28 research outputs found

    Use of single versus multiple biotic communities as indicators of biological integrity in northern prairie wetlands

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    AbstractAs much as 70% of prairie wetlands in Canada have been lost. Although further degradation of natural wetlands is considered to be somewhat offset by wetland construction and restoration, Canada lacks bioassessment tools that can track ecosystem health in prairie wetlands. Indices of biological integrity (IBIs) use one or more biotic communities to compare the biological condition of a particular site to conditions found in least-impacted reference sites. Using the IBI approach, we evaluated the potential of 5 biotic communities to assess wetland health in northern prairie wetlands in Canada. Vegetation in the wet meadow, emergent and open-water zones as well as wetland-dependent songbirds and waterbirds were sampled at 81 semi-permanent/permanent natural and compensation wetlands spanning an environmental stress gradient. Metrics with strong linear relationships to the stress gradient (R2>0.2) were combined into an IBI for each biotic community and were subsequently validated at a suite of test sites. After validation, the entire data set was combined and each IBI was evaluated based on its linear relationship to environmental stress. Wet meadow zone vegetation was a strong indicator of environmental stress (R2=0.68, p<0.001), as was the wetland-dependent songbird community (R2=0.59, p<0.001). The emergent zone vegetation community was a relatively weak and inconsistent indicator of environmental stress, while the open-water zone vegetation and waterbird communities were poor indicators. To evaluate whether monitoring more than one biotic community provided additional information about a site's biological and environmental condition, we produced a two-taxon IBI that combined wet meadow zone vegetation and wetland-dependent songbird metrics. The two-taxon IBI had a marginally stronger linear relationship to the stress gradient (R2=0.72, p<0.001) than any single biotic community alone, although we argue that this added information would not warrant the extra cost, effort, and logistical barriers of sampling both plants and birds. The wet meadow zone vegetation and wetland-dependent songbird IBIs were strong surrogates of one another (R2=0.57), suggesting that wet meadow zone vegetation can be used to predict the health of wetland-dependent songbirds, and visa versa. Our results suggest that habitat for healthy wet meadow zone vegetation and wetland-dependent songbird communities is being degraded as compensation sites are replacing their natural analogs

    Factors controlling sulfur gas exchange in Sphagnum-dominated wetlands

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    Atmosphere-peatland exchange of reduced sulfur gases was determined seasonally in fen in NH, and in an artificially-acidified fen at the Experimental Lakes Area (ELA) in Canada. Dimethyl sulfide (DMS) dominated gas fluxes at rates as high as 400 nmol/m(sup -2)hr(sup -1). DMS fluxes measured using enclosures were much higher than those calculated using a stagnant-film model, suggesting that Sphagnum regulated efflux. Temperature controlled diel and seasonal variability in DMS emissions. Use of differing enclosure techniques indicated that vegetated peatlands consume atmospheric carbonyl sulfide. Sulfate amendments caused DMS and methane thiol concentrations in near-surface pore waters to increase rapidly, but fluxes of these gases to the atmosphere were not affected. However, emission data from sites experiencing large differences in rates of sulfate deposition from the atmosphere suggested that chronic elevated sulfate inputs enhance DMS emissions from northern wetlands

    Human Activity Mediates a Trophic Cascade Caused by Wolves

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    Experimental evidence of trophic cascades initiated by large vertebrate predators is rare in terrestrial ecosystems. A serendipitous natural experiment provided an opportunity to test the trophic cascade hypothesis for wolves (Canis lupus) in Banff National Park, Canada. The first wolf pack recolonized the Bow Valley of Banff National Park in 1986. High human activity partially excluded wolves from one area of the Bow Valley (low-wolf area), whereas wolves made full use of an adjacent area (high-wolf area). We investigated the effects of differential wolf predation between these two areas on elk (Cervus elaphus) population density, adult female survival, and calf recruitment; aspen (Populus tremuloides) recruitment and browse intensity; willow (Salix spp.) production, browsing intensity, and net growth; beaver (Castor canadensis) density; and riparian songbird diversity, evenness, and abundance. We compared effects of recolonizing wolves on these response variables using the log response ratio between the low-wolf and high-wolf treatments. Elk population density diverged over time in the two treatments, such that elk were an order of magnitude more numerous in the low-wolf area compared to the high-wolf area at the end of the study. Annual survival of adult female elk was 62% in the high-wolf area vs. 89% in the low-wolf area. Annual recruitment of calves was 15% in the high-wolf area vs. 27% without wolves. Wolf exclusion decreased aspen recruitment, willow production, and increased willow and aspen browsing intensity. Beaver lodge density was negatively correlated to elk density, and elk herbivory had an indirect negative effect on riparian songbird diversity and abundance. These alternating patterns across trophic levels support the wolf-caused trophic cascade hypothesis. Human activity strongly mediated these cascade effects, through a depressing effect on habitat use by wolves. Thus, conservation strategies based on the trophic importance of large carnivores have increased support in terrestrial ecosystems. Read More: http://www.esajournals.org/doi/full/10.1890/04-126

    QF2011: a protocol to study the effects of the Queensland flood on pregnant women, their pregnancies, and their children's early development

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    Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

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    Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes
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