ArticleJournal of experimental stroke & translational medicine2010
Towards a dynamical network view of brain ischemia and reperfusion. Part II: a post-ischemic neuronal state space.
Article in Journal of experimental stroke & translational medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Inductive and Deductive Approaches to Acute Cell Injury.International scholarly research notices · 2014Review
- A program for solving the brain ischemia problem.Brain sciences · 2013Article
- Neuroprotective effect of penehyclidine hydrochloride on focal cerebral ischemia-reperfusion injury.Neural regeneration research · 2013Article
- Post-stroke depression and the aging brain.Journal of molecular psychiatry · 2013Review
- A nonlinear dynamical theory of cell injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Article
- 'Functional histology' in brain ischemia studies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011Article
- Polyadenylated mRNA staining reveals distinct neuronal phenotypes following endothelin 1, focal brain ischemia, and global brain ischemia/ reperfusion.Neurological research · 2011Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
The general failure of neuroprotectants in clinical trials of ischemic stroke points to the possibility of a fundamental blind spot in the current conception of ischemic brain injury, the "ischemic cascade". This is the second in a series of four papers whose purpose is to work towards a revision of the concept of brain ischemia by applying network concepts to develop a bistable model of brain ischemia. We here build the bistable network model of brain ischemia. The central concept is that of a post-ischemic state space. Ischemia, as a quantitative perturbation, is envisioned to push the brain through a series of four phenotypes as a function of the amount of ischemia: the homeostatic, preconditioned, delayed neuronal death and necrotic phenotypes. The phenotypes are meta-stable attractors in the landscape of the post-ischemic state space. The sequence of the phenotypes derives from the mutual antagonism between damage mechanisms and stress responses, each conceived as aggregate ensemble variables. The competition between damage mechanisms and stress responses is posited to have the form of a bistability. Application of bistability to brain ischemia is grounded in the incontrovertible fact that post-ischemic neurons face the mutually exclusive decision to either live or die.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.