Objective:In order to obtain more effective endoscopic treatment,we analysed 32 cases data of therapeutic ERCP.Methods:Of which 23 were males,9 females with a median age of 56 years.Therapeutic effort was executed in all cases including biliary drainage (n=16)，endoscopic sphincterotomy (EST) (n=15,10 of them received extraction)and extract ascaris(n=1).The discussion focus on the treatment of biliary disease.Results:All common bile-duct stone were cleared up.Satisfactory treatment was achieved in almost all with no severe side effect.Conclusions:Therapeutic ERCP is an effective method for cholangiopancreatic diseases.It is of considerable value and should be promoted in clinical application.

monocarboxylate transporter (MCT) are vital transmembran e transporters involved in multiple cellular functions including the regulation of intracellul ar pH and lactate transport. At least eight isoforms of MCT have been cloned and characterized to date, they constitute a new gene family of mammal transporters . These isoforms have the differences in substrate and inhibitor specificities a nd tissue distribution. Thus it may provide a new way of diagonosis and treating for dieases such as cancer by investigating on the structure and function and r egulational mechanism of MCT.

Chemotherapy for lung cancer is expected to prolong the survival of lung cancer patients. multidrug resistance is considered to be a major cause of failure of treatment. Many multidrug resistance mechanisms have contributed to lung cancer drug resistance, such as P glycoprotein (P gp), multidrug resistance associated protein (MRP), lung resistance related protein (LRP). The drug efflux pump mechanisms are the focus of recent researches.

objective In the former research work, a differential-expressed gene was cloned from multi-drug resistance lung cancer cell line (SPC-A-1/CDDP) with suppression substractive hybridization, and in this study we further analyze the site of this gene on the chromosome, and appraise its function related to multi-drug resistance in lung cancer cells. Methods The cDNA sequence data of the gene was input to computer and analyzed to ascertain its site on human chromosome by screening the gen bank on the www.ncbi.nlm.nih.gov. With DNA recombination technique, the gene was reversedly inserted to the vector pLXSN to get an antisense expression recombinant vector pLXSN-R, which was then transfected into SPC-A-1/CDDP cells with the aid of electroporation technique. And the semi-quantitative RT-PCR technique was used to quantify the mRNA content of gene in the transfected cells. Finally, the chemosensitivity of the transfected cells was tested with MTT method. Results The gene was located on the human chromosome 19q13.3-19q13.4 locus. The antisense gene recombinant vector was successfully constructed and transfected into SPC-A-1/CDDP cells as shown by its inhibitory activity on the mRNA expression of the gene. The drug-resistance indexes of transfected SPC-A-1/CDDP cells for cisplatin, doxorubicin, 5-fluorouracil, vincristin, hydroxycamptothecine and etoposide were obviously decreased. Conclusion The function of this gene is related to multi-drug resistance in human lung cancer cell, and its locus on the human chromosome is at 19q13.3-1913.4.

Objective To construct an effective expression system for secretory canstatin, and to study its biological effects. Methods Canstatin cDNA was ligated with the cDNA of CEA signal peptide by SOE PCR, and the new fused fragment was cloned into eukaryotic expression vector pCMV-Script. The recombination vector pCMV-CEAS-Cans was transferred into human umbilical vein endothelial cells (HUV-EC) and human lung adeno-carcinoma cell line A549 by cationic liposome. The expression of canstatin mRNA together with CEAS mRNA in the transformed cells were detected by real time PCR method. Results Canstatin mRNA was detected in both transformed cells. The 3 H-TdR intake rate in pCMV-CEAS-Cans transformed HUVEC cells is significant lower than that of the pCMV-Script transformed cells (P

Objective To study the expression of a new drug resistance-related gene cDNA fragment from human lung adenocarcinoma cell line in several types of lung cancer and their adjacent normal tissues. Methods The in situ hybridization histochemistry (ISHH) and Northern blot were employed to study the location and expression of the cDNA fragment in lung cancer cells. Results The results of ISHH and Northern blot showed that the expression of the fragment was discovered in 6 cases of 12 patients with lung adenocarcinoma, but not observed in the lung cancer tissues of other types and normal tissues(P

Objective To analyze the effects of annexin Ⅱ antisense expression vector on the growth of the transplanted tumor in nude mice. Methods The SPC-A-1 cells (parental group) and SPC-A-1-annexin Ⅱ cells (antisense group) were inoculated subcutaneously in nude mice respectively. The forming time, volume, and weight of tumor were measured. The tumor cells and the surrounding tissues were observed microscopically. Results The forming time of tumor in the antisense group was later than that in the parental group. The volume and weight of tumor in the antisense group were lower than those in the parental group. Furthermore, invasion of tumor in the surrounding tissues was found in 2 cases in the parental group, but not in the antisense group. Conclusion The annexin Ⅱ gene may be important in promoting tumor cell growth and invading the surrounding tissues.

