Journal of Gastroenterology and Hepatology最新文献

{"title":"Guselkumab in East Asians With Moderate-to-Severe Ulcerative Colitis: Subgroup Analysis of the QUASAR Induction and Maintenance Studies.","authors":"Baili Chen, Byong Duk Ye, Qian Cao, Fumihito Hirai, Masayuki Saruta, Minhu Chen, Susan Pelak, Nicole Shipitofsky, Ye Miao, Keira Herr, Bryan Wahking, Jianmin Zhuo, Tadakazu Hisamatsu","doi":"10.1111/jgh.17036","DOIUrl":"https://doi.org/10.1111/jgh.17036","url":null,"abstract":"<p><strong>Background and aim: </strong>The global QUASAR (NCT04033445) clinical program demonstrated the efficacy and safety of guselkumab, a dual-acting interleukin-23 p19 subunit inhibitor, as induction and maintenance therapy in participants with moderate to severely active ulcerative colitis (UC). We report a subgroup analysis in East Asian participants.</p><p><strong>Methods: </strong>The QUASAR program included two randomized, placebo-controlled, 12-week induction studies of guselkumab 200 mg (and 400 mg, Phase 2b) IV every 4 weeks (q4w) in adults with baseline modified Mayo scores of 5-9 and inadequate response/intolerance to conventional and/or advanced UC therapy. Clinical responders to guselkumab induction were re-randomized (1:1:1) at maintenance study baseline to SC guselkumab 200 mg q4w, 100 mg q8w, or placebo. Primary endpoints were clinical response (Phase 2b) or clinical remission (Phase 3) at induction Week 12 (I-12) and clinical remission at maintenance Week 44 (M-44). Subgroup analyses included participants from sites in China, Japan, Korea, and Taiwan region.</p><p><strong>Results: </strong>Data were from 71 (Phase 2b) and 135 (Phase 3) East Asians in the induction studies and 106 in the maintenance study. At Week I-12, 45.5%-58.8% of guselkumab versus 25.5%-29.2% of placebo participants achieved clinical response and 16.0%-23.8% versus 4.2%-5.5%, respectively, achieved clinical remission. At Week M-44, 37.1%-46.3% of guselkumab versus 13.3% of placebo participants achieved clinical remission. The adverse event profile was generally consistent with the global QUASAR population.</p><p><strong>Conclusions: </strong>Results support the efficacy and safety of guselkumab induction and maintenance in East Asians with moderately to severely active UC, consistent with findings from the global QUASAR studies.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov, NCT04033445; EudraCT, 2018-004002-25.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compositional and Metabolomic Shifts of the Gut Microbiome in Alcohol-Related Liver Disease.","authors":"Cheng-Hao Kuo, Emad El-Omar, Cheng-Yen Kao, Jaw-Town Lin, Chun-Ying Wu","doi":"10.1111/jgh.17038","DOIUrl":"https://doi.org/10.1111/jgh.17038","url":null,"abstract":"<p><p>Alcohol-related liver disease (ALD) is a major global health concern characterized by steatosis and liver inflammation due to chronic alcohol consumption. Emerging evidence suggests that ALD is not solely a liver pathology but also involves dysfunction of the gut-liver axis, where alterations in the gut microbiota play a significant role. Although alcohol-associated dysbiosis has been extensively studied, whether these microbial changes contribute to ALD development or are merely a consequence of alcohol exposure remains unclear. To prove causation, it is essential to decipher which specific taxa and their metabolites drive the maladaptation of host-microbiota interactions upon alcohol exposure. In this review, we summarize the compositional changes in the gut microbiome after alcohol exposure, identifying traits of alcohol-induced dysbiosis and distinguishing them from those associated with liver disease. The effects of alcohol-induced dysbiosis on microbial metabolism and host responses are reviewed, focusing on the key classes of microbiota-derived metabolites, notably free fatty acids, tryptophan and its indole derivatives, and secondary bile acids. We discuss how alterations in these metabolites disrupt intestinal barrier function, immune responses, and metabolic signaling pathways, thereby exacerbating alcohol-induced injury. Advanced omics technologies and microbiome modulation strategies will help further investigation into these mechanisms. Detailed mechanistic insights into host-microbiota interactions could unveil novel therapeutic targets, offering potential strategies to prevent or mitigate ALD by modulating the gut microbiome and its metabolites.