[Summary] Holistic integrative medicine ( HIM ) is an ultimate direction and a new way for medical development. It emphases the organic integration of the most advanced knowledge and theories in medical sciences with the most valuable clinical experiences. Treating ( endocrine and metabolic diseases) patients with the concept of HIM, and implementing practical strategies will greatly accelerate the advancement of HIM.

Gastroenterology ; Humans

Multidrug resistance (MDR) is widely thought to be a major cause of the failure in cancer chemotherapy. The detection of MDR marker is therefore valuabe in studying the mechanisms of MDR and to predict response to chemotherapy in patient with carcinoma. Previous studies have examined MDR marker in gastric cancer, but the major part of the investigation in patients have focused on a single parameter. The purposes of this study were to detect the expression of glutathione S transferase pi(GST ?), multidrug resistance associated protein(MRP), lung resistance protein(LRP) and multidrug resistance gen 1 (MDR1) in the patients with primary gastric cancer, who had not received prior chemotherapy, and evaluate the correlation between GST ?, MRP, LRP and MDR1. The expression of GST ?, MRP, LRP and MDR1 mRNA in carcinoma tissue and the adjacent non cancerous tissue from 50 patients was examined by semiquantitative reverse transcription polymerase chain reaction (RT PCR). The positive rate of GST ? mRNA, MRP mRNA, LRP mRNA and MDR1 mRNA in gastric cancer tissue were 36.00%, 12.00%, 10.00%, and 10.00% respectively. Their expression in gastric cancer tissue was significantly higher than that in the adjacent non cancerous tissue. The overall positive rate of their expression in gastric tissue was 48.00%. The results indicated that GST ? mRNA, MRP mRNA, LRP mRNA and MDR1 mRNA are overexpressed in various degrees and no co expression exists among the studied genes in gastric cancer,and perhaps intrinsic MDR exists in 46% patients with primary gastric cancer .

The aim is to investigate the effects of tumornecrosis factor ?(TNF?0 and interferon a(IFN?) on the cytotoxicity of mitomycin C(MMC) in vitro. The cytotoxicity of the three agents against gastric cancer cell line and freshly isolated gastric cancer cells were determined by the MTT assay. TNF? and/or IFN? (each 0~5000U/ml) showed cytotoxicity effects only on one of ten cell cultures dose-dependently; the combination resulted in a more significant effect. The combination of MMC with TNF? (30U/ml) or IFN?(l00U/ml) could enhance the cytotoxicity of MMC on two of three cell cultures synergisticly. When three agents were used together, the cytotoxicity of MMC against the ten cell cultures was enhanced synergisticly. TNF? and IFN? could enhance the cytotoxicity of MMC synergisticly, and this may make the cancer chemotherapy more effective.

In patients with liver cirrhosis,variceal bleeding is a common fatal complication of portal hypertension.Varices are present in al-most half of patients with cirrhosis at the time of diagnosis.Since transjugular intrahepatic portosystemic shunt (TIPS)was first applied clini-cally in 1988,the relevant information about TIPS has been continually updated and perfected by lots of clinical trials.The role of TIPS in the prevention and treatment of variceal bleeding in cirrhotic patients with portal hypertension,including primary prevention of variceal bleeding,treatment of acute variceal bleeding,and prevention of rebleeding,is reviewed.TIPS is an effective treatment for variceal bleeding in cirrhotic patients with portal hypertension.Along with the technical development,TIPS will be available for more and more patients and will play an increasingly important role in the prevention and treatment of variceal bleeding among cirrhotic patients with portal hypertension.

Objective To generate specific targeting T cells against gastrointestinal cancer, a eukaryotic expression vector encoding carcinoembryonic antigen(CEA) specific single chain variable fragment(scFv) fused to the transmembrane and intracellular domains of the signal transducing chain of CD3? was constructed. Methods Anti CEA scFv cDNA was obtained by RT PCR. The transmembrane and intracellular domains of CD3?cDNA was amplified from human T lymphocyte using RT PCR to clone into a eukaryotic expression vector, and anti CEA scFv cDNA was inserted upstream of CD3?. Finally, the eukaryotic expression vector containing scFv CD3? pcDNA3.0 was constructed and sequenced. Results A 810 base pair of anti CEA scFv was in accordance with sequence concerned, a 438 base pair of cDNA of the transmembrane and intracellular domains of CD3? was confirmed as sequence concerning of GenBank. Further identification was carried out through agarose electrophoresis after enzyme digestion. Conclusion We constructed a fusion molecular with both CEA targeting and CD3? signal transduction perporties, which lay a good foundation for generation of modified cytotoxic T lymphocytes against gastrointestinal tumors.

