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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A detailed description and stepwise evaluation of a procedure that can be used to obtain myelin basic protein (BP) from whole brain is presented. The procedure involved the 0.001 MHC1 extraction of whole brain pre-treated in a sequential manner with chloroform-methanol (2:1 v/v), acetone, and deionized water. This is followed by a precipitation of the extract at pH 9.0, and gel filtration of the supernatant in 0.01 M HC1. Yields of canine and porcine BP and their disc gel evaluations are presented at several key points in the procedure. The final products possessed a high degree of homogeneity when examined on SDS gels stained with commonly used protein stains. When compared with six SDS-gel marker-protein standards, the canine and porcine final products had mobilities that correspond to an apparent molecular weight of 18,5000 +/- 5%. Quantitative binding of 125I-labeled canine and porcine BPs with standardized rabbit anti-BP antisera gave comparable results. Immunoelectrophoretic and immunodiffusion examinations demonstrated single components and complete identity. The canine and porcine BP's also reacted fully with syngeneic anti-BP antisera raised in Lewis-strain rats. The canine BP was tested for encephalitogenicity in Lewis-strain rats and found to be comparable to rat BP in producing experimental allergic encephalomyelitis.
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PMID:An evaluation of a procedure for the isolation of myelin basic protein (BP). 6 Jul 58

Pulse-chase experiments after synchronous initiation of translation indicate that the larger Venzuelan equine encephalomyelitis (VEE) virus membrane glycoprotein E2, is derived by proteolytic cleavage of the precursor, PE2. The structural proteins of VEE virus strains representing each of the antigenic subtypes and varieties have been compared by discontinuous SDS-polyacrylamide gel electrophoresis. Nucleocapsid proteins of all isolates were similar in size (mol. wt. 35 to 36 X 10(3). The mol. wt. of E1 varied from 48 to 51 X 10(3) and the mol. wt. of E2 glycoproteins ranged from 53 to 59 X 10(3). Pixuna virus contained a third envelope glycoprotein of 59 X 10(3) mol. wt. in addition to the two major glycoproteins of mol. wt. 53 X 10(3) and 48 X 10(3) respectively. The isoelectric points (pI) of E1 and E2 for all VEE strains studied were approx. 7 and 9 respectively. Both glycoproteins of TC-83 virus induced precipitating antibodies which reacted only with the homologous purified E1 and E2 glycoproteins. Antibodies to E2 protein of each virus neutralized virus infectivity and inhibited the agglutination of goose erythrocytes by virions. Haemagglutination-inhibition tests using antisera to E2 glycoproteins of prototype viruses, representing each of the antigenic subtypes and varieties, differentiated the viruses into subtypes I, II, III and IV with subtype I divided into variants 1AB, 1C, 1D and 1E.
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PMID:Biochemical and antigenic comparison of the envelope glycoproteins of Venezuelan equine encephalomyelitis virus strains. 11 35

After in vitro incubation of brain slices from guinea pigs in the intermediate (10 days postinduction) stage of experimental allergic encephalomyelitis (EAE), incorporation of [14C]leucine into protein was increased in a glial-enriched fraction. By the late (17-18 days postinduction) stage of the disease, when EAE symptoms were manifest, both the neuronal- and glial-enriched fractions showed increased specific activity of their total protein. SDS polyacrylamide gel electrophoresis showed that the increased leucine incorporation occurred in those proteins which labeled in a control material. After intraperitoneal injection of [3H]leucine the incorporated radioactivity was slightly increased in unfractionated brains from EAE animals. The neuronal-glial ratios for protein-bound radioactivity indicated that the increased incorporation resided mainly in the glial population.
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PMID:Amino acid incorporation into neurons and glia of guinea pigs with experimental allergic encephalomyelitis. 111 9

Mouse hepatitis virus (MHV) strain JHM (MHV-JHM) is a neurotropic coronavirus that causes acute fatal encephalomyelitis in 75-99% of infected mice. The surviving animals may subsequently develop demyelinating disease. We compared the S peplomer protein of the wild type (wt) and five temperature-sensitive (ts) mutants of MHV-JHM. In contrast with the wt, none of these five cause fatal disease (mortality less than 10%). Three of these ts mutants did not induce any demyelinating disease, a fourth caused demyelinating disease in 5% of the animals and a fifth, designated ts8, exhibited strong demyelinating properties and caused demyelination in 99% of the animals. SDS-PAGE analysis revealed no differences in the molecular weight of S peplomer protein of wt or ts MHV-JHM mutants. However, isoelectric focusing of the S protein of these five ts mutants and the wt MHV-JHM, followed by transfer to nitrocellulose sheets and immunoblotting with anti-S specific antibody revealed significant differences in the microheterogeneity of the S protein.
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PMID:Microheterogeneity of S-glycoprotein of mouse hepatitis virus temperature-sensitive mutants. 132 26

Biochemical studies of myelin fractions were undertaken on Lewis rats during various time-points in the development of chronic-relapsing experimental allergic encephalomyelitis (CR-EAE). Lipid and protein composition of myelin fractions obtained by sucrose density gradient centrifugation at 10, 19, 24, and 66 d postinduction (pi) were determined by high-performance thin-layer chromatography (HPTLC) and sodium dodecyl sulfate-polyacrilamide gel electrophoresis (SDS PAGE), respectively. When comparing the myelin fractions of CR-EAE affected animals with those of controls, main differences were observed at 10 d pi. These changes were particularly evident in the light myelin fraction, where a decrease in the percentage of phosphatidylethanolamine and small basic protein relative to the total lipids and proteins of the fraction were observed. At 19 and 24 d pi no biochemical differences were present in both fractions. At 66 d pi, differences in the lipid composition were observed again only in the light myelin fraction. These findings suggest that the light myelin fraction is the most sensitive, particularly at the early stages of the disease, and must play a key role in demyelinating processes.
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PMID:Biochemical changes in central nervous system membranes in chronic-relapsing experimental allergic encephalomyelitis. 209 67