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144484677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carcinoma of Esophagus.","authors":"Joseph Sung, Dongxin Lin, Rebecca Fitzgerald, Prateek Sharma, Simon Law, David Ilson","doi":"10.1111/jgh.16990","DOIUrl":"https://doi.org/10.1111/jgh.16990","url":null,"abstract":"<p><p>Carcinoma of esophagus is one of the most common cancer worldwide, but its epidemiology is changing. Squamous cell carcinoma is declining in the East, but adenocarcinoma is rising in the West, probably related to the pandemic of obesity and changing lifestyle. Screening of esophageal cancer (both endoscopic and nonendoscopic methods) is recommended in patients suffering from long-term acid reflux symptoms associated with high-risk factors and surveillance in patients with Barrett's esophagus. Endoscopy with virtual chromoendoscopy, endoscopic ultrasound, and CT scan is essential for diagnosis and staging of the disease. Endoscopic therapy can be used to treat early diseases. Surgery remains a mainstay treatment. Multimodality treatment strategies involving combinations of chemotherapy, radiotherapy, and more recently immunotherapy and target therapies are gaining momentum.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144484676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"Promotion of Wound Healing by Acetate in Murine Colonic Epithelial Cell via c-Jun N-Terminal Kinase Activation\".","authors":"","doi":"10.1111/jgh.17039","DOIUrl":"https://doi.org/10.1111/jgh.17039","url":null,"abstract":"","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-Diagnosis Alkaline Phosphatase and Antimitochondrial Antibody Positivity Vary by Race/Ethnicity Among Patients With Primary Biliary Cholangitis.","authors":"Allyce Caines, Mei Lu, Trueman Wu, Sheri Trudeau, Christina Melkonian, Humberto C Gonzalez, Amandeep K Sahota, Mark A Schmidt, Yihe Daida, Christopher L Bowlus, Stuart C Gordon","doi":"10.1111/jgh.17035","DOIUrl":"https://doi.org/10.1111/jgh.17035","url":null,"abstract":"<p><strong>Background: </strong>Diagnosis of primary biliary cholangitis (PBC) is made using alkaline phosphatase (ALP) and positive antimitochondrial antibody (AMA), but these biomarkers may vary by race. There is also little known about changes in ALP in the years prior to PBC diagnosis.</p><p><strong>Methods: </strong>Using data from the Fibrotic Liver Disease Consortium, we used matched pairs to evaluate racial differences in ALP for up to 5 years prior to diagnosis. We also compared rates of AMA positivity by race.</p><p><strong>Results: </strong>1335 confirmed PBC patients were included: 769 (58%) non-Hispanic white (NHW); 110 (8%) Black; 138 (11%) Asian American Pacific Islander (AAPI); and 318 (24%) Hispanic. 774 patients had AMA test results. Black patients had significantly lower AMA positivity than NHWs. Black patients were less likely to be AMA-positive compared to NHW patients (OR = 0.50, 95% CI 0.29-0.86, p = 0.012). There were no significant differences in rates of AMA positivity between AAPI or  Hispanic versus NHW patients. All patient groups had elevated ALP for 2-5 years prior to diagnosis. ALP differed between Black and NHW patients only at specific times before diagnosis. There were no significant differences in ALP between Hispanic and NHW patients. AAPI patients had significantly lower ALP compared to NHWs.</p><p><strong>Conclusion: </strong>In a diverse sample of PBC patients, we observed significant differences in AMA positivity and pre-diagnosis ALP levels by race. Future studies to better characterize PBC across racial/ethnic groups are warranted.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thermophiles, Thick-Walled Bacteria, and Pseudomonads in High-Altitude Gut Microbiota.","authors":"Fang Yan, Shi-Min Wu, Wen-Qiang Yuan, Yun-Han Yang, Hao Zhu, De-Jun Cui","doi":"10.1111/jgh.17032","DOIUrl":"https://doi.org/10.1111/jgh.17032","url":null,"abstract":"<p><strong>Background and aim: </strong>High-altitude environments are characterized by low oxygen and reduced low pressure, which impose significant physiological challenges on organisms. Among various adaptive systems, the intestinal flora plays a crucial role in maintaining gut health and barrier integrity function under such conditions. This study aimed to elucidate the regulatory mechanisms of intestinal flora in high-altitude environments, focusing on downregulating intracellular Bone Morphogenetic Protein 4 (BMP4) to influence glycolysis metabolism, thereby affecting intercellular communication of the intestinal mucosal barrier and matrix remodeling.</p><p><strong>Methods: </strong>High-altitude mouse intestinal flora composition and function were analyzed using 16S rRNA and metagenomic sequencing. Additionally, single-cell sequencing was employed to examine cell population communication and gene expression differences between normal and high-altitude mouse intestinal tissues.