Reading view
Research Status and Prospects of <em>Helicobacter pylori</em>-associated gastritis: From Mechanisms to Traditional Chinese Medicine Treatment
Gastroenterol Res Pract. 2026 Sep 7;2026:3413458. doi: 10.1155/grp/3413458. eCollection 2026.
ABSTRACT
Helicobacter pylori-associated gastritis (HPAG) is a chronic inflammatory condition of the gastric mucosa caused by Helicobacter pylori infection, serving as the core etiological factor for peptic ulcers and gastric precancerous lesions. Given the persistently high global infection rates and the escalating burden of antibiotic resistance, conventional eradication therapies are encountering significant challenges. This article systematically delineates the molecular pathogenic mechanisms underlying HPAG, encompassing bacterial virulence factors, host immune responses, aberrant signaling pathways, oxidative stress, epigenetic regulation, and mucosal barrier damage. Building upon this foundation and in alignment with international mainstream diagnostic and therapeutic guidelines, we summarize the research progress of traditional Chinese medicine (TCM) interventions from a novel perspective of microecological homeostasis regulation. Specifically, we clarify the multifaceted roles of TCM monomers and formulas in immunomodulation, mucosal repair, and antibacterial synergism. By systematically synthesizing existing evidence from TCM studies, we construct a whole-course TCM intervention framework for HPAG that integrates "susceptibility prevention, active treatment, and posteradication repair." Furthermore, we critically analyze the current clinical translation bottlenecks and the limitations inherent in the "black-box" research paradigm of TCM monomers and formulas, and propose future research directions driven by multiomics technologies. This work provides both theoretical support and practical references for precise integrated Chinese and Western medicine diagnosis and treatment of HPAG.
PMID:42707495 | PMC:PMC13548316 | DOI:10.1155/grp/3413458
Research Status and Prospects of <em>Helicobacter pylori</em>-associated gastritis: From Mechanisms to Traditional Chinese Medicine Treatment
Gastroenterol Res Pract. 2026 Sep 7;2026:3413458. doi: 10.1155/grp/3413458. eCollection 2026.
ABSTRACT
Helicobacter pylori-associated gastritis (HPAG) is a chronic inflammatory condition of the gastric mucosa caused by Helicobacter pylori infection, serving as the core etiological factor for peptic ulcers and gastric precancerous lesions. Given the persistently high global infection rates and the escalating burden of antibiotic resistance, conventional eradication therapies are encountering significant challenges. This article systematically delineates the molecular pathogenic mechanisms underlying HPAG, encompassing bacterial virulence factors, host immune responses, aberrant signaling pathways, oxidative stress, epigenetic regulation, and mucosal barrier damage. Building upon this foundation and in alignment with international mainstream diagnostic and therapeutic guidelines, we summarize the research progress of traditional Chinese medicine (TCM) interventions from a novel perspective of microecological homeostasis regulation. Specifically, we clarify the multifaceted roles of TCM monomers and formulas in immunomodulation, mucosal repair, and antibacterial synergism. By systematically synthesizing existing evidence from TCM studies, we construct a whole-course TCM intervention framework for HPAG that integrates "susceptibility prevention, active treatment, and posteradication repair." Furthermore, we critically analyze the current clinical translation bottlenecks and the limitations inherent in the "black-box" research paradigm of TCM monomers and formulas, and propose future research directions driven by multiomics technologies. This work provides both theoretical support and practical references for precise integrated Chinese and Western medicine diagnosis and treatment of HPAG.
PMID:42707495 | PMC:PMC13548316 | DOI:10.1155/grp/3413458
High-fidelity identification of guest species in porous materials
Nature, Published online: 20 May 2026; doi:10.1038/s41586-026-10527-2
A reconstruction method based on Gaussian-apodized single-sideband electron ptychography removes artefacts to enable the high-fidelity identification of guest species in porous materials.Pulmonary-Intestinal Axis: Shared Genetic Basis and Mediating Factors Identified Through Multi-Omics Analysis
Int J Chron Obstruct Pulmon Dis. 2026 Apr 7;21:561645. doi: 10.2147/COPD.S561645. eCollection 2026.
ABSTRACT
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a systemic condition with comorbidities beyond the lung (eg, cardiovascular and metabolic disorders), and gastrointestinal (GI) disorders are also common. The shared genetic basis of COPD-GI comorbidity and its mediating factors remain unclear. We hypothesized that COPD and GI diseases share pleiotropic genetic architecture implicating lipid-metabolic pathways, with smoking mediating part of the association.
