Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Actively demyelinating central nervous system (CNS) lesions from a patient with acute multiple sclerosis (MS) were tested for measles antigens using peroxidase-conjugated antimeasles antibody. No evidence of measles antigens was found. Similarly reacted tissue from 2 patients with chronic MS also revealed no evidence of measles antigens. Identically treated and simultaneously tested measles-infected CNS cultures and human SSPE brain tissue stained strongly for measles antigens. The possible reasons underlying the failure to detect measles antigens in MS are discussed.
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PMID:Immunocytochemical studies for the localisation of measles antigens in multiple sclerosis plaques and measles virus-infected CNS tissue. 33 59

The vascular permeability in the nervous system to Evans blue-albumin and horseradish peroxidase was studied in chronic relapsing EAE in strain 13 and Hartley guinea pigs. The disease was induced by single sensitization of immature animal and was characterized clinically by remissions and relapses. Recent and old demyelinating plaques in the spinal cord were present. These showed an increased permeability to the protein tracers. The blood-brain barrier in these plaques are therefore disturbed and also in this respect the condition is similar to the multiple sclerosis lesions.
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PMID:Chronic relapsing experimental allergic encephalomyelitis. Studies in vascular permeability changes. 90 1

Alterations in normal function of the blood-brain barrier (BBB) are important in the pathophysiology of multiple sclerosis and its laboratory counterpart, experimental autoimmune encephalomyelitis (EAE). As part of studies on drugs that affect vascular tone in rats with EAE, we have shown previously that the specific alpha 1-adrenoreceptor antagonist, prazosin, suppressed clinical and pathologic disease. In the present study we used quantitative morphometric analysis of capillary endothelium and the tracer horseradish peroxidase (HRP) to define effects of this drug on vascular events associated with central nervous system edema. In prazosin-treated and saline-treated EAE rats, protein extravasation in the spinal cord correlated with clinical presentation. Consistent with our previous data, the results showed that increased edema was associated with increased vesicular content of capillary endothelium. In prazosin-treated rats with no clinical signs, vesicular content was comparable to that found in normal animals. With increasing severity of disease, vesicular content increased and mitochondrial content decreased. In both prazosin- and saline-treated rats, mitochondrial content was reduced even when clinical signs were slight, and sharply declined when clinical signs increased. These results suggest that damage to mitochondria may be associated with early pathological events. In prazosin-treated animals, HRP accumulated in pericytes, suggesting that these cells were a target for the action of prazosin and may restrict the extravasation of fluid into the perivascular parenchyma. Our results underscore the presence of capillary changes associated with inflammation of the central nervous system, in addition to the well-recognized cellular inflammation that is targeted to the venular bed. The extent of capillary changes was closely associated with extent of tracer leakage in the spinal cord and support the conclusion that transcytotic vesicles are involved in transport of edema fluid during EAE, and that high mitochondrial levels are important for the normal function of BBB endothelium.
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PMID:Effects of prazosin on the blood-brain barrier during experimental autoimmune encephalomyelitis. 145 Sep 49

Phytohemagglutinin-induced lymphocyte activation sequence was studied in monozygotic and dizygotic discordant multiple sclerosis (MS) twin pairs in a quiescent disease phase. The study group included all available 11 pairs listed in a nation-wide twin register. Lymphocyte activation markers, DNA synthesis and gamma-interferon secretion were studied using avidin-biotin-peroxidase complex (ABC) stainings, [3H]thymidine incorporation, and a solid-phase double-antibody immunoradiometric assay (IRMA), respectively. The level and kinetics of interleukin-2 receptor expression, DNA synthesis, gamma-interferon secretion, and major histocompatibility complex (MHC) locus II antigen expression were similar (Wilcoxon's test for paired samples) in both the diseased and healthy monozygotic and dizygotic twins. Our results suggest that the cell-mediated immune system may not be primarily at fault, but rather that both MS itself and its exacerbations are caused by an unknown triggering stimulus facing a properly functioning immune system.
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PMID:Lymphocyte activation in discordant multiple sclerosis twin pairs. 169 Jul 51

Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease. It is widely used as an animal model of multiple sclerosis (MS). We studied the prophylactic effects of FK 506 electrophysiologically and immunohistochemically in acute EAE. Female Lewis rats were sensitized with guinea pig spinal cord in complete Freund's adjuvant. FK 506 suspended in distilled water was orally administered at 1.0, 3.2, 5.0 or 10.0 mg/kg per day for 12 successive days starting from the day of sensitization. A placebo was used as the control. Administration of FK 506 at doses of 3.2 mg/kg per day and over significantly delayed the onset of clinical signs. However, the FK 506 group showed a relapse or a chronic state following the onset of EAE. We made a time course recording of cortical somatosensory evoked potential (cortical SEP: P 15). P 15 latency in the placebo group was significantly delayed in accordance with the clinical signs and showed immediate improvement upon recovery. Prolongation of P 15 latency in the FK 506 group also occurred concomitantly with the clinical signs, but the delay continued after the loss of symptoms as well. After the onset of EAE, the infiltrating lymphocyte subset was examined by the avidin-biotin peroxidase complex (ABC) method in the lumbar spinal cord. In the placebo group, the number of OX3+ (Ia) cells and the W 3 25+: OX8+ (helper/inducer T: suppressor/cytotoxic T) ratio clearly reflected the development and remission of EAE. In the FK 506 group, however, increases in OX8+ lymphocytes were observed irrespective of clinical sign fluctuation, and there were corresponding decreases in the W 3/25+: OX8+ ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of novel immunosuppressant FK 506 in acute experimental allergic encephalomyelitis]. 169 82

