ABSTRACT. As oil transportation worldwide continues to increase, many communities are at risk of oil spill disasters and must anticipate and prepare for them. Factors that influence oil spill consequences are myriad and range from the biophysical to the social. We provide a summary literature review and overview framework to help communities systematically consider the factors and linkages that would influence consequences of a potential oil spill. The focus is on spills from oil tanker accidents. Drawing primarily on empirical studies of previous oil spill disasters, we focused on several main domains of interest: the oil spill itself, disaster management, the physical marine environment, marine biology, human health, economy, and policy. Key variables that influence the severity of consequences are identified, and significant interactions between variables are delineated. The framework can be used to clarify the complexity of oil spill impacts, identify lessons that may be transferable from other oil spill disasters, develop scenarios for planning, and inform risk analysis and policy debates in localities that are seeking to understand and reduce their vulnerability to potential spill disasters. As a case study, the framework is used to consider potential oil spills and consequences in Vancouver, Canada. Major increases in oil tanker traffic are anticipated in this region, creating urgent new demands for risk information, disaster management planning, and policy responses. The case study identifies particular conditions that distinguish the Vancouver context from other historic events; in particular, proximity to a densely populated urban area, the type of oil being transported, financial compensation schemes, and local economic structure. Drawing lessons from other oil spill disasters is important but should be undertaken with recognition of these key differences. Some types of impacts that have been relatively inconsequential in previous events may be very significant in a Vancouver case.
To determine the frequency of LRRK2 mutations in idiopathic Parkinson disease (PD), the authors studied 786 PD probands, 32 affected siblings, 1,044 unaffected siblings, and 278 unrelated controls. The authors designed allelic discrimination assays for nine LRRK2 mutations and identified these in six probands with PD, one affected sibling, one unaffected sibling, and one unrelated control. Thus LRRK2 mutations only rarely cause idiopathic PD.
Genetic variation of the alpha-synuclein gene (SNCA) is known to cause familial parkinsonism, however the role of SNCA variants in sporadic Parkinson's disease (PD) remains elusive. The present study identifies an association of common SNCA polymorphisms with disease susceptibility in a series of Irish PD patients. There is evidence for association with alternate regions, of protection and risk which may act independently/synergistically, within the promoter region (Rep1; OR: 0.59, 95% CI: 0.37-0.84) and the 3'UTR of the gene (rs356165; OR: 1.67, 95% CI: 1.08-2.58). Given previous reports of association a collaborative effort is required which may exploit global linkage disequilibrium patterns for SNCA and standardise polymorphic markers used in each population. It is now crucial to identify the susceptibility allele and elucidate its functionality which may generate a therapeutic target for PD.
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