Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death? - Wikidata - wikimedia - TriplyDB

Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death?

Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death?

http://www.wikidata.org/entity/Q35968596

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Therapeutic window analysis of the neuroprotective effects of cyclosporine A after traumatic brain injury Traumatic brain injury: can the consequences be stopped?MicroRNAs: Key Regulators in the Central Nervous System and Their Implication in Neurological Diseases Brain injury following cardiac arrest: pathophysiology for neurocritical care Role of Glia in Memory Deficits Following Traumatic Brain Injury: Biomarkers of Glia Dysfunction Mitochondrial permeability transition pore is a potential drug target for neurodegeneration Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies Reperfusion promotes mitochondrial biogenesis following focal cerebral ischemia in rats Battery of behavioral tests in mice to study postoperative delirium.Emerging therapies in traumatic brain injury Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature Thioredoxin-Mimetic-Peptides Protect Cognitive Function after Mild Traumatic Brain Injury (mTBI)Dietary fructose aggravates the pathobiology of traumatic brain injury by influencing energy homeostasis and plasticity.Mitochondrial proteomics in experimental autoimmune uveitis oxidative stress Methamphetamine- and trauma-induced brain injuries: comparative cellular and molecular neurobiological substrates Safety and tolerability of cyclosporin a in severe traumatic brain injury patients: results from a prospective randomized trial Early mitochondrial dysfunction after cortical contusion injury Traumatic brain injury: an overview of pathobiology with emphasis on military populations.Chronic treatment with anesthetic propofol improves cognitive function and attenuates caspase activation in both aged and Alzheimer's disease transgenic mice Cyclosporine A, FK506, and NIM811 ameliorate prolonged CBF reduction and impaired neurovascular coupling after cortical spreading depression.Brain metabolism is significantly impaired at blood glucose below 6 mM and brain glucose below 1 mM in patients with severe traumatic brain injury.Acetyl-L-carnitine ameliorates mitochondrial dysfunction following contusion spinal cord injury.Peripheral nerve graft with immunosuppression modifies gene expression in axotomized CNS neurons.Brain-on-a-chip microsystem for investigating traumatic brain injury: Axon diameter and mitochondrial membrane changes play a significant role in axonal response to strain injuries.Role of oxidative stress and the mitochondrial permeability transition in methylmercury cytotoxicity Neuroproteomics: a biochemical means to discriminate the extent and modality of brain injury.Neuroprotective effects of N-acetyl-cysteine and acetyl-L-carnitine after spinal cord injury in adult rats.Mitochondrial protection after traumatic brain injury by scavenging lipid peroxyl radicals.Mitochondria, Amyloid β, and Alzheimer's Disease Mitochondrial mechanisms of cell death and neuroprotection in pediatric ischemic and traumatic brain injury.Post-injury administration of the mitochondrial permeability transition pore inhibitor, NIM811, is neuroprotective and improves cognition after traumatic brain injury in rats Broad-spectrum neuroprotection against traumatic brain injury by agonism of peroxisome proliferator-activated receptors Mitochondria, oxidative stress, and temporal lobe epilepsy Glucose administration after traumatic brain injury exerts some benefits and no adverse effects on behavioral and histological outcomes.Establishing a Clinically Relevant Large Animal Model Platform for TBI Therapy Development: Using Cyclosporin A as a Case Study Ketone bodies mediate antiseizure effects through mitochondrial permeability transition.Lipid peroxidation in brain or spinal cord mitochondria after injury Acetyl-L-carnitine treatment following spinal cord injury improves mitochondrial function correlated with remarkable tissue sparing and functional recovery.The Mitochondrial Permeability Transition Pore: Channel Formation by F-ATP Synthase, Integration in Signal Transduction, and Role in Pathophysiology.Role of calcium and mitochondria in MeHg-mediated cytotoxicity.

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Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death?

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Mitochondrial permeability tra ...... effect of neuronal cell death?

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Journal of Neuroscience Research

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Rabchevsky AG

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Springer JE

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Sullivan PG

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Waldmeier PC

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P2860

Mitochondria in the life and death of neurons.

Inhibition of Ca2(+)-induced large-amplitude swelling of liver and heart mitochondria by cyclosporin is probably caused by the inhibitor binding to mitochondrial-matrix peptidyl-prolyl cis-trans isomerase and preventing it interacting with the adeni

Recruitment of mitochondrial cyclophilin to the mitochondrial inner membrane under conditions of oxidative stress that enhance the opening of a calcium-sensitive non-specific channel.

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231-239

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10.1002/JNR.20292

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1-2

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79

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15573402

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