Objective To discuss the value of TAI, TAE and PEI treatments for intermediate and advanced stages of hepatic cancers.Methods Conventional TAE, TAI, PEI perfusion chemotherapy and mulitiple percutaneous transhepatic injection of pure alcohol under guidance of fluoroscopy and CT were used for different cases. Results Follow up 1-3 year. 1,2,3 year survival rates were 60.3%, 28.6%, 17.3% respectively.Conclusions Combination interventional treatment in intermediate and advanced stages of hepatic is very important outcoming with high efficacy.

Objective:To investigate the efficacy of treatment of primary hepatic carcinoma by three different interventional theraputic methods.Methods:121 cases with moderate and advanced stages of HCC were treated with PEI +LP-TAE,chemoembolization,LP,and SLPGSTAE respectively.All cases were divided into two groups according to the tumor’s size:group A(＞8 cm)and group B(≤8 cm).The efficacy and survial incidence of the three different methods were analyzed.Results:62 of the 76 cases(81%)in group A and 16 of the 45 cases(35.5%)in group B were decreased in size after the same theraputic method,two groups had statistically significant (P＜0.01).In group A,9 cases treated with chemoembolization and LP were invalid.16 of the 36 cases became smaller after SLPGSTAE.The 1,2 and 3 year surval incidence of patients in group B were 77.6%、42.1%、18.4% respectively as compared with group A were 68.8%、40.0%、11.1%.Conclusion:PEI can cause small tumors to form nerosis,SLPGSTAE cn play dual embolization role and had no servious damage to liver function.

Objective To investigate the effect of celecoxib on the cell cycle and cell autophagy of HepG2 cell line and its possible molecular mechanism. Methods HepG2 cells were treated with celecoxib at different concentrations (0, 50, 100, 200, 500μM), then MTT was used to detect the cell proliferation, cell cycle and apoptosis were detected by flow cytometry, the cell autophagy was observed by transmission electron microscopy, and the expressions of cyclin and autophagy protein were determined using Western blot. Results Celecoxib inhibited the proliferation of HepG2 cells in a concentration dependent manner (0, 50, 100, 200 and 500 μM) and time-dependent manner (24,48h)(P<0.05). There was no significant change in necrocytosis and apoptosis after ttreated by different concentrations of (0, 50, 100, 200 and 500 μM). The celecoxib inhibited cell cycle arrest at G1 phase, the cell rate of G1 phase increased, while the cell rate of S phase decreased in a concentration dependent manner (0, 50, 100, 200 and 500 μM) and time-dependent manner (0, 8, 16, 24h)(P<0.05). The protein expressions of cyclin D1,cyclin D3, cyclin E2, CDK2 and CDK4 significantly decreased by 500 μM celecoxib (P<0.05). The celecoxib induced autophagy in HepG2 cells, and transformed autophagy protein LC3-Ⅰto LC3-Ⅱ in a concentration dependent manner. Conclusion Celecoxib can effectively inhibit the proliferation of human malignant hepatocellular carcinoma cell line HepG2, which provides a new idea for the clinical application of celecoxib.