Objective: To investigate the correlation between the expression of vascular endothelial growth factor(VEGF) and angiogenesis in tumor. Methods: VEGF 165 sense and antisense gene recombinants were introduced into human gastric cancer cells, respectively. Then the growth of transfected cells in nude mice and the microvascular density and histological change were examined. Results: The growth rate of tumor in nude mice inoculated with sense VEGF cells was markedly higher than that in nude mice inoculated with antisense-VEGF cells. In histological examination, the microvascular density in tumor caused by sense-VEGF cells was greatly higher than that in tumor caused by antisense VEGF cells. Conclusion: As starting angiogenesis, VEGF might promote the growth of tumor, and the inhibition of VEGF production might prevent solid tumor from growing.

Objective　To investigate the effect of a new cloned full length gene, C2 gene which encodes a translation initiation factor, on cell cycle and the relationship between C2gene and apoptosis. Methods　Construct a eukaryotic vector carrying the full length of C2 gene, then transfected it into a gastric cell line-SGC7901 cells and gained cells expressing C2 protein transiently or stably. Test the expression of C2 protein and the change of cell cycle of the transfected cells using the flurescence activatied cell sorting(FACS) and the changes of their ultra structure electromicroscopically. Results　The C2 gene eukaryotic expression vector was successfully constructed. FACS showed the C2 protein expression ratio of transfected cells was 32.3%, while the empty control group was 0.9%. The test of cell cycle showed that there was appeared apoptosis peak in transiently or stably transfected cells. The apoptosis cells can be seen electromicroscopically among the C2 transfected cells. Conclusions　C2 gene transfection can lead SGC7901 cells to apoptosis, but the mechanism has to be further study.

Objective To synthesize H.pylori bacterial ghosts (BG) and loaded with adriamycin.The cytotoxic effects in gastric cancer cell line were also observed.MethodsThe lysis plasmid was introduced into H.pylori by bacterial conjugation. H.pylori BG were produced by inducing H.pylori lysis at 42 ℃.After suspension and centrifuge, H.pylori BG were loaded with adriamycin.The adriamycin loading quantity was measured with spectrophotometry.The cytotoxic effects of H.pylori BG-adriamycin in gastric cancer cell line SGC7901 were evaluated with MTT assay.ResultsH.pylori BG were successfully synthesized and loaded with adriamycin.The loading quantity of adriamycin was 70.4 μg/mg.H.pylori BG were seen to be adsorbed and internalized by gastric cancer cells under confocal microscope, which distributed on the surface or cytoplasmic of SGC7901 cell line. Carried Adriamycin was delivered into gastric cancer cell line and mainly accumulated in the nucleus.IC50 of SGC7901 to H.pylori BG-adriamycin was 0.32 ± 0.15 by MTT assay, which was significantly lower than that to free adriamycin (0.44 ±0.15, P＜0.05).Conclusions The proliferation of gastric cancer cells were effectively inhibited by H.pylori BG-adriamycin.H.pylori BG are expected to be ideal carrier for anti-gastric cancer medicine.

Objective To investigate the currents impact on delayed rectifier potassium (HERG)regulated by cyclooxygenase (COX)-2 in gastric cancer cells and its mechnism. Methods ① The HERG mRNA, protein and current in gastric cancer cells transfected with or without COX-2 antisense vector were measured by RT-PCR, Western blot and patch-clamp, respectively. ② cAMP concentration in gastric cancer cells transfected with or without COX-2 antisense vector was measured by ELISA. ③ The mutant HERG, which was absence of cAMP-binding domain, was constructed by PCR and transfected into gastric cancer cells. ④ The impact of COX-2 inhibitor and proglandin (PG) E2 on HERG current in gastric cancer cells transfected with or without mutant HERG was investigated by patch clamp. ⑤ The effects of agonist and antagonist of cAMP and inhibitor of protein kinase (PK) A on HERG current in gastric cancer cells transfected with or without HERG mutant were observed by patch clamp. Results ① The expression of HERG mRNA and protein in gastric cancer cells transfected with COX-2 antisense vector were not altered, but the amplitude of HERG current was diminished (P<0.05). ② The cAMP concentration in gastric cancer cells transfected with COX-2 antisense vector was lower than that in parental gastric cancer cells (P<0.05). ③ COX-2 inhibitor and PGE2 had influence on the HERG currents in gastric cancer cells. COX-2 inhibitor reduced and PGE2 enhanced the amplitude of HERG current in gastric cancer cells. However, neither COX-2 inhibitor nor PGE2 showed any negative or positive effects on currents of mutant HERG. ④ cAMP agonist enhanced the amplitude of HERG current and cAMP antagonist reduced the amplitude in gastric cancer cells. Neither agonist nor antagonist had effect on currents of mutant HERG. ⑤ PKA inhibitor did not influence the HERG current of parental gastric cancer cells and gastric cancer cells transfected with mutant. Conclusions COX-2 regulates HERG current through its catalytic product of PGE2, which binds with its receptor on the gastric cancer cells and alters cAMP level in gastric cancer cells, cAMP interacts with HERG protein by binding with cAMP-binding domain of HERG protein and exerts impact on HERG current. PKA does not participate in this process.