This paper summerized the surgical treatment of primary bronchogenic carcinoma in 3568 cases between 1957-1991. The resectability rate was 90. 3%, postoperative morbidity rate 8.32% and operative mortality 0. 89%. Pathological diagnoses of the resected specimens included squa-mous cell carcinoma for 48.7%, adenocarcinoma 22.9%, small cell cancer 15. 4%, large cell cancer 1. 3% and squa-mous-adenocarcinoma in 10.1%. The follow-up rate was 93%. The 5-and 10-year survival rates were 34.6% and 22.79% respectively. Analyses of the data demonstratad that the histologic type, pathological stage and metastasis of mediastinal lymph node are the important factors affecting the prognosis. According to UICC P-TNM,42. 6% of the patients in this group were in stage III. The 5 year survival rate was 19% in IIIa patients and 6% in IIIb. According to authors experience, it is recommended that in IIIa patients with nonsmall cell cardinoma, active surgical treatment should be adopted; in patients with small cell carcinoma, chemotherapy and radiotherapy should be given pre-and postoperatively, in IIIb patients with small cell carcinoma, surgical treatment is generally not indicated.

Objective To observe the changes of serumγ?glutamyl transpeptidase(GGT)levels before and after the patho?gen treatment in patients with subclinical schistosomiasis,and explore its clinical value in the diagnosis and treatment of sub?clinical schistosomiasis. Methods Totally 109 patients with subclinical schistosomiasis,who were found in the endemic inves?tigation of schistosomiasis in Ezhou City,were selected as the investigation subjects,and then they were treated with praziquan?tel. The serum GGT levels of the subjects before and after the treatment were detected and compared. Results Before the treat?ment,the average value of the GGT levels of the 109 patients was(48.1 ± 45.9)IU/L,among which,the GGT levels of 69 cases (63.3%)were normal,and the levels of 40 cases(36.7%)were increased. After the treatment,the average GGT level of the pa?tients was(32.1 ± 23.4)IU/L,which decreased by 33.3%comparing with that before the treatment,and the difference had a statistical significance(U=2.17,P=0.01). The GGT levels of 65 patients decreased in different degrees. Among the 40 pa?tients whose GGT levels had increased before the treatment,the GGT levels of 31 ones returned to the normal. Conclusion The GGT level detection can accurately reflect the liver function in the patients with subclinical schistosomiasis ,and also it has certain clinical application value to judge the liver function damage and recovery of the patients before and after the pathogen treatment.

BACKGROUNDTo study the role of nm23-H1 and CD44v6 gene in non-small cell lung cancer (NSCLC).

METHODSExpressions of nm23-H1 and CD44v6 genes were analyzed in 147 cases of NSCLC by SP immunohistochemistry method.

RESULTSThe overall positive rate of nm23-H1 staining was 62.6% (92/147). Significant differences in the positive rate of nm23-H1 were found between well and poor differentiated groups [68.6% (83/121) [WTBX]vs 34.6% (9/26)], and between adenocarcinoma and squamous cell carcinoma , and between adenocarcinoma and squamous cell carcinoma [78.8% (52/66) [WTBX]vs 50.8% (32/63) ] ( (P < 0.05), but not between stage I+II and stage III+IV [ 65.3% (62/95) [WTBX]vs 57.7% (30/52) ], and between N0 and N1-3 , and between N0 and N1 3 [64.7% (55/85) [WTBX]vs 59.7% (37/62) ]( ( P > 0.05). The positive rate of nm23-H1 of patients who survived for more than 3 years was 71.4% (55/77), which was significantly higher than 52.9% (37/70) of patients who survived for less than 3 years (Chi-square=5.4, P < 0.05). For CD44v6, the overall positive rate was 63.9% (94/147). Significant differences in the positive rate of CD44v6 were found between well and poor differentiated groups [68.6% (83/121) [WTBX]vs 42.3% (11/26)], and between adenocarcinoma and squamous cell carcinoma , and between adenocarcinoma and squamous cell carcinoma [53.0% (35/66) [WTBX]vs 77.8% (49/63) ] ( (P < 0.05), but not between stage I+II and stage III+IV [ 66.3% (63/95) [WTBX]vs 59.6% (31/52) ], and between N0 and N1-3 , and between N0 and N1 3 [63.5% (54/85) [WTBX]vs 64.5% (40/62) ]((P > 0.05). The positive rate of CD44v6 of patients who survived for more than 3 years was much lower than that of patients who survived for less than 3 years (43/74 vs 51/70, P < 0.01 ). The 3-year survival rate in patients with nm23-H1(+)CD4v6(-) was significantly higher than those with nm23-H1(-)CV44v6(+) (22/32 vs 11/34, P < 0.01).

