For groundwater-surface water interactions to be understood in complex wetland settings, the architecture of the underlying deposits requires investigation at a spatial resolution sufficient to characterize significant hydraulic pathways. Discrete intrusive sampling using conventional approaches provides insufficient sample density and can be difficult to deploy on soft ground. Here a noninvasive geophysical imaging approach combining three-dimensional electrical resistivity tomography (ERT) and the novel application of gradient and isosurface-based edge detectors is considered as a means of illuminating wetland deposit architecture. The performance of three edge detectors were compared and evaluated against ground truth data, using a lowland riparian wetland demonstration site. Isosurface-based methods correlated well with intrusive data and were useful for defining the geometries of key geological interfaces (i.e., peat/gravels and gravels/ Chalk). The use of gradient detectors approach was unsuccessful, indicating that the assumption that the steepest resistivity gradient coincides with the associated geological interface can be incorrect. These findings are relevant to the application of this approach in settings with a broadly layered geology with strata of contrasting resistivities. In addition, ERT revealed substantial structures in the gravels related to the depositional environment (i.e., braided fluvial system) and a complex distribution of low-permeability putty Chalk at the bedrock surface-with implications for preferential flow and variable exchange between river and groundwater systems. These results demonstrate that a combined approach using ERT and edge detectors can provide valuable information to support targeted monitoring and inform hydrological modeling of wetlands.

Enteropathogenic Escherichia coli (EPEC) are a class of diarrheagenic organisms that induce a characteristic attaching and effacing lesion in enterocytes and various cultured cell lines. Infection of cultured HEp-2 cells by EPEC isolates 2036-80 (serotype 0119) and E2348-69 (serotype 0127) resulted in significant elevation of intracellular free calcium levels, determined quantitatively with the fluorescent calcium indicator dye 2-{[2-bis (carboxymethyl)amino-5-methylphenoxyjmethyl}-6-methoxy-8-bis(carboxymethyl)aminoquinoline. This effect, which was not observed on infection with non-lesion-forming E. coli strains, was inhibited by dantrolene, a drug that prevents calcium mobilization from intracellular stores. Moreover, activated protein kinase C in infected cells was dissociated from cell membranes by a process that was inhibited by cyclosporin A, suggesting involvement of the calcium-dependent protease calpain. A qualitative method for observing intracellular calcium fluxes by fluorescence microscopy with the recently described fluorescein-based indicator fluo-3 was used to screen a collection of well-characterized E. coli isolates from patients with infantile enteritis. Increased localized calcium-dependent fluo-3 fluorescence was observed only in HEp-2 cells infected with known lesion-forming EPEC strains. We propose that enhancement of intracellular free calcium levels in enterocytes infected with EPEC would result in formation of the characteristic lesion by calcium-dependent activation of actin-depolymerizing proteins, with eventual loss of absorptive capacity.

New synthetic routes to a series of tetra- and pentacyclic acridines related in structure to marine natural products are reported. The novel water-soluble agent dihydroindolizino[7,6,5-kl]acridinium chloride 14 has inhibitory activity in a panel of non-small-cell lung and breast tumor cell lines exceeding that of m-AMSA. The salt inhibited the release of minicircle products of kDNA confirming that disorganization of topoisomerase II partly underlies the activity of the compound. COMPARE analysis of the NCI mean graph profile of compound 14 at the GI(50) level corroborates this conclusion with Pearson correlation coefficients (>0.6) to clinical agents of the topoisomerase II class: however, this correlation was not seen at the LC(50) level. The inhibitory action of 14 on Saccharomyces cerevisiae transfected with human topoisomerase II isoforms showed a 3-fold selectivity against the IIalpha isoform over the IIbeta isoform. Unlike m-AMSA, 14 is not susceptible to P-glycoprotein-mediated drug efflux and retains activity in lung cells with derived resistance to the topoisomerase II inhibitor etoposide.