Pub Date : 2026-01-28DOI: 10.1136/gutjnl-2025-337583
Matam Vijay-Kumar,Beng San Yeoh,Andrew T Gewirtz
{"title":"Hydroxylation matters! Microbial bile acid metabolism and colorectal cancer.","authors":"Matam Vijay-Kumar,Beng San Yeoh,Andrew T Gewirtz","doi":"10.1136/gutjnl-2025-337583","DOIUrl":"https://doi.org/10.1136/gutjnl-2025-337583","url":null,"abstract":"","PeriodicalId":12825,"journal":{"name":"Gut","volume":"31 1","pages":""},"PeriodicalIF":24.5,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146069834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Postoperative recurrence (POR) is a major challenge in the long-term management of Crohn's disease (CD), affecting up to 70% of patients within the first year after surgical resection. The multifactorial pathogenesis of POR complicates prevention, while evolving surgical techniques and different anastomotic configurations further hinder accurate prediction and monitoring.Current surveillance strategies, including standard ileocolonoscopy and faecal calprotectin, remain limited by suboptimal accuracy, the absence of validated scoring systems and the lack of standardised monitoring intervals. Recent advances in high-resolution endoscopic imaging, such as confocal laser endomicroscopy and endocytoscopy, enable real-time, in vivo microstructural assessment of the anastomosis, offering opportunities for earlier and more precise detection of recurrence. In parallel, developments in intestinal ultrasound and cross-sectional imaging are reshaping non-invasive monitoring by providing transmural evaluation. Beyond imaging, multiomics approaches, spanning genomics, transcriptomics, proteomics, metabolomics and metagenomics, are uncovering novel biological pathways linked to POR, providing new mechanistic insights.Artificial intelligence (AI) has the potential to integrate clinical, endoscopic, imaging and omics data into predictive multimodal models for POR, supporting individualised risk stratification, early detection and personalised treatment strategies. While promising, these innovations require prospective validation, methodological standardisation and integration into clinical workflows before translation into routine practice.This review summarises the current understanding of POR, highlights emerging diagnostic and monitoring technologies and explores how AI-enabled endoscopy and multi-omics approaches may transform future management, paving the way towards precision medicine for POR in CD.
{"title":"Shaping the future of postoperative recurrence in Crohn's disease: personalised approaches with AI-enabled imaging and multi-omics.","authors":"Marietta Iacucci,Irene Zammarchi,Cecilia Lina Pugliano,Giovanni Santacroce,Ivan Capobianco,Snehali Majumder,Andrea Ruffa,Valery Naranjo,Enrico Grisan,Olga Maria Nardone,Subrata Ghosh","doi":"10.1136/gutjnl-2025-337171","DOIUrl":"https://doi.org/10.1136/gutjnl-2025-337171","url":null,"abstract":"Postoperative recurrence (POR) is a major challenge in the long-term management of Crohn's disease (CD), affecting up to 70% of patients within the first year after surgical resection. The multifactorial pathogenesis of POR complicates prevention, while evolving surgical techniques and different anastomotic configurations further hinder accurate prediction and monitoring.Current surveillance strategies, including standard ileocolonoscopy and faecal calprotectin, remain limited by suboptimal accuracy, the absence of validated scoring systems and the lack of standardised monitoring intervals. Recent advances in high-resolution endoscopic imaging, such as confocal laser endomicroscopy and endocytoscopy, enable real-time, in vivo microstructural assessment of the anastomosis, offering opportunities for earlier and more precise detection of recurrence. In parallel, developments in intestinal ultrasound and cross-sectional imaging are reshaping non-invasive monitoring by providing transmural evaluation. Beyond imaging, multiomics approaches, spanning genomics, transcriptomics, proteomics, metabolomics