Objective To investigate the best management in treating relapsed biliary calculi after endoscopic sphincterotomy (EST).Methods The clinical data of 96 patients with relapsed biliary calculi after EST in our hospital from February 1999 to February 2009 were retrospectively analysed. The patients were grouped into two groups by the size of calculi under magnetic resonance cholangiopancreatography: surgical group (the size of calculi was bigger than 1.0 cm) in 79 cases and non-surgical group (the size of stone was smaller than 1.0 cm and the patients were performed EST again) in 17 cases. The relapsed biliary calculi rate between two groups were compared. Results In the surgical group, the 79 patients (82.29%) were performed common bile duct exploration, transected common bile duct and choledochojejunostomy with Roux-en-Y anastomosis. In the non-surgical group, the 17 patients (17.17%) were performed EST again. The relapsed biliary calculi rate was 2.63% in the surgical group, 70.59% in the non-surgical group. There was marked difference in the relapsed biliary calculi rate between surgical group and non-surgical group (Plt;0.05). Conclusion The operation treatment is the best way for relapsed biliary calculi after EST, and has good curative effect. The best manner of operation treatment is common bile duct exploration, transected common bile duct and choledochojejunostomy with Roux-en-Y anastomosis.
Objective To investigate the effect of angiostatin gene combined with somastatin on inhibiting proliferation of human pancreatic cancer cell BXPC-3 and endothelial cell of vascular ECV-304 and on inducing their apoptosis in vitro. Methods The pcDNA3/angio was transfected BXPC-3 by liposome-mediated gene transfer method. RT-PCR and Western blot were used to detect the expression of angiostatin gene. In vitro, MTT and flow cytometry (FCM) were used to detect whether angiostatin gene combined with somastatin could effect the growth inhibition of BXPC-3 and ECV-304 cells. Results Angiostatin was expressed and secreted by transfected BXPC-3. The growth of BXPC-3 was inhibited by certain concentration of somatostatin (≥10 μg/ml, P＜0.01）, which was dependent on the dose of somatostatin in a concentration extent; Simultaneity apoptosis was induced （P＜0.01）. But the growth of ECV-304 was not inhibited with somatostation （Pgt;0.05）. Angiostatin could inhibit the growth of ECV-304 and induced apoptosis （P＜0.01）, but it had no effect on the growth of BXPC-3 （Pgt;0.05）. Angiostation gene combined with somatostation could inhibit the growth both of BXPC-3 and ECV-304 （P＜0.01）, and induce apoptosis of them （P＜0.01）; but the effect couldn’t be additived. Conclusions ①Somatostatin directly inhibits the proliferation of human pancreatic cancer cells and induces apoptosis, but it doesn’t directly inhibit angiogenesiso of human pancreatic cancer. ②Angiostatin specially inhibits the proliferation of endothelial cell of vascular and induces apoptosis. Angiostatin could inhibit angiogenesis of human pancreatic cancer to induce necrosis of cancer cell.