Community and public participation: risk communication and improving decision making in flood and coastal defence

PROJECT CLOSING STATEMENT The first phase of a study reviewed the effectiveness of consultation and communication of procedures and practices used in flood and coastal defence in England and Wales. The study puts forward recommendations and a plan for additional work which has not been commissioned within the joint Defra / EA programme, however the Environment Agency is undertaking work on consultation and communication to support a wide range of activities. SUMMARY OBJECTIVE To review the effectiveness of consultation and communication procedures and practices used in flood and coastal defence in England and Wales and, from this, to put forward suggestions for best practice methodologies to enable the public and stakeholder groups to better appreciate flood and coastal defence. KEY CUSTOMER PURPOSE To identify, develop and evaluate methods for communicating flood and erosion risk and uncertainties to a range of stakeholders. This will lead to consistency and best practice in communicating flood and erosion risk and hazard, and to improve understanding of risk and uncertainty among stakeholders, and support moves to risk-based planning guidance

Pathogenesis of Shiga toxin-associated hemolytic uremic syndrome

The aim of this review is to examine recent advances in experimental and clinical research relevant to the pathogenesis of diarrhea-associated hemolytic uremic syndrome with special reference to histopathologic findings, virulence factors of Shiga toxin-producing Escherichia coli, the host response, and the prothrombotic state. Despite significant advances during the past decade, the exact mechanism by which Shiga toxin-producing E. coli leads to hemolytic uremic syndrome remains unclear. Factors such as Shiga toxin, lipopolysaccharide, the adhesins intimin and E. coli-secreted proteins A, B, and D, the 60-MD plasmid, and enterohemolysin likely contribute to the pathogenesis. Data on the inflammatory response of the host, including leukocytes and inflammatory mediators, are updated. The pathogenesis of the prothrombotic state leading to thrombocytopenia secondary to endothelial cell damage and platelet activation is also discussed. A hypothetical sequence of events from ingestion of the bacteria to the development of full-blown hemolytic uremic syndrome is proposed