Influence of Mg+2 and Cu+2 on the interaction between quinolone and calf thymus DNA.

Mg(+2) and Cu(+2) have different binding capacities to quinolone drugs and have different binding modes with calf thymus DNA. Using the method of absorption and fluorescence spectroscopy, the influence of Mg(+2) and Cu(+2) on the binding between calf thymus DNA and each of four quinolone drugs has been studied. The results show that both Mg(+2) and Cu(+2) can bind with the four drugs. In the absence of divalent metal ions, quinolone drugs interact with DNA double helix by forming hydrogen bonds between the carboxyl and carbonyl groups of the drugs and the phosphate groups of the DNA bases, and the binding capacity shows a close relationship with the drug structures. The two metal ions show different influences on the binding between the drug and DNA, which depends on the type of ion, concentration of the metal ions and the structure of drugs. Mg(+2) in lower concentrations (0.01 mM to 3.0 mM) can act as a bridge between the carboxyl group/carbonyl group of the drug and the phosphate group of the DNA by electrostatic interaction, while Cu(+2) can act as an intermediary ion between carboxyl group/carbonyl group of the drug and the DNA bases by a co-ordinate bond. Both actions can increase the interaction of the π electron between the condensed rings of the drugs and the DNA bases. In some conditions, Cu(+2) can weaken the binding between the drug and the DNA by competitive inhibition if there is a site on the drug that can directly bind both DNA bases and Cu(+2).

[Characterization and Health Risk Assessment of Exposure to Odorous Pollutants Emitted from Industrial Odor Sources].

Odor pollution has a high complaint rate with strong public concern, and industrial production is an important source of this type of pollution in China. To understand odor pollution in industrial parks and to protect the safety of work environments, samples were collected from 14 industrial odor sources and then were analyzed for odorous volatile organic compounds (VOCs) and odor concentration. Based on the field data, the main compounds causing odor were assessed and identified. The cancer and non-cancer risk of odor exposure were correspondingly estimated by the health risk model. These following results were noted. ①The substances discharged from 14 sources were the same, but the content varied greatly. Alkanes and alkenes are the major odorous compounds of fibers and batteries manufacturing and in the synthesis of hydrocarbons, anhydrides, esters, and solvents. Benzene and benzene series in waste gases from refineries, purified terephthalic acid (PTA), and latex sources were the highest. Esters are the main pollutants emitted from activated carbon processing, resin synthesis, and spraying. Carbonyl compounds and sulfides are the main exhaust gases from ceramic manufacturing and additive synthesis. ②Exhaust gases from 14 sources caused strong irritation. The synthesis of lubricating oil additives and latex sources result in severe olfactory stimulation. Ethyl mercaptan, ethyl sulfide, n-butanol, and toluene were the major odorous compounds of lubricating oil additives sources. Styrene, propylbenzene, cumene, butyl acrylate, and 1,3-butadiene were the major odorous compounds of latex sources. ③The carcinogenic risk levels for 14 sources ranged from 3.06×10-7 to 1.06×10-2, expressed as life cancer risk (LCR). Refinery, PTA, ester, and latex sources had the highest carcinogenic risk among the 14 emission sources. The non-carcinogenic risk levels for the 14 sources ranged from 0.02 to 51.66, expressed as hazard index (HI). The total HI of latex synthesis, ester synthesis, petroleum refining, PTA synthesis, and fiber manufacturing has certain non-carcinogenic health risks. Factory boundaries for latex, anhydrides synthesis, and resin synthesis sources have potential carcinogenic risk.

[Emission Characteristics of Vehicle Exhaust in Artery and Collector Roads in Nanjing Based on Real-time Traffic Data].

The vehicle emissions were estimated by the Urban High Temporal-Spatial Resolution Vehicle Emission Inventory Model and Decision Support System (hereinafter referred to as the HTSVE system) with the real-time data including traffic flow, average speed and fleet compositions obtained from Radio Frequency Identification (RFID) and emission factors based on COPERT. The study focused on the characteristics of vehicle emissions by means of non-parametric test and cluster analysis with ArcGIS in artery roads and collector roads in Nanjing, 2014. The result showed that the proportion of passenger cars reached up to 80%, and China 3 and China 4 accounted for over 90% while China 3 contributed most. The daily average emissions in special periods including morning, noon and evening were affected by both road types and weekend effect. The artery and collector roads were classified as 5 clusters. Each type had similar emission rates distribution and was affected by spatial position to support traffic management.

Molecular mechanism of fluoroquinolones resistance in Mycoplasma hominis clinical isolates

To evaluate the molecular mechanism of fluoroquinolones resistance in Mycoplasma hominis (MH) clinical strains isolated from urogenital specimens. 15 MH clinical isolates with different phenotypes of resistance to fluoroquinolones antibiotics were screened for mutations in the quinolone resistance-determining regions (QRDRs) of DNA gyrase (gyrA and gyrB) and topoisomerase IV (parC and parE) in comparison with the reference strain PG21, which is susceptible to fluoroquinolones antibiotics. 15 MH isolates with three kinds of quinolone resistance phenotypes were obtained. Thirteen out of these quinolone-resistant isolates were found to carry nucleotide substitutions in either gyrA or parC. There were no alterations in gyrB and no mutations were found in the isolates with a phenotype of resistance to Ofloxacin (OFX), intermediate resistant to Levofloxacin (LVX) and Sparfloxacin (SFX), and those susceptible to all three tested antibiotics. The molecular mechanism of fluoroquinolone resistance in clinical isolates of MH was reported in this study. The single amino acid mutation in ParC of MH may relate to the resistance to OFX and LVX and the high-level resistance to fluoroquinolones for MH is likely associated with mutations in both DNA gyrase and the ParC subunit of topoisomerase IV.