Vibrio parahaemolyticusnaturally occurs in brackish and marine waters and is one of the leading causes of seafood-borne illness. Previous work studying the ecology ofV. parahaemolyticushas often been limited in geographic extent and lacked a full range of environmental measures. This study used a unique large data set of surface water samples in the Chesapeake Bay (n= 1,385) collected from 148 monitoring stations from 2007 to 2010. Water was analyzed for more than 20 environmental parameters, with additional meteorological and surrounding land use data. TheV. parahaemolyticus-specific genetic markers thermolabile hemolysin (tlh), thermostable direct hemolysin (tdh), andtdh-related hemolysin (trh) were assayed using quantitative PCR (qPCR), and interval-censored regression models with nonlinear effects were estimated to account for limits of detection and quantitation.tlhwas detected in 19.6% of water samples;tdhortrhmarkers were not detected. The results confirmed previously reported positive associations forV. parahaemolyticusabundance with temperature and turbidity and negative associations with high salinity (>10 to 23‰). Furthermore, the salinity relationship was determined to be a function of both low temperature and turbidity, with an increase of either nullifying the high salinity effect. Associations with dissolved oxygen and phosphate also appeared stronger when samples were taken near human developments. A renewed focus on theV. parahaemolyticusecological paradigm is warranted to protect public health.IMPORTANCEVibrio parahaemolyticusis one of the leading causes of seafood-borne illness in the United States and across the globe. Exposure is often through consuming raw or undercooked shellfish. Given the natural presence of the bacterium in the marine environment, an improved understanding of its environmental determinants is necessary for future preventative measures. This analysis of environmentalVibrio parahaemolyticusis one of only a few that utilize a large data set measured over a wide geographic and temporal range. The analysis also includes a large number of environmental parameters forVibriomodeling, many of which have previously only been tested sporadically, and some of which have not been considered before. The results of the analysis revealed previously unknown relationships between salinity, turbidity, and temperature that provide significant insight into the abundance and persistence ofV. parahaemolyticusbacterium in the environment. This information will be essential for developing environmental forecast models for the bacterium.

Studies of older persons show consumption of light-to-moderate amounts of alcohol is positively associated with cognitive function and, separately, is negatively associated with total brain volume (TBV). This is paradoxical as generally, cognitive function is positively associated with TBV. We examined the relationships of TBV, global cognitive function (GCF), and alcohol consumption in a population-based cohort of 3,363 men and women (b. 1907–1935) participating in the Age Gene/Environment Susceptibility-Reykjavik Study (2002–2006) and who were free of dementia or mild cognitive impairment Drinking status (never, former, and current) and current amount of alcohol consumed were assessed by questionnaire. GCF is a composite score derived from a battery of cognitive tests. TBV, standardized to head size, is estimated quantitatively from brain magnetic resonance imaging. Among women and not men, adjusting for demographic and cardiovascular risk factors, current drinkers had significantly higher GCF scores than abstainers and former drinkers (p < .0001); and GCF was associated with amount consumed. TBV was not associated with drinking status or amount consumed in men or women. GCF and TBV did significantly differ in their associations across alcohol categories (p_interaction < .001). Within categories of alcohol intake, GCF and TBV were positively associated. The difference in associations of alcohol intake to brain structure and function suggests there may be unmeasured factors that contribute to maintaining better GCF relative to TBV. However, at higher levels of reasonable alcohol consumption, there may be factors leading to reduced brain volume.

High adiposity in midlife might increase risk for late-life brain pathology, including dementia. Using data from the prospective Age, Gene/Environment Susceptibility-Reykjavik Study of men and women (born 1907–1935), we studied the associations of overweight and obesity at midlife (mean age, 50 (standard deviation, 4.7) years) with 1.5-T brain magnetic resonance imaging measures of infarct-like brain lesions, cerebral microbleeds, total brain volume, and white matter lesions volume, as well as dementia, in late life (mean age, 76 (standard deviation, 5.2) years). We used linear and Poisson models to estimate associations in 3,864 persons after adjustment for sociodemographic, health, and lifestyle characteristics. In midlife, the prevalence of overweight was 39% and that of obesity was 8%. After a mean follow-up of 26.2 (standard deviation, 4.9) years, midlife overweight and obesity were not associated with infarct-like brain lesions (relative risk (RR) = 0.82, 95% confidence interval (CI): 0.61, 1.10), cerebral microbleeds (RR = 0.69, 95% CI: 0.37, 1.32), total brain volume (β = 0.05, 95% CI: −0.34, 0.45), white matter lesions volume (β = −0.10, 95% CI: −0.20, 0.01), or dementia (RR = 0.91, 95% CI: 0.49, 1.72) compared with normal weight. These findings do not support the hypothesis that high body mass index in midlife modulates the risk for dementia.