and metagenomics, are uncovering novel biological pathways linked to POR, providing new mechanistic insights.Artificial intelligence (AI) has the potential to integrate clinical, endoscopic, imaging and omics data into predictive multimodal models for POR, supporting individualised risk stratification, early detection and personalised treatment strategies. While promising, these innovations require prospective validation, methodological standardisation and integration into clinical workflows before translation into routine practice.This review summarises the current understanding of POR, highlights emerging diagnostic and monitoring technologies and explores how AI-enabled endoscopy and multi-omics approaches may transform future management, paving the way towards precision medicine for POR in CD.","PeriodicalId":12825,"journal":{"name":"Gut","volume":"293 1","pages":""},"PeriodicalIF":24.5,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146056779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Kupffer cell autophagy emerges as a central regulator of immune dysregulation in primary biliary cholangitis.","authors":"Naths Grazia Sukubo,Chiara Caime,Alessio Gerussi,Pietro Invernizzi","doi":"10.1136/gutjnl-2025-337652","DOIUrl":"https://doi.org/10.1136/gutjnl-2025-337652","url":null,"abstract":"","PeriodicalId":12825,"journal":{"name":"Gut","volume":"74 1","pages":""},"PeriodicalIF":24.5,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146056778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-23DOI: 10.1136/gutjnl-2025-337684
Tommaso Lorenzo Parigi,Fabio Cominelli
{"title":"Role of TL1A in perianal fistulising Crohn's disease: a new therapeutic target?","authors":"Tommaso Lorenzo Parigi,Fabio Cominelli","doi":"10.1136/gutjnl-2025-337684","DOIUrl":"https://doi.org/10.1136/gutjnl-2025-337684","url":null,"abstract":"","PeriodicalId":12825,"journal":{"name":"Gut","volume":"36 1","pages":""},"PeriodicalIF":24.5,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146033619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUNDRNA 5-methylcytosine (m5C) has emerged as a critical epigenetic regulator in cancer biology, yet its role in the tumour immune microenvironment (TME) remains incompletely understood.OBJECTIVEWe aimed to elucidate the functional role and underlying mechanism of NOP2/Sun RNA methyltransferase 6 (NSUN6), an m5C methyltransferase, in shaping the TME of pancreatic ductal adenocarcinoma (PDAC).DESIGNThe clinical significance of NSUN6 was assessed in human PDAC cohorts. The impact of NSUN6 on antitumour immunity was evaluated using murine PDAC models. Single-cell RNA sequencing was employed to characterise the TME landscape of PDAC. RNA bisulfite sequencing and RNA sequencing were used to identify NSUN6 targets. The synergistic effects of C-C motif chemokine ligand 2 (CCL2) blockade combined with immune checkpoint blockade (ICB) therapy were investigated.RESULTSNSUN6 deficiency significantly enhanced macrophage accumulation and polarisation toward immunosuppressive phenotypes, thereby impairing CD8+ T cell-mediated antitumour immunity in PDAC. Mechanistically, NSUN6 deficiency downregulated KDM5A expression in an m5C-dependent manner, resulting in transcriptional activation of CCL2. Elevated CCL2 secretion promoted the accumulation and polarisation of protumorous macrophages, fostering an immunosuppressive TME and inducing resistance to ICB. Notably, CCL2 blockade reversed protumorous macrophage infiltration and restored ICB sensitivity in Nsun6-deficient murine PDAC models. Clinical analysis further revealed a positive correlation between NSUN6 expression and favourable immune responses in ICB-treated cohorts.CONCLUSIONNSUN6 deficiency drives immune suppression through the m5C-KDM5A-CCL2 axis in PDAC. Targeting the NSUN6-CCL2 axis represents a promising strategy to sensitise PDAC to ICB therapy.
