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)

We report the preliminary results of an ongoing study of multiple sclerosis (MS) in childhood. The investigations include an analysis of the clinical picture and course. Multiple sclerosis in early childhood may present atypically, with a symptomatology suggesting diffuse encephalomyelitis, meningeal reaction, brain oedema, seizures, impaired consciousness and in some cases take a lethal course. Imaging studies including MRI and MR-spectroscopy, CSF-analysis, electrophysiology (VEP, BAEP, SER), and virological and immunological investigations are performed. So far 15 children have been studied. Their age at the onset of the disease ranged from 3 to 15 years. Abnormal CSF-findings with pleocytosis and oligoclonal IgG bands were present in 11 and 10 out of 15 patients respectively. MRI revealed numerous white matter lesions in the brain stem and cerebral hemispheres. VEP, BAEP and SER's were abnormal in most children. Proton magnetic resonance spectra from plaques exhibited a 50-80% decrease in N-acetyl aspartate, which is a potential marker of vital neuronal tissue, a decrease of the creatine pool and an increase of choline-containing compounds. Lactate was not increased. Our observations of MS in early childhood cast doubt on some of the previous notions concerning a latency period of several years between the exposure to a still unknown agent and the manifestation of MS. In view of atypical features in the initial phase, it would seem desirable to record cases of encephalomyelitis of undetermined origin as potential cases of MS and to register the further course for verification or exclusion.
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PMID:Multiple sclerosis in childhood: report of 15 cases. 833 16

The histopathologic and virologic features of several mouse strains inoculated with the C strain of lactate dehydrogenase-elevating virus are described. Young C58 and AKR mice were found to develop histologic poliomyelitis when injected with cyclophosphamide prior to peripheral inoculation of lactate dehydrogenase-elevating virus. None of the C58 mice developed serious hindlimb paralysis, but some of the AKR mice did. Chronic poliomyelitis persisted for many weeks after infection in some C58 mice, but a spongioform poliomyopathy of the anterior horn was found in others. In contrast, inoculation of young C57BR/cd mice with lactate dehydrogenase-elevating virus produced inflammatory lesions restricted to central nervous system white matter that could be detected many weeks after infection. The most frequent findings were moderate leptomeningitis and myelitis localized to the white matter, however, radiculitis was also occasionally observed. Severe necrosis of spinal cord white matter was seen rarely. Development of lesions in C57BR/cd mice did not require immunosuppression prior to peripheral inoculation with virus and was not age related, sex linked, or exclusively controlled by the H-2 histocompatibility locus. Lactate dehydrogenase-elevating virus-infected C57L, C57BL/6, and RF mice did not develop poliomyelitis; however, C57L and C57BL/6 mice displayed a low incidence of mild encephalomyelitis. Poliomyelitis-susceptible C58 mice had the highest levels of viral infectivity in plasma and central nervous system tissues. White matter disease-susceptible C57BR/cd mice had viral titers in plasma and central nervous system tissues comparable to poliomyelitis-resistant C57L, C57BL/6, and RF mice. These studies demonstrate that different strains of mice have differing susceptibilities to the development of central nervous system inflammatory diseases.
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PMID:Mouse strain-specific central nervous system lesions associated with lactate dehydrogenase-elevating virus infection. 688 86

Lactic acid bacteria are claimed to have immunomodulating effects. Stimulation as well as suppression of T helper (Th)1 mediated immune responses, have been described for various strains. Experiments involving Lactobacillus casei Shirota (LcS) detected mainly enhancement of innate immune responses and promotion of Th1 mediated immune reactivity. To confirm and further investigate modulation of Th1 responses and development of autoimmune disease by LcS, the consequences of oral administration of LcS were assessed in several experiments. The effect of LcS varied between the different models. No modulation was found in the mitogen-induced cell proliferation and cytokine release assays in mesenteric lymph nodes of Wistar rats. LcS inhibited the Th1 mediated immune response in an adapted murine Local Lymph Node Assay (LLNA) in BALB/c mice, whereas experimental autoimmune encephalomyelitis (EAE) in Lewis rats was aggravated. These varying effects on Th1 responses indicate that beneficial as well as harmful effects on immune related disorders could occur after LcS consumption. Since microarray analysis is suggested to be more sensitive and predictive than functional tests, gene expression profiling was included as an alternative endpoint in the testing of immunomodulation. The detected gene expression profiles did not reflect the effects of LcS on the immune system. Microarray analysis may therefore have no more predictive value than immune function assays when investigating immunomodulation by probiotics. To gain further insight into effects of probiotics on immune function, experiments including cytokine assays and gene expression analysis combined with disease models could be useful.
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PMID:Evaluation of immunomodulation by Lactobacillus casei Shirota: immune function, autoimmunity and gene expression. 1687 51