METHODS: We analyzed publicly available European-ancestry GWAS summary statistics for COPD (Global Biobank Meta-analysis Initiative), 15 GI diseases (FinnGen), and smoking phenotypes (UK Biobank). Genetic correlation was estimated using linkage disequilibrium score regression (LDSC) and high-definition likelihood (HDL). Multi-trait analysis of GWAS (MTAG) boosted COPD discovery by leveraging genetically correlated GI traits. We integrated locus-to-gene mapping with multi-tissue expression quantitative trait loci (eQTL) and plasma protein quantitative trait loci (pQTL) evidence to prioritize shared loci, genes, and proteins. Bidirectional two-sample Mendelian randomization (MR) tested causal directions, and two-step mediation MR evaluated smoking.
RESULTS: COPD showed significant genetic correlation with nine GI diseases. We identified six comorbidity-associated loci (three with CADD > 12.37) and 13 unique candidate pleiotropic genes; APOE was supported by proteomic evidence. Enrichment analyses highlighted lipid-metabolism pathways. MR suggested COPD increases risk of gastroesophageal reflux disease (GERD), irritable bowel syndrome (IBS), acute appendicitis, and gastric ulcer, while diverticular disease showed reverse causality toward COPD. Smoking partially mediated the COPD effect on GERD, acute appendicitis, and gastric ulcer.
CONCLUSION: COPD and multiple GI disorders share a distributed pleiotropic genetic basis within the broader systemic comorbidity spectrum of COPD. Multi-omics evidence supports a genomic pulmonary-intestinal axis in which lipid metabolism and smoking-related mechanisms contribute to COPD and GI comorbidity, providing targets for risk stratification and potential intervention.
PMID:41978582 | PMC:PMC13070119 | DOI:10.2147/COPD.S561645
KLong: Training LLM Agent for Extremely Long-horizon Tasks
S100A6 promotes liver metastasis by activating FGFR3 signaling in <i>BAP1</i>-deficient uveal melanoma
Oncogene, Published online: 04 April 2026; doi:10.1038/s41388-026-03766-0
S100A6 promotes liver metastasis by activating FGFR3 signaling in BAP1-deficient uveal melanomaTwo-step clinical care pathway to predict MASLD-related advanced fibrosis and long-term outcomes in type 2 diabetes
Gut. 2026 Feb 9;75(3):576-587. doi: 10.1136/gutjnl-2025-337506.
ABSTRACT
BACKGROUND: Current guidelines recommend a two-step approach for risk stratification of metabolic dysfunction-associated steatotic liver disease (MASLD), starting with Fibrosis-4 index (FIB-4) followed by liver stiffness measurement (LSM) using vibration-controlled transient elastography (VCTE).
OBJECTIVE: To evaluate this approach for predicting advanced fibrosis and liver-related events (LREs) in patients with type 2 diabetes (T2D).
DESIGN: A prospective liver biopsy cohort of T2D patients with histologically confirmed MASLD from seven centres in China was used to assess diagnostic performance for advanced fibrosis. The international VCTE-Prognosis cohort, including T2D patients with MASLD who underwent VCTE at 16 centres in the USA, Europe and Asia, with longitudinal follow-up, was used to assess LREs, defined as hepatic decompensation or hepatocellular carcinoma.
RESULTS: 4781 participants were included. In the liver biopsy cohort (n=352; 22.2% with advanced fibrosis), applying LSM thresholds of <8 kPa and >12 kPa after FIB-4 classified patients into 63.4% low-risk, 9.4% intermediate-risk and 27.3% high-risk, with a correct classification rate of 71%. In the VCTE-Prognosis cohort (n=4429; median follow-up 51.3 (IQR 27.4-70.7) months), 140 (3.2%) patients developed LREs (110 (2.5%) with hepatic decompensation and 59 (1.3%) with hepatocellular carcinoma). The two-step approach classified 72.6%, 6.8% and 20.6% of patients into low-risk, intermediate-risk and high-risk groups, with corresponding 5-year cumulative LRE incidences of 0.7%, 0.9% and 11.8%. Refining classification of intermediate FIB-4 patients using LSM <10 kPa (low-risk) and >15 kPa (high-risk) reduced the intermediate-risk group to 5.6% while preserving predictive accuracy.
CONCLUSION: The non-invasive two-step approach of FIB-4 followed by LSM effectively stratifies MASLD-related advanced fibrosis and LREs risk in T2D. Applying LSM cut-offs of 10 and 15 kPa further optimises risk stratification for future LREs.
PMID:41911049 | DOI:10.1136/gutjnl-2025-337506