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These agents have been directed towards glutamate homeostasis, apoptosis, oxidative stress and neuroprotection.
Taken together, these results may indicate that homeostasis was progressively lost between days 3 and 5, even though viability was around 100%.
In conjunction, these observations reveal novel mechanisms by which neuroinflammation can alter glutamate homeostasis and trigger oligodendrocyte death.
Even if glucocorticoids act primarily at a peripheral level to maintain homeostasis, the brain represents one of the principal targets for these steroid hormones.
There are changes in other body systems which may affect homeostasis and reduce safety margins.
Astrocytes can dynamically and rapidly change their phenotype in a process known as 'activation', contributing to the maintenance of the central nervous system homeostasis.
These results suggest that heat shock proteins initially try to maintain homeostasis, but on failing, may be involved in cell death.
Under normal situations there is a balance between these two systems placing the body in a state of homeostasis.
These functional changes lead to a progressive loss of the organism's ability to withstand both internal and environmental stresses, causing the failure of cellular homeostasis.
In older patients with disturbed fluid balance homeostasis, this can be problematic as, often, intravascular volume is low.
This work describes novel roles for mast cells in nerve homeostasis and pathology.
Transplantation of pancreatic islets is arguably the most logical approach to restoring metabolic homeostasis in people with diabetes.
But the homeostasis process in the plasma makes the total energy loss almost unchanged.
The homeostasis model's stress on the complex interplay between individual (or host) factors and environmental influences is particularly useful.
Together these findings provide insights into how activation of microglia alters glutamate homeostasis, which results in oligodendrocyte excitotoxicity.
