The transcription activity of ectogenic human carcinoembryonic antigen (CEA) promoter in lung adenocarcinoma cells A549 was investigated for the further gene-targeting therapy. The reporter gene green fluorescent protein (GFP) driven by CEA promoter and human cytomegalovirus (CMV) promoter were relatively constructed and named plasmid pCEA-EGFP and pCMV-GFP respectively. The intensity of fluorescence was detected by fluorescence microscope and flow cytometry analysis after the pCEA-GFP and pSNAV-GFP plasmids were transfected into A549 cells through liposome respectively. The results showed (4.08+/-0.63) % of the A549 cells transfected with pCEA-AFP plasmid expressed, significantly lower than that of the A549 cells transfected with pCMV-GFP [(43.27+/-3.54) %]. It was suggested that ectogenic human CEA promoter in lung adenocarcinoma cells A549 was weakly expressed. The distinct specificity of CEA promoter in CEA high expression cells was regarded as a tool in selective gene therapy, but the transcription activity of ectogenic human CEA promoter was needed to increase in the future.

Objective: To investigate the causes and management of enteral feeding intolerance in patients with severe acute pancreatitis (SAP). Methods: The clinical data were retrospectively analyzed of 128 SAP patients who underwent enteral feeding treatment during the period from January 2006 to January 2008. Results: The rate of enteral feeding intolerance was significantly higher in the group of patients who didn' t use Flocare 800 pump, single-use enteral feeding tube and heater (10/50 or 20.0%) than that in the group of patients who used Flocare 800 pump, single-use enteral feeding tube and heater (5/78 or 6.4%). Conclusion: The possible risk factors of enteral feeding intolerance may be transfusional speed, temperature and concentration of nutritional fluid. Severity of acute pancreatitis is another important factor. Intestinal dysfunction should be noticed during the enteral nutritional support.

OBJECTIVETo investigate the efficacy of IFN-alpha on severe acute pancreatitis (SAP) of IFN-alpha.

METHODSA SAP model was developed in adult male rats by retrograde injection of 5% sodium taurocholate in the pancreatic duct. Serum amylase was measured by the blue-starch method and serum cytokines were determined by ELISA.

RESULTSCompared with to the control group, less pancreatic injury and lower amylase level were observed treat in the rats with IFN-alpha. In contrast, the concentration of IL-10 was higher.

CONCLUSIONIFN-alpha has significant curative effect on SAP.

Animals ; Disease Models, Animal ; Immunologic Factors ; therapeutic use ; Interferon-alpha ; therapeutic use ; Interleukin-10 ; metabolism ; Kidney ; metabolism ; Male ; Pancreatitis, Acute Necrotizing ; drug therapy ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

The transcription activity of ectogenic human carcinoembryonic antigen (CEA) promoter in lung adenocarcinoma cells A549 was investigated for the further gene-targeting therapy. The reporter gene green fluorescent protein (GFP) driven by CEA promoter and human cytomegalovirus (CMV) promoter were relatively constructed and named plasmid pCEA-EGFP and pCMV-GFP respectively. The intensity of fluorescence was detected by fluorescence microscope and flow cytometry analysis after the pCEA-GFP and pSNAV-GFP plasmids were transfected into A549 cells through liposome respectively. The results showed (4.08±0.63) % of the A549 cells transfected with pCEA-AFP plasmid expressed, significantly lower than that of the A549 cells transfected with pCMV-GFP [(43.27±3.54) %]. It was suggested that ectogenic human CEA promoter in lung adenocarcinoma cells A549 was weakly expressed. The distinct specificity of CEA promoter in CEA high expression cells was regarded as a tool in selective gene therapy, but the transcription activity of ectogenic human CEA promoter was needed to increase in the future.