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)

Poly-L-lysin (PLL) given subcutaneously in a dose of 3 mg/day suppresses experimental allergic encephalomyelitis in guinea-pigs. The suppressive effect of PLL can still be demonstrated when administration is begun 8 days post-immunization. The effect is disease- and species-specific since PLL (3 mg/day) does not suppress experimental allergic orchitis in guinea-pigs, nor does it suppress EAE in rats (1-5 mg/day). PLL (0-2 mg/day) does not decrease the severity of graft-versus-host disease (GVH) in mice as judged by the spleen/body weight assay.
Clin Exp Immunol 1975 Dec
PMID:Suppression of experimental allergic encephalomyelitis in guinea-pigs with poly-L-lysine. 0 13

The induction of immunological tolerance with, and for, the caused organotypical antigen is a conception for a specific therapy for neuroimmunological diseases with at least a partial autoallergic pathogenesis. Appropriate to a set step-by-step programme for the development of antigen-specific therapy preventive tolerance experiments were carried out at the model of experimental allergic encephalomyelitis (EAEM) with allogenic myelin basic protein (BP) prepared from rabbits. The result is: 100 ug BP given intravenously simultaneously with 100 ug BP in incomplete Freud's adjuvant given intracutanously twice a week and 40 mg Cyclophosphamid given daily during the minor clinical incidence rate and no signs of EAEM pathomorphologically. A longlasting tolerance for the BP could be obtained as a test proved after 100 days. Hints are given for further potential therapeutic treatments, such as the use of antigen bound chemically to the immunosuppressive drug or the use of chemically modified BP for the induction of a specific tolerance.
Psychiatr Neurol Med Psychol (Leipz) 1975 Dec
PMID:[Experimental allergic encephalomyelitis as a model for the study of therapeutic concepts for encephalomyelitis disseminata]. 5 33

In order to elucidate the role of humoral antibodies in the pathogenesis of myelin lesions in experimental allergic encephalomyelitis (EAE) a combined in vivo and in vitro study was done using rabbits immunized with the purified A1 basic protein. Rabbits injected with whole white matter were used for comparison. Demyelinating activity appeared in the rabbit sera 5 days after injection, as tested in myelinated organotypic tissue cultures. In spite of this no lesions of the myelin preceded the appearance of inflammatory cells in the living animals. In the spinal cord changes in vascular permeability, as revealed by leakage of Evans blue-albumin complex, appeared at the same time as the cells. In contrast to in vitro, the mere presence of circulating antibodies in vivo does not appear to be enough to cause structural changes of the myelin. Possible reasons for this discrepancy are discussed; it is emphasized that the inflammatory changes develope first in areas where the so-called blood-brain barrier to diffusion of proteins is lacking.
Acta Neuropathol 1976 Dec 21
PMID:About demyelinating properties of humoral antibodies in experimental allergic encephalomyelitis. In vivo and in vitro studies. 6

A woman, aged 26 years, who died of progressively worsening demyelinating encephalomyelitis in the course of 4 years is reported. The neuropathological findings included large subcortical softenings in the cerebral hemispheres, tiny perivenous demyelinated foci in their neighborhood and scattered in the white matter. There was an acute vasculitis with fibrinoid exudation in the affected as well as unaffected areas. Focal perivenous mononuclear cell infiltrations are conspicuous in the white matter. The laboratory and postmortem examinations suggested a collagen disease like SLE. The abnormalities included marked increase of serum gamma-globulin, especially of IgG, and elevation of CRP, RA, and ANA titer, moderate thickening of the basement membranes of the renal glomeruli, onion skin-like periarteriolar fibrosis in the spleen, fibrous pericarditis and periadventitial fibrosis of myocardial arteries. Bilateral degeneration of the spinal posterior columns and dorsal roots was also observed. A probable relationship of the modified features in this example of demyelinating encephalomyelitis with abnormal immune mechanisms in the background is discussed.
J Neurol 1977 Dec 01
PMID:A case of demyelinating encephalomyelitis with some resemblance to collagen disease. 7 51

