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)

Experimental autoimmune encephalomyelitis influenced catecholaminergic and indoleaminergic neurotransmitter systems in the central nervous system of Lewis rats. During paralysis, serotonin and noradrenaline were significantly reduced compared to animals injected with complete Freund's adjuvant in the posterior dorsomedial brainstem and in lower spinal cord segments. These diminutions remained after recovery from neurological signs in T11-S1. The serotonin metabolite 5-hydroxyindoleacetic acid was greatly augmented during the attack in all segments but was depleted during recovery in the lumbar spinal cord, which may indicate a normalized turnover at a reduced serotonin level. These results suggest functional impairment of monoaminergic neurons of the brainstem and spinal cord followed by permanent damage to some monoaminergic fibers in the spinal cord.
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PMID:Monoamines and related substances in brainstem and spinal cord of Lewis rats during the attack and recovery of experimental autoimmune encephalomyelitis. 247 12

We reported previously that two different anti-CD4 monoclonal antibodies (W3/25, MRC OX35) were effective in treating experimental allergic encephalomyelitis in the Lewis rat whereas anti-I-A antibody was ineffective. Further studies with other monoclonal antibodies and fragments have now been performed. Anti-I-E antibody was ineffective in shortening the disease duration even when used in combination with anti-I-A antibody. Anti-CD2 (T11) antibody was marginally effective, shortening the duration of disease by only one day on the average. Combination of anti-CD4 antibody with anti-CD2 antibody did not improve the recovery time over the use of anti-CD4 antibody alone. On the other hand, the F (ab')2 fragment of the anti-CD4 antibody was as effective in the treatment of disease as the intact antibody molecule, indicating that it was sufficient to block the CD4 molecules on the cell surface of the EAE effector cells in order to affect the disease course.
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PMID:Treatment of clinical experimental allergic encephalomyelitis in the rat using fragments and combinations of monoclonal antibodies. 325 18

We investigated the effects of chronic relapsing experimental allergic encephalomyelitis (first attack and first recovery) on uric acid (UR) concentrations in Lewis rat spinal cord. Perchloric extracts of 9 regions between spinal cord segments C3 and Co1 were injected into a reversed-phase high-performance liquid chromatographic system, and UR was quantified electrochemically. In all regions UR, which was lower than 0.5 micrograms/g wet tissue in rats injected with adjuvant (controls), increased to a variable extent during the attack (5-12 micrograms/g, maximum in T11-L2) and returned during recovery to a residual level of 1-2 micrograms/g. These findings can be partly attributed to blood-brain barrier damage.
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PMID:Increased concentrations of uric acid in the spinal cord of rats with chronic relapsing experimental allergic encephalomyelitis. 348 7

The patient was a 14-year-old male diagnosed with acute disseminated encephalomyelitis (ADEM) with acute onset of multifocal central nervous system symptoms. He showed increased cerebrospinal fluid cell counts and high myelin basic protein levels, which responded well to steroid pulse therapy. Spinal MRI showed a centrally-located long spinal cord lesion (LCL) involving 17 vertebral bodies from C2 to T11 that later expanded into the white matter, and lesions on the ventral side of the medulla. The cause of LCL has been reported to be heterogeneous. In this case, LCL is considered to be associated with ADEM, an acute autoimmune response to myelin, and vascular inflammation of the gray matter of the spinal cord.
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PMID:A case of ADEM with atypical MRI findings of a centrally-located long spinal cord lesion. 2178 34