Nature Nanotechnology, Published online: 07 September 2026; doi:10.1038/s41565-026-02271-5
Single copper atoms on boron nanosheets dynamically and reversibly switch to clusters, enabling the direct conversion of methane to acetic acid with 97% selectivity and high activity without the requirement for carbon monoxide.
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
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
J Gene Med. 2026 Sep;28(9):e70111. doi: 10.1002/jgm.70111.
ABSTRACT
BACKGROUND: Metabolic pathways are crucial in hepatocellular carcinoma (HCC) pathogenesis, but causal metabolic genes remain unclear. This study used Summary data-based Mendelian Randomization (SMR) and colocalization to identify metabolism-related genetic loci influencing HCC risk.
METHODS: Differentially expressed genes in hepatic malignancy phenotype versus normal tissues from TCGA and GTEx were analyzed. Metabolism-related candidates were examined via SMR and colocalization using multi-omics data: methylation (mQTL), expression (eQTL), and protein (pQTL) quantitative trait loci.
RESULTS: Multi-omics integration identified NIT2 as a key metabolic regulator for HCC. The cg13016775 locus of NIT2 was associated with elevated HCC risk at gene (OR = 1.618, 95% CI: 1.199-2.182) and protein (OR = 4.432, 95% CI: 1.783-11.018) levels. Colocalization supported a shared causal variant (PPH4 > 0.6), linking NIT2 to hepatocarcinogenesis via metabolic regulation.
CONCLUSIONS: This study provides multi-omics evidence for NIT2 as a potential causal gene in HCC, enhancing understanding of metabolic contributions to HCC pathogenesis and highlighting integrative genomics for uncovering causal relationships.
PMID:42681890 | PMC:PMC13534973 | DOI:10.1002/jgm.70111
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