ABSTRACT
@#ObjectiveTo search for a new method of anti-tumor immunity,using mutated tumor cells by spaceflight.MethodsTumor cells were carried in the Shenzhou 4 and the recoverable satellite No.18.After 7 days and 18 days spaceflight respectively,the effects of spaceflight were investigated primarily.Results2382 and 1 strains of mutated tumor cells from the airship No.4 and the recoverable satellite No.18 had been obtained respectively. Comparing with the control group, the growth rate of mutated cells decreased, moreover, the secretion of cytokines also changed.ConclusionSpaceflight may affect physiological characteristics of tumor cells, and that, there was a negative correlation between the ratio of surviving cells and carrying time.
ABSTRACT
Objective To investigate the dynamic expression of nitric oxide synthase(NOS) in the apoptosis of primary cultured rat cortical neruons following hypoxia/reoxygenation(H/R) and the protective role of extract of ginkgo biloba(EGB). Methods The cortical neurons of E16-17 days fetal rat were primarily cultured.The apoptosis model of primary cultured cortical nurons following H/R was established by using W-G staning,electromicroscopy,TUNEL staining.The dynamic expression of NOS different H/R times was investigated with NADPH-diaphorase histochemical method. Results H/R can cause apoptosis of primary cultured rat cortical neurons.In the experiment of H-2R-0,H-4R-0, H-6R-0,H-8R-0 and H-2R 18,H-4R 18,H-6R 18 H-8R 18,the apoptosis cells occurred after 4 hour hypoxia.The increasing of apoptosis cell acted as time-dependence and the peak value was at H-8R 18.The expression of NOS increased both after 2 hour hypoxia and reoxygenation 18 hour after 8 hour hypoxia compared with the normal control group.EGB could inhibit the increasing and decrease the percentage of apoptosis.Conclusion The apoptosis of primary cultured rat cortical neurons could be induced by H/R.The increasing of NO might be one of the mechannisms of apoptosis.EGB could singnificantly inhibit the apoptosis by means of inhibiting the expression of NOS and reducing the production of NO.;