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Impact of LLM-supported patient education on patient perspectives and patient-reported outcomes: a mixed-methods systematic review
npj Digital Medicine, Published online: 10 September 2026; doi:10.1038/s41746-026-03228-7
Impact of LLM-supported patient education on patient perspectives and patient-reported outcomes: a mixed-methods systematic reviewTransduction Efficiency in Clinical CAR T-Cell Products: A Retrospective Study at a Single Center
Wuwei Huanglian Wan inhibits Helicobacter pylori and alleviates associated gastritis: host metabolic remodeling and altered IL-6/STAT3 signaling
J Ethnopharmacol. 2026 Sep 5;374(Pt 1):122370. doi: 10.1016/j.jep.2026.122370. Online ahead of print.
ABSTRACT
ETHNOPHARMACOLOGICAL RELEVANCE: Wuwei Huanglian Wan (WWHLW) is a traditional Tibetan medicine formula developed by Tibetan physician Takpe Pingcuo and officially documented in the Ministry of Health Drug Standards for Tibetan Medicines (Volume I, 1995). It has long been used for the treatment of gastrointestinal disorders, particularly conditions associated with gastrointestinal discomfort and inflammation. Given the overlap between its traditional indications and the clinical manifestations of H. pylori-associated gastritis (HAG), WWHLW represents a promising candidate for the management of H. pylori infection and related gastric inflammation. In addition, several constituent herbs of WWHLW have demonstrated anti-H. pylori and anti-inflammatory activities, providing a pharmacological basis for further investigating its therapeutic effects.
AIM OF THE STUDY: This study aimed to systematically evaluate the therapeutic effects of WWHLW against H. pylori infection and HAG, and to explore the biological processes associated with these effects through integrated multi-omics and experimental validation.
MATERIALS AND METHODS: The therapeutic effects of WWHLW were evaluated through in vitro antibacterial assays and an H. pylori-infected mouse model. UHPLC-HRMS/MS was employed for chemical profiling and identification of serum-absorbed constituents. Serum metabolomics, 16S rRNA gene sequencing, network pharmacology analysis, molecular docking analysis, and molecular biological analyses were integrated to investigate the metabolic, microbial, and signaling changes associated with its therapeutic activity.
RESULTS: WWHLW exhibited anti-H. pylori activity, with minimum inhibitory concentrations (MICs) of 0.2-0.5 mg/mL against both standard strains and multidrug-resistant clinical isolates. At MIC concentrations, WWHLW treatment altered the expression of multiple virulence-associated genes and reduced gastric H. pylori colonization by 93.8% in infected mice. UHPLC-HRMS/MS analysis putatively annotated 121 compounds in the WWHLW extracts, of which 10 prototype constituents were detected in serum after oral administration. Integrated metabolomics and network pharmacology analyses revealed alterations in lipid and amino acid-related metabolic pathways following WWHLW treatment. Gut microbiota analysis showed that WWHLW was associated with less pronounced alterations in microbial diversity and composition than antibiotic treatment. Correlation analysis further revealed statistical associations between microbial taxa and lipid and amino acid-related features. Experimental validation showed that WWHLW reduced inflammatory cytokine expression and suppressed STAT3 phosphorylation, consistent with altered IL-6/STAT3-related molecular changes.
CONCLUSIONS: WWHLW exhibits therapeutic potential against H. pylori infection and HAG through combined antibacterial, anti-inflammatory and metabolic regulatory effects. The protective activity of WWHLW was associated with reduced IL-6/STAT3 signaling, providing pharmacological evidence supporting its traditional use in gastrointestinal disorders.
PMID:42700849 | DOI:10.1016/j.jep.2026.122370
TIAR: Trajectory-Informed Advantage Reweighting for LLM Abstention Learning
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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.
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