Critical role of NADPH oxidase in neuronal oxidative damage and microglia activation following traumatic brain injury. - Wikidata - wikimedia - TriplyDB

Critical role of NADPH oxidase in neuronal oxidative damage and microglia activation following traumatic brain injury.

Critical role of NADPH oxidase in neuronal oxidative damage and microglia activation following traumatic brain injury.

http://www.wikidata.org/entity/Q34224919

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The role of Nox2-derived ROS in the development of cognitive impairment after sepsis NADPH oxidase- and mitochondria-derived reactive oxygen species in proinflammatory microglial activation: a bipartisan affair?Role of Microvascular Disruption in Brain Damage from Traumatic Brain Injury Traumatic brain injury and NADPH oxidase: a deep relationship Association of traumatic brain injury with subsequent neurological and psychiatric disease: a meta-analysis Selective inhibition of matrix metalloproteinase-9 attenuates secondary damage resulting from severe traumatic brain injury Zinc wave during the treatment of hypoxia is required for initial reactive oxygen species activation in mitochondria Histamine induces microglia activation and dopaminergic neuronal toxicity via H1 receptor activation.Effects of low-level blast exposure on the nervous system: is there really a controversy?Acute blast injury reduces brain abeta in two rodent species.New insights on NOX enzymes in the central nervous system.Suppression of oxidative stress and 5-lipoxygenase activation by edaravone improves depressive-like behavior after concussion.Characterization of the expression and inflammatory activity of NADPH oxidase after spinal cord injury.Progressive neurodegeneration after experimental brain trauma: association with chronic microglial activation.Capillary transit time heterogeneity and flow-metabolism coupling after traumatic brain injury.CCR2 antagonism alters brain macrophage polarization and ameliorates cognitive dysfunction induced by traumatic brain injury TSG (2,3,4' ,5-tetrahydroxystilbene 2-O-β-D-glucoside) suppresses induction of pro-inflammatory factors by attenuating the binding activity of nuclear factor-κB in microglia.Selective estrogen receptor modulators (SERMs) enhance neurogenesis and spine density following focal cerebral ischemia Peripheral Blood Mitochondrial DNA as a Biomarker of Cerebral Mitochondrial Dysfunction following Traumatic Brain Injury in a Porcine Model A time-course analysis of changes in cerebral metal levels following a controlled cortical impact.Propofol Attenuates Small Intestinal Ischemia Reperfusion Injury through Inhibiting NADPH Oxidase Mediated Mast Cell Activation NOX2 As a Target for Drug Development: Indications, Possible Complications, and Progress.Systematic Review of Traumatic Brain Injury and the Impact of Antioxidant Therapy on Clinical Outcomes.Epigallocatechin-3-Gallate (EGCG) Attenuates Traumatic Brain Injury by Inhibition of Edema Formation and Oxidative Stress.Age modulates the injury-induced metallomic profile in the brain.Traumatic brain injury in aged animals increases lesion size and chronically alters microglial/macrophage classical and alternative activation states Activation of mGluR5 and inhibition of NADPH oxidase improves functional recovery after traumatic brain injury Microglia activation as a biomarker for traumatic brain injury Strategies Aimed at Nox4 Oxidase Inhibition Employing Peptides from Nox4 B-Loop and C-Terminus and p22 (phox) N-Terminus: An Elusive Target.Age exacerbates the CCR2/5-mediated neuroinflammatory response to traumatic brain injury.Perineuronal nets protect fast-spiking interneurons against oxidative stress.Glucose administration after traumatic brain injury improves cerebral metabolism and reduces secondary neuronal injury.Peripheral Inflammatory Markers and Antioxidant Response during the Post-Acute and Chronic Phase after Severe Traumatic Brain Injury.Cellular and temporal expression of NADPH oxidase (NOX) isotypes after brain injury Resolving Contributions of Oxygen-Consuming and ROS-Generating Enzymes at the Synapse.NADPH oxidase in brain injury and neurodegenerative disorders Rotenone induces neurotoxicity through Rac1-dependent activation of NADPH oxidase in SHSY-5Y cells Antioxidant gene therapy against neuronal cell death.NOX2 deficiency alters macrophage phenotype through an IL-10/STAT3 dependent mechanism: implications for traumatic brain injury Biomarkers in traumatic brain injury.

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Critical role of NADPH oxidase in neuronal oxidative damage and microglia activation following traumatic brain injury.

http://www.wikidata.org/entity/Q34224919

description

2012 nî lūn-bûn

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2012 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2012 թվականի ապրիլին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年论文

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Critical role of NADPH oxidase ...... lowing traumatic brain injury.

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Critical role of NADPH oxidase ...... lowing traumatic brain injury.

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Critical role of NADPH oxidase ...... lowing traumatic brain injury.

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Critical role of NADPH oxidase ...... lowing traumatic brain injury.

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Critical role of NADPH oxidase ...... lowing traumatic brain injury.

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Critical role of NADPH oxidase ...... lowing traumatic brain injury.

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Critical role of NADPH oxidase ...... lowing traumatic brain injury.

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Darrell W Brann

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Dong Han

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Erin Scott

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Khoi Nguyen

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Krishnan M Dhandapani

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Melissa D Laird

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Quan-Guang Zhang

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Yan Dong

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P2860

The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology

NADPH oxidase as a therapeutic target in Alzheimer's disease.

Edema and brain trauma.

Estrogen attenuates ischemic oxidative damage via an estrogen receptor alpha-mediated inhibition of NADPH oxidase activation

Role of Rac1 GTPase in NADPH oxidase activation and cognitive impairment following cerebral ischemia in the rat

Chronic upregulation of activated microglia immunoreactive for galectin-3/Mac-2 and nerve growth factor following diffuse axonal injury.

Traumatic brain injury and Alzheimer's disease: a review.

Curcumin attenuates cerebral edema following traumatic brain injury in mice: a possible role for aquaporin-4?

Gp91phox (NOX2) in classically activated microglia exacerbates traumatic brain injury.

Absolute number and size of pigmented locus coeruleus neurons in young and aged individuals.

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traumatic brain injury

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