The past decade has witnessed a tremendous profusion of data on the luminal contents of the gastrointestinal tract and their interactions with the host, many of which have been implicated in the pathophysiology of Disorders of Gut-Brain Interaction (DGBI). The role of food in DGBI-related symptoms has attracted much attention and while many alterations in gut microbiome composition have been described, the multitude of factors that confound study design and interpretation in DGBI has precluded the discovery of a specific microbial "signature". The complexities of the gut barrier, its immune and enteroendocrine systems, so critical to the transmission of signals from lumen to host, continue to be revealed. Along the way, concepts such as the microbiome-gut-brain axis have emerged to explain symptom generation in DGBI, forming the basis for novel diagnostic approaches and therapeutic interventions. Taken together, recent research findings have renewed interest in luminal and enteric phenomena in DGBI.

We identify three centrally mediated disorders of gastrointestinal pain in the context of epidemiology, pathophysiology, clinical evaluation and treatment, including pharmacotherapy, brain-gut behavioral therapy and neuromodulation, with emphasis on the importance of a physician-patient relationship. Centrally mediated abdominal pain syndrome is characterized by chronic continuous abdominal pain. It has two main categories: Category A, where the pain occurs without association with physiological events, while in Category B, there is a variable association of pain with physiological events. It is thought to be predominantly a result of central sensitization with altered processing of visceral pain by spinal and brain networks rather than heightened peripheral afferent nerve excitability. Abdominal migraine is newly recognized in adults with paroxysmal, stereotypical episodes of intense abdominal pain. Narcotic bowel syndrome/opioid-induced gastrointestinal hyperalgesia is characterized by the paradoxical development of, or increases in, abdominal pain associated with continuous or increasing dosages of opioids.

Chimeric antigen receptor (CAR) T cells have shown great potential in hematological cancers, but lack efficacy in solid tumors, highlighting the need for novel strategies. Stimulator of interferon genes (STING) activation was shown to inflame the tumor microenvironment, but combination of STING agonists and CAR-T cells might be limited by detrimental outcomes of T cell-intrinsic STING activation. In this study, we evaluated the potential of combining STING agonists and CAR-T cells in the context of pancreatic cancer METHODS: We assessed the synergy of CRISPR-Cas9-edited CAR-T cells and the STING agonist diABZI within a T cell exhaustion model in vitro and both xenograft and syngeneic mouse models in vivo.

The variability of pancreatic vasculature, especially the dorsal pancreatic artery (DPA), increase surgical difficulty and may elevate the risk of intra- and postoperative bleeding. This study aimed to establish a precise preoperative vascular assessment protocol for pancreatic surgery, summarize DPA variant patterns, and evaluate their impact on pancreatic surgery-related bleeding.

Current indicators lack the precision required to accurately predict the PM(peritoneal metastasis) of gastric cancer (GC). The accurate prediction of GC with PM and the implementation of targeted therapeutic strategies hold substantial clinical significance. This study aimed to evaluate the prognostic value of galectin-1 expression and peritoneal fibrosis in predicting PM in GC patients. Immunohistochemical and Masson's trichrome staining were conducted on GC tissues and peritoneal tissues from 125 patients who underwent radical gastrectomy. The correlations among galectin-1 expression in GC tissues, peritoneal fibrosis, and PM were analyzed. Univariate and multivariate regression analyses were performed, incorporating clinicopathological parameters, to assess predictors of PM of GC. Both univariate and multivariate analyses revealed significant correlations among pathological Tumor (pT) stage, galectin-1 expression, peritoneal fibrosis, and PM. Patients with pathological pT3-4 stage GC, who had high galectin-1 expression and who were positive for peritoneal fibrosis had a greater risk of PM after pairwise superposition. This study represents the first to systematically elucidate that galectin-1 expression in GC tissues and peritoneal fibrosis are independent predictors of the risk of PM in patients with GC. These two indicators coordinate with pT stage, and the combination of these two indicators increases their predictive accuracy.

This study investigates the protective effects of citraconic acid (CA) on radiation-induced intestinal injury (RIII) and elucidates its relationship with the interleukin-17 (IL-17) signaling pathway.

Gastric bronchogenic cyst constitutes a rare form of ectopic bronchogenic cyst, with an estimated incidence of less than 1 in 68,000 to 1 in 42,000. This study reported a case who was preoperatively misdiagnosed as gastrointestinal stromal tumor and reviewed the literature on gastric bronchogenic cyst to summarize its clinical features, diagnosis, treatment, pathological manifestations, and prognosis.

No consensus exists on optimal post-conversion therapy for initially unresectable hepatocellular carcinoma (uHCC) patients responding to a combination of immune checkpoint inhibitors (ICIs) and tyrosine kinase inhibitors (TKIs). This study evaluated surgical benefits and prognostic factors in such patients.

Chronic colonic inflammation can lead to colitis-associated cancer (CAC) in ulcerative colitis (UC) patients. The host-microbiome interface plays a critical role in CAC development. Quorum-sensing molecules (QSMs) are bacterial products that regulate bacterial processes. We investigated whether QSMs are related to risk factors for CAC in UC patients and drive CAC development in mouse models.

Primary biliary cholangitis (PBC) is a chronic, progressive autoimmune disease characterized by the destruction of intrahepatic biliary epithelial cells, progressive fibrosis, and the expression of anti-mitochondrial antibodies. Although ursodeoxycholic acid (UDCA) can significantly improve liver biochemical parameters and delay disease progression as a first-line treatment, 40% of patients still have a poor response to UDCA treatment. Inflammation involving different regions of the hepatic lobule may be related to the therapeutic effect of UDCA. The aim of this study is to investigate the relationship between liver inflammation zones and UDCA treatment response in PBC patients, and to further analyze the predictive value of liver lobular zones for treatment response.

Precise staging is essential for treatment options and patient benefits in individuals with unresectable pancreatic ductal adenocarcinoma (PDAC). Laparoscopic biopsy is a minimally invasive procedure used to identify radiographically occult metastases and accurately stage unresectable PDAC. The cancer antigen 125 (CA125) levels change rule after laparoscopic biopsy and its correlation with overall survival (OS) in patients with unresectable PDAC remains unclear.

The underlying mechanisms of incomplete response to ursodeoxycholic acid (UDCA) therapy in patients with primary biliary cholangitis (PBC) remain unclear. This study aimed to investigate the clinicopathological characteristics and potential mechanisms of hepatobiliary (HB) cells in PBC patients with an incomplete response to UDCA.

Peptic ulcer disease (PUD) remains a cause of gastrointestinal mortality despite advances in Helicobacter pylori eradication and gastroprotection.

Severe acute pancreatitis (SAP) is a critical gastrointestinal disorder associated with high mortality. Dysregulated ferroptosis, an iron-dependent form of cell death, is recognized as a pivotal mechanism driving SAP progression. Although Homoplantaginin (Homo) exhibits notable anti-inflammatory and antioxidant properties, its specific role in modulating ferroptosis during SAP remains unclear.