Objective To study the effects of short-term and long-term exposure to extremely low frequency electromagnetic field(ELFEMF)on Morris learning and memory among rats. Methods Both younger(2-3 months old)and adult(18 months old)male SD rats were exposed to 50 Hz uniform ELFEMF with continuously adjusted intensities(0.1,1.2,1.6 mT) developed by Helmholtz coil pair for 10 days to 8 months. The levels of escape latency and the crossing annulus coefficients reflecting the behavioral changes in place navigation ability and spatial probe ability were examined by Morris water maze after exposure to ELFEMF among rats. Results The escape latency was shortened and the crossing annulus coefficients were increased compared with those of control group when the younger rats were exposed to 0.1,1.2 and 1.6 mT ELFEMF for 10 days respectively,and only revealed significant differences in 1.2 and 1.6 mT ELFEMF exposure groups compared with those of control group. In the younger rats of 1.6 mT ELFEMF exposure group with 10-day exposure ,their escape latencies were prolonged and the crossing annulus coefficients were decreased gradually and showed no significant differences compared with those of control group after the 30-day blank exposure period without ELFEMF.The younger rats of 1.2 mT ELFEMF exposure group showed significantly longer escape latency and lower crossing annulus coefficient compared those of control group after continuous 90-day exposure to 1.2 mT ELFEMF. The escape latency of adult rats in 0.1 mT ELFEMF exposure group showed no significant difference after 10-day exposure,was prolonged after 4-month exposure,and was significantly prolonged further more after 8-month exposure. Conclusion The learning and memory ability could be promoted by short-term ELFEMF exposure and impaired by long-term ELFEMF exposure for the young rats,and could be obviously inhibited by long-term ELFEMF exposure for the adult rats.

1)were up-regulated in test and 184 genes(RA1.5)and down-regulation(RA

Objective To examine the expression of metastasis-associated in colon cancer 1 (MACC1) gene in ovarian cancer cell lines and investigate its effect on biological behaviors of ovarian cancer cells.Methods The expression of MACC1 was examined by qRT-PCR and Western blot analysis in four ovarian cancer cell lines inculding OVCAR3,ES-2,SKOV3 and HO-8910.When the MACC1 was transfected to OVCAR3 cells,fluorogenic quantitative PCR was used to filter and identify MACC1 gene after the efficient silencing.Changes of adhesion in the cells were analyzed by an adhesion assay.Transwell migration and invasion assay and in vitro vascular mimicry assay were used to detect migration,invasion and angiogenesis of OVCAR3 cells in vitro.Results The expression of MACC1 gene was higher in OVCAR3 compared to other cell lines.qRT-PCR confirmed that the expression of MACC1 was silenced successfully after transient transfected MACC1-siRNA into OVCAR3 cells.After successful silencing the MACC1 expression,the adhesion ability was inhibited to some degree.In transwell migration assay,the numbers of cells in upper chamber passing through the membrane in transfected group were less than control groups (245.5 ±12.8,500.3±16.5 and 496.3±13.1 respectively),while in transwell invasion assay,the numbers of cells in upper chamber passing through the membrane in transfected group were less than the negative group and control group (185.3±14.1,405.7±9.1 and 416.3±11.5 respectively),both with markedly differences among the three groups.In tube formation assay,the distrubition of HUVECs was diffused with less junctions,and the average number of complete tubular structure was decreased in transfected group compared to the corresponding controls.Conclusion RNA interference inhibits the expression of MACC1 and effectively inhibits the metastasis and invasion abilities of ovarian cancer cells in vitro,and MACC1 is expected to become the target gene of ovarian cancer treatment.

Objective To construct replication deficient recombinant adenovirus of human monocyte chemoattractant protein-1(MCP-1) by homologous recombination.Methods The cDNA of MCP-1 gene was obtained from human liver tissue by using RT-PCR,and was subcloned into a transfer plasmid pAdTrack-CMV.The linearized recombinant transfer plasmid pAdTrack-CMV-MCP-1 was co-transformed with backbone vector pAdEasy-1 into bacteria BJ5183 for recombinant adenoviral plasmid.The recombinant adenoviral plasmid was linearized and then transfected into HEK293 packing cells to produce virus particles.The recombinant adenovirus was detected by using PCR.Results The recombinant adenoviral plasmid was successfully established and confirmed by restriction endonuclease digestion.The expression of green fluorescent protein(GFP) was observed on the 5th day after transfection.The fragment of MCP1 gene was amplified by PCR.Conclusion The achievement of recombinant adenoviral plasmid and recombinant adenovirus of MCP-1 lay a foundation for further investigation of the function and application of MCP-1.

