Objective:To find out the apoptosis mechanism of HT-29 colon cancer cell induced by NDGA,the lipoxygenase inhibitor in vitro.Methods:We applied respectively:RT-PCR to detect colon cancer cell’s expression of 5-LOX messenger ribonucleic acid(5-LOXmRNA) and that of messenger ribonucleic acid about human telomerase reverse transcriptase(hTERTmRNA)respectively,confocal laser scanning electron microscope to examine intracellular free calcium.Results:Colon cancer cell lines HT-29 showed positive expression of 5-LOXmRNA.This expression became weaker following the rise of cell’s apoptosis and so were hTERTmRNA.Intracellular Free calcium increased following the rise of cell’s apoptosis.Conclusion:The apoptosis of tumor cell is caused by a combination of factors,with 5-LOX,telomerase and free calcium all active in the course.

Objective To investigate whether there is any consistent evidence of linkage across multiple studies,and to identify novel AS susceptibility loci by using GSMA method.Methods Genome-search Meta-analysis(GSMA)method was applied to genome scans of AS and spondyloarthropathy(SpA)to assess evidence for linkage across studies.Results Four AS genome scans including 479 families with 1151 affected individuals were used.Suggesting these BINS most likely contain AS-linked loci;BINS 6p22.3-p21.1,6pter-p22.3,17pter-p12,2p12-q22.1 and 5q34-qter.Four AS genome scans and one SpA scan including 544 families with 1,331 affected individuals were used.The GSMA produced genome-wide evidence for linkage on bin 6p22.3-p21 and 16q23.1-qter.Conclusion This GSMA added the evidence of the HLA loci as the greatest susceptibility factor to AS and shows evidences of chromosome 6,17p,2,5q and 16q as non-HLA susceptibility loci.

Objective To investigate the therapeutic effect of 4-1BB monoclone antibodies on mice hepatitis induced by Coneanavalin A (ConA) and its influenes on CD4+CD25+T lymphoeytes during the course. Methods The miee model of hepatic injury was indueed by ConA and monitored by hepatic function tests and hepatic pathology. The expressions of 4-1BB were examined by flow eytometry. 4-1BB monoelone antibodies were intravenously injected to the mice. The therapeutic efficacy was then examined by hepatic function tests and hepatic pathology. The expressions of CD4+CD25+T lymphoeytes were also examined by flow eytometry. Results The group of immune hepatic injury induced by ConA showed damage and marked increase of ALT and AST which were (139±22) U/L and (130±16) U/L respectively. The expression level of 4-1BB was 8.1±2.6. Compared with the eontrol group, the difference was significant (P<0.05). The overall eondition of the miee was improved after being treated with 4-1BB monoelone antibodies. ALT and AST were lowed down to (98±14) U/L and (89±11) U/L respectively and the differenee was signifieant (P<0.01). The expression of 4-1BB of the control group was 3.0±0.8 and that of the treatment group was 8.3±3.0. The difference was significant (P<0.01). Conclusion 4-1BB eontributes to the immune-mediated hepatic injury induced by Con-A.

Objective To investigate the therapeutic effect of 4-1BB monoclonal antibodies (4-1BBmAb) and glucocorticosteroid and the affect of the expression of CD4+CD25+T lymphocytes on the mouse hepatitis induced by ConA.Methods Mouse model of hepatic injury was induced by the application of ConA and checked by hepatic function tests and hepatic pathology.Mter the animal models were constructed,the mice in the group of therapeutic alliance were treated with glucocorticosteroid and 4-1BBmAb.In contrast,mice in the control group were treated with 4-1BBmAb or glucocorticosteroid alone.The groups were then compared.After blood was collected respectively from the control group,the model group and the therapy group,flow cytometry was used to examine CD4+CD25+T lymphocytes.Chi-square test and t-test were used for statistical analysis.Results Compared with the control group,the conditions of the mice were improved after being disposed with 4-1BBmAb.The conditions became even better when 4-1BBmAb were used combined with glucocorticosteroid.ALT and AST of the control group were (140±22) U/L and (131±16) U/L respectively,that of 4-1BBmAb group were (98±14) U/L and (89±11) U/L respectively.The ALT and AST of the glucocorticosteroid treatment group were (76±11) U/L and (71±10) U/L respectively,ALT was (61±8) U/L and AST was (55±7) U/L in the combination treatment group.Differences among groups was statistically significant (P＜0.01).The expression of CD4+CD25+T lymphocytes was (3.0±0.8)％ in the control group,(8.5±2.9)％ in the gluco-corticosteroid treatment group,(8.4±3.5)％ in the 4-1BBmAb treatment group and was (11.2±3.5)％ in the combination treatment group.The difference was significant among the groups (P＜0.05).Conclusion 4-1BB-mAb have therapeutic effect for hepatic injury.The effectiveness will become even more evident when 4-1BB monoclonal antibodies are used together with glucocorticosteroid.During the course of treatment,4-1BBmAb and glucocorticosteroid can impact the expressions of CD4+CD25+T lymphocytes and this is the mechanism for the effectiveness in treating immune-mediated hepatic injury.

AIM: To study the anti-invasive effect of NS-398 on colon cancer cell line HT-29 in vitro an its regulation by CD44v6 and nm23-H1 genes. METHODS: Flow cytometry was used to detect the expression of COX-2 and CD44v6 in HT-29 cells. MTT was used for cell survival rate tests. The modified Boyden chamber model was used for quantitative invasion assay. RT-PCR was used to detect the expression of nm23-H1 mRNA. RESULTS: Flow cytometry analysis showed that COX-2 was positive in HT-29 cells. NS-398 had significant inhibitory effects on invasion of HT-29 cells, which had no relation with its cytotoxicity. NS-398 down-regulated the expression of CD44v6 and up-regulated the expression of nm23-H1 mRNA. CONCLUSION: NS-398 has an anti-invasive effect on HT-29 cells in vitro. Down-regulation of CD44v6 and up-regulation of nm23-H1 may be its underlying mechanisms.