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We describe studies of the pressure driven flow of several classical fluids through lithographically produced channels in which one dimension, the channel height h, is in the micron or nanometer size range. The measured flow rates are compared with theoretical predictions assuming no-slip boundary conditions at the walls of the channel. The results for water agree well with this prediction for h as small as 40 nm ͑our smallest channels͒. However, for hexane, decane, hexadecane, and silicone oil we find deviations from this theory when h is reduced below about 100 nm. The observed flow rates for small h are larger than theoretical expectations, implying significant slip at the walls, and values of the slip length are estimated. The results are compared with previous experimental and theoretical work.

Objective Epidemiological and recent clinical studies implicate periodontitis as an independent risk factor for cardiovascular disease. Previously, we demonstrated that rabbits with experimental periodontitis and cholesterol diet exhibit more aortic plaque compared to diet alone. We also showed that a proresolution mediator, Resolvin E1 (RvE1), reverses the experimental periodontitis. Here, we determined whether oral/topical application of RvE1 attenuates aortic atherosclerosis induced by both diet and periodontal inflammation. Approach and Results Thirty-nine rabbits on a 13-week regimen of 0.5% cholesterol diet were included. Periodontitis was induced by P. gingivalis in 24 rabbits and 15 rabbits were placed in no-periodontitis groups. Interventions were no-treatment, vehicle, and RvE1 treatment (4μg/site or 0.4 μg/site) topically applied 3-times/ week. At 13 weeks, both periodontitis and atherosclerosis were quantified. Atherosclerotic plaques were assessed by Sudan IV staining, histology and ex vivo MRI. Serum levels of C-reactive protein (CRP) were evaluated as a measure of systemic inflammation.RvE1, used as an oral/topical agent, significantly diminished atherogenesis and prevented periodontitis (p<0.05). In the absence of periodontal inflammation, oral/topical application of RvE1 resulted in significantly less arterial plaque, a lower intima/media ratio, and decreased inflammatory cell infiltration compared to no-treatment (p<0.001). Local oral RvE1 application significantly reduced systemic levels of CRP (p<0.05). Conclusions The results suggest that oral/topical RvE1 attenuates enhanced atherogenesis induced by periodontitis and prevents vascular inflammation and atherogenesis in the absence of periodontitis. The inhibition of vascular inflammation with endogenous mediators of resolution of inflammation provides a novel approach in the prevention of atherogenic events.