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)

Cellular clone (MAK 14-7), producing antibodies against the virus of Venezuela equine encephalomyelitis (VEE), strain 230, was isolated using the standard hybridomata technology. Monoclonal antibodies neutralized the viral hemagglutinating activity leaving the infectious one intact. Monoclonal antibodies from MAD 14-7 reacted specifically with viral glycoprotein E1 as registered by the immunoprecipitation technique. The topography of antigenic determinants of viral E1/E2 glycoprotein dimer forming the virions outer spikes is discussed in connection with the results obtained.
Mol Gen Mikrobiol Virusol 1985 Aug
PMID:[Identification of monoclonal antibodies against protein E1 of venezuelan equine encephalomyelitis virus blocking the hemagglutinating but not the infective activity of virions]. 384 54

A substrain of the Lewis rat, Lew/Mol, differing from ordinary Lewis rats in that it is hardly susceptible to the induction of experimental autoimmune encephalomyelitis (EAE) is described. The Lew/Mol rats did not mount a host-vs.-graft response towards cells from an EAE-susceptible substrain of Lewis rats (Lew/Mai) and vice versa. This argues against the possibility that the origin of Lew/Mol rats involves accidental cross-breeding with other rat strains. Thus the EAE-resistance in Lew/Mol rats in interpreted as being due to a mutation(s) in a gene(s) regulating the susceptibility to EAE. Specific pathogen-free Lew/Mol rats were more resistant to EAE induction than Lew/Mol rats bred under conventional conditions, emphasizing the importance of environmental factors. Neither cyclophosphamide treatment nor increased age resulted in marked susceptibility in the Lew/Mol rats, although aging apparently had some effect, as a few animals did show neurological signs. Approximately half of (Lew/Mol x Lew/Mai)F1 hybrids developed EAE with neurological signs. In this respect, Lew/Mol rats differ from another recently described EAE-resistant substrain of the Lewis rat (LeR).
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PMID:Low susceptibility to the induction of experimental autoimmune encephalomyelitis in a substrain of the otherwise susceptible Lewis rat. 618 Sep 8

An explanation of experimental allergic encephalomyelitis prevention and suppression is presented based upon evidence that the active unit in disease induction is an encephalitogen-adjuvant complex. The stereochemical complementarity in structure of the encephalitogen and adjuvant is mirrored in complementarity in the recognition sites of lymphocyte populations activated against encephalitogen and adjuvant. Since two complementary lymphocyte populations are necessary for disease induction, any procedure that prevents the development of one of these populations will prevent disease induction. Any procedure that eliminates one population after induction has occurred will suppress the disease. We argue that all extant data support the hypothesis. Several new experiments are proposed to further test it.
Mol Immunol 1983 Feb
PMID:An explanation of prevention and suppression of experimental allergic encephalomyelitis. 618 49

Immunoaffinity chromatography has been developed for the isolation of the human myelin basic protein (MBP). The method is based on the use of a monoclonal antibody which was produced to bovine MBP, cross-reacting with human MBP. The protein isolated from acidic extracts of the brain proteins was shown to be native MBP by its immunochemical reactivity, by its ability to elicit experimental allergic encephalomyelitis and by its mol. wt (18,600 +/- 400). It represented a single-band purity after hypersensitive silver staining. The MBP isolated by the method described represents a higher purity than that of the MBP purified by conventional multistep biochemical separation techniques.
Mol Immunol 1984 Oct
PMID:Isolation of the human myelin basic protein by immunoaffinity chromatography with a monoclonal antibody. 620 61

Cardiovirus specific sequences located in the 5' NTR are used to amplify viral RNA by PCR. General primers were selected for the amplification of cardioviruses, including encephalomyocarditis virus (EMCV), mengovirus and Theiler's murine encephalomyelitis virus (TMEV. Additionally, ECHO virus type 22, an atypical enterovirus, could also be detected with the general cardiovirus primers. An internal encephalomyocarditis virus specific probe and a general cardiovirus probe are used to discriminate EMCV from other cardioviruses. The sensitivity of the PCR was determined at 10 pfu after hybridization with an internal oligonucleotide probe. Specificity was tested with a broad range of picornaviruses and other nonrelated RNA and DNA viruses. The applicability of the assay was demonstrated by the detection of TMEV RNA in tissue samples from experimentally-infected mice.
Mol Cell Probes 1993 Dec
PMID:Molecular identification of cardioviruses by enzymatic amplification. 751 89