</p><p><strong>Results: </strong>Single-cell sequencing showed significantly reduced interactions between intestinal fibroblasts and epithelial cells in high-altitude mice, accompanied by a marked increase in BMP4 expression. Overexpression of BMP4 was found to activate the glycolysis pathway. Gut microbiota metabolites, including secondary bile acids, lactic acid, and butyrate, exhibited protective effects on hypoxia-induced intestinal mucosal barrier injury, with butyrate showing the most prominent effect. Under hypoxic conditions, butyrate suppressed the BMP4/glycolysis pathway, thereby alleviating hypoxia-induced intestinal mucosal barrier damage.</p><p><strong>Conclusion: </strong>This study uncovered a novel mechanism by which the gut microbiota in high-altitude environments modulate glycolysis metabolism through BMP4 downregulation, thereby affecting intercellular communication and matrix remodeling within the intestinal mucosal barrier.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of Semaglutide in MASLD Treatment: Where Is the Master Key?","authors":"Devaraj Ezhilarasan","doi":"10.1111/jgh.17037","DOIUrl":"10.1111/jgh.17037","url":null,"abstract":"<p><strong>Background: </strong>Semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1 RA), is used for weight reduction and metabolic improvement. Semaglutide effectively improves MASH but not confers histological fibrosis resolution. The key question remains whether semaglutide exerts direct, independent effects in ameliorating MASH or if its benefits are merely secondary to improvements in weight, insulin resistance, and glycemic control. The exact mechanisms of action through which semaglutide or other GLP-1 RAs offer liver protection are not entirely clear.</p><p><strong>Methods: </strong>A comprehensive search in PubMed and EMBASE was conducted using the keywords \"Semaglutide and NAFLD/MASLD\", \"glucagon-like peptide-1 receptor agonist and MASLD/NALFD\", and \"Semaglutide and type II diabetes/obesity and hypertension\". Relevant papers published before February, 2025, were included.</p><p><strong>Results: </strong>Semaglutide modulates several lipid-associated molecular pathways through unknown mechanisms. Preclinical and clinical studies suggest that semaglutide acts by (i) reducing appetite and increasing satiety, thereby decreasing dietary intake and subsequent free fatty acid export to the liver; (ii) reducing insulin resistance and improving insulin sensitivity and adipose dysfunction; (iii) reducing de novo lipogenesis by downregulating ChREBP and SREBP-1c signaling, as well as the expression of lipid-synthesizing genes; (iv) reducing the weight of white and brown adipose tissue; and (v) reducing inflammation by decreasing pro-inflammatory markers in GLP-1-expressing macrophages and favorably altering the gut microbiota.</p><p><strong>Conclusion: </strong>While this review explores the potential mechanisms of semaglutide action, the lack of GLP-1 receptor expression in the livers of mice and humans suggests that these mechanisms are associated with indirect modulation. Consequently, further mechanistic studies are needed to elucidate these pathways.</p><p><strong>Trial registration: </strong>NOT APPLICABLE.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of the Pro-Tumorigenic Role of the ELK4-METTL3-CEMIP Axis in Colorectal Carcinoma: Promotion of Cancer Cell Stemness and Malignant Phenotypes.","authors":"Lanfang Zhang, Fang Yang, Xiaoling Zhang, Daiyuan Dong, Xiangjie Fang, Lijun Meng, Tingmin Chang","doi":"10.1111/jgh.17030","DOIUrl":"https://doi.org/10.1111/jgh.17030","url":null,"abstract":"<p><strong>Background: </strong>Colorectal carcinoma (CRC) is the third most prevalent and deadly malignancy worldwide. CEMIP has emerged as a significant player in colorectal tumorigenesis and CRC metastasis. Here, we explored the specific role of CEMIP in the malignant phenotypes and stemness of CRC cells.</p><p><strong>Methods: </strong>The expression analysis was performed by quantitative PCR, immunohistochemistry, or immunoblot methods. The effect on CRC cell malignant phenotypes was determined by detecting cell colony formation, invasion, and migration. The influence on CRC cell stemness was evaluated by analyzing cell spheroid formation potential and related protein expression. The METTL3-CEMIP relationship was confirmed by RIP, luciferase, and mRNA stability assays. The ELK4-METTL3 relationship was verified by ChIP and luciferase assays.</p><p><strong>Results: </strong>High levels of CEMIP in CRC were associated with poor patient outcomes. CEMIP downregulation inhibited CRC cell growth, migration, invasion, and stemness while promoting apoptosis. Moreover, METTL3 stabilized CEMIP mRNA to upregulate its expression. CEMIP restoration reversed METTL3 knockdown-driven alterations in cell phenotypes and stemness. The transcription factor (TF) ELK4 transcriptionally upregulated METTL3, thereby influencing the stemness and malignant behaviors of CRC cells. Furthermore, ELK4 increased CEMIP expression through METTL3 in CRC cells. Additionally, ELK4 depletion hindered the in vivo tumorigenesis of SW620 CRC cells.