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This exposure has induced a gradual change in consumption desires and expectations regarding standards of living.
Metal exposure has induced metabolic changes that have been suggested to be compensatory, in order to facilitate metal tolerance and detoxification.
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In control cells, exposure to DNP (10 mM) has induced a significant increase in whole cell K+ current flowed through KATP channels [see also 4,5], but this was more pronounced in cells infected with SUR2A (Fig. 2).
In animal models, exposure to water disinfection byproducts (WDBPs) has induced a variety of malformations (reviewed in [ 9]).
Upon exposure to blood plasma, Ca2+-modified surface has induced surface clot formation, platelet adsorption, and activation [6].
In experimental animals, exposure to neurotoxic chemicals during critical periods of brain development has induced permanent functional disturbances in the CNS.
Exposure has also induced lipotoxicity responses in the ovaries, which shown as an increase of interstitial ectopic lipid accumulation and total lipids.
Animal model of COPD using cigarette smoke exposure has been induced in guinea pigs which leads to emphysematous lung destruction and lung inflammation [ 8- 10].
However, like the REG IV gene, it is likely that repeated exposure to cytotoxic chemotherapeutic reagents had induced the expression of the antiapoptotic REG Iα gene (Violette et al, 2003).
The observation that novelty-exposed and home-staying rats differed in competitive success during senescence implies that neonatal novelty exposure must have induced permanent changes within the brain.
It is possible that our CAPs exposures would have induced similar effects on conduit arterial tone because this may not be reflected in changes in basal forearm blood flow measured by venous occlusion plethysmography.
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