0.05). ②Plasma endothelin in the two groups was remarkably decreased after treatment(P0.05).③ NO in the two groups was significantly increased after treatment(P0.05). Conclusion TFL can reduce blood pressure and improve endothelial cell function.

Objective: To investigate the role of Smads signaling pathway in the transdifferentiation of airway epithelial cells into myofibroblasts induced by rhTGF-?1 in vitro.Methods: We exposed cultured 16HBE cells to rhTGF-?1(10?g/L),detected the levels of Phosphorylated Smad2 and Smad3 in nucleus proteins by Western blot at different time points,treated with rhTGF-?1 the 16HBE cells pre-transfected with either the expression plasmid of Smad7(pCDNA3.0/Smad7) or the blank vector(pCDNA3.0),and determined the expression of ?-SMA by immunofluorescent staining and RT-PCR and that of E-cadherin by RT-PCR.Results: The expression of Phosphorylated Smad2 was observed and that of Smad3 increased in the TGF-?1-treated group,with the levels of Phosphorylated Smad2 and Smad3 elevated in a time-dependent manner.The level of ?-SMA was significantly decreased while that of E-cadherin markedly increased in the Smad7 transfection group as compared with the blank vector transfection group 24 h after TGF-?1 stimulation,and no differences were found between the two groups at 36 h.Correspondingly,the number of ?-SMA-positive cells was reduced in the Smad7 group compared with the blank vector group(P

Objective To investigate pathogens and drug resistance of lower respiratory tract infection(LRTI)in Intensive Care Unit(ICU).Methods Retrospective study of the clinical data,the distribution and the drug-sensitivity of pathogens of 220 cases with LRTI in ICU.Results Totally 280 strains of pathogens were identified by bacterial culturing.The ratio of G-bacteria to total pathogens isolated was 63.5%,of the G+ bacteria was 25.1%,and of the fungi was 11.4%.The main kinds of the G-bacteria were Klebsiella pneumoniae(17.1%),Pseudomonas aeruginosa(13.2%),Acinetobacter baumannii(12.5%),and Stenotrophomonas maltophilia(10.4%).Staphylococcus aureus(SA)(91.4%)was the most prominent in G+ bacteria,and MRSA was 98.4% in SA.The result of drug sensitive test in vitro showed the multiple drug fast rate of Pseudomonas aeruginosa was comparatively high,Stenotrophomonas maltophilia to Levofloxacin was low,Klebsiella pneumoniae and Acinetobacter baumannii were highly sensitive to carbapenems.The susceptibility rate of MRSA to vancomycin was 100%.Conclusion G-bacteria are the majority of the pathogens,isolated from patients with LRTI in ICU.Klebsiella pneumoniae,Pseudomonas aeruginosa,Acinetobacter baumannii,and Stenotrophomonas maltophilia are the chief G-pathogens.Except Stenotrophomonas maltophilia,imipenem and merpenem are relatively active against the G-bacilli.The proportion of MRSA and fungal infection is increasing.It is suggested that there be urgent need for surveillance of bacterial resistance and rational use of antimicrobial agents during clinical therapy.

Objective: To observe the expression changes of Notch and nuclear factor-κB (NF-κB) signaling pathways in rat myocardium post myocardial infarction. Methods: Myocardial infarction was established by ligation of the left anterior descending coronary artery(MI group), sham rats (similar surgical procedure without coronary artery ligation) served as control, the rats were sacrificed at first week, 4th and 8th week after operation, the non-infarct myocardial tissue in both groups was obtained to detect the mRNA expression of Notch1, Dll4 and Hes1 by RT-PCR, the protein expression of NICD1 was detected by Western blot, the nuclear protein p65 content was detected to reflect the activation degree of NF-κB signaling in the cardiomyocytes. Results: The myocardial mRNA expression of Notch1 in MI group was significantly higher than in control group (1.68±0.35 vs. 0.47±0.12, P<0.05) at first week, and tended to be higher at the 4th week and 8th week (P>0.05). The mRNA expression of Dll4 and Hes1 was similar between the two groups at the three time points. NICD1 protein level was increased at the first week in MI group as compared with control group (1.31±0.33 vs.0.45±0.11, P<0.05), which tended also to be higher at the 4th week and 8th week post operation (P>0.05). For NF-κB activation study, the nuclear protein p65 content was higher at first week, 4th week and 8th week in MI group as compared with respective control groups (0.286±0.052 vs.0.049±0.016 (P<0.01), 0.247±0.056 vs. 0.043±0.018 (P<0.01), 0.120±0.033 vs. 0.044±0.009 (P<0.05)), the most significant increase was found in the first week. Conclusions Notch and NF-κB signaling pathways are actively involved in the process of ventricular remodeling after myocardial infarction. Notch1 and NF-κB signaling pathways are both activated at the first week after myocardial infarction, NF-κB signaling pathway activation after myocardial infarction continues up to 8 weeks. These two signal transduction pathways may thus serve as new targets for future intervention studies to prevent heart failure.