Objective To detect cytokeratin in routine pathology negative regional lymph nodes postoperatively in non-small cell lung carcinoma (NSCLC). To investigate the relationship of lymph node micrometastasis in P-TNM stages NSCLC and survival rates. Methods From Jan. 1996 to Dec. 2003, 107 paraffin-embedded specimens of T1-T4N0-N1M0 NSCLC patients were collected. Anti-cytokeratin(CK) an- tibody AE1/AE3 was applied to detect cytokeratin with Envision~(TM) method in routine pathological negative re- gion lymph nodes in NSCLC, and selected negative control, positive control and blank control. The pulmo- nary hilar lymph node micrometastasis was upward regulated with stage pCK-N1, mediastinal lymph node mi- crometastatsis was upward regulated with stage pCK-N2. The result applied to SPSS11.0 software to process. Results The CK positive rate was 29.9% in all the patients. The CK positive rate was 27% (21/78), 30% (7/23), 67% (4/6)in stage p-Ⅰ, p-Ⅱand p-Ⅲ, respectively. All these data showed the tendency by which detectable rate increased and was accompanied by disease progress. Comparing the annual survival rate and median survival time of the non-micrometastasis group with the mierometastasis group in two groups, the survival rate difference was statistically significant. Comparing the annual survival rate and median sur- vival time in pCK-ⅢA stage with p-Ⅰ-Ⅱstage, pCK-ⅢA stage annual survival rate and median survival time was significantly different (P=0.020). Similarly, comparing the survival rate in pCK-ⅡB stage with p-ⅠB stage, pCK-ⅡB stage survival rate was significantly different(P=0.059). Comparing the survival time of pCK-ⅢA stage with p-Ⅲstage, pCK-ⅡB stage, with p-ⅡB stage, euther survival time difference was statistically significant (P=0.838, 0.518). Conclusions The rate of positive cytokeratin increase is ac- companied by the disease progress in NSCLC. Positive cytokeratin has disadvantagious prognosis. It is showed that pCK-N1 may be equal to p-N1 and pCK-N2 which also may be equal to p-N2. Micrometastasis may affect the UICC staging currently in use.

AIM: To study the role of TGF-?/Smad pathway in the development of renal fibrosis in diabetic nephropathy.METHODS: Rats were induced to diabetic nephropathy by using tail intravenous injection of STZ.The expression of TGF-?_1,Smad2/3 protein and mRNA in kidney were examined at 2,4,8 and 16 weeks after STZ induction.CTGF,collagen-Ⅲ,PAI-1 mRNA expression in kidney at 16 weeks of STZ-induced diabetic nephropathy and normal rats were studied by RT-PCR.RESULTS: Weak TGF-?_1,Smad2/3 protein were detected in normal renal tissues while strong TGF-?_1,Smad2/3 staining were observed in renal tissues of diabetic nephropathy(0.057?0.030/0.223?0.040;0.017?0.010/0.153?0.010,respectively,P