Long-term outcomes of endoscopic submucosal dissection for early esophageal adenocarcinoma in the Eastern population: a comprehensive analysis.

BACKGROUND: Endoscopic submucosal dissection (ESD) is a preferred method for early esophageal cancer, yet its application to esophageal adenocarcinoma (EAC), especially in the Eastern population with its relative rarity, lacks sufficient literature. This study evaluated ESD's long-term outcomes for EAC, focusing on noncurative resections and diagnostic accuracy. METHODS: Between 2012 and 2022, a retrospective study included 68 patients undergoing ESD for early EAC at Jiangsu Province Hospital. Primary outcomes encompassed ESD efficacy, en bloc resection, R0 resection, curative resection rates, and follow-up. Secondary outcomes involved noncurative ESD, T1a/T1b stage comparison, and diagnostic consistency. RESULTS: Postoperative staging revealed T1a (n = 53) and T1b tumors (n = 15). En bloc resection rate was 97.1%, R0 resection rate was 79.4%, and noncurative rate was 30.9%. T1a had significantly higher R0 rate and curative resection rate. Among noncurative ESDs, 33.3% underwent esophagectomy, 42.9% had surveillance endoscopies, 19.1% repeated curative ESD, and 4.7% were lost to follow-up. Average follow-up was 63.76 ± 28.47 months. Furthermore, 6 patients had recurrence, 3 had residual lesions, and 6 deaths occurred, unrelated to ESD. No significant difference in survival or recurrence rates between curative and noncurative ESD groups was observed. ESD led to a histologic diagnosis change in 70.6% of cases, all upstaged. CONCLUSION: ESD is effective for EAC, with higher curative rates for T1a than T1b. Noncurative ESD cases may benefit from conservative approaches. Long-term follow-up underscores poor consistency between residual lesions and positive margins. ESD serves as a valuable diagnostic staging tool, particularly for T1b cases, considering the low accuracy of endoscopic ultrasound and preoperative biopsy.

Catalase catalyzed tannic acid-Fe3+ network coating: A theranostic strategy for intestinal barrier restoration.

Epithelial barrier impairment of intestinal inflammation leads to the leakage of bacteria, antigens and consequent persistent immune imbalance. Restoring the barrier function holds promise for management of intestinal inflammation, while the theragnostic strategies are limited. In this study, we developed a novel coating by catalase (CAT)-catalyzed polymerization of tannic acid (TA) and combined chelation network with Fe3+. TA-Fe3+ coating was self-polymerized in situ along the small intestinal mucosa, demonstrating persistent adhesion properties and protective function. In enteritis models, sequential administration of TA-Fe3+ complex solution effectively restored the barrier function and alleviated the intestinal inflammation. Overexpressed CAT in inflammatory lesion is more favorable for the in situ targeting growth of TA-Fe3+ coating onto the defective barrier. Based on the high longitudinal relaxivity of Fe3+, the pathologically catalyzed coating facilitated the visualization of intestinal barrier impairment through MRI. In conclusion, the novel TA-Fe3+ delivery coating proposed an alternative approach to promote theranostic intervention for intestinal diseases.

Corrigendum: Unveiling the key genes, environmental toxins, and drug exposures in modulating the severity of ulcerative colitis: a comprehensive analysis.

[This corrects the article DOI: 10.3389/fimmu.2023.1162458.].

Unveiling the key genes, environmental toxins, and drug exposures in modulating the severity of ulcerative colitis: a comprehensive analysis.

Background: As yet, the genetic abnormalities involved in the exacerbation of Ulcerative colitis (UC) have not been adequately explored based on bioinformatic methods. Materials and methods: The gene microarray data and clinical information were downloaded from Gene Expression Omnibus (GEO) repository. The scale-free gene co-expression networks were constructed by R package "WGCNA". Gene enrichment analysis was performed via Metascape database. Differential expression analysis was performed using "Limma" R package. The "randomForest" packages in R was used to construct the random forest model. Unsupervised clustering analysis performed by "ConsensusClusterPlus"R package was utilized to identify different subtypes of UC patients. Heat map was established using the R package "pheatmap". Diagnostic parameter capability was evaluated by ROC curve. The"XSum"packages in R was used to screen out small-molecule drugs for the exacerbation of UC based on cMap database. Molecular docking was performed with Schrodinger molecular docking software. Results: Via WGCNA, a total 77 high Mayo score-associated genes specific in UC were identified. Subsequently, the 9 gene signatures of the exacerbation of UC was screened out by random forest algorithm and Limma analysis, including BGN,CHST15,CYYR1,GPR137B,GPR4,ITGA5,LILRB1,SLFN11 and ST3GAL2. The ROC curve suggested good predictive performance of the signatures for exacerbation of UC in both the training set and the validation set. We generated a novel genotyping scheme based on the 9 signatures. The percentage of patients achieved remission after 4 weeks intravenous corticosteroids (CS-IV) treatment was higher in cluster C1 than that in cluster C2 (54% vs. 27%, Chi-square test, p=0.02). Energy metabolism-associated signaling pathways were significantly up-regulated in cluster C1, including the oxidative phosphorylation, pentose and glucuronate interconversions and citrate cycle TCA cycle pathways. The cluster C2 had a significant higher level of CD4+ T cells. The"XSum"algorithm revealed that Exisulind has a therapeutic potential for UC. Exisulind showed a good binding affinity for GPR4, ST3GAL2 and LILRB1 protein with the docking glide scores of -7.400 kcal/mol, -7.191 kcal/mol and -6.721 kcal/mol, respectively.We also provided a comprehensive review of the environmental toxins and drug exposures that potentially impact the progression of UC. Conclusion: Using WGCNA and random forest algorithm, we identified 9 gene signatures of the exacerbation of UC. A novel genotyping scheme was constructed to predict the severity of UC and screen UC patients suitable for CS-IV treatment. Subsequently, we identified a small molecule drug (Exisulind) with potential therapeutic effects for UC. Thus, our study provided new ideas and materials for the personalized clinical treatment plans for patients with UC.