19 research outputs found

    Correlating Remote Sensing Data with the Abundance of Pupae of the Dengue Virus Mosquito Vector, Aedes aegypti, in Central Mexico

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    Using a geographic transect in Central Mexico, with an elevation/climate gradient, but uniformity in socio-economic conditions among study sites, this study evaluates the applicability of three widely-used remote sensing (RS) products to link weather conditions with the local abundance of the dengue virus mosquito vector, Aedes aegypti (Ae. aegypti). Field-derived entomological measures included estimates for the percentage of premises with the presence of Ae. aegypti pupae and the abundance of Ae. aegypti pupae per premises. Data on mosquito abundance from field surveys were matched with RS data and analyzed for correlation. Daily daytime and nighttime land surface temperature (LST) values were obtained from Moderate Resolution Imaging Spectroradiometer (MODIS)/Aqua cloud-free images within the four weeks preceding the field survey. Tropical Rainfall Measuring Mission (TRMM)-estimated rainfall accumulation was calculated for the four weeks preceding the field survey. Elevation was estimated through a digital elevation model (DEM). Strong correlations were found between mosquito abundance and RS-derived night LST, elevation and rainfall along the elevation/climate gradient. These findings show that RS data can be used to predict Ae. aegypti abundance, but further studies are needed to define the climatic and socio-economic conditions under which the correlations observed herein can be assumed to apply

    Insulin and IGF1 signalling pathways in human astrocytes <i>in vitro</i> and <i>in vivo</i>; characterisation, subcellular localisation and modulation of the receptors.

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    Background The insulin/IGF1 signalling (IIS) pathways are involved in longevity regulation and are dysregulated in neurons in Alzheimer’s disease (AD). We previously showed downregulation in IIS gene expression in astrocytes with AD-neuropathology progression, but IIS in astrocytes remains poorly understood. We therefore examined the IIS pathway in human astrocytes and developed models to reduce IIS at the level of the insulin or the IGF1 receptor (IGF1R). Results We determined IIS was present and functional in human astrocytes by immunoblotting and showed astrocytes express the insulin receptor (IR)-B isoform of Ir. Immunocytochemistry and cell fractionation followed by western blotting revealed the phosphorylation status of insulin receptor substrate (IRS1) affects its subcellular localisation. To validate IRS1 expression patterns observed in culture, expression of key pathway components was assessed on post-mortem AD and control tissue using immunohistochemistry. Insulin signalling was impaired in cultured astrocytes by treatment with insulin + fructose and resulted in decreased IR and Akt phosphorylation (pAkt S473). A monoclonal antibody against IGF1R (MAB391) induced degradation of IGF1R receptor with an associated decrease in downstream pAkt S473. Neither treatment affected cell growth or viability as measured by MTT and Cyquant® assays or GFAP immunoreactivity. Discussion IIS is functional in astrocytes. IR-B is expressed in astrocytes which differs from the pattern in neurons, and may be important in differential susceptibility of astrocytes and neurons to insulin resistance. The variable presence of IRS1 in the nucleus, dependent on phosphorylation pattern, suggests the function of signalling molecules is not confined to cytoplasmic cascades. Down-regulation of IR and IGF1R, achieved by insulin + fructose and monoclonal antibody treatments, results in decreased downstream signalling, though the lack of effect on viability suggests that astrocytes can compensate for changes in single pathways. Changes in signalling in astrocytes, as well as in neurons, may be important in ageing and neurodegeneration

    Combining targeted sampling and bacterial source tracking (bst) during calm and stormy conditions

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    In April 2004, high numbers of fecal enterococci triggered a beach advisory on Sea Island, GA. Targeted sampling, which finds fecal contamination much like the children’s game of “hot” and “cold,” was combined with three bacterial source tracking (BST) methods: Enterococcus speciation, the presence or absence of a human virulence factor in Enterococcus faecium, and fluorometry. During calm (i.e non-runoff) conditions, the likely contamination sources were wildlife feces and leaking sewer lines located on a creek of St. Simons Island, GA. Fluorometry quickly identified malfunctioning sewer lines. A test for human virulence factor was positive. During stormflow (i.e. runoff) conditions, the likely contamination sources were wildlife feces and effluent from two pipes. A test for human virulence factor was negative. Because the percentage of Ent. faecalis from the pipes was high (>30%), fecal contamination from wild birds was likely. This is the first report of targeted sampling during stormy conditions, and the first time fluorometry has been combined with targeted sampling.Sponsored by: Georgia Environmental Protection Division U.S. Geological Survey, Georgia Water Science Center U.S. Department of Agriculture, Natural Resources Conservation Service Georgia Institute of Technology, Georgia Water Resources Institute The University of Georgia, Water Resources Facult

    Fine Particulate Matter and Incident Cognitive Impairment in the REasons for Geographic and Racial Differences in Stroke (REGARDS) Cohort

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    <div><p>Studies of the effect of air pollution on cognitive health are often limited to populations living near cities that have air monitoring stations. Little is known about whether the estimates from such studies can be generalized to the U.S. population, or whether the relationship differs between urban and rural areas. To address these questions, we used a satellite-derived estimate of fine particulate matter (PM<sub>2.5</sub>) concentration to determine whether PM<sub>2.5</sub> was associated with incident cognitive impairment in a geographically diverse, biracial US cohort of men and women (n = 20,150). A 1-year mean baseline PM<sub>2.5</sub> concentration was estimated for each participant, and cognitive status at the most recent follow-up was assessed over the telephone using the Six-Item Screener (SIS) in a subsample that was cognitively intact at baseline. Logistic regression was used to determine whether PM<sub>2.5</sub> was related to the odds of incident cognitive impairment. A 10 µg/m<sup>3</sup> increase in PM<sub>2.5</sub> concentration was not reliably associated with an increased odds of incident impairment, after adjusting for temperature, season, incident stroke, and length of follow-up [OR (95% CI): 1.26 (0.97, 1.64)]. The odds ratio was attenuated towards 1 after adding demographic covariates, behavioral factors, and known comorbidities of cognitive impairment. A 10 µg/m<sup>3</sup> increase in PM<sub>2.5</sub> concentration was slightly associated with incident impairment in urban areas (1.40 [1.06–1.85]), but this relationship was also attenuated after including additional covariates in the model. Evidence is lacking that the effect of PM<sub>2.5</sub> on incident cognitive impairment is robust in a heterogeneous US cohort, even in urban areas.</p></div
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