To assess the distribution of insulin-like growth-factor-related proteins during autoimmune CNS demyelination and remyelination, experimental autoimmune encephalomyelitis was produced by injecting Lewis rats with an emulsion containing guinea pig spinal cord and complete Freund's adjuvant. Tail weakness appeared at 10-12 days and was followed by hind and forelimb weakness. Paraplegia and incontinence were observed in some animals. From 8-40 days postinoculation (dpi), spinal cord sections were used to correlate lesion location and severity with mRNA distributions of insulin-like growth factor I (IGF-I), IGF-binding protein 2 (IGFBP-2), IGF-I-receptor (IGFR-I), glial fibrillary acidic protein (GFAP), and myelin basic protein (MBP). These were determined semiquantitatively by in situ hybridization. Fourteen dpi, there were inflammatory infiltrates and demyelination in both white matter (WM) and grey matter (GM). IGF-I and GFAP mRNAs were increased in these lesions and transcripts encoding myelin basic protein (MBP) were greatly reduced. Large lesions with extensive demyelination were evident in both WM and GM when mRNA levels of GFAP and IGF-I peaked 26 dpi. MBP mRNA levels began increasing 21 dpi and peaked 26 dpi, when a few thin regenerating myelin sheaths were found morphologically. Astrocytes, identified by their morphology and GFAP immunoreactivity, expressed very low levels of IGFBP-2 mRNA and peptide in normal controls; their levels were significantly higher 14 dpi, peaked 26 dpi, and then gradually decreased. Some neurons, as well as oligodendroglia in areas undergoing remyelination, expressed IGFR-I. Although levels of IGF-I, IGFBP-2, and GFAP mRNAs were highest in lesion areas, levels were also elevated around lesions and in some normal-appearing areas of WM and GM 14-40 dpi. The gene expression of both IGF-I and IGFBP-2 by hypertrophic GFAP-positive astrocytes was demonstrated 14-40 dpi by combined in situ hybridization and immunocytochemistry as well as by double immunostaining. Coexpression of IGF-I and IGFBP-2 in the same astrocyte was a frequent finding. Relative increases in both IGF-I, GFAP, IGFBP-2, IGFR-I, and MBP mRNAs peaked at about the same time. This suggests that during lesion progression and recovery, astrocytic expression of IGF-I-related peptides may reduce immune-mediated myelin injury. We also suggest that astrocytic IGFBP-2 in lesions may help target IGF-I to IGFR-I-expressing oligodendrocytes and promote remyelination of demyelinated axons.
Mol Cell Neurosci 1994 Oct
PMID:Astrocytes express insulin-like growth factor-I (IGF-I) and its binding protein, IGFBP-2, during demyelination induced by experimental autoimmune encephalomyelitis. 752 31

Reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI) are toxic molecules that are thought to play a pathogenic role in many disease states, and data from prior studies indicate a role for ROI and RNI in the pathogenesis of experimental allergic encephalomyelitis (EAE). ROI and RNI can elicit tissue damage by initiating the chain reaction of lipid peroxidation. Lazaroids are a series of compounds that have been shown to interrupt lipid peroxidation. In the present study, the lazaroids, U-74389G and U-83836E, were administered to Lewis rats with EAE in order to evaluate their therapeutic effectiveness. Several different doses and administration routes, which were based on the manufacturer's (Upjohn) recommendations and a prior experimental study, were employed: 1) intraperitoneal injection (IP), 1mg drug/kg body weight, 1x/day from 7-18 days postencephalitogen injection (diseases onset approximately 9 day), male; 2) IP, 1mg/kg, 1x/day from 0-18 days, male; 3) intravenous (IV) cannula, 3mg/kg, 2x/day from 7-18 days, female; 4) IV cannula, 3mg/kg, 2x/day from 7-18 days, male; and 5) IV cannula, 10mg/kg, 2x/day from 7-18 days, female. The weights and clinical signs were evaluated on a daily basis. In all treatment regimens, there was an absence of a statistically significant difference between the vehicle-treated animals and the two groups of drug-treated animals. These data imply that lipid peroxidation may not be an effective therapeutic site in EAE. It is important to note that there are several different types of EAE and our study only explored the EAE model in the Lewis rat.(ABSTRACT TRUNCATED AT 250 WORDS)
Res Commun Mol Pathol Pharmacol 1995 Mar
PMID:Testing lazaroids U-74389G and U-83836E for therapeutic value in experimental allergic encephalomyelitis in the Lewis rat. 762 Aug 28

