Stochastic synthesis of a ligand coupled to a nanoparticle results in a distribution of populations with different numbers of ligands per nanoparticle. This distribution was resolved and quantified using HPLC, and is in excellent agreement with the ligand/nanoparticle average measured by 1H NMR, GPC, and potentiometric titration, yet significantly more disperse than commonly held perceptions of monodispersity. Two statistical models were employed to confirm that the observed heterogeneity is consistent with theoretical expectations.

Aromatic hydrocarbon fuels, such as toluene, are important components in real jet fuels. In this work, reactive molecular dynamics (MD) simulations employing the ReaxFF reactive force field have been performed to study the high-temperature oxidation mechanisms of toluene at different temperatures and densities with equivalence ratios ranging from 0.5 to 2.0. From the ReaxFF MD simulations, we have found that the initiation consumption of toluene is mainly through three ways, (1) the hydrogen abstraction reactions by oxygen molecules or other small radicals to form the benzyl radical, (2) the cleavage of the C-H bond to form benzyl and hydrogen radicals, and (3) the cleavage of the C-C bond to form phenyl and methyl radicals. These basic reaction mechanisms are in good agreement with available chemical kinetic models. The temperatures and densities have composite effects on toluene oxidation; concerning the effect of the equivalence ratio, the oxidation reaction rate is found to decrease with the increasing of equivalence ratio. The analysis of the initiation reaction of toluene shows that the hydrogen abstraction reaction dominates the initial reaction stage at low equivalence ratio (0.5-1.0), while the contribution from the pyrolysis reaction increases significantly as the equivalence ratio increases to 2.0. The apparent activation energies, E(a), for combustion of toluene extracted from ReaxFF MD simulations are consistent with experimental results.

BackgroundGlutathione S-transferases (GSTs) are multifunctional detoxification enzymes that play important roles in insects. The completion of several insect genome projects has enabled the identification and characterization of GST genes over recent years. This study presents a genome-wide investigation of the diamondback moth (DBM), Plutella xylostella, a species in which the GSTs are of special importance because this pest is highly resistant to many insecticides.ResultsA total of 22 putative cytosolic GSTs were identified from a published P. xylostella genome and grouped into 6 subclasses (with two unclassified). Delta, Epsilon and Omega GSTs were numerically superior with 5 genes for each of the subclasses. The resulting phylogenetic tree showed that the P. xylostella GSTs were all clustered into Lepidoptera-specific branches. Intron sites and phases as well as GSH binding sites were strongly conserved within each of the subclasses in the GSTs of P. xylostella. Transcriptome-, RNA-seq- and qRT-PCR-based analyses showed that the GST genes were developmental stage- and strain-specifically expressed. Most of the highly expressed genes in insecticide resistant strains were also predominantly expressed in the Malpighian tubules, midgut or epidermis.ConclusionsTo date, this is the most comprehensive study on genome-wide identification, characterization and expression profiling of the GST family in P. xylostella. The diversified features and expression patterns of the GSTs are inferred to be associated with the capacity of this species to develop resistance to a wide range of pesticides and biological toxins. Our findings provide a base for functional research on specific GST genes, a better understanding of the evolution of insecticide resistance, and strategies for more sustainable management of the pest.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1343-5) contains supplementary material, which is available to authorized users.

The potent vasoconstrictor endothelin (ET) is implicated in several human disease states including hypertension, congestive heart failure, renal failure, pulmonary hypertension, ischemia, and cerebral vasospasm.1-9Two subtypes of ET receptors known as ETa and ETb have been cloned and characterized in animal and mammalian systems.10-13 A third endothelin receptor subtype has been cloned from Xenopus dermal melanophores and heart,14•15 although this subtype has not yet been described in mammalian tissues.Both ETa and ETb receptors are widely distributed in animal and human tissues.16-26 In a wide variety of animal tissues, vasoconstriction occurs via activation of ETa and/or ETb receptors depending upon the species and vascular bed under study.17-26 However, there is some controversy as to whether ETb receptors play an important role in mediating vasoconstrictor responses in mammalian tissues.20-23 Davenport et al. have reported that ETA-mediated vasoconstriction plays a major role in some human vessels, such as coronary artery, but have been unable to demonstrate ETb receptor-mediated contractions in human tissues using ETB-selective agonists such as [Ala 1,3,11,15]ET-1 and BQ 3020.20 However, Luscher et al. have reported that ETb receptor mRNA was detected by Northern blot analysis in human internal mammary artery and aortic smooth muscle cells.23 Several groups have shown that the ETb receptor agonist SRTX-6c can elicit vasoconstriction in human vessels although the magnitude of the response has been found to be considerably less than that observed for ET-1 itself.24-26 It is possible that downregulation of ETb receptors in isolated tissues is responsible for these observations.A number of peptide ET antagonists have been reported including BQ-12327•28 and FR 139317,29 which are potent ETA-selective antagonists; balanced ETa/ETb antagonists including PD 14289330 and PD 14506531 and the recently reported ETB-selective antagonist, BQ-788.32 A number of non-peptide endothelin antagonists have also been reported. These include the Shionogi steroid analog 97-13933 and several balanced ETa/ETb non-peptide antagonists, including Ro 46-2005,9 Ro 47t Department of Therapeutics.