encephalomyelitis

(redirected from experimental allergic encephalomyelitis)
Also found in: Thesaurus, Medical, Acronyms, Encyclopedia.

en·ceph·a·lo·my·e·li·tis

 (ĕn-sĕf′ə-lō-mī′ə-lī′tĭs)
n.
Inflammation of the brain and spinal cord.

encephalomyelitis

(ɛnˌsɛfələʊˌmaɪəˈlaɪtɪs)
n
(Pathology) acute inflammation of the brain and spinal cord
encephalomyelitic adj

en•ceph•a•lo•my•e•li•tis

(ɛnˌsɛf ə loʊˌmaɪ əˈlaɪ tɪs)

n.
inflammation of the brain and spinal cord.
[1905–10]
en•ceph`a•lo•my`e•lit′ic (-ˈlɪt ɪk) adj.
ThesaurusAntonymsRelated WordsSynonymsLegend:
Noun1.encephalomyelitis - inflammation of the brain and spinal cord
inflammation, redness, rubor - a response of body tissues to injury or irritation; characterized by pain and swelling and redness and heat
Translations

en·ceph·a·lo·my·e·li·tis

n. encefalomielitis, infl. del encéfalo y de la médula espinal, que puede ser letal.
References in periodicals archive ?
Two minor determinants of myelin basic protein induce experimental allergic encephalomyelitis in SJL/J mice.
Peroxisome proliferator-activated receptor-gamma-deficient heterozygous mice develop an exacerbated neural antigen-induced Th1 response and experimental allergic encephalomyelitis.
Cognitive deficit associated with cholinergic and nerve growth factor down-regulation in experimental allergic encephalomyelitis in rats.
Immune response after experimental allergic encephalomyelitis in rats subjected to calorie restriction.
Resveratrol (trans-3,5,4'-trihydroxystilbene) ameliorates experimental allergic encephalomyelitis, primarily via induction of apoptosis in T cells involving activation of aryl hydrocarbon receptor and estrogen receptor.
Key words: apoptosis, caspases, complement C5, complement complex C5b-9, experimental allergic encephalomyelitis, Fas ligand, oligodendrocyte, multiple sclerosis, phosphatidylinositol-3 kinase, T lymphocyte.
University of Alabama at Birmingham) showed that introducing high levels of a protein (C-reactive protein or CRP, which is regulated by testosterone) in female mice can delay the onset of experimental allergic encephalomyelitis (EAE), indicating that sex hormones might in part, through this path, control immune function and disease--a potential link between hormones, immune function, and MS disease course.
HLA-DR4-1E chimeric class II transgenic, murine class II-deficient mice are susceptible to experimental allergic encephalomyelitis.

Full browser ?