Aims to characterize e-cigarette use, users, and effects, in a sample of Electronic Cigarette Causacian, 44% educated to degree level or above. Findings 74% reported not smoking for at least a few weeks since using the e-cigarette and 70% reported reduced urge to smoke.72% of participants used a 'tank' system, most commonly, the eGo-C (23%). Mean duration of use was 10 months. Only 1% reported exclusive use of non-nicotine (0mg) containing liquid. E-cigarettes were generally considered to: be satisfying to use; elicit few side effects; be healthier than smoking; improve cough/breathing; and be associated with low levels of craving. Among ex-smokers, 'time to first vape' was significantly longer than 'time to first cigarette' (t 1104 =11.16, P <0.001) suggesting a lower level of dependence to e-cigarettes. Exsmokers reported significantly greater reduction in craving than current smokers (χ 2 1 =133.66, P<0.0007) although few other differences emerged between these groups.Compared to males, females opted more for chocolate/sweet flavours (χ 2 1 =16.16, P< 0.001) and liked the e-cigarette because it resembles a cigarette(χ 2 3 = 42.65, P< 0.001). Conclusions E-cigarettes tend to be used for smoking cessation but for a longer duration than NRT and were generally regarded as efficacious. Future research should focus on possible long-term health risks, abuse liability and cessation efficacy.

The therapeutic application of siRNA shows promise as an alternative approach to small molecule inhibitors for the treatment of human disease. However, the major obstacle to its use has been the difficulty in delivering these large anionic molecules in vivo. In this study, we have investigated whether siRNA-mediated knockdown of p38 MAP kinase mRNA in mouse lung is influenced by conjugation to the non-viral delivery vector cholesterol and the cell penetrating peptides (CPP) TAT(48-60) and penetratin. Initial studies in the mouse fibroblast L929 cell line, showed that siRNA conjugated to cholesterol, TAT(48-60) and penetratin but not siRNA alone achieved a limited reduction of p38 MAP kinase mRNA expression. Intratracheal administration of siRNA resulted in localisation within macrophages and scattered epithelial cells and produced a 30-45% knockdown of p38 MAP kinase mRNA at 6hrs. As with increasing doses of siRNA, conjugation to cholesterol improved upon the duration but not the magnitude of mRNA knockdown whilst penetratin and TAT(48-60) had no effect. Importantly, administration of the penetratin or TAT(48-60) peptides alone caused significant reduction in p38 MAP kinase mRNA expression whilst the penetratin-siRNA conjugate activated the innate immune response. Overall, these studies suggest that conjugation to cholesterol may extend but not increase siRNA mediated p38 Figure S1, dose-dependent percentile p38 MAP kinase mRNA levels in vitro following lipofection with three mouse p38 MAP kinase siRNA or two mismatch controls; Figure S2, analytical HPLC and electrospray mass spectrograms of peptide-and cholesteryl-RNA constructs; Figure S3, analytical gels of CPP and cholesterol conjugate annealing products; Figure S4, cell viability following incubation with siRNA, CPP or siRNA conjugates; Figure S5, MAP kinase mRNA knockdown in the lung. Furthermore, the use of CPP may be limited due to as yet uncharacterized effects upon gene expression and a potential for immune activation.