Spontaneous exfoliation of single‐walled carbon nanotubes on dilution of dispersions in a common solvent, N‐methyl‐pyrrolidone, is demonstrated. The free‐energy of mixing is negative, confirming athermal solubility. Scanning tunneling microscopy measurements show physisorption of the solvent to the nanotube (see figure). Experiments, supported by a simple model, show that successful solvents for nanotubes are those with surface tensions close to that of graphite.

Clinical evidence suggests that many cases of serious idiosyncratic drug-induced liver injury are mediated by the adaptive immune system in response to hepatic drug-protein adducts, also referred to as "drug-induced allergic hepatitis"; but detailed mechanistic proof has remained elusive due to the lack of animal models. We have hypothesized that drug-induced allergic hepatitis is as rare in animals as it is in humans due at least in part to the tolerogenic nature of the liver. We provide evidence that immune tolerance can be overcome in a murine model of halothane-induced liver injury initiated by trifluoroacetylated protein adducts of halothane formed in the liver. Twenty-four hours after female Balb/cJ mice were initially treated with halothane, perivenous necrosis and an infiltration of CD11b Gr-1 high cells were depleted from the liver with Gr-1 antibody treatment, enhanced liver injury was observed at 9 days after halothane rechallenge. Toxicity was associated with increased serum levels of interleukin-4 and immunoglobulins G1 and E directed against hepatic trifluoroacetylated protein adducts, as well as increased hepatic infiltration of eosinophils and CD41 T cells, all features of an allergic reaction. When hepatic CD41 T cells were depleted 5 days after halothane rechallenge, trifluoroacetylated protein adduct-specific serum immunoglobulin and hepatotoxicity were reduced. Conclusion: Our data provide a rational approach for developing animal models of drug-induced allergic hepatitis mediated by the adaptive immune system and suggest that impaired liver tolerance may predispose patients to this disease. (HEPATOLOGY 2015;62:546-557)

The utilisation of recycled concrete aggregate (RCA) in Self-Compacting Concrete (SCC) has the potential to reduce both the environmental impact and financial cost associated with this increasingly popular concrete type. However, to date limited research exists exploring the use of coarse RCA in SCC. The work presented in this paper seeks to build on the existing knowledge in this area by examining the workability, strength, and fracture properties of SCCs containing 0%, 25%, 50%, 75%, and 100% coarse RCA. The experimental programme indicated that at RCA utilisation levels of 25% to 50% little or no negative impact was observed for strength, workability, or fracture properties, with the exception of a slight reduction in Young's modulus.

In a recent study, we reported that interleukin (IL)-4 had a protective role against acetaminophen (APAP)-induced liver injury (AILI), although the mechanism of protection was unclear. Here, we carried out more detailed investigations and have shown that one way IL-4 may control the severity of AILI is by regulating glutathione (GSH) synthesis. In the present studies, the protective role of IL-4 in AILI was established definitively by showing that C57BL/6J mice made deficient in IL-4 genetically (IL-4−/−) or by depletion with an antibody, were more susceptible to AILI than mice not depleted of IL-4. The increased susceptibility of IL-4−/− mice was not due to elevated levels of hepatic APAP-protein adducts, but was associated with a prolonged reduction in hepatic GSH that was attributed to decreased gene expression of γ-glutamylcysteine ligase (γ-GCL). Moreover, administration of recombinant IL-4 to IL-4−/− mice post-acetaminophen treatment diminished the severity of liver injury and increased γ-GCL and GSH levels. We also report that the prolonged reduction of GSH in APAP-treated IL-4−/− mice appeared to contribute towards increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK), since levels of phosphorylated JNK remained significantly higher in the IL-4−/− mice up to 24 hours after APAP treatment Conclusion Overall these results show for the first time that IL-4 has a role in regulating the synthesis of GSH in the liver under conditions of cellular stress. This mechanism appears to be responsible at least in part for the protective role of IL-4 against AILI in mice and may have a similar role not only in AILI in humans, but also in pathologies of the liver caused by other drugs and etiologies.