Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways. - Wikidata - awgldk - TriplyDB

Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways.

Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways.

http://www.wikidata.org/entity/Q34037588

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Neuroprotective and Neurorestorative Processes after Spinal Cord Injury: The Case of the Bulbospinal Respiratory Neurons Multiple organ dysfunction and systemic inflammation after spinal cord injury: a complex relationship Extrinsic and Intrinsic Regulation of Axon Regeneration by MicroRNAs after Spinal Cord Injury Bryostatin-1 Restores Blood Brain Barrier Integrity following Blast-Induced Traumatic Brain Injury A novel closed-body model of spinal cord injury caused by high-pressure air blasts produces extensive axonal injury and motor impairments Potential natural products for Alzheimer's disease: targeted search using the internal ribosome entry site of tau and amyloid-β precursor protein.Inflammation is increased with anxiety- and depression-like signs in a rat model of spinal cord injury.Progressive inflammation-mediated neurodegeneration after traumatic brain or spinal cord injury.Ablation of the transcription factors E2F1-2 limits neuroinflammation and associated neurological deficits after contusive spinal cord injury Age-dependent differences in microglial responses to systemic inflammation are evident as early as middle age Cell cycle inhibition limits development and maintenance of neuropathic pain following spinal cord injury.Neuroinflammation as Fuel for Axonal Regeneration in the Injured Vertebrate Central Nervous System.Effect of ZBD-2 on chronic pain, depressive-like behaviors, and recovery of motor function following spinal cord injury in mice.Endogenous recovery after brain damage: molecular mechanisms that balance neuronal life/death fate.Does time heal all wounds? Experimental diffuse traumatic brain injury results in persisting histopathology in the thalamus.Microstructural and microglial changes after repetitive mild traumatic brain injury in mice.Truncated TrkB.T1-Mediated Astrocyte Dysfunction Contributes to Impaired Motor Function and Neuropathic Pain after Spinal Cord Injury Neuropathic pain following traumatic spinal cord injury: Models, measurement, and mechanisms.Reward, motivation, and emotion of pain and its relief.NOX2 drives M1-like microglial/macrophage activation and neurodegeneration following experimental traumatic brain injury.Modulating the immune response in spinal cord injury.Huanglian-Jie-Du-Tang Extract Ameliorates Depression-Like Behaviors through BDNF-TrkB-CREB Pathway in Rats with Chronic Unpredictable Stress.Spinal cord injury drives chronic brain changes.Salubrinal reduces oxidative stress, neuroinflammation and impulsive-like behavior in a rodent model of traumatic brain injury.Multiple Kernel Based Region Importance Learning for Neural Classification of Gait States from EEG Signals.Cell cycle inhibition reduces inflammatory responses, neuronal loss, and cognitive deficits induced by hypobaria exposure following traumatic brain injury.Endoplasmic Reticulum Stress and Disrupted Neurogenesis in the Brain Are Associated with Cognitive Impairment and Depressive-Like Behavior after Spinal Cord Injury.Neuronal Nitric Oxide Synthase Contributes to PTZ Kindling-Induced Cognitive Impairment and Depressive-Like Behavior.Neural Stem Cell-Conditioned Medium Suppresses Inflammation and Promotes Spinal Cord Injury Recovery.Elucidation of Gene Expression Patterns in the Brain after Spinal Cord Injury.Histamine H3 Receptor Antagonist Prevents Memory Deficits and Synaptic Plasticity Disruption Following Isoflurane Exposure.Hedonic and motivational responses to food reward are unchanged in rats with neuropathic pain.Ciproxifan, an H3 receptor antagonist, improves short-term recognition memory impaired by isoflurane anesthesia.Unique sensory and motor behavior in Thy1-GFP-M mice before and after spinal cord injury.Delayed Influence of Spinal Cord Injury on the Amino Acids of NO• Metabolism in Rat Cerebral Cortex Is Attenuated by Thiamine.Spinal Cord Injury Impairs Neurogenesis and Induces Glial Reactivity in the Hippocampus.Copolymer-1 enhances cognitive performance in young adult rats.Chronic pain impairs cognitive flexibility and engages novel learning strategies in rats.The Biology of Regeneration Failure and Success After Spinal Cord Injury.Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.

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Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways.

http://www.wikidata.org/entity/Q34037588

description

2014 nî lūn-bûn

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2014 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի օգոստոսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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JNEUROSCI.5110-13.2014

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Journal of Neuroscience

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Spinal cord injury causes brai ...... : role of cell cycle pathways.

@en

P2093

Alok Kumar

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Boris Sabirzhanov

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Jacob Skovira

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Junfang Wu

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Tao Luo

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Zaorui Zhao

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P2860

Mechanisms of chronic central neuropathic pain after spinal cord injury

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Alternative activation of macrophages

Modulation of thalamic nociceptive processing after spinal cord injury through remote activation of thalamic microglia by cysteine cysteine chemokine ligand 21

Inhibition of E2F1/CDK1 pathway attenuates neuronal apoptosis in vitro and confers neuroprotection after spinal cord injury in vivo

Unbiased stereological estimation of the total number of neurons in thesubdivisions of the rat hippocampus using the optical fractionator

CR8, a selective and potent CDK inhibitor, provides neuroprotection in experimental traumatic brain injury.

Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury.

Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury.

A reassessment of whether cortical motor neurons die following spinal cord injury.

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scholarly article

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10.1523/JNEUROSCI.5110-13.2014

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33

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34

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Bogdan A Stoica

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2014-08-01T00:00:00Z

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25122899

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4131014

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