Differential effects of the mitochondrial uncoupling agent, 2,4-dinitrophenol, or the nitroxide antioxidant, Tempol, on synaptic or nonsynaptic mitochondria after spinal cord injury
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Effects of tempol and redox-cycling nitroxides in models of oxidative stress.The role of pharmacotherapy in modifying the neurological status of patients with spinal and spinal cord injuriesMitochondrial function in hypoxic ischemic injury and influence of agingImaging mass spectrometry reveals loss of polyunsaturated cardiolipins in the cortical contusion, hippocampus, and thalamus after traumatic brain injuryAge-related changes in mitochondrial respiration and oxidative damage in the cerebral cortex of the Fischer 344 rat.N-acetylcysteine amide preserves mitochondrial bioenergetics and improves functional recovery following spinal traumaAcetyl-L-carnitine ameliorates mitochondrial dysfunction following contusion spinal cord injury.Rat diaphragm mitochondria have lower intrinsic respiratory rates than mitochondria in limb musclesMitochondria-associated microRNAs in rat hippocampus following traumatic brain injury.N-acetylcysteine treatment following spinal cord trauma reduces neural tissue damage and improves locomotor function in mice.Light Chain Amyloid Fibrils Cause Metabolic Dysfunction in Human CardiomyocytesAcetyl-L-carnitine treatment following spinal cord injury improves mitochondrial function correlated with remarkable tissue sparing and functional recovery.Cellular and subcellular oxidative stress parameters following severe spinal cord injury.Trichloroethylene induces dopaminergic neurodegeneration in Fisher 344 ratsVitamins and nutrients as primary treatments in experimental brain injury: Clinical implications for nutraceutical therapies.MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection.Tempol protection of spinal cord mitochondria from peroxynitrite-induced oxidative damage.PPAR agonists as therapeutics for CNS trauma and neurological diseasesChemically induced pheochromocytomas in rats: mechanisms and relevance for human risk assessment.Targeting mitochondrial function for the treatment of acute spinal cord injury.Changes in mitochondrial bioenergetics in the brain versus spinal cord become more apparent with age.Prospects for therapeutic mitochondrial transplantation.Caged mitochondrial uncouplers that are released in response to hydrogen peroxide.Concentration dependent effect of calcium on brain mitochondrial bioenergetics and oxidative stress parameters.Tempol reduces injury area in rat model of spinal cord contusion injury through suppression of iNOS and COX-2 expression.Pioglitazone treatment following spinal cord injury maintains acute mitochondrial integrity and increases chronic tissue sparing and functional recovery.Mitochondrial-Based Therapeutics for the Treatment of Spinal Cord Injury: Mitochondrial Biogenesis as a Potential Pharmacological Target.FM19G11 favors spinal cord injury regeneration and stem cell self-renewal by mitochondrial uncoupling and glucose metabolism induction.Optimization of mitochondrial isolation techniques for intraspinal transplantation procedures.Synaptic Mitochondria Sustain More Damage than Non-Synaptic Mitochondria after Traumatic Brain Injury and Are Protected by Cyclosporine A.Mitochondria in Excitatory and Inhibitory Synapses have Similar Susceptibility to Amyloid-β Peptides Modeling Alzheimer's Disease.Intrathecal Administration of Tempol Reduces Chronic Constriction Injury-Induced Neuropathic Pain in Rats by Increasing SOD Activity and Inhibiting NGF Expression.D-β-hydroxybutyrate promotes functional recovery and relieves pain hypersensitivity in mice with spinal cord injury.Deletion of mammalian sterile 20-like kinase 1 attenuates neuronal loss and improves locomotor function in a mouse model of spinal cord trauma.Effects of Mitochondrial Transplantation on Bioenergetics, Cellular Incorporation, and Functional Recovery after Spinal Cord Injury.
P2860
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P2860
Differential effects of the mitochondrial uncoupling agent, 2,4-dinitrophenol, or the nitroxide antioxidant, Tempol, on synaptic or nonsynaptic mitochondria after spinal cord injury
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on January 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Differential effects of the mi ...... ndria after spinal cord injury
@en
Differential effects of the mi ...... dria after spinal cord injury.
@nl
type
label
Differential effects of the mi ...... ndria after spinal cord injury
@en
Differential effects of the mi ...... dria after spinal cord injury.
@nl
prefLabel
Differential effects of the mi ...... ndria after spinal cord injury
@en
Differential effects of the mi ...... dria after spinal cord injury.
@nl
P2093
P2860
P356
P1476
Differential effects of the mi ...... ndria after spinal cord injury
@en
P2093
Alexander G Rabchevsky
Jignesh D Pandya
Patrick G Sullivan
Samir P Patel
P2860
P304
P356
10.1002/JNR.21814
P577
2009-01-01T00:00:00Z