Post-infection disorders of gut-brain interaction (PI-DGBI) are a subset of chronic gastrointestinal disorders triggered by acute infectious gastroenteritis. These conditions impose a significant burden on patients' quality of life.

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.

RNA 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.

Coexistence of metabolic dysfunction-associated steatotic liver disease (MASLD) increases hepatocellular carcinoma (HCC) risk after HCV cure.

Genetic studies of stool frequency (SF), an indirect proxy for gastrointestinal transit, may reveal therapeutically tractable pathways relevant to IBS and other dysmotility disorders.

The pathogenesis of liver fibrosis centres on the activation of hepatic stellate cells (HSCs). Adenosine-to-inosine RNA editing, primarily catalysed by adenosine deaminase acting on RNA1 (ADAR1), is the most prevalent post-transcriptional modification that increases transcriptome diversity.

IBD is characterised by recurrent flares, but evidence on whether modifiable dietary factors influence flare risk is limited.

Oncological principles favour en bloc R0 excision for curative endoscopic resection. In Barrett's neoplasia, endoscopically curable cancers include T1a and selected early T1b disease. Although endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD) are established treatments, optimal lesion selection remains debated.

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterised by remarkable cellular heterogeneity, which emerges early from the interplay of oncogenic KRAS signalling and inflammatory injury. However, the transcriptional, metabolic and functional properties of these pre-malignant cell states that initiate and drive PDAC progression remain elusive.

Why alcohol-associated liver disease (ALD) resolves after abstinence in most people but progresses to liver failure in others remains poorly understood. Experimental models show that increased exposure to proinflammatory cytokines exacerbates ALD, yet clinical trials targeting these cytokines have failed. The tumour necrosis factor alpha (TNFα)-inducible zinc finger protein 36 (ZFP 36) family of RNA binding proteins controls the outcomes of TNFα exposure by destabilising suites of messenger RNAs (mRNAs) that execute the pleiotropic downstream actions of TNFα.

Accumulating evidence has demonstrated that distinct tumour-promoting and tumour-restraining cancer-associated fibroblast (CAF) subtypes coexist in pancreatic ductal adenocarcinoma.