{"title":"NSUN6 deficiency drives immune suppression in pancreatic cancer via the KDM5A-CCL2-macrophage axis.","authors":"Lingxing Zeng,Shuang Liu,Xinyi Peng,Chunling Xue,Daoyuan Wang,Ruihong Bai,Shaoqiu Liu,Ziming Chen,Hongzhe Zhao,Zilan Xu,Sihan Zhao,Yifan Zhou,Xiaoyu Wu,Shaojia Wu,Mei Li,Ji Liu,Jialiang Zhang,Qi Zhou,Xudong Huang,Jiachun Su","doi":"10.1136/gutjnl-2025-336541","DOIUrl":"https://doi.org/10.1136/gutjnl-2025-336541","url":null,"abstract":"BACKGROUNDRNA 5-methylcytosine (m5C) has emerged as a critical epigenetic regulator in cancer biology, yet its role in the tumour immune microenvironment (TME) remains incompletely understood.OBJECTIVEWe aimed to elucidate the functional role and underlying mechanism of NOP2/Sun RNA methyltransferase 6 (NSUN6), an m5C methyltransferase, in shaping the TME of pancreatic ductal adenocarcinoma (PDAC).DESIGNThe clinical significance of NSUN6 was assessed in human PDAC cohorts. The impact of NSUN6 on antitumour immunity was evaluated using murine PDAC models. Single-cell RNA sequencing was employed to characterise the TME landscape of PDAC. RNA bisulfite sequencing and RNA sequencing were used to identify NSUN6 targets. The synergistic effects of C-C motif chemokine ligand 2 (CCL2) blockade combined with immune checkpoint blockade (ICB) therapy were investigated.RESULTSNSUN6 deficiency significantly enhanced macrophage accumulation and polarisation toward immunosuppressive phenotypes, thereby impairing CD8+ T cell-mediated antitumour immunity in PDAC. Mechanistically, NSUN6 deficiency downregulated KDM5A expression in an m5C-dependent manner, resulting in transcriptional activation of CCL2. Elevated CCL2 secretion promoted the accumulation and polarisation of protumorous macrophages, fostering an immunosuppressive TME and inducing resistance to ICB. Notably, CCL2 blockade reversed protumorous macrophage infiltration and restored ICB sensitivity in Nsun6-deficient murine PDAC models. Clinical analysis further revealed a positive correlation between NSUN6 expression and favourable immune responses in ICB-treated cohorts.CONCLUSIONNSUN6 deficiency drives immune suppression through the m5C-KDM5A-CCL2 axis in PDAC. Targeting the NSUN6-CCL2 axis represents a promising strategy to sensitise PDAC to ICB therapy.","PeriodicalId":12825,"journal":{"name":"Gut","volume":"9 1","pages":""},"PeriodicalIF":24.5,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUNDCoexistence of metabolic dysfunction-associated steatotic liver disease (MASLD) increases hepatocellular carcinoma (HCC) risk after HCV cure.OBJECTIVEThe specific impacts of steatosis grade and cardiometabolic burden on HCC risk among patients with MASLD remain unclear.DESIGNWe enrolled 700 patients who underwent biannual HCC surveillance after HCV cure. Steatosis was graded by vibration-controlled transient elastography using controlled attenuation parameter cut-offs of 248-267, 268-279 and ≥280 dB/m, corresponding to S1, S2 and S3, respectively. Cardiometabolic risk factors (CMRFs) were assessed at the time of viral cure. Cumulative HCC incidence was compared across steatosis grades and cardiometabolic burdens using the log-rank test. Multivariable Cox proportional hazards models with Akaike Information Criterion-based selection evaluated the effects of steatosis grade, cardiometabolic burden and individual CMRFs on HCC risk, expressed as adjusted HRs (aHRs) with 95% CIs. Fine-Gray subdistribution hazard models were used for sensitivity analyses.RESULTSCumulative HCC incidence differed significantly across steatosis grades (p=0.035) but not across cardiometabolic burdens (p=0.62). In multivariable analysis adjusted for age, sex, liver stiffness and alpha-fetoprotein, advanced steatosis remained independently associated with HCC risk (S3 vs S1: aHR 2.15, 95% CI 1.25 to 3.69, p=0.005). Among individual CMRFs, pre-diabetes or type 2 diabetes was significantly associated with HCC risk (aHR 2.33, 95% CI 1.38 to 3.94, p=0.002). Fine-Gray analyses confirmed these associations.CONCLUSIONAdvanced hepatic steatosis and glycaemic abnormalities, rather than overall cardiometabolic burden, are independently associated with increased HCC risk after HCV cure.
