0.05), and the mean ADCC activity was 43.0?21.44% (P 0.05) .The NK activity in 15/24(62.5%)cases with low NK and ADCC activity in 4/25(16.0%)cases with low ADCC were enhanced to normal level by HuIFN- ?.The results suggest that HuIFN-? enhanced the NK activity more efficiently than the ADCC activity in bladder cancer patients after surgery.

Objective:To analyze the lymphocyte activation from patients with different activities of multiple sclerosis (MS) and its clinical signifiance. Methods: The positive percentage of CD69 and HLA-DR were determined on peripheral blood (PB) or cerebrospinal fluid (CSF) lymphocytes by flow cytometry from 28 patients with relapsing-remitting MS (relapses n - 20, remission n = 8) , 12 patients with relapse MS and 11 patients with relapse MS after glucocorticoid treatment. ResultS:The percentage of HLA-DR+ and CD3+ /HLA-DR+ on PB lymphocytes in relapses MS group were higher than in remission MS group and controls. The percentage of CD3+ /HLA-DR+ on PB lymphocytes in remission MS group were higher than in controls. The percentage of CD69+ , HLA-DR+ and CD3+ /HLA-DR+ were higher in CSF than in PB of patients with relapse MS. There was no significant correlation between the levels of CD69+ , HLA-DR+ , CDS+ /HLA-DR+ and the time of onset of clinical relapse, duration, clinical disability scale score(EDSS) . In patients with relapse MS, there was significant positive correlation between CD69+ expression on CSF lymphocytes and blood brain barrier damage, intravenous glucocorticoid treatment caused a significant changes in the positive percentage of HLA-DR on PB lymphocytes. Conclusion:The findings support that lymphocyte activation involvement of MS pathogenesis. Lymphocyte activation may be as a marker of disease activity in MS.

The change of PKC activity and cytosolic free Ca 2+ induced by oxLDL and simvastatin in ASMC were measured by its ability to transfer phosphate from 32P-ATP to lysine-rich histone and flow cytometric analysis loading with the Ca 2+ dye fluo-3/Am, respectively. As a result, oxLDL increased total PKC activity in a dose-dependent manner with phase peaking at 14 min, then decreased slowly and maintained for at least 30 min, while oxLDL induced biphasic [Ca 2+]i responses including rapid initial transient phase and sustained phase. Removal of extracellular Ca 2+did not inhibit the rapid phase of oxLDL-induced rise in [Ca 2+]i, but abolished the sustained phase of [Ca 2+]i in response to oxLDL. Activity of PKC was markedly decreased and simvastatin did not impair the initial peak in response to oxLDL but significantly reduced the subsequent plateau phase when simvastatin was added. The results suggested that oxLDL can induce dynamic changes of signal transduction of PKC and cytosolic free Ca 2+in ASMC. The rapid initial transient phase was due to the mobilization of [Ca 2+]i from intracellular Ca 2+ pool and the sustained phase resulted from the influx of extracellular Ca 2+. The inhibition of PKC activity induced by simvastatin may contribute to the changes of intracellular Ca 2+.

AIM: To investigate whether human umbilical vein endothelial cells and human atherosclerotic plaque lesions can coexpress CD40 and CD40 ligand . METHODS: The expression of CD40 and its ligand CD40L on human endothelia cells were measured by fluorescence microscope , flow cytometry(FCM), reverse transcription PCR(RT-PCR) and Western blotting, respectively. Both CD40 and CD40L expression in atheroma plaques were determined by immunohistochemistry. RESULTS: Cultured human endothelial cells constitutively coexpressed CD40 and CD40L in mRNA and protein levels. Stimulation with interleukin-1?, interleukin-6, tumor necrosis factor-? and interferon-? increased expression of CD40 and CD40L on endothelial cells . Human atherosclerotic lesions( n =6) showed coexpression of immunoreactive CD40 and CD40L. However, no expression of CD40 and CD40L in nonatherosclerotic human arteries. CD40L mainly expressed on the shoulder and base of the plaque. But CD40 was widespreadly expressed in plaque. CONCLUSION: Our results demonstrated that CD40 and CD40L coexpressed on human umbilical vein endothelial cells and in human atherosclerotic plaque lesions. These findings suggest a previously unsuspected role for CD40-CD40L interactions in atherosclerosis.

