OBJECTIVE: To detect the ability of polysaccharide nucleic acid fraction of bacillus calmette guerin(BCG-PSN) in inducing mIFN? in mouse. METHODS: The Balb/c mice were treated with saline, BCG-PSN and lipopolysaccharide(LPS) respectively, and mIFN? cDNA was amplified by RT-PCR. The ability of BCG-PSN in inducing mIFN? in mouse was identified through RT-PCR product with ?-actin as control. RESULTS: In normal sodium group, only ?-actin but not the mIFN? cDNA was detected, but in groups treated with BCG-PSN or LPS, mIFN? and ?-actin cDNA were all detected in RT-PCR amplification products. As compared with LPS group, there was stronger expression of mIFN? in BCG-PSN group (P

OBJECTIVE:To prepare PTD modified mice interferon gamma(PTD-mIFN-?) in order to prepare for its function research.METHODS:The code of PTD-mIFN-? fragment was amplified by PCR for 3 times,using pUC19/mIFN-? as template.The PCR product was cloned into pUC19 plasmid and then constructed into expression plasmid vector pQE80L after sequencing.After double digestion with BamH Ⅰ and Hind Ⅲ,the recombinant vector was identified in 1.2% agarose gel.The target protein and PTD-mIFN-? was checked by SDS-PAGE,Western blot method and ELISA assay,respectively.Recombinant protein was purified by nikel ion-triglycollamic acid(Ni2+-NTA) Agarose affinity chromatogram.RESULTS:The cDNA fragment encoding PTD-mIFN-? amplified by PCR was obtained.The high-level expression of recombinant protein was noted in SDS-PAGE and Western blot assay.The target protein was obtained by ELISA assay.CONCLUSION:PTD-mIFN-? was prepared successfully.

Objective To investigate the clinical effect of anterior internal fixation plus vacuum sealing drainage in the treatment of ulnar and radial fractures of Gustilo type Ⅲ.Methods Twenty-eight patients with open ulnar and radial fracture of Gustilo type Ⅲ were managed from April 2007 to March 2014,and were divided into four groups(n =4).Group A were managed with external fixator and conventional changing dressings.Group B were managed with internal fixation and vacuum sealing drainage.Group C were managed with external fixator and vacuum sealing drainage.Group D were managed with internal fixation and conventional changing dressings.Result Twenty-eight cases were adopted telephone follow-up for 6 to 27 months.The soft tissue recovery time of each group respectively was (20.5 ± 2.37) days,(14.7 ±2.16) days,(15.6 ±2.17) days and(19.7 ±2.18) days.The hospital stay of each group respectively was (9.7 ± 2.54) weeks,(4.7 ± 1.46) weeks,(5.2 ± 2.34) weeks and 8.6 ± 2.16) weeks.The fracture healing time of each group respectively was (19.6 ± 2.74) weeks,(13.1±1.84) weeks,(18.1 ±2.54) weeks and (14.7 ± 1.74) weeks.There was significant difference of these data between the two groups(P ＜ 0.05).Conclusions Anterior internal fixation plus vacuum sealing drainage is a better way to treat ulnar and radial fractures of Gustilo type Ⅲ.The technique has short period,less complications,less painful and less expense.

AIM: To explore interaction and biological behaviou r changes of two kinds of cells-blastocysts and hepatocarcinoma cells in the same microenvi ronment. METHODS:The models of mouse blastocysts co-cultured wit h human hepatoca rcinoma cell lines were established, then biological behaviours and mutual effe c ts of the two kinds of cells in co-culture system were observed. RESULTS: Co mpared with control group, hepatocarcinoma cells with differently invasive and met astatic potential significantly enhanced the rates of blastocyst hatchment , at t achment and outgrowth(P0 05). The blastocyst ha tched and attached to hepatocarcinoma cells with differently invasive and metast atic p otential. Then, differential trophoblasts invaded hepatocarcinoma cells. The clear-cut interfaces were gradually formed between both sides. Hepatocarcinoma cells o n interface showed changes of growth direction and cell shapes and did not inv ade blastocysts. CONCLUSIONS: Hepatocarcinoma cells promoted bla stocyst develo pment. Blastocysts implanted and invaded hepatocarcinoma cells with differentl y i nvasive and metastatic potential in vitro, which indicate that blastocyst i mplan tation in vitro does not relate with the kinds and differential level of int erac tional cells and the low selectivity maybe relate with high adaptability of earl y life.

