Developing a Conceptual Framework for Environmental Health Tracking in Victoria, Australia.

Victoria's (Australia) Environment Protection Authority (EPA), the state's environmental regulator, has recognized the need to develop an Environmental Health Tracking System (EHTS) to better understand environmental health relationships. To facilitate the process of developing an EHTS; a linkage-based conceptual framework was developed to link routinely collected environmental and health data to better understand environmental health relationships. This involved researching and drawing on knowledge from previous similar projects. While several conceptual frameworks have been used to organize data to support the development of an environmental health tracking system, Driving Force-Pressure-State-Exposure-Effect-Action (DPSEEA) was identified as the most broadly applied conceptual framework. Exposure and effects are two important components of DPSEEA, and currently, exposure data are not available for the EHTS. Therefore, DPSEEA was modified to the Driving Force-Pressure-Environmental Condition-Health Impact-Action (DPEHA) conceptual framework for the proposed Victorian EHTS as there is relevant data available for tracking. The potential application of DPEHA for environmental health tracking was demonstrated through case studies. DPEHA will be a useful tool to support the implementation of Victoria's environmental health tracking system for providing timely and scientific evidence for EPA and other decision makers in developing and evaluating policies for protecting public health and the environment in Victoria.

Nitric oxide inhibits platelet adhesion to collagen through cGMP-dependent and independent mechanisms: the potential role for S-nitrosylation.

Nitric oxide (NO)-mediated inhibition of platelet function occurs primarily through elevations in cGMP, although cGMP-independent mechanisms such as S-nitrosylation have been suggested as alternative NO-signaling pathways. In the present study we investigated the potential for S-nitrosylation to act as a NO-mediated cGMP-independent signaling mechanism in platelets. The NO-donor, S-nitrosoglutathione (GSNO), induced a concentration-dependent inhibition of platelet adhesion to immobilized collagen. In the presence of the soluble guanylyl cyclase inhibitor, ODQ, NO-mediated activation of the cGMP/protein kinase G signaling pathway was ablated. However, ODQ failed to completely abolish the inhibitory effect of NO on collagen-mediated adhesion, confirming that cGMP-independent signaling events contribute to the regulation of platelet adhesion by NO. Biotin-switch analysis of platelets demonstrated the presence of several S-nitrosylated proteins under basal conditions. Treatment of platelets with exogenous NO-donors, at concentrations that inhibited platelet adhesion, increased the number of S-nitrosylated bands and led to hyper-nitrosylation of basally S-nitrosylated proteins. The extent of S-nitrosylation in response to exogenous NO was unaffected by platelet activation. Importantly, platelet activation in the absence of exogenous NO failed to increase S-nitrosylation beyond basal levels, indicating that platelet-derived NO was unable to induce this type of protein modification. Our data demonstrate that S-nitrosylation of platelet proteins in response to exogenous NO may act as a potentially important cGMP-independent signaling mechanism for controlling platelet adhesion.