One hundred and ninety one patients with esophageal carcinoma underwent surgical resection from January 2004 to January 2009. The gastroesophageal anastomosis was performed with auto suture instrument at superior aperture of the thorax in 107 cases (group A) and the instrument anastomosis was performed above or below the aorta arch in 84 cases ( group B ). The electron gastroscopy was performed and biopsy of mucosa at 3cm above the anastomosis was taken during the postoperative follow-up in all patients. Results showed that the incidence rate of reflux esophagitis in group A ( 5% ) was much lower than that in group B (51% ).

Objective To investigate of the MMI-166 on the expression of MMP-2,MMP-9 and the cell apoptosis of nude mouse xenografts of SW1990 human pancreatic cancer cells.Methods Establishment of control and experimental groups,randomly,the human pancreatic cancer xenograft model of SW1990 was constructed.The control group was treated with normal saline,and experimental group was treated with MML-166 (200 mg · kg-1 · d-1).The tumor volume and tumor inhibition rate was measured by vernier caliper through length and short diameter.The expression of MMP-2 and MMP-9 protein was observed using immunohistochemistry in the tumor tissues.Apoptosis index was detected by deoxynucleotidyl transferase-mediated nick end labeling (TUNEL method).Results The tumor volume of MMI-166 group (1252.30± 464.84) mm3 was less than the control group (2241.82±208.06) mm3,significantly.The inhibition rate was 34.47％ between the experimental groups (treat with MMI-166) (1.42±0.15) g and control group (2.17±0.20) g.The expression of MMP-2 (2.80 ± 1.10) ％ and MMP-9 (2.60 ± 1.52) ％ protein was significantly downregulated in MMI-166 group,compared with the control group.Apoptotic index in the experimental group (75.60±9.71) ％ was higher than the control group (17.40 ± 10.14) ％,significantly.Conclusion The mechanism of MMI-166 inhibiting pancreatic tumor growth and inducing apoptosis may be related to the suppression of MMP-2 and MMP-9 protein expression.

Objective:To analize the mechanism of Xiaoxianxiong Decoction on myocardial ischemiareperfusion injury by network pharmacological method and molecular docking technology. Methods:The effective components and corresponding target proteins of Xiaoxianxiong Decoction were screened by TCMSP, and the predicted target protein names were converted to gene names in UniProt database. The gene target of myocardial ischemia reperfusion injury was screened through the GeneCards and OMIM database. Venn online software was used to obtain the common target of drugs and diseases, then the visual analysis and the "compound-target" network diagram was constructed by using Cytoscape software. The protein interaction network was made by using STRING database and Cytoscape software, and the network topology was analyzed. Molecular docking software (autodock Vina) was used to verify the molecular docking between the top five active components and the top ten core targets, and the GO function of target genes and enrichment analysis of KEGG pathway were analyzed by Bioconductor R software package. Results:After the screening, 38 effective chemical components and 187 target genes of Xiaoxianxiong Decoction and 511 disease-related target genes were obtained. 72 common target genes of drug diseases were obtained. The core targets involved AKT1, MMP9, IL1B, EGF, etc. Go function analysis showed 1 095 biological processes, 24 cell components, 61 molecular functions, and KEGG pathway analysis found 111 related signal pathways. Conclusion:This study predicted that Xiaoxianxiong Decoction could treat myocardial ischemia-reperfusion injury through multiple targets such as AKT1, MMP9, IL1B, EGF, and multiple pathways such as IL-17 signaling pathway and PI3K-Akt signaling pathway, which laid a foundation for further study on the material basis and molecular mechanism of this compound.