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Stress-induced neuroinflammation: mechanisms and new pharmacological targets.
Data is presented supporting the hypothesis that stress-related events are characterized by modifications of oxidative/nitrosative pathways in the brain in response to the activation of inflammatory mediators.
Chronic Unpredictable Stress Exacerbates Lipopolysaccharide-Induced Activation of Nuclear Factor-κB in the Frontal Cortex and Hippocampus via Glucocorticoid Secretion
It is indicated that stress, via GC secretion, can increase LPS-induced NF-κB activation in the frontal cortex and hippocampus, agreeing with a growing literature demonstrating proinflammatory effects of GCs.
Glucocorticoids Exacerbate Lipopolysaccharide-Induced Signaling in the Frontal Cortex and Hippocampus in a Dose-Dependent Manner
Findings suggest that GCs do not uniformly suppress neuroinflammation and can even enhance it at multiple levels in the pathway linking LPS exposure to inflammation.
Intermittent fasting attenuates lipopolysaccharide-induced neuroinflammation and memory impairment
It is suggested that intermittent fasting induces adaptive responses in the brain and periphery that can suppress inflammation and preserve cognitive function in an animal model of systemic bacterial infection.
Nitric oxide, cGMP, and hormone regulation of active sodium transport.
Evidence is reported that NO, produced in response to various hormones and cytokines, can effect long-term alterations in the activity of the membrane sodium pump, which represents a mechanism for hormonal modulation of ion gradients not only in kidney but also in other organs, including brain, where NO and cGMP play a prominent role in cellular function.
Cocaine as a naturally occurring insecticide.
It is demonstrated that cocaine exerts insecticidal effects at concentrations which occur naturally in coca leaves, and that octopamine transporters may be useful sites for targeting pesticides with selectivity toward invertebrates.
Neutrophil function and metabolism in individuals with diabetes mellitus.
Lowering of blood glucose levels by insulin treatment of diabetic patients or experimental animals has been reported to have significant correlation with improvement of neutrophil functional activity, which might be primarily linked to a continuing insulin deficiency or to secondary hyperglycemia occurring in the diabetic individual.