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)

Fluorescent antibody study showed persistent infection of egg-adapted avian encephalomyelitis virus in the central nervous system and pancreatic tissues of infected embryos and chickens hatched from them. The limited organ tropism of the egg-adapted virus in hatched chickens was in striking contrast to the systemic infection that occurs with a field strain. In chidkens orally infected with egg-adapted virus strains, transient infection of a few organs was found despite occurrence of viremia.
Am J Vet Res 1977 Dec
PMID:Immunofluorescent study on egg-adapted avian encephalomyelitis virus infection in chickens. 20 77

We demonstrated antibodies to isolated oligodendrocytes and to oligodendroglia in brain sections by indirect immunofluorescence technic in serums of 19 of 21 patients with multiple sclerosis. We also found such antibodies in three of five patients with subacute sclerosing panencephalitis and one of four patients with acute disseminated encephalomyelitis, but not in patients with other neurologic diseases or normal persons. The antibodies were absorbed by preincubation of serum with isolated oligodendrocytes or whole white matter, but not with purified myelin or liver tissue. Immunofluorescent staining was blocked by either rabbit anti-oligodendrocyte serum or non-fluoresceinated goat anti-human immunoglobulin. These findings suggest that antibodies to oligodendroglia are distinct from antibodies to myelin and that demyelination in multiple sclerosis could be a consequence of an immunopathologic reaction directed against oligodendroglial cells.
N Engl J Med 1977 Dec 01
PMID:Antibodies to oligodendroglia in patients with multiple sclerosis. 33 46

Lewis rats with experimental allergic encephalomyelitis (EAE) exhibited cell-mediated immunity to myelin basic protein as determined both with in vivo and in vitro assays. Positive skin test reactions and production of migration inhibitory factor (MIF) were observed before onset and after recovery from EAE. Rats rendered unresponsive to EAE exhibited in vitro cell-mediated immunity to basic protein, although in vivo manifestations were depressed. However, tolerant rats failed to respond to the encephalitogenic determinant; rats with EAE exhibited cell-mediated immunity to this region of the molecule. The results indicate that EAE-unresponsive rats possess lymphocytes capable of responding to basic protein, but that reactivity to the encephalitogenic peptide is suppressed.
Eur J Immunol 1978 Dec
PMID:Cell-mediated immunity to myelin basic protein in Lewis rats made unresponsive to experimental allergic encephalomyelitis. 36 47

Dynamics of emergence of specific reactive cell (SRC) with respect to the brain antigen in the draining regional lymph nodes and peripheral blood was studied in experimental whooping cough allergic encephalomyelitis (EAE) in guinea pigs. The greatest number of SRC in the regional lymph nodes, that markedly decreased by the 9th day of sensitization, was revealed in the middle of the EAE incubation period (the 6-7th day), whereas the peripheral blood showed the highest SRC number during this period. The SRC number rose in the regional lymph nodes and dropped in the peripheral blood at the height of EAE progress (the 20th day). It is concluded that SRC found may be attributed to T lymphocyte population.
Biull Eksp Biol Med 1979 Dec
PMID:[Specifically reactive cells in experimental allergic pertussis encephalomyelitis]. 39 Dec 96

Previous studies have shown that Strain 13 guinea pigs sensitised for experimental allergic encephalomyelitis (EAE) as adults usually develop an acute, fatal form of disease while animals inoculated as juveniles usually display a chronic relapsing form. The present study reports that following repeated short-interval blood sampling by cardiac puncture for the estimation of lymphocyte populations, some adult Strain 13 guinea pigs sensitised for acute EAE unexpectedly survived and developed chronic EAE, while a group of juveniles sensitised for chronic EAE and bled under the same conditions, developed a more severe, acute form of EAE. It is suggested that this reversal of disease course was related to the depletion of circulating factors.
Acta Neuropathol 1979 Dec
PMID:Experimental allergic encephalomyelitis. Frequent sampling of blood alters disease course. 52 58

Numerous drugs were tested for ability to suppress the hyperacute form of experimental allergic encephalomyelitis (EAE). This very severe disease produced clinical signs after 7-9 days which progressed rapidly to paralysis and death. Treatment during the first five days of the incubation period with cycloleucine, cyclophosphamide EN3638, 6-mercaptopurine, methotrexate and procarbazine produced important delays in onset. Corticosteroids, nonsteroidal antiinflammatory drugs, antilymphocyte serum, asparaginase, gold, cytarabine and tilorone, all previously reported to suppress ordinary EAE, had moderate, little or no effect in hyperacute EAE. Proteacted treatment was of no avail with some of these drugs, but it revealed the remarkable suppressive effect of EN3638, equal to cyclophosphamide. Hyperacute EAE was a rapid and economical screening test for immunosuppressive drugs, and a highly discriminating tool for comparison of potent agents.
Arch Int Pharmacodyn Ther 1977 Dec
PMID:Suppression of the hyperacute form of experimental allergic encephalomyelitis by drugs. 60 23

