Fish productivity in the lower lakes and Coorong, Australia, during severe drought

Anthropogenic modification of catchments and river flow can significantly alter estuarine habitats, hydrology and nutrient delivery with implications for fisheries productivity. The Coorong estuary at the terminus of Australia's River Murray supports an economically important fishery as well as being recognised internationally as a critical site for migratory birds. Salinity near the Murray Mouth varies between fresh and marine depending upon river flow, but the Coorong becomes increasingly saline along its 120km length. Freshwater flow to the Coorong is naturally variable but has significantly reduced by extraction for irrigated agriculture and domestic use upstream. Extreme drought from 2000 to 2010 and over-allocation of water resources resulted in the cessation of freshwater flow to the Coorong, significantly increasing salinity. During this period the diversity and abundance of organisms in the Coorong declined which reduced food web complexity. During lower flows the system generally becomes less productive as evidenced by: lower nutrient concentrations and loads, lower chlorophyll and primary productivity, a decrease in the abundance of fish-prey items (zooplankton, macroinvertebrates and small fish), a decrease in fish abundance, although this is not well reflected in fishery catch data because of the concentration of fishing in available habitat. The maintenance of flow is the only management strategy that stimulates recruitment, delivers nutrient resources to the estuary and ensures maintenance of habitable area by maintaining appropriate salinity

Morphometric analysis of inflammation in bronchial biopsies following exposure to inhaled diesel exhaust and allergen challenge in atopic subjects

BACKGROUND: Allergen exposure and air pollution are two risk factors for asthma development and airway inflammation that have been examined extensively in isolation. The impact of combined allergen and diesel exhaust exposure has received considerably less attention. Diesel exhaust (DE) is a major contributor to ambient particulate matter (PM) air pollution, which can act as an adjuvant to immune responses and augment allergic inflammation. We aimed to clarify whether DE increases allergen-induced inflammation and cellular immune response in the airways of atopic human subjects. METHODS: Twelve atopic subjects were exposed to DE 300 μg.m-³ or filtered air for 2 h in a blinded crossover study design with a four-week washout period between arms. One hour following either filtered air or DE exposure, subjects were exposed to allergen or saline (vehicle control) via segmental challenge. Forty-eight hours post-allergen or control exposure, bronchial biopsies were collected. The study design generated 4 different conditions: filtered air + saline (FAS), DE + saline (DES), filtered air + allergen (FAA) and DE + allergen (DEA). Biopsies sections were immunostained for tryptase, eosinophil cationic protein (ECP), neutrophil elastase (NE), CD138, CD4 and interleukin (IL)-4. The percent positivity of positive cells were quantified in the bronchial submucosa. RESULTS: The percent positivity for tryptase expression and ECP expression remained unchanged in the bronchial submucosa in all conditions. CD4 % positive staining in DEA (0.311 ± 0.060) was elevated relative to FAS (0.087 ± 0.018; p = 0.035). IL-4 % positive staining in DEA (0.548 ± 0.143) was elevated relative to FAS (0.127 ± 0.062; p = 0.034). CD138 % positive staining in DEA (0.120 ± 0.031) was elevated relative to FAS (0.017 ± 0.006; p = 0.015), DES (0.044 ± 0.024; p = 0.040), and FAA (0.044 ± 0.008; p = 0.037). CD138 % positive staining in FAA (0.044 ± 0.008) was elevated relative to FAS (0.017 ± 0.006; p = 0.049). NE percent positive staining in DEA (0.224 ± 0.047) was elevated relative to FAS (0.045 ± 0.014; p = 0.031). CONCLUSIONS: In vivo allergen and DE co-exposure results in elevated CD4, IL-4, CD138 and NE in the respiratory submucosa of atopic subjects, while eosinophils and mast cells are not changed. TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov . Unique identifier: NCT01792232 .Medicine, Department ofMedicine, Faculty ofOther UBCNon UBCReviewedGraduateFacultyResearche