ABSTRACT
Objective To evaluate the causes,prevention and treatment of mesh infection after abdominal wall hernia mesh repair.Methods The clinical data of 14 mesh infections admitted from De-cember 1997 to December 2013 were analyzed retrospectively.There were one case of inguinal hernia with Lichtenstein repair,eleven cases of inguinal hernia with preperitoneal repair,one case of incisional hernia with Bard Composix Mesh and 1 case of parastomal hernia with mesh repair above the abdominal muscle. Based on prothetic materials and infection status,the infection meshes were removed in 4 cases and open dressing change were operated in 10 cases.Results All patients were healed and discharged without peri-operative death.There was no hemorrhage and bladder injury during the procedures.The time of dressing change ranged from 3 weeks to 6 months,with a median of 4 weeks.All patients were followed up for 8 to 64 months.One patient had a recurrence of abdominal incisional hernia.Conclusion There are many fac-tors related to mesh infection after mesh repair and preventing mesh infection is the most important.Once the infection occurs,the management should be individualized.Antibiotic treatment and surgical drainage can be effective in most polypropylene mesh(PPM)infection However,infected expanded polytetrafluoro-ethylene(ePTFE)mesh should be removed completely.
ABSTRACT
Objective To determine the effect of signal transducers and activators of transcription 3 (STAT3) gene silencing by shRNA mediated by lentiviral vector for the treatment of colorectal cancer. Methods The recombinant lentiviral vector pRNAT-shSTAT3, empty lentiviral vector pRNAT-GFP, and lentiviral packaging plasmids in supernatant were collected to transfect HT-29 cells for harvesting the HT-29-shSTAT3 cells and HT29-GFP cells. Fifteen male rats were divided into three groups (n = 5 ), and then they were inoculated with HT-29cells, HT-29-GFP cells and HT-29-shSTAT3 cells, respectively. Cell growth was assessed by MTT assay and the changes in cell cycle were detected by flow cytometry. The changes in microvessel density (MVD) of tumors were detected by immunohistochemistry. All data were analysed by one-way analysis of variance. Results The growth of HT-29-shSTAT3 cells was significantly suppressed compared with HT-29 and HT-29-GFP cells (F = 632.50,P ＜ 0. 05 ). The proportions of cells at the G0/G1 phase were 68.7% ± 2.9% in HT-29-shSTAT3 cells, 38.5% ±1.6% in HT-29-GFP cells and 38.7% ± 2.3% in HT-29 cells, with a significant difference among the three groups (F = 166.53, P ＜ 0.05 ). The MVDs of HT-29 cells, HT-29-GFP cells and HT-29-shSTAT3 cells were 29 ±5, 28 ±4 and 10 ±3, respectively, with a significant difference among the three groups (F=31.60, P ＜0.05). Conclusion STAT3 gene silencing by shRNA mediated by lentiviral vector can significantly inhibit the growth of colorectal cancer cells.