Objective To establish lung adenocarcinoma drug resistance cell strain induced by cis-diaminodichloroplatin and investigate the biologic characteristics and chromosome karyotype of cell strain.Methods Large dosage impact and step by step inducing method were used to establish A549 and SPC-A-1 drug resistance cells: A549/CDDP and SPC-A-1/CDDP.MTT was used to detect the cell drug resistance index. Bioluminescence was used to detect the energy metabolism.Cell cycle was analysed by flow cytometer.The differential staining technique and SKY were used to analyze the chromatosome of A549/CDDP and SPC-A-1/CDDP.Results The drug resistance index of A549/CDDP and SPC-A-1/CDDP were 14.0 and 12.0. The content of ATP,ADP and AMP decreased significantly.The cell cycle of A549/CDDP and SPC-A-1/CDDP were of no notable changes.The results of the differential staining technique and SKY showed that the chromatosome of A549/CDDP and SPC-A-1/CDDP had several derivative chromosomes.Both cells had the same derivative chromosome: der(21)t(21;22).Conclusion CDDP can induce lung adenocarcinoma cell strain drug resistance.The derivative chromosome,including der(21)t(21;22) may have relationship with the drug resistance of cell strains.

Objective To analyze the unbalanced state of hereditary material of squamous carcinoma, adenocarcinoma and other lung cancers. Methods Fifty-five patients suffered from lung cancer were included in this study, including 24 of squamous carcinoma, 13 of adenocarcinoma, 5 of adenosquanous carcinoma, 8 of bronchioalveolar carcinoma, 4 of small cell lung cancer and 1 of atypical carcinoma. The technology of comparative genomic hybridization (CGH) was used. The normal DNA was obtained from 20 healthy male volunteers. Results The common extension region of squamous carcinoma was 2q, 5p, 11q and 22q, and the common deletion region was 1p, 4q, 5q, 6q, 8p, 9p, 10q, 11p, 13q, 18q and 21q. The common extension region of adenocarcinoma was 5p, 8q and 11q, and the common deletion region was 10p and 19. Conclusion The hereditary material of squamous carcinoma, adenocarcinoma and other lung cancers was unbalanced. The extension and deletion of chromatosome were the base of the occurrence of different lung cancer.

Purpose:To study the biological effects of high secreted canstatin on human umbilical vein endothelial cells (HUVEC) and tumor model. Methods:Hypoxic responsive elements (HREs) were inserted in the upper stream of canstatin cDNA of a recombinant vector we constructed in a former research. The new recombinant vector named pCMV-3HRE-CEAS-Cans was transferred into A549 cells by cationic liposome; canstatin mRNA expression in the transformed cells under oxic and anoxic condition was detected by Taqman PCR. Then we designed a co-cultured assay: HUVECs were co-cultured with recombinant vector transformed A549 cells with Transwell plates, and the proliferation and apoptosis of co-cultured HUVECs were evaluated with 3H-thymidine incorporation method, TUNEL method respectively. Finally the vector was introduced into tumor tissues of lung cancer-bearing nude mice, and the biological activity in the tumor tissues was tested by micro-vessel count (MVC). A vector of canstatin we constructed before was used as controls in above experiments.Results:The pCMV-3HRE-CEAS-Cans vector was successfully constructed and transferred into A549 cells. canstatin mRNA was detected both in the recombinant vector transformed A549 cells and the pCMV-CEAS-Cans transformed A549 cells, moreover the expression of canstatin in the new vector transformed A549 was significantly higher than that of the controls under hypoxic condition. ~(3)H-TdR intake rate of HUVECs was decreased markedly, and a large amount of them underwent apoptosis when they were co-cultured with recombinant vector transformed A549 cells. Significant differences of ~(3)H-TdR intake rate and apoptotic rate of co-cultured HUVEC were found between pCMV-3HRE-CEAS-Cans group and any of the controls (P