Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity? - Wikidata - awgldk - TriplyDB

Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity?

Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity?

http://www.wikidata.org/entity/Q29042454

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Mitochondrial defects in acute multiple sclerosis lesions Imaging Axonal Degeneration and Repair in Preclinical Animal Models of Multiple Sclerosis Breaking boundaries-coagulation and fibrinolysis at the neurovascular interface Brain innate immunity in the regulation of neuroinflammation: therapeutic strategies by modulating CD200-CD200R interaction involve the cannabinoid system Redox control of microglial function: molecular mechanisms and functional significance Positive or negative involvement of heat shock proteins in multiple sclerosis pathogenesis: an overview Multiple sclerosis: molecular mechanisms and therapeutic opportunities Pathophysiological processes in multiple sclerosis: focus on nuclear factor erythroid-2-related factor 2 and emerging pathways Mechanisms of oxidative damage in multiple sclerosis and neurodegenerative diseases: therapeutic modulation via fumaric acid esters In vitro and in vivo induction and activation of nNOS by LPS in oligodendrocytes Excessive biologic response to IFNβ is associated with poor treatment response in patients with multiple sclerosis Hypochlorite modification of sphingomyelin generates chlorinated lipid species that induce apoptosis and proteome alterations in dopaminergic PC12 neurons in vitro.Early detection of thrombin activity in neuroinflammatory disease.Importance of oligodendrocyte protection, BBB breakdown and inflammation for remyelination.Antibodies produced by clonally expanded plasma cells in multiple sclerosis cerebrospinal fluid.Mouse brain plasmalogens are targets for hypochlorous acid-mediated modification in vitro and in vivo.Thrombotic processes in multiple sclerosis as manifestation of innate immune activation.Fibrinogen triggers astrocyte scar formation by promoting the availability of active TGF-beta after vascular damage Fibrinogen signal transduction in the nervous system.The role of infections in the pathogenesis and course of multiple sclerosis.Inhibiting poly(ADP-ribose) polymerase: a potential therapy against oligodendrocyte death.Myelin debris regulates inflammatory responses in an experimental demyelination animal model and multiple sclerosis lesions.Review: Mitochondria and disease progression in multiple sclerosis Initiation and progression of axonopathy in experimental autoimmune encephalomyelitis.Iron and neurodegeneration in the multiple sclerosis brain.Thrombin mutant W215A/E217A treatment improves neurological outcome and attenuates central nervous system damage in experimental autoimmune encephalomyelitis.An updated histological classification system for multiple sclerosis lesions.Short-term cuprizone feeding induces selective amino acid deprivation with concomitant activation of an integrated stress response in oligodendrocytes.Oxidative damage in multiple sclerosis lesions.Relationship between iron accumulation and white matter injury in multiple sclerosis: a case-control study NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury.Hypoxia Inducible Factor-1α in Astrocytes and/or Myeloid Cells Is Not Required for the Development of Autoimmune Demyelinating Disease(,.)Demyelination and axonal preservation in a transgenic mouse model of Pelizaeus-Merzbacher disease.Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation Clusters of activated microglia in normal-appearing white matter show signs of innate immune activation Inflammatory response and chemokine expression in the white matter corpus callosum and gray matter cortex region during cuprizone-induced demyelination Demyelination patterns in a mathematical model of multiple sclerosis.Mannitol induces selective astroglial death in the CA1 region of the rat hippocampus following status epilepticus.Fibrinogen-induced perivascular microglial clustering is required for the development of axonal damage in neuroinflammation.The formation of inflammatory demyelinated lesions in cerebral white matter.

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P2860

Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity?

http://www.wikidata.org/entity/Q29042454

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2007 nî lūn-bûn

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2007 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2007 թվականի ապրիլին հրատարակված գիտական հոդված

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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Lesion genesis in a subset of ...... s: a role for innate immunity?

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Lesion genesis in a subset of ...... s: a role for innate immunity?

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Lesion genesis in a subset of ...... s: a role for innate immunity?

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Hans Lassmann

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P2860

The allograft inflammatory factor-1 family of proteins

Relapsing and remitting multiple sclerosis: pathology of the newly forming lesion

Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination

Axonal transection in the lesions of multiple sclerosis

Leukocyte engagement of fibrin(ogen) via the integrin receptor alphaMbeta2/Mac-1 is critical for host inflammatory response in vivo

Destruction of neurons by cytotoxic T cells: a new pathogenic mechanism in Rasmussen's encephalitis.

Fibrin depletion decreases inflammation and delays the onset of demyelination in a tumor necrosis factor transgenic mouse model for multiple sclerosis.

A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica.

Magnetization transfer changes in the normal appearing white matter precede the appearance of enhancing lesions in patients with multiple sclerosis.

Heat shock factor 1 and heat shock proteins: critical partners in protection against acute cell injury.

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2800-2815

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10.1093/BRAIN/AWM236

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Pt 11

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130

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Kenneth J Smith

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2007-11-01T00:00:00Z

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5888735

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17956913

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multiple sclerosis

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2981817

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