ABSTRACT
Objective To explore the vascular endothelial function in individuals with normal glucose tolerance (NGT),impaired glucose tolerance (IGT),and type 2 diabetes mellitus,and to study the role played by PPARγcoactivator 1 α (PGC-1 α) in diabetic macrovascular function.Methods A total of 94 subjects with NGT,87with IGT,and 306 with type 2 diabetes mellitus were recruited in the study.Carotid flow-mediated vasodilatation (FMD),glyceryl trinitrate dilatation (GTN),and carotid intima-media thickness (CIMT) were assessed by highresolution B-mode color vascular Doppler instrument.Finally,correlation analysis was conducted.NO,Akt-Ser473phosphorylation levels,IL-β,and PGC-1 α mRNA expression levels were measured by means of nitrate reductase,western blot,and reverse transcriptase real-time fluorescence quantitative PCR assay methods in peripheral blood mononuclear cells respectively.Results FMD in newly-diagnosed type 2 diabetic group was significantly lower than that in NGT and IGT groups(P＜0.01).GTN and CIMT showed no difference.PGC-1 α mRNA transcription level in diabetic group was significantly lower than that in non-diabetic groups (P＜0.01).Correlation analysis showed that PGC-1 α was positively correlated with FMD and GTN (P＜0.05 or P＜0.01).Logistic regression analysis revealed that PGC-1 α was independently associated with FMD (P ＜ 0.01) after adjusting other influencing factors.Conclusion FMD is a more sensitive early warning indicator of endothelial function than CIMT and GTN.As indices of atherosclerosis,CIMT and GTN are more or less focused on the progression of macrovascular complications.PGC-1 α is a protective factor of macro-vasculature in diabetes mellitus,and its effect may be achieved through the protection of the vascular endothelium.
ABSTRACT
To observe its proliferation and cytolytic activity in vitro induced by autologous soluble tumor antigen and IL-2, PBMC costimulated with TSA extracted from gastric tumor by biochemical procedure and IL-2 was cultured. The proliferation and cytotoxicity were evaluated by MTT method and the phenotype was analysed by APAAP method. TSA alone did not induce PBMC proliferation while TSA (10?g/ml) with IL-2 presented syngenic stimulating effect which was time and concentration dependent. The cytolytic unit of PBMC induced with IL-2/TSA was 86.3% vs 48.6% with IL-2 alone. The phenotypic measurement demonstrated that TSA enhanced CD25 and CD8 expression significantly. The observation offered experimental data for further research work about tumor activated killer(TAK) cells. The results indicated that TAK cells would be a new type of immunoactive cells in adoptive immunotherapy against tumor.