Many bacteria spread over surfaces by "swarming" in groups. A problem for scientists who study swarming is the acquisition of statistically significant data that distinguish two observations or detail the temporal patterns and two-dimensional heterogeneities that occur. It is currently difficult to quantify differences between observed swarm phenotypes. Here, we present a method for acquisition of temporal surface motility data using time-lapse fluorescence and bioluminescence imaging. We specifically demonstrate three applications of our technique with the bacterium Pseudomonas aeruginosa. First, we quantify the temporal distribution of P. aeruginosa cells tagged with green fluorescent protein (GFP) and the surfactant rhamnolipid stained with the lipid dye Nile red. Second, we distinguish swarming of P. aeruginosa and Salmonella enterica serovar Typhimurium in a coswarming experiment. Lastly, we quantify differences in swarming and rhamnolipid production of several P. aeruginosa strains. While the best swarming strains produced the most rhamnolipid on surfaces, planktonic culture rhamnolipid production did not correlate with surface growth rhamnolipid production.

We used a novel approach for molecular quantification in standard fixed and embedded tissue to measure Aβ42 and paired helical filament-τ) (PHF-τ) in frontal, temporal, and parietal cortex from 325 consecutive brain autopsies collected as part of a population-based study of brain aging and incident dementia in the Seattle area. We observed significant effects of APOE ε4 on Aβ42 levels in both diagnostic groups by disease stage and region. In contrast, we did not observe a significant effect of APOE ε4 on PHF-τ levels by disease stage in any region. Aβ42 and PHF-τ levels in cerebral cortex were correlated more strongly in the Dementia group, and these measures had independent explanatory power for dementia beyond those of standard neuropathologic indices. Associations between Lewy body disease and levels of Aβ42 or PHF-τ and between Aβ42 levels and microvascular brain injury suggested that these co-morbid diseases enhanced the penetrance of AD. Our novel approach brings additional insights into the molecular pathogenesis of common causes of dementia and may serve as a platform for future studies that pursue associations between molecular changes of AD and genetic or environmental risk.

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