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.

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.

From March 2002 to February 2006, 12 patients with soft tissue defects of lower third of leg, ankle and dorsum of foot, who were repaired with reversed island flap pedicled with nutrient vessels of sural nerve, were enrolled at Department of Plastic and Burn Surgery, Affiliated Hospital of Luzhou Medical College. Of the 12 patients, 6 cases were achilles tendon exposure caused by soft tissue necrosis after trauma, 6 cases chronic ulcer in leg ,ankle and dorsum of foot, respectively. All patients knew and agreed to participate in the experiment. The areas of soft tissue defect from 6 cm?7.5 cm-10 cm?12 cm. The maximal area of flap was 12 cm?14 cm. After debridement, the flap which designed based on the size and shape of defect, the line from fibular head to the middle point of lateral malleolus and achilles as axes was transfered to repair the defect, taking 6 cm on lateral malleolus as swivel. Eleven flaps survived postoperatively, and raw surface was primary healing. Margin necrosis was occurred in 1 patient, and healed after changing drugs. Follow-up was performed from 6-18 months in all cases. The texture and color of skin flap is similar to that normal skin, and the function and shape of recipient and donor site were satisfied. No secondary ulcer or functional disturbance, wear-resisting were found. The patients could walk and load normally. The reversed island flap pedicled with nutrient vessels of sural nerve is ideal donor site for soft tissue defect repairing of lower third of leg, heel, dorsum of foot and ankle.

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 To explore the relationship between the microsatellite markers on chromosome 6 and the phenotypes of atopy. Methods Sixteen microsatellite markers on chromosome 6 were evaluated in 20 affected sib pair and trios families. Linkage disequilibrium analysis was conducted according to asthmatic phenotypes (total IgE, skin prick test, bronchial hyper responsiveness and eosinophil) by ETDT software system. Results Significant P value( P

Objective To explore the effects of antisense vector of annexinⅡ gene on the growth of SPC A 1, a human lung cancer cell line. Methods The total RNA was isolated from human lung cancer cell line SPC A 1 and the target DNA fragments were amplified by RT PCR. The antisense expression vector was constructed by double restriction endonuclease cleavage directional clone method. Annexin Ⅱ antisense expression vector was introduced into SPC A 1 cells by liposome transfection reagent. The expression of annexin Ⅱ mRNA was analyzed by semi quantitative RT PCR. The effects of antisense vector of annexinⅡ gene on the growth of SPC A 1 were observed. Results The antisense vector of annexinⅡ gene was constructed and introduced into SPC A 1 cells successfully. Semi quantitative RT PCR showed that the annexin Ⅱ mRNA expression reduced by about two thirds in the transfected cells as compared with that in the untransfected cells. Compared with the untransfected cells, transfected cells decreased significantly in cell growth, clone formation efficiency in plating and DNA synthesis. Cell cycle was blocked in G 0 G 1 phase. Conclusion Annexin Ⅱ could promote the growth of lung cancer cells and may be helpful for the development of lung cancer.

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.

To study the possibility of enhancing IFN ? level in the lung of rats by gene transfection. The recombined IFN ? expression vector in eukaryotic cell was constructed, and it was transfected into lungs of immunocompromised rats. The expression of pLXSN IFN and pLXSN in the genomic DNA of the transfected cells was investigated, and the level and activity of IFN ? in the BALF and sera was assessed. The results showed that the sequence of the IFN ? gene in the constructed recombinant pLXSN IFN eukaryotic cell was the same as that of the IFN ? of rats found in the Gene Bank. The band of transfected plasmid was found when the eletrophoresis analysis of PCR product of genomic DNA of the transfected cells in BALF was done. It could still be the found 21 days after transfection. The level and activity of IFN ? in the BALF of the transfected pLXSN IFN group were markedly higher than those of transfected pLXSN group.On the other hand, the level and activity of IFN ? in sera showed no difference between the two groups. It was suggested that the constructed recombinant IFN ? exprossion vector in eukaryotic cell could be transfected into the cells of the lungs of rats successfully, inserted into the genomic DNA, resulting in active secretion of IFN ?, and prolongation of its expression.

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