Metachromatic leukodystrophy (MLD) is an autosomal recessive progressive demyelination disorder caused by the deficiency of arylsulfatase A (ASA). However, there exist individuals with low ASA activity without clinical symptoms. This state is described as ASA pseudodeficiency (PD). A number of patients with low ASA activity and various neuropsychiatric symptoms have been observed. It is controversial to what extent low ASA activity predisposes for neurological and/or psychiatric symptomatology. Therefore, persons with low ASA activity who were collected from a large-scale screening among neuropsychiatric patients and healthy controls are presently being extensively evaluated using biochemical, genetic, and clinical methods. Here we present a female patient, who had been first hospitalized with the diagnosis encephalomyelitis disseminata. Her ASA activity determined in fibroblast extracts is intermediate between adult MLD and PD. Sulfatide degradation in cultured fibroblasts is diminished. The subunit pattern obtained after SDS-polyacrylamide gel electrophoresis and immunoblotting was determined in the index patient and 2 sibs. It is compatible with a compound genotype ASA-/ASAp in the index case. It appears probable that in this patient low ASA activity leads to the accumulation of sulfatide and either causes the appearance of neuropsychiatric symptoms or at least contributes to the demyelination process.
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PMID:Probable metachromatic leukodystrophy/pseudodeficiency compound heterozygote at the arylsulfatase A locus with neurological and psychiatric symptomatology. 290 25

We have previously shown that astrocytes produce and secrete plasminogen activator (PA) and that this function is responsive to various modulating agents. When astrocyte conditioned medium (CM) is subjected to SDS-PAGE and PA activity localized by fibrin-agar gel overlay, the activity in the CM is found to comigrate with control t-PA. On affinity chromatography CM PA specifically binds to t-PA antibody. The latter also inhibits fibrinolytic activity of CM PA. When incubated with a fibrin clot, CM PA activity can be shown to bind to fibrin. These observations help identify the enzyme in astrocyte CM as t-PA. A possible role of astrocyte PA in myelin injury could provide an explanation for the previously observed correlation between fibrin deposition and demyelination as well as inhibition of demyelination by ancrod and heparin in experimental allergic encephalomyelitis.
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PMID:Characterization of astrocyte plasminogen activator. 311 79

Experimental allergic encephalomyelitis (EAE) was successfully induced in BALB/c mice with DM-20, a protein component of proteolipid apoprotein. DM-20 was separated by ion exchange column chromatography with CM-Trisacryl from proteolipid apoprotein obtained from bovine spinal cords. Its purity was ascertained by SDS-polyacrylamide gel electrophoresis, a dot immunobinding procedure, and amino acid analysis. Nine of 15 animals with a single injection of 100 micrograms of DM-20 and five of seven animals with a booster injection developed hind leg paralysis or axial rotatory movement 16 to 27 days after sensitization (mean 21.3 days). Five of the 14 animals relapsed 2 to 6 wk after the first attack. Histological examination revealed inflammatory lesion, with significant demyelination in the central nervous system. Antibody levels to DM-20 were not related to the clinical signs. Five of 11 BALB/c nude mice reconstituted with T cells developed similar clinical and pathologic signs. This DM-20-induced EAE in mice may provide a valuable model because it is similar to multiple sclerosis and because it can be induced in inbred mice in which immune mechanisms can be easily studied.
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PMID:DM-20, a proteolipid apoprotein, is an encephalitogen of acute and relapsing autoimmune encephalomyelitis in mice. 349 Nov 50

Retinal S antigen is a potent autoantigen used for the induction of experimental allergic uveoretinitis (EAU). EAU is an organ-specific disease and shows many similarities to other autoimmune diseases such as experimental encephalomyelitis. This paper describes the preparation of highly purified S antigen by using a one-step ion-exchange method. High yields of the protein were obtained. S antigen prepared by this method induces a prolonged posterior uveoretinitis with cellular infiltration in the vitreous and specific loss of retinal photoreceptor cells. The purity of the protein was checked by silver-stained SDS-polyacrylamide gels and immunoblotting techniques.
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PMID:A simplified method for the isolation of highly purified bovine retinal S antigen. 380 62

Experimental allergic neuritis has been produced in the inbred Lewis rat in the absence of experimental allergic encephalomyelitis (EAE) using bovine intradural root myelin. The lack of EAE is probably because P1 is only weakly encephalitogenic in the rat. One of the basic proteins of bovine peripheral myelin, P2, was isolated and demonstrated to be pure by amino acid analysis and SDS PAGE. It was found to have a molecular weight of 15,400 and contained 4 mol 1/2-cystine/mol. This P2 was found to be highly neuritogenic and is probably the sole neuritogenic antigen in this system. The successful demonstration of its neuritogenicity must be due in large part to the use of the inbred Lewis rat and bovine P2, but an explanation could also involve the omission of denaturing organic solvents, the prevention of oxidative denaturation and presumably the fact that any changes which may occur are not sufficient to prevent recognition of the active site by the immune system of the inbred Lewis rat. P2 was neuritogenic down to 5 micrograms/animal. Its activity was enhanced by but not dependent on the presence of Mycobacterium in the adjuvant. This suggested that release of P2 could possibly break tolerance and produce an auto-immune disease such as the Guillain--Barre syndrome.
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PMID:Experimental allergic neuritis in the Lewis rat: characterization of the activity of peripheral myelin and its major basic protein,P2. 615 87


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