In this case, reducing the replication level to four

cultures per learn more dose would have a negligible effect on resolving power (30–40%). Data from individual experiments could be combined into one larger analysis. However, care should be taken with this approach. The methods discussed here were powered and designed to find differences within an experiment, not across several experiments. By combining experiments, small differences that are not scientifically relevant, might acquire statistical significance. This statistical approach was developed to compare PMs, but could also be applied to comparing other products’ in vitro genotoxicities. It could add confidence to any differences observed and limit apparent similarities to the resolving power of the assay. While in vitro tests alone cannot measure human risk, they can contribute to a Weight of Evidence paradigm for the risk assessment of

Reduced Toxicant Prototype (RTP) tobacco products. Together with smoke composition, in vitro disease models, CP-868596 manufacturer appropriate in vivo data, bio-markers of exposure and of biological effect, and smoking behaviour data, in vitro genotoxicity studies can help to test the hypothesis that the biological significance of exposure to tobacco and/or tobacco smoke toxicants from RTP tobacco products has been reduced, without introducing new genotoxic hazards. The authors are employees of British American Tobacco, except for J Saul who is employed by Covance click here Laboratories. British American Tobacco funded this research as part of its tobacco harm reduction scientific programme. The authors declare

that no financial or personal conflicts of interest exist with regard to the submission of the manuscript entitled “The resolving power of in vitro genotoxicity assays for cigarette smoke particulate matter”. The Ames test, IVMNT and MLA were performed by Covance Laboratories. “
“Allergic contact dermatitis (ACD) is a type IV hypersensitivity reaction, mediated by effector CD8+ and CD4+ T cells (Fonacier et al., 2010). The disease is caused by low molecular weight (LMW) compounds, which act as haptens that form a functional allergen after binding to endogenous proteins present in skin. During the sensitization phase of ACD, the protein is taken up by dermal dendritic cells (DCs) that are present in the epidermis at the site of exposure. Consequently, DCs will mature and migrate to local lymph nodes, presenting fragments of the LMW complex on either MHC class I or II, depending on the route of antigen uptake (Friedmann, 2006). Provided that the DCs also become activated and signal using co-stimulatory molecules, as reviewed in (Martin et al., 2011), this antigen presentation will lead to differentiation of naïve T cells into specific effector and memory T cells.