Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy. - Wikidata - awgldk - TriplyDB

Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

http://www.wikidata.org/entity/Q35116558

about

Mechanical and cellular processes driving cervical myelopathy Role of MK2 signaling pathway in the chronic compression of cervical spinal cord The incidence of cervical spondylosis decreases with aging in the elderly, and increases with aging in the young and adult population: a hospital-based clinical analysis.Magnetic Resonance Imaging Biomarker of Axon Loss Reflects Cervical Spondylotic Myelopathy Severity Treatment considerations of cervical spondylotic myelopathy.Degenerative Cervical Myelopathy: A Clinical Review.Association between Cervical Spondylosis and Migraine: A Nationwide Retrospective Cohort Study.

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Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

http://www.wikidata.org/entity/Q35116558

description

2011 nî lūn-bûn

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2011 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2011 թվականի մայիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

@zh-hant

2011年論文

@zh-hk

2011年論文

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2011年論文

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2011年论文

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name

Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

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Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

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Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

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Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

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Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

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Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

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Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.

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Geoffrey T Manley

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Michael S Beattie

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P2860

Inhibition of Fas-mediated apoptosis through administration of soluble Fas receptor improves functional outcome and reduces posttraumatic axonal degeneration after acute spinal cord injury

ProNGF induces p75-mediated death of oligodendrocytes following spinal cord injury

Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord

Minocycline treatment reduces delayed oligodendrocyte death, attenuates axonal dieback, and improves functional outcome after spinal cord injury.

Inflammation and apoptosis: linked therapeutic targets in spinal cord injury.

Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury.

Cell death after spinal cord injury is exacerbated by rapid TNF alpha-induced trafficking of GluR2-lacking AMPARs to the plasma membrane

Neutralization of CD95 ligand promotes regeneration and functional recovery after spinal cord injury.

A review of the pathophysiology of cervical spondylotic myelopathy with insights for potential novel mechanisms drawn from traumatic spinal cord injury.

Developmental stage of oligodendrocytes determines their response to activated microglia in vitro.

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1259-1261

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scholarly article

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10.1093/BRAIN/AWR088

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Pt 5

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134

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2011-05-01T00:00:00Z

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51150615

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