Objective： To investigate the effect of oxLDL and VitE on the expression of CD40 and CD40 ligand(CD40L) in cultured human monoc ytes. Methods： The expression of CD40 and CD40L on monocytes su rface were measured by indirect immunorescence technique in combination with flo w cytometry. Results： Low concentration of oxLDL（≤200 μg/L） significantly increased the expression of CD40 and CD40L in a dose and time dep endent manner. High concentration (>200 μg/L）of oxLDL markedly reduced the exp ression of CD40 and CD40L. When VitE was added, it significantly reduced the ex pression of CD40 and CD40L on monocytes surface induced by oxLDL in a dose-depe ndent manner. Conclusion：It is an important mechanism that the high expression of CD40 and CD40L induced by oxLDL may be contributed to the for mation of atherosclerosis. Antioxidan VitE can partially inhibit the high expres sion of CD40 and CD40L on monocytes surface induced by oxLDL.

Objective: To investigate the effects of hyaluroni dase (HAase) and hyaluronan (HA) on proliferation of vascular endothelial cells and its mechanism. Methods: The cultured bovine aortic endothel ial cells (BAEC) were treated with HAase or HA. Cell proliferation rate was dete cted by MTT assay. The expression of CD44 and DNA content of the cells were meas ured by flow cytometry (FCM). Results: HAase (50 μg/ml) stimula ted cell proliferation ［(50.10±1.23）% vs control, P<0.01］, incre ased S phase cell rate and induced the expression of CD44, but HA (100 μg/ml) i nhibited cell proliferation and the expression of CD44. Conclusion: HAase may degrade antiangiogenic HA of extracellular matrix, which may stim ulate proliferation of endothelial cells and enhance the curative effect of grow th factors to myocardial ischemia.

Objectives:To investigate the method of generating recombinant adenovirus vector containing human p16(Ad-p16) efficiently.　Methods:Recombinant adenovirus vector was generated with HEK 293 cells, and the titer of the adenovirus was detected.　Results:The titer of generated adenovirus is about 5×108 PFU/ml.　Conclusions:Recombinant adenovirus vector was generated with HEK 293 cells with high titer. This set the foundation of adenovirus mediated gene-transfer.

Objective:To explore the levels of adhesion molecules in peripheral blood leucocyte from patients with multiple sclerosis(MS) and after intravenous methylprednisolone(MP) treatment.Methods:The positive percentag of intercellular adhesion molecule 1(CD54)?integrin LFA 1 ? subunit(CD18)?very late antigen 4 ??? subunit(CD49d?CD29) and L selectin(CD62L) were determined on lymphocytes and monocytes by flow cytometry from 28 patients with relapsing remitting MS (relapses n=20,remission n=8) and 20 controls.Results:The positive percentage of CD49d?CD29 on lymphocytes and monocytes,CD54 and CD62L on monocytes in relapses MS group were higher than in remission MS group and controls(P0.05).Conclusion:The adhesion molecules expression on peripheral blood leucocyte were elevated in MS patients and it may be suitable to be as a marker of MS activity.

Objective: To investigate the influence of mental stress on platelet function in patients received coronary angiography(CAG). Methods: With flow cytometry the expressions of platelet membrane glycoproteinⅡb Ⅲa complex ? subunit(CD41) and P selectin(CD62p) were measured in 24 CAG patients before,immediately after and 10 min after mental stress, respectively. Results: Compared with that before mental stress, the positive rate of CD41 [from(74.15?22.24)% to (87.41? 9.24)%, P

Objective: To investigate the effects of hyaluronidase (HAase) and hyaluronan (HA) on proliferation of vascular endothelial cells and its mechanism. Methods: The cultured bovine aortic endothelial cells (BAEC) were treated with HAase or HA. Cell proliferation rate was detected by MTT assay. The expression of CD44 and DNA content of the cells were measured by flow cytometry (FCM). Results: HAase (50 ?g/ml) stimulated cell proliferation [(50.10? 1.23)% vs control, P