Recent research has shown that Toxoplasma gondii, the cause of human toxoplasmosis, is a protozoan close to the genus Isospora, whose life cycle involves cats as the definitive host, and other mammals, including man, and birds as intermediate hosts. Cats shed oocysts in their faeces; these are infective to the intermediate hosts when ingested. But the non-felid intermediate hosts can also become infected by eating other intermediate hosts. Probably most human infections occur in this manner and result from eating raw or insufficiently cooked meats. Most people become infected during their life time, but most infections are benign and unnoticed. Occasionally the disease picture may simulate infectious mononucleosis. However, in intrauterine or neonatal infections the disease may be most severe and chorioretinitis, encephalomyelitis, hydrocephalus or microcephaly may result. Diagnosis depends upon demonstrating the parasite in biopsy material or through changing titres in serological tests.
Aust Fam Physician 1977 Dec
PMID:Toxoplasmosis. 60 49

Experimental allergic encephalomyelitis (EAE) was induced in rats of the Lewis strain fed diets adequate or deficient in essential fatty acids (EFA). After induction of the disease, the diets were supplemented with aspirin (3.75 g/kg diet), and the effects of the drug on the course of EAE and on the synthesis of prostaglandin F (PGF) by brain slices from diseased animals and their Freund controls were examined. Aspirin supplementation delayed the onset of EAE in both dietary groups. EFA-deficient rats experienced an incidence and severity of the disease similar to that of aspirin-free, EFA-deficiet rats, while the EFA-adequate group showed a greater severity but not an increased incidence, compared to aspirin-free controls. Aspirin treatment led to an increased PGF production by brain slices from rats on either diet and not subjected to an immunochallenge. When the diet was deficient in EFA, challenge with antigen plus adjuvant or adjuvant alone tended to decrease PGF synthesis by brain slices, and when the diet was adequate in EFA, immunochallenge caused a marked depression on PGF synthesis. It was concluded that the PG synthetase inhibitor aspirin can alter the course of EAE in the rat, providing further evidence that PGs or related metabolites may be involved in the immune response in this disease.
Lipids 1978 Dec
PMID:Incidence and severity of experimental allergic encephalomyelitis and cerebral prostaglandin synthesis in essential fatty acid deficient and aspirin-treated rats. 75 Aug 27

Theiler's virus infection in SJL/J mice was studied ultrastructurally at subsequent intervals after intracerebral inoculation. Extensive spinal cord lesions consisting of leptomeningeal and white matter mononuclear cell infiltrates with concomitant primary demylination were seen by 15 days. Stripping of myelin lamellae by invading mononuclear cell processes and vesicular disruption of myelin were demonstrated to be the patterns of myelin breakdown. Oligodendrocytes in the vicinity of demyelinating lesions never showed degenerative changes, and viral inclusions could not be found in any cells in the central nervous system. Remyelinating axons, first detected 21 days after infections, were more frequently seen in the late phase of the disease when conspicuous gliosis was also present. Active demyelination could still be observed as late as one year after infection at which time inflammation was decreased. However, plasma cells were relatively more numerous at later times after infection. These ultrastructural findings are similar to experimental allergic encephalomyelitis, and suggest an immune-mediated mechanism of demyelination in Theiler's virus infection.
Lab Invest 1975 Dec
PMID:Primary demyelination in Theiler's virus infection. An ultrastructural study. 120 82

Treatment of Lewis rats with a single dose of OX19 antibody, specific for rat CD5, uniformly prevented the development of experimental autoimmune encephalomyelitis (EAE). This protective effect had several notable characteristics: (1) it persisted for at least 10 days; (2) it could be achieved with either high doses of the antibody (> 200 micrograms) or lower doses (100-200 micrograms), which did not deplete T cell populations; and (3) the treated animals were able to mount comparable T cell responses to both myelin basic protein and myelin-unrelated antigens. In addition, antibody treatment consistently prevented the development of adoptively transferred EAE, suggesting that enhanced suppressor cell activity may have contributed to the protection. Antibodies such as OX19 appear capable of blocking the development of EAE, and perhaps other autoimmune diseases as well.
Cell Immunol 1992 Dec
PMID:Prevention of experimental autoimmune encephalomyelitis in Lewis rats by treatment with an anti-rat CD5 antibody (OX19). 128 May 33


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