Arsenic in the Water, Soil Bedrock, and Plants of the Ester Dome Area of Alaska

Concentrations of arsenic as large as 10 ppm (200 times the safe limit for drinking water) occur in the groundwater of a mineralized residential area near Fairbanks. Bedrock of the area contains 750 ppm As, primarily as arsenopyrite and scorodite. The oxygen-poor groundwater is enriched in As(III) and ferrous iron while the surface waters are iron free and contain less than 50 ppb As(V). Arsenic is removed from the water by coprecipitation with ferric hydroxide. Some iron-rich stream sediments contain as much as 1,400 ppm arsenic. The distribution of arsenic in the groundwater is controlled by the distribution of arsenic in the bedrock. The arsenic content of the B soil horizon over mineralized veins is about 150 ppm, while that over barren rock is 30 ppm. The vegetation over the veins is not significantly enriched in arsenic. Lettuce, radishes and tomatoes grown with arsenic-rich water (5 ppm) contain 16, 8 and 1 ppm As, respectively; these amounts are significantly greater than plants not treated with arsenic. Preliminary studies by state and federal health agencies show no detrimental effects on the health of persons drinking these arsenic-rich waters.The work upon which this publication is based was supported in part by funds provided by the Office of Water Research and Technology (Project B-037-ALAS, Agreement No. 14-34-0001-8056), U.S. Department of the Interior, Washington, D.C., as authorized by the Water Research and Development Act of 1978

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Treatment of Alaska-produced food products by ionizing radiation may benefit the seafood and agricultural industries and the Alaskan consumer. A feasibility study to evaluate the potential social and economic benefits and risks as well as the costs of using the process in Alaska on Alaskan products is being coordinated by the Institute of Northern Engineering. A research and development project to determine effects on the quality o f Alaskan products could be the next phase in the introduction o f a new food-preservation technique to Alaska

CSF proteome profiling across the Alzheimer’s disease spectrum reflects the multifactorial nature of the disease and identifies specific biomarker panels

Development of disease-modifying therapies against Alzheimer’s disease (AD) requires biomarkers reflecting the diverse pathological pathways specific for AD. We measured 665 proteins in 797 cerebrospinal fluid (CSF) samples from patients with mild cognitive impairment with abnormal amyloid (MCI(Aβ+): n = 50), AD-dementia (n = 230), non-AD dementias (n = 322) and cognitively unimpaired controls (n = 195) using proximity ligation-based immunoassays. Here we identified >100 CSF proteins dysregulated in MCI(Aβ+) or AD compared to controls or non-AD dementias. Proteins dysregulated in MCI(Aβ+) were primarily related to protein catabolism, energy metabolism and oxidative stress, whereas those specifically dysregulated in AD dementia were related to cell remodeling, vascular function and immune system. Classification modeling unveiled biomarker panels discriminating clinical groups with high accuracies (area under the curve (AUC): 0.85–0.99), which were translated into custom multiplex assays and validated in external and independent cohorts (AUC: 0.8–0.99). Overall, this study provides novel pathophysiological leads delineating the multifactorial nature of AD and potential biomarker tools for diagnostic settings or clinical trials

CSF proteome profiling across the Alzheimer’s disease spectrum reflects the multifactorial nature of the disease and identifies specific biomarker panels

Development of disease-modifying therapies against Alzheimer’s disease (AD) requires biomarkers reflecting the diverse pathological pathways specific for AD. We measured 665 proteins in 797 cerebrospinal fluid (CSF) samples from patients with mild cognitive impairment with abnormal amyloid (MCI(Aβ+): n = 50), AD-dementia (n = 230), non-AD dementias (n = 322) and cognitively unimpaired controls (n = 195) using proximity ligation-based immunoassays. Here we identified &gt;100 CSF proteins dysregulated in MCI(Aβ+) or AD compared to controls or non-AD dementias. Proteins dysregulated in MCI(Aβ+) were primarily related to protein catabolism, energy metabolism and oxidative stress, whereas those specifically dysregulated in AD dementia were related to cell remodeling, vascular function and immune system. Classification modeling unveiled biomarker panels discriminating clinical groups with high accuracies (area under the curve (AUC): 0.85–0.99), which were translated into custom multiplex assays and validated in external and independent cohorts (AUC: 0.8–0.99). Overall, this study provides novel pathophysiological leads delineating the multifactorial nature of AD and potential biomarker tools for diagnostic settings or clinical trials.</p

CSF proteome profiling across the Alzheimer’s disease spectrum reflects the multifactorial nature of the disease and identifies specific biomarker panels

Development of disease-modifying therapies against Alzheimer’s disease (AD) requires biomarkers reflecting the diverse pathological pathways specific for AD. We measured 665 proteins in 797 cerebrospinal fluid (CSF) samples from patients with mild cognitive impairment with abnormal amyloid (MCI(Aβ+): n = 50), AD-dementia (n = 230), non-AD dementias (n = 322) and cognitively unimpaired controls (n = 195) using proximity ligation-based immunoassays. Here we identified &gt;100 CSF proteins dysregulated in MCI(Aβ+) or AD compared to controls or non-AD dementias. Proteins dysregulated in MCI(Aβ+) were primarily related to protein catabolism, energy metabolism and oxidative stress, whereas those specifically dysregulated in AD dementia were related to cell remodeling, vascular function and immune system. Classification modeling unveiled biomarker panels discriminating clinical groups with high accuracies (area under the curve (AUC): 0.85–0.99), which were translated into custom multiplex assays and validated in external and independent cohorts (AUC: 0.8–0.99). Overall, this study provides novel pathophysiological leads delineating the multifactorial nature of AD and potential biomarker tools for diagnostic settings or clinical trials.</p