Microfluidic electrochemical sensor for on-line monitoring of aerosol oxidative activity.

Particulate matter (PM) air pollution has a significant impact on human morbidity and mortality; however, the mechanisms of PM-induced toxicity are poorly defined. A leading hypothesis states that airborne PM induces harm by generating reactive oxygen species in and around human tissues, leading to oxidative stress. We report here a system employing a microfluidic electrochemical sensor coupled directly to a particle-into-liquid sampler (PILS) system to measure aerosol oxidative activity in an on-line format. The oxidative activity measurement is based on the dithiothreitol (DTT) assay, where, after being oxidized by PM, the remaining reduced DTT is analyzed by the microfluidic sensor. The sensor consists of an array of working, reference, and auxiliary electrodes fabricated in a poly(dimethylsiloxane)-based microfluidic device. Cobalt(II) phthalocyanine-modified carbon paste was used as the working electrode material, allowing selective detection of reduced DTT. The electrochemical sensor was validated off-line against the traditional DTT assay using filter samples taken from urban environments and biomass burning events. After off-line characterization, the sensor was coupled to a PILS to enable on-line sampling/analysis of aerosol oxidative activity. Urban dust and industrial incinerator ash samples were aerosolized in an aerosol chamber and analyzed for their oxidative activity. The on-line sensor reported DTT consumption rates (oxidative activity) in good correlation with aerosol concentration (R(2) from 0.86 to 0.97) with a time resolution of approximately 3 min.

Experimental demonstration of a two-phase population extinction hazard.

Population extinction is a fundamental biological process with applications to ecology, epidemiology, immunology, conservation biology and genetics. Although a monotonic relationship between initial population size and mean extinction time is predicted by virtually all theoretical models, attempts at empirical demonstration have been equivocal. We suggest that this anomaly is best explained with reference to the transient properties of ensembles of populations. Specifically, we submit that under experimental conditions, many populations escape their initially vulnerable state to reach quasi-stationarity, where effects of initial conditions are erased. Thus, extinction of populations initialized far from quasi-stationarity may be exposed to a two-phase extinction hazard. An empirical prediction of this theory is that the fit Cox proportional hazards regression model for the observed survival time distribution of a group of populations will be shown to violate the proportional hazards assumption early in the experiment, but not at later times. We report results of two experiments with the cladoceran zooplankton Daphnia magna designed to exhibit this phenomenon. In one experiment, habitat size was also varied. Statistical analysis showed that in one of these experiments a transformation occurred so that very early in the experiment there existed a transient phase during which the extinction hazard was primarily owing to the initial population size, and that this was gradually replaced by a more stable quasi-stationary phase. In the second experiment, only habitat size unambiguously displayed an effect. Analysis of data pooled from both experiments suggests that the overall extinction time distribution in this system results from the mixture of extinctions during the initial rapid phase, during which the effects of initial population size can be considerable, and a longer quasi-stationary phase, during which only habitat size has an effect. These are the first results, to our knowledge, of a two-phase population extinction process.

Indanylacetic acids as PPAR-delta activator insulin sensitizers.

A series of indane acetic acid derivatives were prepared which show a spectrum of activity as insulin sensitizers and PPAR-alpha and PPAR-delta ligands. In vivo data are presented for insulin sensitizers with selectivity for PPAR-delta over PPAR-alpha.