Objective To develop a capillary electrophoresis method for the determination of methamidopho residue in water.Methods Methamidopho in water was determined by micellar electrokinetic capillary chromatograph.The qualitative analysis was done by retention time and quantitative analysis by external standard curve.Results The optimum conditions for methamidopho determination were: pH= 7.5,20 mmol/L phosphate buffer,30 mmol/L SDS,wavelength of 254 nm,separate voltage 25 kV,inject duration of 9 s.The linear range was 1.0-200 ?g/ml,the correlation coefficient was 0.999 1,the rates of recovery were 91.5%-105.2%,the relative standard deviations were 1.35%-3.24% for this method.The limit of determination was 0.007 1 ?g/ml(capillary volume was 3 ?l).Conclusion This method was sensitive,accurate and applicable to rapid the determination of methamidopho.

Objective:A study was conducted to determine the expression of acetyl-coa carboxylase product of phosphorylation (P-ACC) and an enzyme called cyclooxygenase 2 (COX-2) in non-small cell lung cancer (NSCLC) tissue, as well as the relationship and correlations between tumor size, lymph node metastasis, clinical stage, and pathological type. Methods: Sixty-two patients with NSCLC lung cancer tissues were included in the patient group, whereas 20 patients who underwent lobectomy for other reasons and had normal lung tissues were included in the control group. Immunohistochemical streptavidin peroxidase method was used to detect the expression of P-ACC and COX-2 in lung cancer and normal lung tissues. Results:The positive expressions of P-ACC and COX-2 in NSCLC lung cancer and normal lung tissues were significantly different (P<0.05). In NSCLC tissues, the positive expression of P-ACC was significantly associated with tumor size (P<0.05), but was not significantly associated with lymph node metastasis, clinical stage, and pathological type. We found no correlation between the positive expression of COX-2 and tumor size, lymph node metasta-sis, clinical stage and pathological type. Further analysis revealed that the positive expression of P-ACC and COX-2 in NSCLC was sig-nificantly and negatively correlated (r=-2.37, P=0.032). Conclusion:The positive expression of COX-2 in NSCLC greatly increased compared with that of P-ACC, and a significantly negative correlation was observed between them. We propose that the positive expres-sion of P-ACC reduction may activate the positive expression of COX-2 and promote the occurrence, development, invasion, and metas-tasis of NSCLC.

Objective To establish a stable lung cancer A549 cell line transfected by AMP-activated protein kinase (AMPK) expression vector,and to observe the effect of AMPK on proliferation as well as on the invasive ability of A549 cells.Methods Full-length of AMPK gene was amplified and its target gene was digested,then inserted into the GV358 plasmid.Co-tranfected 293T cells were subjected to the lentivirus equipment package.Subsequently,we collected the lentivirus supernatant to infect the A549 cells and establish a stably,overexpressed cell line A549.The mRNA and protein of AMPK were examined by real-time quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western blotting.The proliferation and invasion abilities of A549 cells were detected by methyl thiazolyl thiazolium (MTT) and Transwell assay.Results GV358-AMPK lentivirus vectors was successfully constructed by restrictive enzyme digestion and plasmid sequencing.There were significantly increased expressions of AMPK protein (5.87 times,P =0.002) and mRNA (16.12 times,P ＜ 0.001) after transfected with GV358-AMPK compared with the Vector group.Meanwhile,AMPK overexpression showed significantly lower proliferation (the forth day:0.53 ± 0.03 vs.0.64 ±0.05,P=0.021;the fifth day:0.58 ± 0.04 vs.0.80 ± 0.07,P =0.002) and weaken invasive ability [(1.6±0.5) ×l05 vs.(3.4±0.3) ×105,P=0.004] ofA549 cells.Conclusion The lentiviralAMPK expression vector and its A549 cell line is successfully constructed.AMPK overexpression inhibits the proliferation and invasive ability of A549 cells.