Intrathecally produced antibodies specific for the infectious agent can be shown by immunoblot. A quantification is practicable by titration. Densitometric evaluation of the immunoblot by a new technique, IDEA (immunoblot for densitometric estimation of antibodies), does not only render titration unnecessary, but also has the advantage of presenting the differentiated local immune response against individual antigens of the infectious agent. Preliminary studies for the densitometric evaluation were performed with a measles virus immunoblot which had been developed with a cerebrospinal fluid (CSF) sample of a patient suffering from multiple sclerosis containing high antibody titers. A peroxidase-labeled anti-immunoglobulin antibody had been added. The intensity of the color reaction on the membrane dependent on the antibody concentration follows a saturation kinetics comparable to the Michaelis-Menten kinetics in enzymology. Thus, indices for the intrathecal antibody synthesis of each individual viral antigen can be calculated by taking the permeability of the blood-CSF barrier into consideration. This method is illustrated in a patient with zoster meningoencephalitis.
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PMID:Immunoblot for densitometric estimation of antibodies (IDEA): a useful method for quantification of intrathecally produced antibodies against individual antigens in infectious diseases of the central nervous system. 191 24

The non-specific peroxidase (donor: H2O2-oxidoreductase, EC 1.11.1.7) activity of red blood cells in patients with multiple sclerosis, patients with other neurological diseases, and healthy control individuals was investigated. To this end, a simple method was developed. No significant difference was found in the non-specific peroxidase activity of red blood cells from patients with multiple sclerosis and controls.
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PMID:Non-specific peroxidase (donor: H2O2-oxidoreductase, EC 1.11.1.7) activity in multiple sclerosis. 196 28

We studied anti-oligodendrocyte antibody in sera and CSF from patients with multiple sclerosis (MS) and other neurological diseases (OND) by enzyme-linked immunosorbent assay (ELISA). Oligodendrocytes were isolated by percoll density gradient from brains of 4 week-old rat and cultured in poly-1-lysine-coated 96 well microwell plate. After overnight culture, oligodendrocytes were fixed in 0.5% glutaraldehyde and stored at -20 degrees C. ELISA was performed using peroxidase-conjugated goat anti-human IgG (Fab')2 as usual. Serum and CSF were examined at dilution of 1:400 and 1:2 respectively, and O.D. was read at 490 nM. In sera from patients with MS and OND, the titer of anti-oligodendrocyte antibody was significantly higher than those from normal controls. However, there was no significant difference between MS and OND. Significantly higher titer of anti-oligodendrocyte antibody was observed in CSF from patients with meningoencephalitis and polyradiculoneuropathy. However, comparing CSF anti-oligodendrocyte antibody per CSF IgG, there was no significant difference among each group. There was no significant correlation between the cytotoxicity index of sera and anti-oligodendrocyte antibody level. There might be additional cytotoxic factor other than anti-oligodendrocyte antibody. Our data support the idea anti-oligodendrocyte antibody is not specific to MS, and the role of anti-oligodendrocyte antibody in the pathogenesis of MS is secondary.
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PMID:[The study of anti-oligodendrocyte antibody in sera, and CSF of patients with multiple sclerosis]. 236 27

To detect immunoglobulin G (IgG) oligoclonal bands in unconcentrated cerebrospinal fluid (CSF) we used a recently developed method combining agarose isoelectric focusing (IEF) and double immunofixation peroxidase staining with Avidin-Biotin amplification. We studied 65 CSF and serum paired specimens from normals, multiple sclerosis (MS), other neurological diseases (OND) and benign monoclonal gammopathies (BMG). We found that the oligoclonal IgG pattern can be demonstrated after IEF of 15 microliter of CSF specimens with an IgG concentration of 15 mg/L. In 98% of CSF from patients with clinically definite MS a sharp oligoclonal band pattern was detected. The reliability and the sensitivity of this powerful technique is compared to agarose IEF of concentrated CSF, followed by Coomassie Brilliant Blue staining. This method constitutes a real improvement in the detection of CSF IgG oligoclonal bands because it avoids CSF concentration and allows the detection of IgG bands only.
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PMID:Detection of IgG oligoclonal bands in unconcentrated CSF by means of agarose isoelectric focusing, double immunofixation peroxidase staining and avidin-biotin amplification. 241 79

Unconcentrated cerebrospinal fluid (CSF) and corresponding serum from 30 patients with multiple sclerosis (MS), 30 with other neurological disease and 30 controls suffering from tension headache or psychoneurosis, were examined for oligoclonal IgG bands by initial separation employing agarose isoelectric focusing (AIF) followed by a modified procedure of immunofixation with monospecific antiserum and silver staining. This method is specific for demonstration of IgG and has a limit for detection of 0.4 microgram of IgG. Comparing the results with those obtained by AIF followed by capillary blotting to nitrocellulose membrane, double antibody peroxidase labeling and avidin-biotin amplification, both methods revealed similar frequencies of positive findings for oligoclonal IgG bands in the three patient groups. AIF followed by antiserum immunofixation and silver staining is a simple, sensitive and specific method for detection of oligoclonal IgG in unconcentrated CSF.
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PMID:Agarose isoelectric focusing, antiserum immunofixation and silver staining for detection of oligoclonal bands in unconcentrated cerebrospinal fluid. 242 67


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