[Enhancement effect of polychlorinated biphenyl on benzo (a) pyrene-induced DNA damage in HepG2 cells].

OBJECTIVE: To study the effect of polychlorinated biphenyl, Aroclor1254 on benzo (a) pyrene [B (a) P]-induced DNA damage in HepG2 cells. METHODS: HepG2 cells were pretreated with Aroclor1254 (11.5, 23 and 46 micromol/L) for 24 hours and then exposed to B (a) P (50 micromol/L). DMSO (10 ml/L) was used as solvent control. Single cell gel electrophoresis (SCGE) and high-performance liquid chromatography-electrochemical detection (HPLC-EC) assays were applied to detect DNA single-strand breaks and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in HepG2 cells, respectively. RESULTS: Average Oliver tail moment (OTM) and 8-OHdG level in HepG2 cells were significantly increased in B (a) P treated group (1.66 +/- 0.21), (23.31 +/- 6.02) 8-OHdG/10(6)dG than that in solvent control (0.79 +/- 0.15), (12.31 +/- 3.24) 8-OHdG/10(6)dG, respectively. In Aroclor 1254 treated group (11.5, 23.0, 46.0 micromol/L), average OTM were 0.88 +/- 0.20, 1.01 +/- 0.15 and 1.10 +/- 0.16, and 8-OHdG levels were (19.57 +/- 7.57), (22.80 +/- 9.16) and (31.74 +/- 9.25) 8-OHdG/10(6)dG, respectively. A concentration of 46 micromol/L Aroclor1254 caused a significant increase of 8-OHdG level as compared with the solvent control. After pretreatment of HepG2 cells with Aroclor1254 (11.5, 23.0 and 46.0 micromol/L), B (a) P induced more DNA strand breaks (OTM: 2.14 +/- 0.22, 2.43 +/- 0.32 and 2.71 +/- 0.31) and 8-OHdG [(32.50 +/- 3.81), (49.23 +/- 16.66) and (60.36 +/- 18.04) 8-OHdG/10(6)dG] in HepG2 cells than B (a) P alone. CONCLUSION: Aroclor1254 might enhance B (a) P-induced DNA damage in HepG2 cells, which should imply a synergistic effect of Aroclor1254 on the genotoxicity of B (a) P.

Ventilator-associated pneumonia in intensive care units in Hubei Province, China: a multicentre prospective cohort survey.

A multicentre prospective cohort study was performed in 17 intensive care units (ICUs) in tertiary care hospitals in Hubei Province, China. Ventilator-associated pneumonia (VAP) was defined according to modified criteria from the published literature. Among 4155 ventilated patients, the crude incidence and incidence rate of VAP were 20.9% and 28.9 cases per 1000 ventilator-days. Multivariate analysis using logistic regression revealed risk factors including male sex [risk ratio (RR): 1.5; P<0.001], coma (RR: 2.1; P<0.001), chronic obstructive pulmonary disease (RR: 1.4; P<0.001), infections at other sites (RR: 1.6; P=0.001), serious disease predating the onset of VAP (RR: 1.6; P<0.001) and interventions including antacid treatment (RR: 1.4; P<0.001), antimicrobial treatment (RR: 5.1; P<0.001), bronchoscopy (RR: 1.5; P=0.041) and tracheostomy (RR: 1.4; P=0.014). The most frequently isolated causative pathogens were Pseudomonas aeruginosa and Acinetobacter baumannii. Of all Staphylococcus aureus isolates, 45.7% were meticillin resistant. Rates, risk factors and causal pathogens of VAP in ICUs in Hubei differ from those reported from developed countries. These data show the need for more effective infection control interventions in Hubei, China.