[Detecting the isoflurane in the air of workplaces with chromatographic method].

OBJECTIVE: To establish a solvent desorption Gas chromatographic method for detecting the isoflurane in air of workplaces. METHODS: This method is based on "Standardization of methods for determination of toxic substances in workplace air". RESULTS: This method presents the linear relation with the minimum detectable limit 1.0 µg/ml and the minimum detectable concentration 0.07 mg/m(3). The precision (RSD) was 0.5% ∼ 5.0%, the mean dsorption efficiencies were 96.7% ∼ 98.9%, the absorption efficiencies were 92.1% ∼ 100%, the breakthrough volume was 3.7 mg isoflurane/100 mg active carbon. Other volatile organic solvents (Sevoflurane, Enflurane and Ethyl Alcohol) did not interfere the detection. The sample could be stored in the active carbon tube at least for 10 days. CONCLUSION: This method is meet the requirement of GBZ/T 210.4-2008 "Guide for establishing occupational health standards-Part4: Determination methods of air chemicals in workplace" and is feasible for determining the isoflurane in the air of workplaces.

Metabolic engineering of the carotenoid biosynthetic pathway toward a specific and sensitive inorganic mercury biosensor.

The toxicity of mercury (Hg) mainly depends on its form. Whole-cell biosensors respond selectively to toxic Hg(ii), efficiently transformed by environmental microbes into methylmercury, a highly toxic form that builds up in aquatic animals. Metabolically engineered Escherichia coli (E. coli) have successfully produced rainbow colorants. By de novo reconstruction of the carotenoid synthetic pathway, the Hg(ii)-responsive production of lycopene and ß-carotene enabled programmed E. coli to potentially become an optical biosensor for the qualitative and quantitative detection of ecotoxic Hg(ii). The red color of the lycopene-based biosensor cell pellet was visible upon exposure to 49 nM Hg(ii) and above. The orange ß-carotene-based biosensor responded to a simple colorimetric assay as low as 12 nM Hg(ii). A linear response was observed at Hg(ii) concentrations ranging from 12 to 195 nM. Importantly, high specificity and good anti-interference capability suggested that metabolic engineering of the carotenoid biosynthesis was an alternative to developing a visual platform for the rapid analysis of the concentration and toxicity of Hg(ii) in environmentally polluted water.

Arsenic exposure assists ccm3 genetic polymorphism in elevating blood pressure.

Epidemiologic study has suggested that arsenic exposure is positively related to increased blood pressure. However, the underlying mechanism concerning interaction between genetic polymorphisms and arsenic exposure remains unclear. In present study, within 395 Chinese, the effects of interaction between arsenic exposure and CCM3 gene polymorphisms on elevation of blood pressure were probed by multiple Logistic regression models after adjusting for confounding factors. Firstly, we found that serum arsenic was positively associated with blood pressure, cholesterol, glucose and C-reactive protein. Then, adjusted for confounding factors of age, gender, smoking, alcohol consumption, BMI and degree of education, arsenic exposure incurred the hazard of increased systolic pressure and diastolic pressure, with odds ratios (ORs) being 1.725 and 1.425, respectively. Distinctly, we found that interactions between rs3804610* rs9818496, rs6784267*rs9818496, and rs3804610* rs6784267 variant genotype can increase significantly risks of SBP. Additionally, interactions between rs9818496, rs3804610 and rs6784267 genotypic variantions and arsenic exposure boosted the hazard of increased systolic pressure, with ORs being 1.496, 1.496 and 1.312. In conclusion, our fingdings suggest that As exposure of population can assist CCM3 polymorphism in elevating SBP.