Objective To investigate the role of miR-125b-1 gene in oncogenesis and progression of human lung cancer. Methods PCR-SSCP was used to detect miR-125b-1 gene mutation in 121 specimens from primary site of lung cancer tissues and 22 samples of nor- real adjacent lung tissues. Results There were 40 cases of miR-125b-1 gene mutation, and gene mutation was positively correlated to the status of lymph node metastasis ( r,=0.285, P＜0.01 ) and clinical stage metastasis( r, =0. 241, P ＜0. 01 ), but no relationship between miR-125b-1 mutation and other clinical features was found. The postoperative survival time in patients with miR-125b-1 gene mutation was significantly longer than those with low expression ( P＜0.05). Conclusion There exist miR-125b-1 gene mutation in lung cancer, miR- 125b-1 gene mutation probably plays a crucial role in lung carcinogenesis.

OBJECTIVE: To analyze status quo of utilization of liver-protective medicines in our hospital. METHODS: Consumption sum and DDDs of liver-protective medicines were analyzed statistically in our hospital during 2004～2008. RESULTS: The proportion of consumption sum of liver-protective medicines in total was 21.09%. The main medicines was inosine to prevent antituberculosis drug-induced hepatic lesion during 2004～2005. The utilization of new and expensive liver-protective medicines was used more than before during 2006～2008. The consumption sum was increased greatly. CONCLUSION: The utilization of liver-protective medicines is rational and economical in the previous two years. But the price of used liver-protective medicines is higher than before during 2006～2008. So some interventions should be adopted to control the utilization of liver-protective medicines rationally and economically.

AIM:To investigate the inhibitory effect of ground dragon on the expression of ?-SMA and FN in the lung tissue with asthma.METHODS:The BALB/c mice were divided into four groups:control group(group A,n=20),asthmatic model group(group B,n=20),large-dose ground dragon treatment group(group C,n=20)and low-dose ground dragon treatment group(group D,n=20).To establish a mouse model of chronic asthma,we sensitized the mouse with 0.02% ovalbumin(OVA)by intraperitoneal injection,and stimulated the mice with 1% OVA by atomization.The treatment groups were given ground dragon before stimulation every time.After the last time of stimulation,the mice were subjected to laboratory tests.Inflammatory cells in bronchoalveolar lavage fluid were counted.Total level of IgE in serum was detected by ELISA.FN mRNA and ?-SMA mRNA in the lung tissue were measured by RT-PCR and AlphaImager 2200 semi-quantitation analysis system.Expressions of FN and ?-SMA were measured by the method of two-step immunohistochemistry and leica QWIN V3 analysis system.RESULTS:(1)Compared with those in group A,the expressions of ?-SMA and FN in group B were significantly increased(P0.05).(2)Compared with those in group A,the expression levels of ?-SMA mRNA and FN mRNA in group B had a great increase(P0.05).CONCLUSION:The ground dragon inhibits ?-SMA and FN expression in the lung tissue of mice with chronic asthma,indicating that ground dragon may inhibit airway remodeling in asthma through the inhibition of ?-SMA and FN expressions.

Objective To investigate the effect of gefitinib on mucus hypersecretion by inhibiting epidermal growth factor receptor (EGFR) activity in chronic obstructive pulmonary disease (COPD).Methods Human airway epithelail cell lines 16HBE cells were exposed to cigarette smoke extraction (CSE) to establish the COPD model.EGFR activity was inhibited by tyrosine kinase inhibitor gefitinib.The mRNA expressions of EGFR and MUC5AC were detected by real-time PCR.EGFR,p-EGFR and MUC5AC protein levels were determined by Western blot and ELISA.Results EGFR mRNA level was increased by 12.7％ in CSE and 8.6％ in gefitinib group,but had no significant differences among CSE,gefitinib group and control group (all P＞ 0.05).MUC5AC mRNA levels were enhanced by 141.7％,26.4％ in CSE group and gefitinib group respectively,and there were significant differences among CSE,gefitinib group and control group (all P＜0.05).EGFR protein levels were (600.34±64.58) μg/mg,(632.58±72.94) μg/mg,(584.57±67.39) μg/mg,in control,CSE and gefitinib groups,respectively,and there were no significant differences between groups (all P＞0.05).p-EGFR protein levels were (338.62±45.28) μg/mg,(679.43±78.23) μg/mg,(292.74±59.17) μg/mg in control,CSE and gefitinib groups,respectively.MUC5AC protein levels were(72.80±6.25)μg/mg,(187.00±±10.26)μg/mg,(92.57±8.32)μg/mg in control,CSE and gefitinib groups respectively.Compared with control group,p-EGFR and MUC5AC protein levels were increased significantly in CSE group (both P＜0.05),and had no significant differences in p EGFR and MUC5AC protein levels between control group and gefitinib group.Conclusions CSE may lead to mucus hypersecretion through activating the EGFR-mediated signaling pathways.Gefitinib may inhibit mucus hypersecretion by inhibiting EGFR tyrosine kinanse activity.EGFR may serve as a potential target for COPD.