Objective To explore the effect of glucocorticoid on disbalance of the Th 1/Th 2 cytokines to investigate the mechanism of treatment of breathing in glucocorticoid in asthmatic patients. Methods The peripheral blood was drawn and the plasma IL-4,IL-12 and IgE of control group and patients were detected by ELISA method before and after glucocorticoid treatment. The results were analysed statistically. Results ⑴In asthmatic group, plasma IL-4 and IgE levels, and PEF variant rate after treatment were lower than those before treatment (P0.05); and ⑷ Correlation analysis showed that IL-4 level positively correlated with the IgE level and PEF variant rate(r=0.64,r=0.52;P

BACKGROUNDTo study the expression of Skp2 and c-myc in non-small cell lung cancer (NSCLC) and to investigate their relationship and clinical significance.

METHODSThe expression of Skp2 and c-myc was detected in 42 NSCLC, 10 pulmonary benign disease and 8 epithelial dysplasia tissues by immuno-histochemistry.

RESULTSThe positive rate of Skp2 stain was 24.83%±13.64% in NSCLC tissues, which was significantly higher than that in pulmonary benign disease tissues (3.07%±1.32%)(P < 0.001) and that in dysplasia tissues (13.89%±3.95%)(P < 0.05). The expression level of Skp2 was closely related to cell differentiation (P < 0.001), TNM stages (P < 0.01) and lymph node metastasis (P < 0.05), but not to pathological type of NSCLC. There was a positive correlation between Skp2 and c-myc expression (r=0.448, P=0.003). The concurrent high expression rate of Skp2 and c-myc was 38.1% (16/42), which was closely rela- ted to TNM stage (P < 0.05), but not to cell differentiation, pathological type or lymph node metastasis.

CONCLUSIONSOverexpression of Skp2 may play important roles in carcinogenesis and development of NSCLC, and it may cooperate with c-myc protein.

BACKGROUNDTo investigate the expression of survivin and its relation with apoptosis in non-small cell lung cancer.

METHODSSurvivin expression was examined in sixty paraffin-embedded NSCLC samples and 16 benign pulmonary disease tissues by immunohistochemistry methods.Apoptosis of NSCLC cells was detected by TUNEL technique.

RESULTSSurvivin was expressed in 38 of 60 (63.3%) NSCLC tissues.In contrast, benign pulmonary disease tissues did not express survivin. The expression of survivin protein was closely related to TNM stages (P < 0.05), lymph node involvement (P < 0.05) and cell differentiation (P < 0.01), but not to histological classification, gender and ages (P > 0.05). A correlation coefficient test showed a negative correlation between the AI and survivin expression (r=-0.231,P < 0.05).

CONCLUSIONSApoptosis inhibition caused by abnormal survivin expression may participate in the oncogenesis and progression of NSCLC. The over-expression of survivin suggest the bad prognosis in NSCLC. Survivin gene may be indentified as a potential therapeutic target in NSCLC.

BACKGROUNDTo investigate the relation between FLIP expression and apoptosis in non-small cell lung cancer (NSCLC).

METHODSFLIP expression was examined in forty-eight paraffin-embeded NSCLC samples and 16 benign pulmonary disease tissues by immunohistochemistry method. Apoptosis of NSCLC cells was detected by TUNEL technique.

RESULTSThe positive rate of FLIP expression in NSCLC was 83.33%(40/48), which was significantly higher than that in benign pulmonary disease tissues (P < 0.01). The expression level of FLIP was closely related to TNM stages and lymph node involvement, but not to histological classification and cell differentiation. No correlation was observed between the expression of FLIP and apoptosis index of tumor cells (r=-0.211,P > 0.05 ).

CONCLUSIONSOverexpression of FLIP may be involved in the progression of NSCLC, but its expression may not be related to cell apoptosis in NSCLC.

BACKGROUNDIt has been known that different degrees of hypoxia can produce different effects on tumor. The study is to investigate the effect of hypoxia on the infiltration and migration of lung adenocarcinoma cells.

METHODSLung adenocarcinoma cells were exposed to normoxic (air, 5%O₂), hypoxic (1%O₂, 5%CO₂, 94%N₂) or anoxic (95%N₂, 5%CO₂) condition for 48 hours. The migration ability of the cells was assayed by wound healing methods. The infiltration ability was assayed by HABM-HEM model. The cells exposed to hypoxia were planted subcutaneously in nude mice, and the growth of cells and the rate of metastasis to lymph node or lung were observed. The levels of matrix metalloproteinase 2 (MMP-2) and tissue inhibitor of metalloproteinase II (TIMP-2) in culture media were assayed by ELISA.

RESULTSComparing with normoxia group, the infiltration, migration and metastasis of hypoxia group were increased significantly (P < 0.05) , as well as the level of MMP-2 (P < 0.01), and the TIMP-2 level was remarkably decreased (P < 0.05) . In anoxia group, the levels of MMP-2 and TIMP-2 were both significantly decreased (P < 0.01).

CONCLUSIONSModerate hypoxia can up-regulate the expression of MMP-2, down-regulate the expression of TIMP-2, and increase the infiltration and migration of lung cancer cells. But serious hypoxia can decrease the expression of MMP-2 and TIMP-2, and inhibit the proliferation, infiltration and migration of lung cancer cells.