A set of Theiler's murine encephalomyelitis virus mutants with engineered alterations in the conserved oligopyrimidine/AUG tandem (E. V. Pilipenko, A. P. Gmyl, S. V. Maslova, G. A. Belov, A. N. Sinyakov, M. Huang, T. D. K. Brown, and V. I. Agol, J. Mol. Biol. 241:398-414, 1994) were assayed for their growth potential in BHK-21 cells (as reflected in plaque size) and for neurovirulence upon intracerebral inoculation of mice. Tandem-destroying mutations, which included substitutions in the oligopyrimidine moiety and extended insertions into the oligopyrimidine/AUG spacer, exerted relatively little effect on the plaque size but ensured a high level of attenuation. The attenuated mutants exhibited remarkable genetic stability upon growth in BHK-21 cells. However, the brains of rare animals that developed symptoms after the inoculation with high doses of these mutants invariably contained pseudorevertants with the oligopyrimidine/AUG tandem restored by diverse deletions or an AUG-generating point mutation. The AUG moiety of the tandem in the revertant genomes was represented by either a cryptic codon or initiator codon. The results demonstrate that the tandem, while dispensable for the Theiler's murine encephalomyelitis virus growth in BHK-21 cells, is essential for neurovirulence in mice. Thus, the oligopyrimidine/AUG tandem is a host-dependent cis-acting control element that may be essential for virus replication under certain conditions. The functional activity of the tandem was retained when its oligopyrimidine or AUG moieties were made double stranded. A possible role of the tandem in the cap-independent internal initiation of translation on the picornavirus RNA templates is discussed.
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PMID:Attenuation of Theiler's murine encephalomyelitis virus by modifications of the oligopyrimidine/AUG tandem, a host-dependent translational cis element. 781 54

Regional changes in percent water content, a measure of regional levels of edema, were determined in female Lewis rats during key stages of recurrent experimental autoimmune encephalomyelitis (rEAE). The changes in percent water content of the spinal cord and brainstem closely paralleled the clinical and, to a lesser extent, histological course of rEAE (increasing during exacerbations and decreasing during remissions), whereas the percent water content of the forebrain, thalamus/midbrain, hypothalamus, and cerebellum remained constant and equal to control levels at all stages of the disease process. These results suggest that edema formation and resolution in the brainstem and spinal cord may be significant determinants of the transient and recurrent course of neurological dysfunction exhibited by rats with rEAE.
Mol Chem Neuropathol 1994 Aug
PMID:Changes in brain and spinal cord water content during recurrent experimental autoimmune encephalomyelitis in female Lewis rats. 799 27

Initiation of translation on picornaviral RNA templates occurs via cap-independent ribosome binding to a cis-acting element, internal ribosome entry site (IRES). Mapping of the starting point of translation relative to the IRES was attempted using Theiler's murine encephalomyelitis virus (TMEV) RNA as a model. The possibility that the starting point is determined by the conserved oligopyrimidine upstream of the initiator codon was studied. In contrast to poliovirus, neither the conserved oligopyrimidine nor an AUG at a fixed distance downstream of this oligopyrimidine are required for efficient translation of the TMEV RNA in Krebs-2 extracts or reticulocyte lysates or for viral infectivity; mutants lacking the oligopyrimidine/AUG tandem were stable upon passage in BHK-21 cells. A short template segment, the starting window, was defined, wherefrom ribosomes begin translation or downstream scanning depending, respectively, on the presence or absence of a good-context AUG within this window. Using a collection of the engineered TMEV mutant RNAs, the starting window was mapped to 16-17 nt downstream of the IRES and was found to be approximately a dozen nt long. The efficiency of translation initiation from an AUG linearly increased upon the 5'-->3' displacement of the initiator codon within the window. The competence of the starting window did not appear to depend markedly on its primary structure; however, it was completely inactivated ("closed") with concomitant dramatic inhibition of total protein synthesis upon conversion of the corresponding RNA segment into a double-stranded form.
J Mol Biol 1994 Aug 19
PMID:Starting window, a distinct element in the cap-independent internal initiation of translation on picornaviral RNA. 806 56


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