Facile in situ synthesis of nanofluids based on ionic liquids and copper oxide clusters and nanoparticles

Two stable nanofluids comprising of mixed valent copper(_I,_II) oxide clusters (<1 nm) suspended in 1-butyl-3-methylimidazolium acetate, [C(₄)mim][OAc], and copper(_II) oxide nanoparticles (<50 nm) suspended in trioctyl(dodecyl) phosphonium acetate, [P-₈₈₈₁₂][OAc], were synthesised in a facile one-pot reaction from solutions of copper(_II) acetate hydrate in the corresponding ionic liquids. Formation of the nanostructures was studied using ¹³C NMR spectroscopy and differential scanning calorimetry (DSC). From a solution of Cu(OAc)₂ in 1-ethyl-3-methylimidazolium acetate, [C₂mim][OAc], crystals were obtained that revealed the structure of [C₂mim][Cu₃(OAc)₅(OH)₂(H₂O)]center dot H₂O, indicating the formation of copper hydroxo-clusters in the course of the reaction. Synthesised nanostructures were studied using transmission electron microscopy (TEM) and X-ray photoelectron spectroscopy (XPS). Physical properties of the prepared IL-nanofluids were examined using IR and UV-VIS spectroscopy, thermogravimetric analysis (TGA), differential scanning calorimetry (DSC) and densitometry. 

Telephone survey evaluation of the educational impact of a distance learning course

The educational impact of a distance learning (DL) course entitled ''Health Screening for Health Promotion, was investigated using a telephone questionnaire survey. An introduction to the DL course was distributed to all community pharmacists in England (16,400); the main body of the course, on which pharmacists were examined, was distributed free of charge to all pharmacists who requested it (1,485). Pharmacists participating in the survey (868) were organized by random selection into groups and stratified according to age, sex and postcode. A matched control group was randomly drawn from those pharmacists who had not participated in the course. The DL course improved pharmacists' knowledge about health screening/health promotion issues (e.g., mean score of 66 percent achieved by a group who had completed the course; 51 percent achieved by the control group; P<0.001). Factors influencing score achieved included sex and year of registration. Males performed better than females (P<0.008) while performance decreased with number of years on the register (P<0.001).

Intravenous tolerance effectively overcomes enhanced pro-inflammatory responses and EAE severity in the absence of IL-12 receptor signaling

Intravenous (i.v.) administration of autoantigen effectively induces Ag-specific tolerance against experimental autoimmune encephalomyelitis (EAE). We and others have shown enhanced EAE severity in mice lacking IL-12 or its receptor, strongly suggesting an immunoregulatory effect of IL-12 signaling. To examine the role of IL-12 responsiveness in autoantigen-induced tolerance in EAE, we administered autoantigen i.v. in two distinct treatment regimes to wildtype and IL-12Rβ2(-/-) mice, immunized to develop EAE. Administration at the induction phase suppressed EAE in wildtype and IL-12Rβ2(-/-) mice however the effect was somewhat less potent in the absence of IL-12Rβ2. Expression of pro-inflammatory cytokines such as IFN-γ, IL-17 and IL-2, was inhibited in wild-type tolerized mice but less so in IL-12Rβ2(-/-) mice. I.v. antigen was also effective in suppressing disease in both genotypes when given during the clinical phase of disease with similar CNS inflammation, demyelination and peripheral inflammatory cytokine profiles observed in both genotypes. There was however a mild impact of a lack of IL-12 signaling on Treg induction during tolerance induction compared to WT mice in this treatment regime. These findings show that the enhanced severity of EAE that occurs in the absence of IL-12 signaling can be effectively overcome by i.v. autoantigen, indicating that this therapeutic effect is not primarily mediated by IL-12 and that i.v. tolerance could be a powerful approach in suppressing severe and aggressive MS.

IL-31 does not induce normal human ciliated epithelial cells to differentiate into a phenotype consistent with the pathophysiology of asthma

Abstract Background IL-31 is a novel cytokine that has been implicated in allergic diseases such as atopic dermatitis and more recently asthma. While IL-31 has been well studied in skin conditions such as atopic dermatitis, little is known about the role IL-31 plays in asthma and specifically the differentiation process of the bronchial epithelium, which is central to the pathogenesis of allergic asthma. Methods We examined the effects of IL-13 (20 ng/ml), IL-31 (20 ng/ml) and an IL-13/IL-31 combination stimulation (20 ng/ml each) on the in vitro mucociliary differentiation of paediatric bronchial epithelial cells (PBECs) from healthy patients (n=6). IL-31 receptor (IL-31-RA) expression, markers of differentiation (goblet and ciliated cells), transepithelial electrical resistance (TEER), quantification of goblet and ciliated cells, real time PCR for MUC5AC, ELISA for VEGF, EGF and MCP-1 (CCL-2) and ELISA for MUC5AC were assessed. Results We found that well-differentiated PBECs expressed IL-31-RA however it's expression did not increase upon stimulation with IL-31 or either of the other treatments. TEER indicated good formation of tight junctions which was found to be similar across all treatment groups (p=0.9). We found that IL-13 alone significantly reduced the number of ciliated cells compared with unstimulated (IL-13 stimuation: mean=4.8% (SD=2.5); unstimulated: mean=15.9%, (SD=7.4), p

Burkholderia cenocepacia O polysaccharide chain contributes to caspase-1-dependent IL-1 beta production in macrophages

Burkholderia cenocepacia infections in CF patients involve heightened inflammation, fatal sepsis, and high antibiotic resistance. Proinflammatory IL-1 beta secretion is important in airway inflammation and tissue damage. However, little is known about this pathway in macrophages upon B. cenocepacia infection. We report here that murine macrophages infected with B. cenocepacia K56-2 produce proinflammatory cytokine IL-1 beta in a TLR4 and caspase-1-mediated manner. We also determined that the OPS (O antigen) of B. cenocepacia LPS contributes to IL-1 beta production and pyroptotic cell death. Furthermore, we showed that the malfunction of the CFTR channel augmented IL-1 beta production upon B. cenocepacia infection of murine macrophages. Taken together, we identified eukaryotic and bacterial factors that contribute to inflammation during B. cenocepacia infection, which may aid in the design of novel approaches to control pulmonary inflammation. J. Leukoc. Biol. 89: 481-488; 2011.