背景：代谢功能障碍相关脂肪变性肝病（MASLD）的共存增加了HCV治愈后发生肝细胞癌（HCC）的风险。目的：脂肪变性等级和心脏代谢负担对MASLD患者HCC风险的具体影响尚不清楚。设计：我们招募了700名HCV治愈后接受半年HCC监测的患者。通过振动控制瞬态弹性学对脂肪变性进行分级，采用控制衰减参数截止值为248-267、268-279和≥280 dB/m，分别对应S1、S2和S3。在病毒治愈时评估心脏代谢危险因素（CMRFs）。使用log-rank检验比较不同脂肪变性等级和心脏代谢负荷的累积HCC发病率。基于赤道信息标准选择的多变量Cox比例风险模型评估了脂肪变性等级、心脏代谢负担和个体cmrf对HCC风险的影响，以校正hr （aHRs）表示，ci为95%。敏感性分析采用细灰色亚分布风险模型。结果肝细胞癌的累积发病率在脂肪变性分级中有显著差异（p=0.035），但在心脏代谢负荷组中无显著差异（p=0.62）。在调整了年龄、性别、肝脏硬度和甲胎蛋白的多变量分析中，晚期脂肪变性仍然与HCC风险独立相关（S3 vs S1: aHR 2.15, 95% CI 1.25 ~ 3.69, p=0.005）。在个体cmrf中，糖尿病前期或2型糖尿病与HCC风险显著相关（aHR 2.33, 95% CI 1.38至3.94,p=0.002）。精细灰色分析证实了这些关联。结论：晚期肝脂肪变性和血糖异常与HCV治愈后HCC风险增加独立相关，而非总体心脏代谢负担。
{"title":"Steatosis grade and cardiometabolic burden as determinants of hepatocellular carcinoma risk after hepatitis C cure in patients with metabolic dysfunction-associated steatotic liver disease.","authors":"Yu-Ping Chang,Yun-Chu Chen,Pin-Nan Cheng,Yu-Jen Fang,Chi-Yi Chen,Wei-Yu Kao,Chih-Lin Lin,Sheng-Shun Yang,Yu-Lueng Shih,Cheng-Yuan Peng,Fu-Jen Lee,Ming-Chang Tsai,Shang-Chin Huang,Tung-Hung Su,Tai-Chung Tseng,Chun-Jen Liu,Pei-Jer Chen,Jia-Horng Kao,Chen-Hua Liu","doi":"10.1136/gutjnl-2025-337275","DOIUrl":"https://doi.org/10.1136/gutjnl-2025-337275","url":null,"abstract":"BACKGROUNDCoexistence of metabolic dysfunction-associated steatotic liver disease (MASLD) increases hepatocellular carcinoma (HCC) risk after HCV cure.OBJECTIVEThe specific impacts of steatosis grade and cardiometabolic burden on HCC risk among patients with MASLD remain unclear.DESIGNWe enrolled 700 patients who underwent biannual HCC surveillance after HCV cure. Steatosis was graded by vibration-controlled transient elastography using controlled attenuation parameter cut-offs of 248-267, 268-279 and ≥280 dB/m, corresponding to S1, S2 and S3, respectively. Cardiometabolic risk factors (CMRFs) were assessed at the time of viral cure. Cumulative HCC incidence was compared across steatosis grades and cardiometabolic burdens using the log-rank test. Multivariable Cox proportional hazards models with Akaike Information Criterion-based selection evaluated the effects of steatosis grade, cardiometabolic burden and individual CMRFs on HCC risk, expressed as adjusted HRs (aHRs) with 95% CIs. Fine-Gray subdistribution hazard models were used for sensitivity analyses.RESULTSCumulative HCC incidence differed significantly across steatosis grades (p=0.035) but not across cardiometabolic burdens (p=0.62). In multivariable analysis adjusted for age, sex, liver stiffness and alpha-fetoprotein, advanced steatosis remained independently associated with HCC risk (S3 vs S1: aHR 2.15, 95% CI 1.25 to 3.69, p=0.005). Among individual CMRFs, pre-diabetes or type 2 diabetes was significantly associated with HCC risk (aHR 2.33, 95% CI 1.38 to 3.94, p=0.002). Fine-Gray analyses confirmed these associations.CONCLUSIONAdvanced hepatic steatosis and glycaemic abnormalities, rather than overall cardiometabolic burden, are independently associated with increased HCC risk after HCV cure.","PeriodicalId":12825,"journal":{"name":"Gut","volume":"142 1","pages":""},"PeriodicalIF":24.5,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146005009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-20DOI: 10.1136/gutjnl-2025-337059
Cristian Díaz-Muñoz,Isotta Bozzarelli,Esteban Alexander Lopera-Maya,Lazaros Belbasis,Valeria Lo Faro,Leticia Camargo Tavares,Francisco Heredia-Fernández,Biagio Di Lorenzo,Trishla Sinha,Cristina Esteban Blanco,Marie-Julie Favé,Philip Awadalla,Robin G Walters,Ferdinando Bonfiglio,Alexandra Zhernakova,Serena Sanna,Mauro D'Amato
BACKGROUNDGenetic studies of stool frequency (SF), an indirect proxy for gastrointestinal transit, may reveal therapeutically tractable pathways relevant to IBS and other dysmotility disorders.OBJECTIVETo identify genes and mechanisms involved in gut motility, providing a foundation for clinical translation.DESIGNWe performed a multiancestry genome-wide association study (GWAS) meta-analysis of SF in 268 606 European and East Asian individuals. Heritability and genetic correlations with other traits were estimated, and Mendelian randomisation was used to test causal relationships. GWAS signals were fine-mapped and functionally annotated to prioritise candidate genes and pathways. Findings implicating thiamine metabolism were followed-up with dietary interaction analyses in UK Biobank (UKB).RESULTSSF heritability was comparable in Europeans (7.0%) and East Asians (5.6%). We observed strong genetic correlations with gastrointestinal and psychiatric disorders (rg=0.18-0.47), and causal effects on IBS. Novel correlations with cardiovascular traits (rg=0.12-0.14) were supported by drug signature enrichment analyses. We identified 21 independent loci, including 10 novel signals implicating bile acid synthesis (KLB) and cholinergic signalling (COLQ). Fine-mapping converged on vitamin B1 metabolism, highlighting single-variant causal effects at SLC35F3 (a thiamine transporter) and XPR1 (phosphate exporter essential for thiamine activation). In 98 449 UKB participants, thiamine intake was positively associated with SF (p<0.0001), and a combined SLC35F3/XPR1 genotype score significantly modulated this effect (p<0.0001).CONCLUSIONSWe identify therapeutically tractable mechanisms involved in the control of gut motility, including a previously unrecognised role for vitamin B1. These findings warrant mechanistic and clinical studies to evaluate their translational potential in IBS and other dysmotility syndromes.
