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Increased IAH caused a significant damage to the intestinal epithelium and a marked dilatation of intestinal tight junction, leading to the increased mucosal barrier permeability. It may explain why IAH was often associated with bacterial translocation and sepsis.

Background Liver metastasis (LIM) of gastrointestinal stromal tumor (GIST) is associated with poor prognosis. The present study aimed at developing and validating nomogram to predict LIM in patients with GIST, thus helping clinical diagnosis and treatment. Methods The data of GIST patients derived from Surveillance, Epidemiology, and End Results (SEER) database from 2010 to 2016, which were then screened by univariate and multivariate logistic regression for the construction of LIM nomogram. The model discrimination of LIM nomogram was evaluated by concordance index (C-index) and calibration plots, while the predictive accuracy and clinical values were measured by decision curve analysis (DCA) and clinical impact plot. Furthermore, we validated predictive nomogram in the internal testing set. Results A total of 3797 patients were enrolled and divided randomly into training and validating groups in a 3-to-1 ratio. After logistic regression, the significant variables were sex, tumor location, tumor size, N stage and mitotic rate. The calibration curves showed the perfect agreement between nomogram predictions and actual observations, while the DCA and clinical impact plot showed the clinical utility of LIM nomogram. C-index of the nomogram was 0.812. What’s more, receiver operating characteristic curves (ROC) also showed good discrimination and calibration in the training set (AUC = 0.794, 95% CI 0.778–0.808) and the testing set (AUC = 0.775, 95% CI 0.748–0.802). Conclusion The nomogram for patients with GIST can effectively predict the individualized risk of liver metastasis and provide insightful information to clinicians to optimize therapeutic regimens.

<b><i>Background:</i></b> Due to a combination of high morbidity and lack of effective treatments, gastric cancer (GC) remains a major cause of cancer-related death all over the world. H19, as a paternally imprinted long noncoding RNA (lncRNA), has been found dysregulated in GC. <b><i>Aim:</i></b> The aim of this study is to elucidate the specific mechanism of H19 in GC. <b><i>Methods:</i></b> Bioinformatic analysis and quantitative real-time PCR analysis were utilized to test the expression pattern of H19 in GC tissues and cell lines. Wound healing, transwell, immunofluorescence assay, and Western blot assays were conducted to test cell malignant phenotypes. Meanwhile, TOP/FOP flash assay was to analyze the relationship of H19 and Wnt/β-catenin signaling. Also, mice xenograft models were to evaluate the influence of H19 on tumor growth. <b><i>Results:</i></b> H19 was overexpressed in GC tissues and cell lines and related to poor prognosis for GC patients. In vitro and in vivo assays verified the promotion of H19 on GC cell epithelial to mesenchymal transition (EMT) and metastasis. Mechanistically, H19 could induce β-catenin to transfer into nucleus and activate Wnt/β-catenin signaling, thus promoting EMT and metastasis of GC cells. <b><i>Conclusion:</i></b> Our findings proved the mechanism of H19-mediated metastasis via activating Wnt/β-catenin signaling, which provides a promising target for developing new therapeutic strategies in GC.