AIM: We hypothesized that PPAR? ligands stimulate endothelial-derived nitric oxide(NO) release to protect the vascular wall.Thus,the purpose of this study is to investigate the effects of ciglitazone(Cig) and fenofibrate(Fen) on angiotensin Ⅱ(AngⅡ)-induced decrease in endothelial NO synthase(eNOS) expression and NO production in human umbilical vein endothelial cells(HUVECs).METHODS: HUVECs were preincubated for 24 h with Cig(10~(-7), 10~(-6),10~(-5),10~(-4) mol/L) or Fen(10~(-5) and 10~(-4) mol/L),then incubated for 12 h with 10~(-7) mol/L AngⅡ.Total RNA was extracted,and the expression of mRNA and protein of eNOS was assessed by RT-PCR and Western blotting.NO production was measured by Griees method.RESULTS: In the presence of 10~(-7) mol/L AngⅡ for 12 h,NO production in cultured HUVECs was decreased(P

AIM:To observe the influence of adenovirus latent infection on the oxidant/antioxidant balance in rat alveolar epithelial cells.METHODS:The rat alveolar epithelial cells were stably transfected with the plasmid pE1Aneo and control plasmid pneo.GSH and MDA contents,the activities of major anti-oxidative enzymes including SOD,CAT,GPx,GST and ?-GCS were detected in oxidant stress.RESULTS:Adenovirus E1A expression repressed the activity of ?-GCS,and decreased GSH contents in oxidant stress.As a result,the activity of GPx and GST was decreased.The contents of MDA maintained high in oxidant stress.CONCLUSION:Adenovirus latent infection amplifies the oxidant/antioxidant imbalance in rat alveolar epithelial cells in oxidants stress,and adenovirus E1A protein decreases the activity of ?-GCS,which plays an important role in this process.

Objective:To construct tumor cell model by determination of the pIRES2-EGFP/MAGE-A3 eukaryotic expression plasmid expressing steadily in mouse melanoma B16 cells.Methods:The pIRES2-EGFP/MAGE-A3 eukaryotic expression plasmid being constructed from the melanoma-associated antigen A3 genes sourcing laryngocarcinoma in advance was translated into the mouse melanoma B16 cells under the mediation of lipofectamine,and the positive clones were detected with G418.The expression of enhanced green fluorescent protein( EGFP) and MAGE-A3 mRNA in positive clones were detected by fluorescence microscopy and fluorescence quantitative PCR ( qRT-PCR ) assay, respectively.Results:The pIRES2-EGFP/MAGE-A3 eukaryotic expression plasmid has been transfected into B16 cells successfully, the green fluorescence of fusion protein expression was found, and MAGE-A3 mRNA transcription in B16 cells expressions were detected in positive clones.Conclusion:The pIRES2-EGFP/MAGE-A3 eukaryotic expression plasmid has been transfected effectively and expressed stably by liposome method in the B16 cells.The expression of MAGE-A3 tumor cell model has been successfully established,which provide data for the study of laryngocarcinoma immunotherapy.

Objective To analyze the influence of adenovirus latent infection on gamma-glutamylcysteine systhetase(γ-GCS) in rat alveolar epithelial cells. Methods The rat alveolar epithelial cells were stably transfected with the plasmid pE1Aneo and control plasmid. Glutathione(GSH) contents, the activity of γ-GCS were detected in oxidant stress. Then the leuel of protein expression, mRNA expression, and promoter transcriptional activity of glutamate-cysteine ligase catalytic subunit(GCLC) were further detected. Results GSH contents decreased because of adenovirus E1A expression in oxidant stress. E1A repressed the expression and activity of γ-GCS, messenger RNA expression, and promoter transcriptional activity of GCLC. Conclusion Adenovirus E1A decreased the activity of γ-GCS probably by repressed promoter transcriptional activity of GCLC. As a result, GSH contents were downregulated in oxidant stress. Thus Adenovirus latent infection amplified the oxidant/antioxidant imbalance in rat alveolar epithelial cells in oxidants stress, which may be an important mechanism of COPD.

Objective To strengthen the capability of emergent supply in field medical point.Methods The common application program was designed by using PowerBuilder.The database program was Oracle.Results The assistant conduction and management of information were realized including the information of staff,war materials,equipment,wounded soldiers in the field medicine.Conclusion Information management system in field hospital can rapidly and accurately provide all kinds of information for users.It can be extensively applied in all levels of field hospitals.

Ras is best known for its ability to regulate cell growth, proliferation and differentiation. Mutations in Ras are associated with the abnormal cell proliferation which can result in incidence of all human cancers. Extracellular signal-regulated kinase (ERK) is a downstream effector of Ras and plays important roles in prognosis of tumors. Recently, evidence has gradually accumulated to demonstrate that there are other effectors between Ras and ERK, these proteins interact each other and constitute the thorough Ras/Raf/MEK/ERK signaling pathway. The pathway has profound effects on incidence of esophageal carcinoma and clinical applications of some chemotherapeutic drugs targeting the pathway. Further understanding of the relevant molecular mechanisms of Ras/Raf/MEK/ERK signaling pathway can be helpful for the development of efficient targeting therapeutic approaches which contribute to the treatment of esophageal cancer. In this article, roles of Ras/Raf/MEK/ERK signaling pathway in esophageal carcinoma as well as pharmacological targeting point in the pathway are reviewed.