BACKGROUND Magnetic resonance imaging (MRI) is contraindicated in patients with an ingested video capsule endoscopy (VCE) due to the theoretical risk of mechanical and thermal harm. However, isolated cases of inadvertent scanning have not shown clear harm. Manufacturers advise against performing VCE in patients with an MRI scheduled within the next 14 days, yet asymptomatic retention for up to 12 years has been reported. With the increasing use of VCEs, the likelihood of incidental MRI exposure is rising. To date, no systematic data have been published on the forces exerted on VCEs in an MRI environment. AIM To quantify magnetically induced forces on VCEs in a 3-Tesla (3-T) scanner to assess clinical safety risks. METHODS Displacement forces on 11 commercially available VCE models were measured in a 3-T MRI scanner according to the American Society of Testing Materials (ASTM) F2052-21. Following ASTM F2213-17, torque was measured by the pulley method for eight VCEs and calculated for three magnet-containing gastric capsules with high displacement forces. The lengths of internal metallic components of the VCEs, as indicators of potential thermal effects, were determined using X-ray images. RESULTS VCEs containing magnets showed significantly higher median displacement forces than those without magnets (2366 mN vs 293.92 mN, P = 0.012). Magnetically induced displacement forces were 50.7-fold higher than the individual gravitational force for magnet-containing devices (2366 mN vs 46.66 mN), compared to a 9.7-fold excess for capsules without a magnet (293.92 mN vs 30.20 mN). Median torque was 19.2 mNm for capsules without integrated magnets vs 289.02 mNm with magnets (P = 0.017). For all but one VCE, the forces exceeded the safety threshold defined by the capsule’s gravitational force. The mean length of internal metallic components was 21.3 mm (range: 18.2-25.4 mm); only two capsules slightly exceeded the 24-mm threshold for possible thermal effects. CONCLUSION In a 3-T MRI, all but one VCE, particularly magnet-containing capsules, exceeded accepted safety thresholds for displacement force and torque but remained below perforation-relevant levels.
The increasing prevalence of metabolic syndrome (MetS) among patients with inflammatory bowel disease (IBD) has prompted renewed interest in their poorly defined bidirectional relationship, underpinned by shared mechanisms such as epithelial barrier disruption, chronic low-grade inflammation, and microbial dysbiosis. In this review, we comprehensively synthesize current evidence on the relationship between MetS and IBD, highlighting their shared pathophysiological mechanisms. We further propose a biphasic model of the MetS-IBD interaction, supported by original immunological data obtained from patients with ulcerative colitis (UC) and concomitant MetS. Early-stage MetS appears to promote a regulatory immune phenotype characterized by increased interleukin-10 and galectin-3-related pathways, which is associated with attenuated UC, whereas advanced MetS appears to be associated with a pro-inflammatory phenotype, increased interleukin-6 and C-X-C motif chemokine ligand 8 signaling, cytotoxic immune-cell infiltration, mucosal damage, and more severe UC. This paradigm should be regarded as hypothesis-generating and requires validation in independent longitudinal cohorts. Nevertheless, it provides a translational framework for future biomarker development, metabolic stratification, and stage-adapted therapeutic research in patients with IBD and metabolic comorbidity.
Biodegradable stents (BDS) are optimal for the prevention of post-endoscopic retrograde cholangiopancreatography pancreatitis and for the management of benign biliary leaks, where the clinical problem resolves within the device’s degradation window and the mandatory retrieval procedure required by conventional plastic stents becomes unnecessary; for postoperative pancreatic fistula, BDS use is currently justified only within clinical trials targeting high-risk patients, and routine implantation for primary sclerosing cholangitis is not advisable under present evidence. Conventional plastic pancreatobiliary stents provide effective short-term drainage but require follow-up imaging and, frequently, a second endoscopic procedure for removal – a burden that limits uptake of otherwise guideline-endorsed therapy. BDS dissolve in situ by hydrolysis, providing temporary ductal support without retrieval. We conducted a structured search of four databases (2000-2026) and appraised the certainty of evidence for four indications using the Grading of Recommendations Assessment, Development and Evaluation framework. Evidence is most mature for pancreatic prophylaxis and supportive for bile leaks; evidence for pancreatic fistula and sclerosing cholangitis remains preliminary. With regulatory clearance now achieved, the field is positioned for definitive randomized comparisons.
BACKGROUND Cholangiocarcinoma (CCA) remains one of the most aggressive malignancies within the digestive tract, and identifying novel biomarkers and therapeutic targets is essential to improve patient survival. Recent studies have highlighted UPB1 as a predictive biomarker across multiple tumor types, but its biological involvement in CCA development and progression remains unclear. AIM To clarify the expression and prognostic value of UPB1 in CCA, its biological functions in tumor growth and immune infiltration. METHODS A combination of bioinformatics analyses and clinical data evaluation was applied to investigate UPB1 expression in CCA. Functional assays in cell models and xenograft mouse experiments were carried out to assess the influence of UPB1 on CCA growth. Co-culture assays were utilized to examine how UPB1 expression influences tumor immune infiltration. RESULTS Reduced UPB1 expression in CCA was correlated with unfavorable clinical manifestations and poor survival outcomes. In vitro studies demonstrated that UPB1 overexpression enhanced apoptosis and triggered G1/S cell cycle arrest in CCA cells. Reduced expression of BCL-2 and BIRC5 , as well as down-regulation of CDK2 and CCNA2 , were observed in UPB1 overexpressing cells. In vivo experiments further confirmed that UPB1 exerts a moderate tumor-suppressive effect on CCA xenograft development. Moreover, UPB1 expression showed a positive correlation with tumor-infiltrating lymphocytes, and in vitro co-culture assays suggested that UPB1 overexpression upregulated T-cell activation related transcripts and increased the release of immune factors. CONCLUSION UPB1 functions as a tumor suppressor in CCA and is associated with tumor immune infiltration. These results deepen understanding of CCA biology and highlight UPB1 as a promising therapeutic candidate.
BACKGROUND A substantial proportion of patients with ulcerative colitis experience clinical relapse despite achieving endoscopic improvement. While it is known that serum total cholesterol (TC) levels fluctuate with inflammatory activity, the clinical significance of longitudinal changes in serum TC after endoscopic improvement remains unclear. AIM To investigate longitudinal serum TC trajectories after endoscopic improvement and their association with subsequent clinical relapse. METHODS This single-center retrospective cohort study at a tertiary hospital included 452 patients with ulcerative colitis who achieved endoscopic improvement (Mayo endoscopic subscore, 0-1) between 2018 and 2019. Patients were observed until clinical relapse or the last outpatient visit. Relapse was defined as worsening symptoms requiring systemic corticosteroids or step-up medical therapy. Serial serum TC levels were analyzed using generalized estimating equations, time-varying Cox models, and 1-year, 2-year, and 3-year landmark analyses. RESULTS During a median follow-up of 67.3 months, 199 patients (44%) experienced clinical relapse. Baseline serum TC levels at endoscopic improvement were similar between the groups; however, the longitudinal patterns differed significantly, showing a progressive increase in patients who later relapsed (time-by-group interaction, P = 0.002). In the time-varying Cox model, each 1 mmol/L increase in updated TC was associated with a higher hazard of clinical relapse (adjusted hazard ratio = 1.31; 95%CI: 1.03-1.66; P = 0.026). Supportive landmark analyses showed that higher maximal TC levels before each landmark were associated with subsequent clinical relapse. CONCLUSION Longitudinal serum TC patterns after endoscopic improvement are associated with the risk of subsequent clinical relapse and may provide complementary information regarding relapse risk.