Objective T9 provide candidate molecules for developing recombinant anti-idiotypic antibody (anti-Id) vaccine of gastric carcinoma by selection of recombinant anti-Id to monoclonal antibody ( McAb) MGb1 directed against the cancer with phage display technique.Methods Balb/c mice were immunized with MGb1 and the mRNA was isolated from the spleens of the immunized mice. The VL and VH cDNAs of the antibody were amplified separately by RT-PCR and assembled into ScFv DNAs with a linker DNA. The ScFv DNAs were ligated into the phagemid vector pCANTAB5E and the ligated sample was transformed into competent E. coli TG1. The transformed cells were infected with M13KO7 helper phage to yield recombinant phage antibody ScFv library. After four rounds of biopanning to the library with MGb1, the MGb1-positive clones were selected from the enriched phages by ELISA. The types of the anti-Id ScFv displayed on the selected phage clones were preliminarily identified by competition ELISA. Results The VL and VH cDNAs was about 320 bp and 340 bp, respectively. The ScFv DNA were about 750 bp. After four rounds panning to the phage antibody ScFv library with MGb1, 18 MGb1-positive phage clones displayed anti-Id ScFv were selected from 50 pre-selected phage clones, among which 4 clones displayed β or γ type anti-Id ScFv. Conclusion The phagedisplayed anti-Id ScFvs to McAb MGb1 are successfully selected by recombinant phage antibody technique, which might lay a foundation for screening the anti-Id ScFv possessing the characteristics of inducing anti-gastric carcinoma immunity.

Experimental research of injury on tumor tissue in vitro is conducted with homemade energy-controllable steep pulse device. With the comparison of histological assay results between treatment group and non-treatment group, basic phenomenon of electrochemical reaction and pathology reaction of tumor tissue during the experiment is observed. The results showed the irreversible breakdown penetrating effect of energy-controllable steep pulse on tumor cells and the feasibility of this therapy are also demonstrated. These results provide a consolidate theoretic and applicable basis for further study on mechanism and animal experiment in vivo.
Electric Stimulation Therapy ; instrumentation ; methods ; Electromagnetic Fields ; Female ; Humans ; In Vitro Techniques ; Male ; Middle Aged ; Neoplasms ; pathology ; therapy

Objective    To compare the 5-year survival rates between two different follow-up patterns of postoperative stage Ⅰ-ⅢA non-small cell lung cancer (NSCLC) patients. Methods    Pathological stage Ⅰ-ⅢA NSCLC 11 958 patients who underwent surgical resection and received follow-up within 6 months after initial diagnosis through telephone follow-up system were included in nine hospitals from July 2014 to July 2020. The patients were divided into two groups including a proactive follow-up group (n=3 825) and a passive follow-up group (n=8 133) according to the way of following-up. There were 6 939 males and 5 019 females aged 59.8±9.5 years. The Kaplan-Meier and Cox proportional hazards regression model were used. Results    The median follow-up frequency was 8.0 times in the proactive follow-up group and 7.0 times in the passive follow-up group. The median call duration was 3.77 minutes in the proactive follow-up group and 3.58 minutes in the passive follow-up group. The 5-year survival rate was 81.8% and 74.2% (HR=0.60, 95CI 0.53-0.67, P<0.001) in the proactive follow-up group and the passive follow-up group, respectively. Multivariate analysis showed that follow-up pattern, age, gender and operation mode were independent prognostic factors, and the results were consistent in all subgroups stratified by clinical stages. Conclusion    The proactive follow-up leads to better overall survival for resected stage Ⅰ-ⅢA NSCLC patients, especially in the stage ⅢA.