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Autonomic and HPA patterns, inflammatory cascades and energy/redox metabolic arrays will be presented, on the one hand, as promoters of allostasis, leading towards adaptation to psychosocial stress and homeostasis, on the other as possible vulnerability factors for allostatic overload and non-adaptive reactions. The existence of allostasis buffering systems will be also underscored. Finally, we will prospect that the combined uses of cell cultures, animal models and wide-omics investigations may constitute a powerful tool to entangle the