Beach Response to a Total Exclusion Barrage: Cardiff Bay, South Wales, UK

The regeneration of 1100 ha of derelict industrial land to the south of Cardiff included the construction of the 1.1-km-long Cardiff Bay Barrage (completed November 1999), which impounded two major South Wales rivers. A 160 m groyned beach, composed of four groynes and three bays, adjacent to and seaward of the barrage breakwater was monitored between September 1997 and September 2002 to assess pre- and postconstruction beach evolution. Overall, mean beach levels increased throughout the five-year period, resulting in a net gain of beach covering equivalent to 818.8 m3 (1800 tonnes). After barrage completion, both longshore and cross-shore gradients became less volatile and increased beach levels in the bay nearest the breakwater, prevented tidal action and erosion at the cliff toe. This was a significant change from initial conditions that was verified by parametric and nonparametric tests at the 99% confidence level. Regression analysis determined that there were significant temporal relationships. Spatial analysis identified two highly significant longshore trends with respect to distance from the breakwater and showed that this influence decreased with distance. More than 72 m from the breakwater, the regression equation (R2 = 96%) modelled a trend of falling beach levels caused by net sediment transport. Conversely, from 72 m to the breakwater, beach levels increased at a rate greater than twice the fall in the previous section (R2 = 92%). These trends were further supported by significantly greater level differences across the second groyne. Impacts of temporal and spatial trends, especially subsequent to barrage completion, were evidenced by the change in beach morphology and similar contour orientation in all three bays. Models were developed and proposed as management tools to identify potential changes in coastal processes, as well as the rate of change of the barrage's upstream influence with respect to net sediment flow. Groyne removal was suggested to provide recreational beach space

Differential induction of innate immune signaling by genetically related parasite species.

<p>a) Microarray-based expression profiling of human foreskin fibroblasts (HFF) infected with <i>Neospora caninum</i> (NcLiv isolate) or <i>Toxoplasma</i> (GT1, Prugniaud or VEG strains). Heat map shows hierarchical clustering analysis of 822 genes differentially regulated relative to uninfected cells by ≥2-fold (FDR≤5%), in any of these experiments. Each row in heatmap represents average of duplicate (NcLiv and GT1) or triplicate arrays (VEG, PRU, uninf). Color pattern on heatmaps represents column Z-score. b) A cluster of 66 genes (Fig. 1a, asterisk) induced by <i>Neospora</i> but not any strain of <i>Toxoplasma</i>, including several well-known type I interferon response genes (arrows). c) Gene Ontology (GO) enrichment analysis of 66 <i>Neospora</i>-induced genes. Bar graph shows fold enrichment for top five GO Biological Process terms enriched at <i>P</i>≤0.05 and represented by ≥5 genes. Number of genes and GO term name is shown at the right of each bar. d) Fluorescence micrographs of uninfected HFF cells, or cells infected with <i>Neospora</i> or <i>Toxoplasma</i>, then challenged with GFP-tagged vesicular stomatitis virus. Representative images are shown. Experiment was repeated three times with similar results.</p

The Type I interferon response to Neospora infection is dependent on <i>Tlr3</i> and <i>Trif.</i>

<p>QPCR analysis of <i>Mx1</i> expression in <i>Neospora</i> infected bone marrow macrophages derived from wild-type (WT), <i>Myd88^−/−</i>, <i>Myd88^−/−/Trif^−/−, Tlr2^−/−/Tlr4^−/−</i> and <i>Tlr3^−/−</i> mice. Error bars indicate standard deviations for three biological replicates; * = <i>P</i>≤0.01. Experiment was repeated three times with similar results.</p

Toxoplasma actively suppresses anti-viral host responses via a soluble factor.

<p>(a) co-infection assay in HFF cells showing <i>Mx1</i> gene expression in <i>Toxoplasma</i> infected cultures (Tg), cultures inoculated with heat-killed <i>Neospora</i> (HK Nc; striped bar), or infected with <i>Toxoplasma</i> for one hr before challenge with heat-killed <i>Neospora</i> (black bar). (b) QPCR analysis of <i>IRF7</i> (open bars) and <i>HERC5</i> (striped bars) expression in HFF cells pre-treated with fresh media or conditioned media from <i>T. gondii</i> infected cells (1° treatment) prior to infection with <i>N. caninum</i> (2° treatment). c) HFF cells were pretreated with supernatants from experiment in panel a, then infected with VSV-GFP. Representative fluorescence micrographs are shown. Error bars indicate standard deviations for three biological replicates; * = <i>P</i>≤0.01. Experiment was repeated two times with similar results.</p

Macrophage transcriptional responses to Neospora infection are Ifnar1-dependent.

<p>Microarray-based expression profiling of <i>Neospora</i> (<i>Nc</i>) or <i>Toxoplasma</i> (<i>Tg</i>) infected wild-type or <i>Ifnar1-/-</i> bone marrow-derived mouse macrophages. a) heat map shows hierarchical clustering analysis of 833 genes differentially regulated by either Nc or Tg on either cell type relative to uninfected cells by ≥2-fold (FDR≤5%). Two clusters of co-regulated genes are indicated. Each column in heatmap represents an average of duplicate arrays, and color pattern represents row Z-score. b) Venn diagrams showing number of differentially regulated genes for each condition. c and e) GO enrichment results for cluster 1 and 2, respectively. d and f) heatmaps showing top ten most strongly induced genes in cluster 1 and 2, respectively. Gene symbol and fold change of infected WT relative to uninfected WT control are shown for each gene.</p

Active invasion is not required for innate recognition of parasites.

<p>QPCR analysis of the expression of the antiviral gene <i>Mx1</i> following (a) infection of HFF cells or (b) treatment of cells with heat-killed strains of <i>Toxoplasma</i> (open bars) or <i>Neospora</i> (shaded bars). (c) confocal fluorescence microscopy of HFF cells treated with live (top row) or heat killed (bottom row) <i>Toxoplasma</i>-mCherry. Lysosomes are stained with LysoTracker dye. Representative images are shown. Error bars indicate standard deviations for three biological replicates; * = <i>P</i>≤0.01. Experiments were repeated three times with similar results.</p

<i>Neospora</i> RNA elicits a TLR3-dependent type I interferon response.

<p>a) QPCR analysis of <i>Irf7</i> gene expression in wild-type mouse bone marrow-derived macrophages pretreated for 1 hr with either DMSO (control) or 100 nM bafilomycin A1 prior to 24 hr infection with live (Nc) or heat-killed <i>Neospora</i> (HK Nc). b) <i>Irf7</i> expression in <i>Myd88^−/−</i> macrophages incubated with 1 µg/ml of either poly(I:C) or total RNA from HFF cells (host), or <i>Neospora</i> parasites, either alone (white) or in complex with DOTAP transfection reagent (striped), to enhance targeting of RNA to endosomes. c) <i>Irf7</i> expression in <i>Myd88^−/−</i> macrophages incubated with 1 µg/ml of either <i>Toxoplasma</i> or <i>Neospora</i> RNA with DOTAP in cells pretreated with either DMSO or a small molecule inhibitor of TLR3/dsRNA complex formation. Error bars indicate standard deviations for three biological replicates; * = <i>P</i>≤0.01. Experiments were repeated two or three times with similar results.</p