Reservoir safety risk assessment - a new guide

Since the House of Lords Select Committee review of dam safety in 1982 there have been various attempts to introduce a more quantified approach to the assessment of dams and reservoirs, including the CIRIA guide to risk assessment methods for UK reservoirs and the Interim Guide to Quantitative risk assessment for UK reservoirs. Unfortunately none of these have gained universal acceptance. The need for a commonly agreed and widely accepted risk assessment method for reservoir safety is now a pressing requirement, both in terms of supporting asset and business management as well as minimising risk to lives and the environment and the increasing use of a risk based approach in government management and regulation of risk to society (HSE, 2001). The main objective of this project is to develop a risk assessment method that is technically robust, scalable and proportionate across the wide range of UK reservoirs. This paper reports on the framework and associated methods that have built upon existing Environment Agency, British Standards (and other) concepts and projects, providing continuity of assessment from small flood control structures through to large dams. The methodology has evolved through initial scoping, method development and pilot testing, taking into account industry feedback via questionnaires and a series of team and industry workshops

Urocortin-1 within the Centrally-Projecting Edinger-Westphal Nucleus Is Critical for Ethanol Preference

Converging lines of evidence point to the involvement of neurons of the centrally projecting Edinger-Westphal nucleus (EWcp) containing the neuropeptide Urocortin-1 (Ucn1) in excessive ethanol (EtOH) intake and EtOH sensitivity. Here, we expanded these previous findings by using a continuous-access, two-bottle choice drinking paradigm (3%, 6%, and 10% EtOH vs. tap water) to compare EtOH intake and EtOH preference in Ucn1 genetic knockout (KO) and wild-type (WT) mice. Based on previous studies demonstrating that electrolytic lesion of the EWcp attenuated EtOH intake and preference in high-drinking C57BL/6J mice, we also set out to determine whether EWcp lesion would differentially alter EtOH consumption in Ucn1 KO and WT mice. Finally, we implemented well-established place conditioning procedures in KO and WT mice to determine whether Ucn1 and the corticotropin-releasing factor type-2 receptor (CRF-R2) were involved in the rewarding and aversive effects of EtOH (2 g/kg, i.p.). Results from these studies revealed that (1) genetic deletion of Ucn1 dampened EtOH preference only in mice with an intact EWcp, but not in mice that received lesion of the EWcp, (2) lesion of the EWcp dampened EtOH intake in Ucn1 KO and WT mice, but dampened EtOH preference only in WT mice expressing Ucn1, and (3) genetic deletion of Ucn1 or CRF-R2 abolished the conditioned rewarding effects of EtOH, but deletion of Ucn1 had no effect on the conditioned aversive effects of EtOH. The current findings provide strong support for the hypothesis that EWcp-Ucn1 neurons play an important role in EtOH intake, preference, and reward