Publications by authors named "Alba Rossi-George"

Microglia, the primary resident immune cells of the central nervous system (CNS), responds rapidly to pathogens and injury by secreting immune mediators including nitric oxide (NO). The reaction of NO with the anti-oxidant glutathione forms S-nitrosoglutathione (GSNO), the major pool of biologic NO in the body. GSNO is degraded by GSNO reductase (GSNOR).

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The role of S-nitrosylation in cellular signaling has been clearly demonstrated. There a number of mechanisms whereby this post-translational modification can occur and the number of protein targets continue to expand. The need to be able to monitor when this important signaling process occurs within cells is increasingly important.

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Microglia are resident immune cells of the central nervous system. Their persistent activation in neurodegenerative diseases, traditionally attributed to neuronal dysfunction, may be due to a microglial failure to modulate the release of cytotoxic mediators such as nitric oxide (NO). The persistent activation of microglia with the subsequent release of NO vis-á-vis the accumulation of redox transition metals such as copper (Cu) in neurodegenerative diseases, prompted the hypothesis that copper would alter NO signaling by changing the redox environment of the cell and that, by altering the fate of NO, microglia would adopt a different phenotype.

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Elevated lead (Pb) exposure and high stress both target low socio-economic status populations. Both also act on the hypothalamic-pituitary-adrenal (HPA) axis. Pb disrupts cognition through effects on the mesocorticolimbic dopamine pathway.

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Staphylococcal enterotoxin A (SEA) is a microbial superantigen that activates T-lymphocytes and induces production of various cytokines, including tumor necrosis factor-alpha (TNFalpha). Previously, it was shown that SEA activates the hypothalamic-pituitary-adrenal axis and augments gustatory neophobic behaviors. In the present study, it was hypothesized that these effects involve neuronal activation in forebrain regions mediating fear and/or anxiety and are dependent on the production of TNFalpha.

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Bacterial superantigens, such as staphylococcal enteroxins A and B (SEA/SEB) stimulate T cells to produce high levels of cytokines in blood. Previously it had been shown that these toxins were capable of stimulating increased neuroendocrine activity and enhanced behavioral reactivity to novel gustatory and non-gustatory stimuli. Therefore, it was suggested that these superantigens may promote anxiety-like behavior.

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The present paper reviews recent studies on the effects of stress on immune function in laboratory animals. The emphasis is on those studies where a simultaneous comparison of acute and chronic stress regimens was determined, although additional relevant studies are also reviewed. The effects of stress on basic measurements of cellular and humoral immune measures are discussed, including the growing number of studies that have reported alterations in macrophage functions.

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In 3 experiments with 85 human 3-month-olds, the authors asked whether retroactive interference with their memory of the original training stimulus is temporary or permanent. Infants learned to move a mobile by kicking and then were exposed to a different mobile (Experiment 1) or context (Experiment 2) immediately or 3 days afterward (Experiment 3). They were tested after increasing delays with the original stimulus, the exposed stimulus, or a completely novel stimulus.

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In three experiments with 164 individuals between 4 and 80 years old, we examined age-related changes in explicit memory for three perceptual features--item identity, color, and location. In Experiments 1-2, feature recognition was assessed in an incidental learning, gamelike task resembling the game Concentration. In Experiment 3, feature recognition was assessed using a pencil-and-paper task after intentional learning instructions.

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