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Townsend, T.

Publications and source records attributed to Townsend, T..

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An innovative approach in identifying a network of priority wetland sites in the East Asian-Australasian Flyway for a new sustainable management investment programme

The East Asian-Australasian Flyway (EAAF) is widely recognised to be the most threatened of the eight flyways in the world, with wetlands rapidly lost due to land cover change, unsustainable use, and the wider impacts of climate change. The recently established Regional Flyway Initiative aims to bring a network of priority wetlands in the EAAF under improved protection, management, and restoration in 10 Asian countries, while mobilising resources for sustainable agriculture, aquaculture, ecotourism, and other livelihoods for local communities. A major step in the development of this initiative is the identification of priority wetland sites through the application of international criteria, based on modern waterbird count data collated from wetland sites across Asia. Through existing analyses and stakeholder consultations, we short-listed 400 internationally important wetlands as candidate sites for further assessment. Count data of EAAF waterbird species was then assessed against international criteria aligned with the Convention on Wetlands (Ramsar Convention), the EAAF Partnerships Flyway Site Network and Important Bird Areas and Biodiversity for each site to iteratively identify a subset of priority sites, drawing on newly available species population thresholds. Each site was scored and ranked using a metric (Prioritisation Criterion1) calculated from the proportions of every occurring EAAF species against published population thresholds. We identified a total of 147 wetland sites of high conservation priority across the 10 countries, thereby representing the full suite of wetland landscapes and habitats in Asia, both freshwater and coastal, all critical sites for the conservation of migratory waterbirds in the flyway. At least 34 threatened species, including significant proportions of their global populations are represented in this network of 147 sites. To ensure that conservation opportunities are maximised for species and ecosystem services, there is a need to ensure that selected sites and landscapes are reconciled with the conservation and development priorities of each country, and to evaluate priority sites for their ecosystem services.

ecology↗

Mice lacking NF-κB1 exhibit marked DNA damage responses and more severe gastric pathology in response to parenteral tamoxifen administration.

BackgroundTamoxifen (TAM) has recently been shown to cause acute gastric atrophy and metaplasia in mice. We have previously demonstrated that the outcome of Helicobacter felis infection, which induces similar gastric lesions in mice, is altered by deletion of specific NF-{kappa}B subunits. Nfkb1-/- mice developed more severe gastric atrophy than wild-type (WT) mice 6 weeks after H. felis infection. In contrast, Nfkb2-/- mice were protected from this pathology. We therefore hypothesized that gastric lesions induced by TAM may be similarly regulated by signaling via NF-{kappa}B subunits.\n\nMethodsGroups of 5 female C57BL/6 (WT), Nfkb1-/-, Nfkb2-/- and c-Rel-/- mice were administered 150mg/kg TAM by IP injection. 72 hours later, gastric corpus tissues were taken for quantitative histological assessment. In addition, groups of 6 female WT and Nfkb1-/- mice were exposed to 12Gy {gamma}-irradiation. Gastric epithelial apoptosis was quantified 6 and 48 hours after irradiation.\n\nResultsTAM induced gastric epithelial lesions in all strains of mice, but this was more severe in Nfkb1-/- mice than WT mice. Nfkb1-/- mice exhibited more severe parietal cell loss than WT mice, had increased gastric epithelial expression of Ki67 and had an exaggerated gastric epithelial DNA damage response as quantified by {gamma}H2AX. To determine investigate whether the difference in gastric epithelial DNA damage response of Nfkb1-/- mice was unique to TAM induced DNA damage, or a generic consequence of DNA damage, we also assessed gastric epithelial apoptosis following {gamma}-irradiation. 6 hours after {gamma}-irradiation, gastric epithelial apoptosis was increased in the gastric corpus and antrum of Nfkb1-/- mice.\n\nConclusionsNF-{kappa}B1 mediated signaling regulates the development of gastric mucosal pathology following TAM administration. This is associated with an exaggerated gastric epithelial DNA damage response. This aberrant response appears to reflect a more generic sensitization of the gastric mucosa of Nfkb1-/- mice to DNA damage.

immunology↗