Therefore, retrievable SEM can be a better option for the management of benign oesophageal stricture,needs
to be established from large series of similar intervention. Key Word(s): 1. Upper GI Tract; 2. Corrosive Stricture; Presenting Author: HONGLI YE Additional Authors: FENG XIAO, HAIHONG YU, BIN LIU Corresponding Author: FENG XIAO Affiliations: jinggangshan university Objective: To investigate the effects of Gensenoside Rg3 on growth and induction of apoptosis in human gastric cancer cell line SGC-7901 in vitro. Methods: Human gastric cancer cells SGC-7901 at logarithmic phase were obtained, and were treated with different concentrations (0,10,40,80,120 μg/ml) RGFP966 of Gensenoside Rg3 for 24~72 h. Cells cultured without ginsenoside Rg3 were served as control group. Cell proliferation was determined by MTT assay. Morphology change of SGC-7901 cell nucleus was observed by dying with the fluorescence (AO/EB). The apoptosis rate and Cell cycles were evaluated by flow cytometry. Results: MTT and flow cytometry demonstrated that Ginsenoside Rg3 caused dose and time dependent inhibition on cell proliferation and induction
of apoptosis in vitro. The apoptosis rates of different treatment groups (0,10,40,80,120 μg/ml) are3.46%,4.64%,30.91%,69.34%,83.99% (P < 0.05). Cell cycle analysis revealed a increased percentages of cells in G0/G1, while a decreased propotion at S. AO/EB double fluorescent labeling showed that the control group appeared blue fluorescence CDK inhibitor without apoptosis morphology change, while the experiment groups presented yellow or jacinth fluorescence in which cell nucleus were pyknosis and asymmetrical.The fluorescence microscope showed clearly apoptosis cells with apoptotic body.
As the dose and time of Ginsenoside Rg3 treated with SGC-7901 increased, cell nucleus morphology change appeared to be more Adenylyl cyclase apparently. Conclusion: Ginsenoside Rg3 has a significantly growth-inhibitory and apoptosis -inducing effects in gastric cancer cells in vitro. As for the inhibitory effect of proliferation, its mechanism may be explained that ginsenoside Rg3 restrains the DNA chemical synthesis and blocks cell cycles at G0/G1. In order clarify the apoptosis pathway, more in-depth molecule research are needed. Key Word(s): 1. Ginsenoside Rg3; 2. proliferation; 3. apoptosis; 4. gastric cancer cell; Presenting Author: NIANDI TAN Additional Authors: YINGLIAN XIAO, JINHUI WANG, MINHU CHEN Corresponding Author: MINHU CHEN Affiliations: the first affiliated hospital of SYSU Objective: To evaluate the clinical, manometric and esophagographic characteristics of untreated achalasia patients. Methods: Patients diagnosed with achalasia in our hospital were retrospectively and prospectively enrolled from July 2010 to Dec. 2012. High resolution manometry (HRM) and esophagographic results were analyzed.