{"title":"Genetic dissection of stool frequency implicates vitamin B1 metabolism and other actionable pathways in the modulation of gut motility.","authors":"Cristian Díaz-Muñoz,Isotta Bozzarelli,Esteban Alexander Lopera-Maya,Lazaros Belbasis,Valeria Lo Faro,Leticia Camargo Tavares,Francisco Heredia-Fernández,Biagio Di Lorenzo,Trishla Sinha,Cristina Esteban Blanco,Marie-Julie Favé,Philip Awadalla,Robin G Walters,Ferdinando Bonfiglio,Alexandra Zhernakova,Serena Sanna,Mauro D'Amato","doi":"10.1136/gutjnl-2025-337059","DOIUrl":"https://doi.org/10.1136/gutjnl-2025-337059","url":null,"abstract":"BACKGROUNDGenetic studies of stool frequency (SF), an indirect proxy for gastrointestinal transit, may reveal therapeutically tractable pathways relevant to IBS and other dysmotility disorders.OBJECTIVETo identify genes and mechanisms involved in gut motility, providing a foundation for clinical translation.DESIGNWe performed a multiancestry genome-wide association study (GWAS) meta-analysis of SF in 268 606 European and East Asian individuals. Heritability and genetic correlations with other traits were estimated, and Mendelian randomisation was used to test causal relationships. GWAS signals were fine-mapped and functionally annotated to prioritise candidate genes and pathways. Findings implicating thiamine metabolism were followed-up with dietary interaction analyses in UK Biobank (UKB).RESULTSSF heritability was comparable in Europeans (7.0%) and East Asians (5.6%). We observed strong genetic correlations with gastrointestinal and psychiatric disorders (rg=0.18-0.47), and causal effects on IBS. Novel correlations with cardiovascular traits (rg=0.12-0.14) were supported by drug signature enrichment analyses. We identified 21 independent loci, including 10 novel signals implicating bile acid synthesis (KLB) and cholinergic signalling (COLQ). Fine-mapping converged on vitamin B1 metabolism, highlighting single-variant causal effects at SLC35F3 (a thiamine transporter) and XPR1 (phosphate exporter essential for thiamine activation). In 98 449 UKB participants, thiamine intake was positively associated with SF (p<0.0001), and a combined SLC35F3/XPR1 genotype score significantly modulated this effect (p<0.0001).CONCLUSIONSWe identify therapeutically tractable mechanisms involved in the control of gut motility, including a previously unrecognised role for vitamin B1. These findings warrant mechanistic and clinical studies to evaluate their translational potential in IBS and other dysmotility syndromes.","PeriodicalId":12825,"journal":{"name":"Gut","volume":"64 1","pages":""},"PeriodicalIF":24.5,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146005011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-20DOI: 10.1136/gutjnl-2026-338118
Qing-Bao Jiang,Guo-Ming Zhang
{"title":"Clarifying the stopping rule and clinical value of AI-guided PEG titration for bowel preparation.","authors":"Qing-Bao Jiang,Guo-Ming Zhang","doi":"10.1136/gutjnl-2026-338118","DOIUrl":"https://doi.org/10.1136/gutjnl-2026-338118","url":null,"abstract":"","PeriodicalId":12825,"journal":{"name":"Gut","volume":"49 1","pages":""},"PeriodicalIF":24.5,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146005078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：