FAT10 may be involved in gastric carcinogenesis, and is a potential marker for the prognosis of gastric cancer patients. FAT10 and mutant p53 may play a common role in the carcinogenesis of gastric cancer.

Introduction The role of double filtration plasmapheresis (DFPP) in hypertriglyceridemic pancreatitis (HTGP) is still not well established. Our study aimed to investigate the efficacy of DFPP in reducing triglyceride levels as well as their effects on the outcomes of HTGP. Material and methods We retrospectively evaluated the data of patients with HTGP presenting within 72 hours from symptom onset between January 2016 and February 2019. Patients with DFPP treatment were compared with those without DFPP treatment. We used a propensity score matching analysis to reduce confounding factors. Results Of the 249 patients enrolled, 88 (35.3%) were treated with DFPP. The DFPP was initiated at a median of 7.7 hours from the time of presentation. In the propensity score‐matched cohort (n = 100), patients with DFPP had a significantly lower level of triglyceride (P = .034), higher triglyceride reduction (P = .005), and the proportion of triglyceride <5.65 mmol/L (P = .002) by 24 hours after admission when compared with those without DFPP. However, this efficacy did not last until 48 hours after admission. No differences were found in terms of the majority of the clinical outcomes between the two groups, including persistent organ failure (P = .098), local complications (P = .213), hospital stay (P = .657), and in‐hospital mortality (P > .999). Conclusions HTGP patients with early initiation of DFPP were associated with rapidly and efficiently reduction of triglyceride levels compared with those without DFPP. However, DFPP showed no beneficial effects on improving the clinical outcomes of HTGP.

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Abstract. Hepatocellular carcinoma (HCC) is the second leading cause of cancer-associated mortality in China and the third leading cause worldwide. A number of microRNAs (miRNAs) have been implicated in cell cycle progression, growth, apoptosis, angiogenesis and metastasis in HCC. In the present study, reverse transcription-quantitative polymerase chain reaction analysis was used to detect the levels of miR-302d expression in the tissues of 30 patients with HCC. Cell cycle, growth, apoptosis and migration were analyzed using a cell counting kit, flow cytometry and a Transwell migration assay. Dual-luciferase reporter assays and western blotting were also used to analyze the expression levels of transforming growth factor beta type II receptor (TGFBR2) in HCC cells. The present study evaluated the role of miR-302d in the development and progression of HCC. Abnormally high expression of miR-302d was observed in 80% of HCC specimens. Moreover, patients with lower levels of miR-302d expression experienced a longer survival time than those with higher levels of miR-302d expression. It was demonstrated that miR-302d promoted HCC cell growth and migration, suppressed cell apoptosis and affected cell cycle distribution in vitro, and augmented tumorigenicity in vivo. Furthermore, TGFBR2, which is a tumor suppressor, was confirmed as a target of miR-302d in HCC cells. Dual-luciferase reporter assays indicated that TGFBR2 expression was negatively regulated by miR-302d. Taken together, the results of the present study suggest that miR-302d may serve as a valuable tool for predicting the prognosis of patients with HCC.