Age-related concentrations of myelin basic protein serum factor (MBP-SF), an endogenous neuroantigen detected and quantitated by inhibition of binding of rat myelin basic protein (RMBP) antibody with 125I-RMBP reagent antigen and immunochemically indistinguishable from native RMBP in this respect, reach peak levels as high as 21 ng/microliter among 2-3-wk-old normal suckling Lewis rats. Levels then progressively decline to low, usually undetectable levels of less than or equal to 0.6 ng/microliter MBP-equivalents in adult animals by 7 wk of age. MBP-SF levels are inversely related to the age-related increasing capacity of maturing Lewis rats to develop experimental allergic encephalomyelitis (EAE) after sensitization to MBP of syngeneic, but not xenogeneic, origin. MBP-SF appears to be an endogenous neuroimmunoregulatory product of potential importance for immunologic tolerance to autologous RMBP in Lewis rats.
J Exp Med 1978 Dec 01
PMID:Myelin basic protein serum factor. An endogenous neuroantigen influencing development of experimental allergic encephalomyelitis in Lewis rats. 8 7

After intracranial replication of a neurotropic strain of vaccinia in mouse brain, analysis of the purified virus preparation reveals the presence of at least one host protein on the virus which was identified as the myelin basic protein. Vaccinia virus Elstree, a dermotropic virus may substitute for complete Freund's adjuvant (CFA) in inducing experimental allergic encephalomyelitis (EAE). Guinea pigs challenged with virus-myelin emulsions without CFA developed clinical and histological signs of EAE.
Neurosci Lett 1979 Dec
PMID:Mechanisms in the pathogenesis of post-infectious vaccinia virus encephalomyelitis in the mouse. 9 31

Autosensitization to some central nervous system antigen still remains one of the best hypotheses for the continuing pathogenesis of multiple sclerosis (MS). Enough is now known about the cause, pathogenesis, and treatment of experimental allergic encephalomyelitis (EAE) to test this hypothesis. Reports of therapeutic failure of the encephalitogen myelin basic protein (BP) in the treatment of MS have their counterparts in similar therapeutic failures in EAE. Only highly inbred strain 13 guinea pigs respond consistently to BP therapy, and this only when BP is administered in relatively high doses. Noninbred guinea pigs respond much less well to simple BP therapy, and monkeys hardly at all. In both strains of monkeys so far studied, a nonspecific adjunctive factor--an antibiotic in Macaca mulatta and a steroid in Macaca fascicularis--is also required. Accordingly, human trials of the therapeutic efficacy of BP in MS should include its administration in large concentrations together with an adjunctive agent.
Ann Neurol 1979 Dec
PMID:Has myelin basic protein received a fair trial in the treatment of multiple sclerosis? 9 73

Treatment of experimental allergic encephalomyelitis (EAE) in two strains of monkeys with large amounts of myelin basic basic protein (BP) fails unless an adjunct is also used. In both strains the adjunct by itself is more effective than BP by itself, but in the one strain which could be investigated sufficiently, the combination can be made almost totally effective in reversing EAE. The adjunct varies with the strain of monkey, an antibiotic in Macaca mulatta and a steroid in Macaca fascicularis. Similar adjunctive treatments should be considered in the management of multiple sclerosis, for EAE remains one of the best studied models.
Ann Neurol 1979 Dec
PMID:Myelin basic protein treatment of experimental allergic encephalomyelitis in monkeys. 9 74

Treatment with rabbit anti-moneky thymus cell sera whether limited (3 days) or extensive (15 days), did not alter the development of experimental allergic encephalomyelitis (EAE) in rhesus monkeys challenged with myelin basic protein or central nervous system tissue (CNS) when compared to similarly challenged control monkeys treated with normal rabbit serum. No consistent difference in disease incidence or intensity as measured by incubation period, neurologic signs or CNS pathology was observed between experimental and control monkeys. This finding is in contrast to previous reports on the efficacy of ATS treatment in prevention of EAE in rodents.
J Neurol Sci 1979 Dec
PMID:Induction of allergic encephalomyelitis in rhesus monkeys treated with anti monkey thymocyte sera. 11 83

Pigs inoculated intravenously with swine vesicular disease virus (UKG strain), those inoculated with coxsackievirus B5, and other pigs exposed by pen contact to the same viruses developed diffuse encephalomyelitis. Perivascular cuffing, with lymphocytes and formation of neuroglia cell foci, were most prominent in telencephalon, diencephalon, and mesencephalon. Encephalitis was of mild to severe intensity. Severity of lesions was more extensive and severe in the pigs exposed to swine vesicular disease virus. Pen contact exposure to either of the 2 viruses caused a more severe central nervous system reaction than did intravenous inoculation. The type and the distribution of lesions produced by the 2 viruses indicate that they may be related.
Am J Vet Res 1975 Dec
PMID:Brain and spinal cord lesions in pigs inoculated with swine vesicular disease (UKG strain) virus and coxsackievirus B5. 12 5


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