</p><p><strong>Conclusion: </strong>Our findings demonstrate that the ELK4-METTL3-CEMIP axis enhances the development of CRC. Targeting the axis may lead to the development of novel strategies against CRC.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sanguisorba officinalis L. and Sophora japonica L. Inhibit Angiogenesis in Ulcerative Colitis.","authors":"Wei Yuzhuo, Liu Li, Bu Shu, Yan Jing, Wang Yongqi, Miao Zhiwei, Xu Yi","doi":"10.1111/jgh.17034","DOIUrl":"https://doi.org/10.1111/jgh.17034","url":null,"abstract":"<p><strong>Background and aim: </strong>Sanguisorba officinalis L. and Sophora japonica L. (SOSJ) have been frequently used as medicinal pairs for treating ulcerative colitis (UC) due to their hemostatic properties. However, the mechanisms underlying their therapeutic effects remain unclear. This study aims to predict the targets of SOSJ for UC treatment using liquid chromatography-quadrupole time-of-flight tandem mass spectrometry (LC-QTOF-MS) and network pharmacology.</p><p><strong>Methods: </strong>The efficacy of SOSJ was evaluated using a 3% dextrose sodium sulfate (DSS)-induced UC mice model. The general condition of the mice, histopathology, and expression of colonic inflammatory factors were assessed. Additionally, the effect of SOSJ on angiogenesis was evaluated by detecting the mRNA of colonic angiogenesis-related mediators, measuring microvessel density, and using transmission electron microscopy.</p><p><strong>Results: </strong>SOSJ significantly attenuated inflammation and inhibited pathological angiogenesis in UC mice. It alleviated weight loss, colon shortening, and the presence of pus and blood in stools. SOSJ also reduced the mRNA expression levels of IL-6, IL-1β, TNF-α, VEGF, VCAM1, Ang1, MMP1, MMP2, and MMP9. Furthermore, SOSJ decreased the protein expression of the PI3K-Akt pathway, an effect that could be reversed by 740Y-P, a specific PI3K activator.</p><p><strong>Conclusion: </strong>S. officinalis L. and S. japonica L. exert therapeutic effects on mice with ulcerative colitis, potentially through the modulation of angiogenesis and the PI3K-Akt signalling pathway.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Increased Epstein-Barr Virus Reactivation With Imbalanced Immunity and Myenteric Neuron Loss in Achalasia.","authors":"Li-Yun Ma, Ling Du, Lu Yao, Wei-Feng Chen, Meng-Jiang He, Yun Wang, Jia-Qi Xu, Zi-Han Geng, Xiao-Qing Li, Zhao-Chao Zhang, Li Wang, Ke-Hao Wang, Quan-Lin Li, Ping-Hong Zhou, Zu-Qiang Liu","doi":"10.1111/jgh.17018","DOIUrl":"https://doi.org/10.1111/jgh.17018","url":null,"abstract":"<p><strong>Background and aim: </strong>Viral infection has been postulated as a potential etiology of achalasia, yet the definitive role of viral involvement remains elusive. This study aims to elucidate virus infections and to analyze their relationships with clinical characteristics, immunological alterations, and neuron loss.</p><p><strong>Methods: </strong>We investigated viral infections in achalasia patients (n = 288) and controls (n = 71). Propensity score matching (PSM) was employed to mitigate selection bias. Flow cytometry and ELISA were performed to characterize the immunological changes. In situ hybridization and immunofluorescence staining were used to detect viral infections within lower esophageal sphincter (LES).</p><p><strong>Results: </strong>No significant differences in the infection rates of HSV-1, HSV-2, CMV, or EBV were detected between two groups. Notably, EBV reactivation was greater in patients with achalasia than in controls (15.3% vs. 5.6%, p = 0.032), especially in Type I achalasia (21.0% vs. 5.6%, p = 0.008). Following PSM, EBV reactivation was associated with an increase in B cells (p = 0.001), a decrease in NK cells (p = 0.005), and lower levels of IL-6 (p = 0.02) and IL-8 (p = 0.05). Additionally, EBV reactivation group presented a greater EBV infection rate in LES (68.8% vs. 31.3%, p = 0.034), which was associated with increased neuron loss. EBV infection was detected in B and T cells of the LES, rather than neurons.</p><p><strong>Conclusions: </strong>Although relatively low, our findings reveal an increased frequency of EBV reactivation in patients with achalasia, which may be associated with imbalanced immunity and neuron loss in LES in these subpopulations. This study provides novel insights into the role of EBV reactivation in achalasia.</p>","PeriodicalId":15877,"journal":{"name":"Journal of Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}