CONCLUSIONSThere are some relationships among expressions of nm23-H1 and CD44v6 in NSCLC and cell differentiation, histological classification and prognosis, and no relation in stage and lymph node metastasis.

Background:Previous study has found that harmine inhibited the proliferation of gastric cancer cells by down-regulating cyclooxygenase-2(COX-2)expression. However,its molecular mechanism is not fully clear. Aims:To investigate the effect of harmine on proliferation and apoptosis of gastric cancer cells,and explore the role of PTEN/Akt/MDM2 signaling pathway in this process. Methods:Human gastric adenocarcinoma cell line SGC-7901 and MKN-45 were treated with harmine at different concentrations(2,4,8,16,32 μg/mL)for 24,48,and 72 hours. The cell proliferation and apoptosis were detected by MTT assay and Hoechst staining,respectively. The expressions of PTEN,COX-2, phosphorylated Akt(p-Akt)and p-MDM2 were measured by Western blotting. Results:Harmine dose- and time-dependently inhibited proliferation and induced apoptosis of SGC-7901 and MKN-45 cells. Also,harmine dose-dependently increased PTEN expression,and inhibited p-Akt,p-MDM2 and COX-2 expressions in SGC-7901 and MKN-45 cells. Conclusions:Harmine may inhibit proliferation and induce apoptosis of gastric cancer cells via down-regulating COX-2 expression through PTEN/Akt/MDM2 signaling pathway.

OBJECTIVE: To evaluate the regulatory effect of berberine on autophagy and apoptosis balance of fibroblast-like synoviocytes (FLSs) from patients with in rheumatoid arthritis (RA) and explore the mechanism. METHODS: The inhibitory effect of 10, 20, 30, 40, 50, 60, 70, and 80 μmol/L berberine on RA-FLS proliferation was assessed using CCK-8 method. Annexin V/PI and JC-1 immunofluorescence staining was used to analyze the effect of berberine (30 μmol/L) on apoptosis of 25 ng/mL TNF-α- induced RA-FLSs, and Western blotting was performed to detect the changes in the expression levels of autophagy- and apoptosis-related proteins. The cells were further treated with the autophagy inducer RAPA and the autophagy inhibitor chloroquine to observe the changes in autophagic flow by laser confocal detection of mCherry-EGFP-LC3B. RA-FLSs were treated with the reactive oxygen species (ROS) mimic H₂O₂ or the ROS inhibitor NAC, and the effects of berberine on ROS, mTOR and p-mTOR levels were observed. RESULTS: The results of CCK-8 assay showed that berberine significantly inhibited the proliferation of RA-FLSs in a time- and concentration-dependent manner. Flow cytometry and JC-1 staining showed that berberine (30 μmol/L) significantly increased apoptosis rate (P < 0.01) and reduced the mitochondrial membrane potential of RA-FLSs (P < 0.05). Berberine treatment obviously decreased the ratios of Bcl-2/Bax (P < 0.05) and LC3B-II/I (P < 0.01) and increased the expression of p62 protein in the cells (P < 0.05). Detection of mCherry-EGFP-LC3B autophagy flow revealed obvious autophagy flow block in berberine-treated RA-FLSs. Berberine significantly reduced the level of ROS in TNF-α-induced RA-FLSs and upregulated the expression level of autophagy-related protein p-mTOR (P < 0.01); this effect was regulated by ROS level, and the combined use of RAPA significantly reduced the pro-apoptotic effect of berberine in RA-FLSs (P < 0.01). CONCLUSION Berberine can inhibit autophagy and promote apoptosis of RA-FLSs by regulating the ROS-mTOR pathway.
Humans ; Synoviocytes ; Berberine/metabolism* ; Reactive Oxygen Species/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Hydrogen Peroxide/metabolism* ; Sincalide/metabolism* ; Cell Proliferation ; Arthritis, Rheumatoid/metabolism* ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism* ; Apoptosis ; Fibroblasts ; Autophagy ; Cells, Cultured