Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 42-year-old woman demonstrated recurrent, progressive neurological symptoms of peripheral and central nervous system damage of undefined infectious origin. Laboratory investigations showed abnormalities in the CSF and serum, suggesting subacute viral infection. Neuropathological examination revealed complete, widespread necrosis in the cervical and thoracic segments of the spinal cord with mononuclear and microglial infiltrations. There was pronounced thickening and fibrinoid necrosis of the vessel walls with mononuclear cuffs along the spinal cord. Dispersed, similar but less intensive inflammatory changes were present in the medulla oblongata, midbrain and basal ganglia. Surprisingly, there was diffuse demyelination with only slight glial and inflammatory reactions throughout the white matter of both hemispheres. The finding of coarse- and fine-grained deposits of IgG and C3 component of complement in the vessel walls of the spinal cord and vasa nervorum of cervical roots and peripheral spinal nerves, together with positive heterologous complement binding and the results of glycine-HC1 buffer elution, suggested immune-complex-mediated disseminated vasculomyelinopathy of the CNS and PNS. Consequent local ischemic changes and hypersensitivity phenomena led to frank necrosis of the cervical spinal cord and to extreme white matter demyelination in the brain. The case was diagnosed as allergic encephalomyelitis in which diffuse demyelination occurred coincidentally with spinal cord necrosis.
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PMID:Necrotic changes of the spinal cord with immune-complex-mediated disseminated vasculitis in a case of atypical allergic encephalomyelitis. 390 21

A 42 year-old woman developed paraplegia that resolved in six months, followed by sudden right hemiparesis and dysphasia two years later. The clinical work-up, including CT and MR scans, visual evoked potential, CSF examination and cerebral biopsy suggested the possibility of either multiple sclerosis or multiphasic disseminated encephalomyelitis. The differential diagnosis between both conditions is discussed.
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PMID:Multiple sclerosis or multiphasic disseminated encephalomyelitis? A new question about an old problem. Case report. 911

The alphavirus Sindbis virus (SINV) causes encephalomyelitis in mice. Lipid-containing membranes, particularly cholesterol and sphingomyelin (SM), play important roles in virus entry, RNA replication, glycoprotein transport, and budding. Levels of SM are regulated by sphingomyelinases (SMases). Acid SMase (ASMase) deficiency results in the lipid storage disease type A Niemann-Pick disease (NPD-A), mimicked in mice by interruption of the ASMase gene. We previously demonstrated that ASMase-deficient mice are more susceptible to fatal SINV encephalomyelitis, with increased viral replication, spread, and neuronal death. To determine the mechanisms by which ASMase deficiency enhances SINV replication, we compared NPD-A fibroblasts (NPAF) to normal human fibroblasts (NHF). NPAF accumulated cholesterol- and sphingolipid-rich late endosomes/lysosomes in the perinuclear region. SINV replication was faster and reached higher titer in NPAF than in NHF, and NPAF died more quickly. SINV RNA and protein synthesis was greater in NHF than in NPAF, but virions budding from NPAF were 26 times more infectious and were regular dense particles whereas virions from NHF were larger particles containing substantial amounts of CD63. Cellular regulation of alphavirus morphogenesis is a previously unrecognized mechanism for control of virus replication and spread.
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PMID:Effect of host cell lipid metabolism on alphavirus replication, virion morphogenesis, and infectivity. 1884 81