Publications by authors named "F F RUST"

Hydroelectric reservoirs emit carbon dioxide (CO) and methane (CH) to the atmosphere, yet there is still much uncertainty concerning the magnitude and drivers of these greenhouse gas (GHG) emissions. This uncertainty is particularly large over the initial years after flooding and in complex, cascade reservoir systems where studies are rare. We assessed the spatial and temporal patterns of CO and CH concentrations in the newly created La Romaine complex, which is composed of three consecutive reservoirs (RO1, RO2, RO3) along the La Romaine River.

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Reservoir sediment can work as both sink and source for contaminants. Once released into the water column, contaminants can be toxic to biota and humans. We investigate potential ecological risk to benthic organisms by metals contamination in six reservoirs in Southeast Brazil.

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Recent studies from temperate lakes indicate that eutrophic systems tend to emit less carbon dioxide (CO2) and bury more organic carbon (OC) than oligotrophic ones, rendering them CO2 sinks in some cases. However, the scarcity of data from tropical systems is critical for a complete understanding of the interplay between eutrophication and aquatic carbon (C) fluxes in warm waters. We test the hypothesis that a warm eutrophic system is a source of both CO2 and CH4 to the atmosphere, and that atmospheric emissions are larger than the burial of OC in sediments.

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Disrupting homeostasis has negative health outcomes, yet disruption routinely occurs with weight homeostasis. This cross-sectional study of nurses found a majority overriding hunger and fullness cues due to situational, dieting, and emotional reasons. Because either splurging or starving can lead to excess weight, preventing homeostasis disruption through intuitive eating is healthier and more holistic.

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The endoplasmic reticulum chaperone GRP78/BIP plays a central role in the prosurvival machinery, and its enhanced expression has been implicated in drug resistance, carcinogenesis, and metastasis. E2F1, as part of an antitumor safeguard mechanism, promotes apoptosis regardless of functional p53. Using cells that are defective in p53, we show that E2F1 represses GRP78/BIP at the transcriptional level, and this requires its DNA binding domain.

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