Background: The roles of circRNA and N6‐methyladenosine (m⁶A) methylation in Crohn's disease (CD) have drawn much attention. Therefore, this investigation aimed to discover how the m⁶A modification of circRNAs contributes to CD progression.Methods: The study performed circRNA sequencing on colon samples from four CD patients and four normal controls (NCs) to screen for dysregulated circRNAs. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was performed to validate the candidate circRNA expression and determine its correlation to CD‐associated inflammatory indicators. In vivo and in vitro investigations were conducted to examine the functions and pathways of circPRKAR1B in CD, besides investigating the m⁶A modification role in circRNA expression modulation.Results: The RNA‐seq revealed that hsa_circ_0008039 (circPRKAR1B) was the most significant upregulated circRNA and was identified as the candidate circRNA for further examinations. Relative circPRKAR1B expression was significantly upregulated in CD colon tissues and closely related to CD‐associated inflammatory indices. The circPRKAR1B expression and function were regulated by methyltransferase‐like 3 (METTL3)‐mediated m⁶A methylation. In vitro studies indicated that circPRKAR1B promoted pyroptosis mediated by NLRP3 inflammasome (NLRP3; nucleotide‐binding oligomerization domain, leucine‐rich repeat and pyrin domain‐containing 3) and impaired autophagy by interacting with the RNA‐binding protein (RBP) SPTBN1, (SPTBN1; spectrin beta, non‐erythrocytic 1). The in vivo investigations revealed the treatment effects of si‐circPRKAR1B and si‐METTL3 in colitis models of IL‐10‐deficient mice.Conclusion: Our study reveals that METTL3‐mediated m⁶A modification of circPRKAR1B promotes Crohn's colitis by aggravating NLRP3 inflammasome‐mediated pyroptosis via autophagy impairment in colonic epithelial cells.

Parenteral nutrition-associated liver disease, a common and life-threating complication among people who require long-term parenteral nutrition, has been associated with abnormal liver function, cholestasis, steatosis and fibrosis. Intravenous soybean lipids may be associated with the development of liver disease. We therefore examined whether different doses of parenteral lipids would affect the development of liver disease, and further investigated the possible pathogenesis of it. C57BL/6J mice with a central catheter placed in the right jugular vein were divided into three groups. The control group received normal mouse chow with intravenous normal saline; The lipids group received parenteral nutrition solution (0.14 g lipids per day); the H-lipids group received parenteral nutrition solution with twice the amount of lipids (0.3 g lipids per day). Changes in body weight, serum biochemical parameters, liver histology and farnesoid X receptor gene expression in the liver were assessed. The values of serum direct bilirubin, total bilirubin and cholesterol were markedly increased in the H-lipids group at day 7. The predominant histologic finding in the H-lipids group was steatosis, and the steatosis score in the H-lipids group was much higher than in the other two groups at either day 5 or day 7. Hepatic expression of farnesoid X receptor mRNA decreased after 7 d of parenteral nutrition. High doses of parenteral lipids are more likely to develop liver disease in a mouse model of parenteral nutrition. Farnesoid X receptor may play a key role in the development of parenteral nutrition-associated liver disease.

Introduction: Aggressive fibromatosis (AF), also known as desmoid tumor, is a rare condition characterized by the proliferation of monoclonal fibroblasts, primarily originating from connective tissue. Despite being histologically benign, AF exhibits malignant-like behavior, including local invasion and a high recurrence rate. AF can be classified based on its location into extra-abdominal, abdominal wall, and intra-abdominal types. Intra-abdominal AF (IAF), though least common, has the worst prognosis and highest mortality rate. Traditionally, complete surgical resection (R0) was the preferred treatment, but recent strategies favor conservative management, especially for asymptomatic patients. Emergency surgery is reserved for complications like bleeding, perforation, or obstruction. Case Presentation: This report details a rare case of IAF in the retroperitoneum of a 39-year-old woman presenting with hemorrhagic shock. Emergency surgery, including partial distal pancreatectomy and partial gastrectomy, was performed. The tumor was β-catenin positive, confirming the diagnosis of IAF. Postoperatively, the patient recovered well and showed no recurrence after 2 years without additional therapy. Conclusion: In summary, IAF presents significant diagnostic and therapeutic challenges. Effective management relies on a multidisciplinary approach, combining various diagnostic tools to improve early detection and patient outcomes. Continued research is essential to understand the pathogenesis of AF and to develop less invasive treatment options.