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OBJECTIVE: To investigate the prognosis of patients with early gastric carcinoma (EGC) treated by endoscopic submucosal dissection (ESD) and the risk factors for additional postoperative surgery. METHODS: A retrospective analysis was performed on 100 patients with EGC admitted to our hospital from January 2017 to May 2019. According to different surgical methods, patients were divided into the ESD (n=60) and endoscopic mucosal resection (EMR) groups (n=40). Clinical efficacy, perioperative indexes, incidence of complications and risk factors for additional postoperative surgery were compared. RESULTS: The ESD group had evidently prolonged operation time (P<0.01) but similar intraoperative blood loss (P>0.05) as compared with the EMR group. In comparison to the EMR group, the gastrointestinal recovery time and length of stay in the ESD group were notably shorter (P<0.01), the rates of en bloc resection and complete resection of lesions were markedly higher (P<0.05), and the postoperative fever/infection rate was noticeably lower (P<0.05). The two surgical methods had no significant difference on the overall survival rate of patients (P=0.302). It was identified that the infiltration depth and the positive surgical margin were independent risk factors for postoperative additional surgery (all P<0.05). ROC analysis revealed that positive surgical margin was quite valuable in judging the need for additional postoperative surgery. CONCLUSION: ESD can accelerate the postoperative recovery of patients with EGC, and positive surgical margin is independently tied to additional postoperative surgery in patients after ESD.
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BACKGROUND: Necrotizing enterocolitis (NEC) is an acquired disease, which mainly occurs in premature infants or sick newborns. microRNA (miR), as a common non-coding RNA in recent years, is found in many diseases. In this research, miR usefulin NEC is analyzed by GEO. METHOD: The differentially expressed miRs in NEC were screened by analyzing GSE68054, and miR-200a-3p in IEC-6 cells induced by lipopolysaccharide (LPS) and serum of NEC children were detected by qRT-PCR. The role of miR-200a-3p in LPS-induced IEC-6 cells was tested using CCK-8, PI dyeing, and inflammatory cytokine detection. The direct downstream molecules of miR-200a-3p were identified using TargetScanHuman and verified by luciferase reporter gene assay. The mechanism of action was explored using western blot. RESULTS: miR-200a-3p in IEC-6 treated with NEC and LPS was significantly decreased. In vitro experiments revealed that miR-200a-3p mimetic could inhibit IL-6 and TNF-α in IEC-6 cells induced by LPS and reduce the positive rate of PI. In addition, it was determined that receptor-interacting protein kinase 1 (RIPK1) was a downstream molecule of miR-200a-3p, and overexpression of RIPK1 could aggravate LPS-induced IEC-6 injury, while miR-200a-3p mimics could alleviate the overexpression of RIPK1. miR-200a-3p mimics inhibited the elevation of necrosis-related molecules and the interaction between RIPK1 and RIPK3 in LPS-induced IEC-6 cells. CONCLUSION: miR-200a-3p can protect intestinal epithelial cells from LPS injury by inhibiting inflammation and necrosis mediated by RIPK1, which provides a possible target for NEC.
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A novel series of quinolone derivatives (6a-n) were designed and synthesized, and their biological activities were evaluated as potential antitumor topoisomerase I (Top I) inhibitors. Among these compounds, 6j exhibited the most potent antitumor activities against multiple cancer cell lines. Docking simulation was performed to insert compound 6j into the crystal structure of DNA-Top I to determine the probable binding model.
