP and CUT3R teachers. The predictive branch shapes internal representations without inference overhead. Experiments on VLN-CE benchmarks and real-robot deployment demonstrate state-of-the-art performance and improved long-horizon robustness under diverse lighting. We will release code for the community soon.
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