Objective To explore the feasibility,efficacy and safety of endoscopic submucosal dissection (ESD) for tumors originating from gastric muscularis propria.Methods A total of 20 patients with tumors originating from gastric muscularis propria confirmed by EUS and CT scan underwent ESD.Laparoscopic intervention was applied in 3 cases when difficulties in en bloc removal or perforation occurred.Results The mean ESD procedure time was 74.8 min (40-120 min),and the mean resected tumor size was 2.6 cm (1.5-3.5 cm).No severe complication occurred.Pathological findings were 17 cases of gastrointestinal stromal tumors and 3 cases of leiomyoma.Conclusion ESD is an effective method for treating the tumors originating from gastric muscularis propria,and laparoscopic intervention is necessary for en bloc resection in some cases.

Objective To evaluate the role of phosphatidylinositol 3-kinase/serine-threonine kinase(PI3K/Akt) signaling pathway in mitochondrial fission in endotoxin-challenged alveolar type Ⅱ epithelial cells of rats.Methods Rat alveolar type Ⅱ epithelial cells CCL-149 were seeded in 6-well plates at a density of 2×105 cells/ml.CCL-149 cells were divided into 6 groups (n =10 each) using a random number table:control group (group C),lipopolysaccharide (LPS) group (group L),LPS plus CO-releasing molecule-2 (CORM-2) group (group L+CO),LPS plus PI3K inhibitor LY294002 group (group L+LY),LPS plus iCORM-2 group (group L+iCO) and LPS plus dimethyl sulfoxide (DMSO) group (group L+D).CCL149 cells were stimulated with 10 μg/ml LPS for 24 h in L,L+CO,L+LY,L+iCO and L+D groups.CORM-2 100 μmol,LY294002 25 μg and iCORM-2 100 μmol were added at 1 h before stimulation with LPS in L+CO,L+LY and LPS+iC0 groups,respectively.In group L+D,0.1％ DMSO 100 μmol was added at 1 h before stimulation with LPS.After the end of incubation,the concentrations of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the culture medium were determined by enzyme-linked immunosorbent assay,and the expression of phosphorylated-Akt (p-Akt),heme oxygenase-1 (HO-1),dynamin-related protein 1 (Drpl) and fissionl (Fisl) was detected by Western blot.Results Compared with group C,IL-6 and TNF-α concentrations in the culture medium were significantly increased,and the expression ofp-Akt,HO-1,Drp1and FIS1 was up-regulated in L,L+CO,L+LY,L+iCO and L+D groups (P＜0.05).Compared with group L,IL-6 and TNF-α concentrations in the culture medium were significantly decreased,the expression of p-Akt and HO-1 was up-regulated,and the expression of Drp1 and Fis1 was down-regulated in group L+CO,and IL-6 and TNF-α concentrations in the culture medium were significantly increased,the expression of p-Akt and HO-l was down-regulated,and the expression of Drpl and Fisl was up-regulated in group L+LY (P＜0.05).Conclusion Activation of PI3K/Akt signaling pathway can inhibit mitochondrial fission in endotoxin-challenged alveolar type Ⅱ epithelial cells of rats.

Objective:To investigate the mechanism of curcumin affecting HIV-1 infection co-receptor CCR5 by regulating transcription factor FOXP3.Methods:Binding sites of transcription factor FOXP3 on CCR5 promoter were predicted and analyzed by bioinformatics method.AutoDock 4.2 software was used to connect curcumin and FOXP3 flexibly.MTT assay was used to detect cyto-toxcity of curcumin on activity of Jurkat cells.qRT-PCR and Western blot were used to detect expression levels of CCR5 and FOXP3 mRNA and protein in Jurkat cells that were treated with different concentrations of curcumin.pcDNA3.1-FOXP3 expression vector was built and combined with the prediction results of transcription factors.The mutant CCR5 gene fragment was amplified by Overlap PCR,and the mutant CCR5 promoter recombinant vector pFireRluc-Mt-CCR5 was constructed.Binding site between transcription fac-tor FOXP3 and CCR5 promoter was verified by double luciferase reporter gene assay.Results:Results of JASPAR transcription factor prediction showed that there was a binding site between CCR5 promoter and transcription factor FOXP3;molecular docking results showed that curcumin could bind to the active region of FOXP3;MTT results showed that curcumin inhibited the activity of Jurkat cells after 24 hours,and the IC50 was 34.48 μmol/L.qRT-PCR and Western blot showed that expression levels of CCR5 and FOXP3 mRNA and protein were decreased in a dose-dependent manner after different concentrations of curcumin treated Jurkat cells;double luciferase reporter gene confirmed that FOXP3 could bind to CCR5 promoter,and the transcription factor FOXP3 could regulate the activity of CCR5 promoter;results of the recovery experiment of FOXP3 on curcumin showed that when the curcumin concentration was 60 μmol/L,relative value of luciferase activity in HEK293T cells with pcDNA3.1-FOXP3 and pFireRluc-Wt-CCR5 was signifi-cantly higher than that in pFireRluc-Wt-CCR5+curcumin-60 group(P<0.01).Conclusion:FOXP3 can regulate the activity of CCR5 promoter,and the mechanism may be that curcumin affects activity of CCR5 promoter by acting on binding site of FOXP3 and CCR5 promoter.