Hydrophobic compounds interfere in radioimmunoassay for basic protein in myelin.

1981 ◽  
Vol 27 (5) ◽  
pp. 742-744 ◽  
Author(s):  
W B Macklin ◽  
M B Lees ◽  
S R Cohen ◽  
S B Ayella
Keyword(s):  
White Matter ◽  
Stearic Acid ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Gm1 Ganglioside ◽  
Hydrophobic Compounds ◽  
Low Concentrations ◽  
High Concentrations ◽  
Protein Assays

Abstract Hydrophobic compounds influenced the accuracy of the radioimmunoassay for myelin basic protein when lipids (stearic acid, phosphatidylcholine, cholesterol, cerebroside, sulfatide, or GM1 ganglioside) or proteolipids (white-matter proteolipid apoprotein, kidney proteolipid apoproteins, or heart proteolipid apoproteins) were added to a known amount of basic protein and the samples assayed. All of these interfere with the assay, but the direction of the error depends on the quantity added: low concentrations of lipid decrease apparent basic protein, high concentrations enhance it. Obviously, results of basic-protein assays must be interpreted carefully.

scholarly journals Proteolytic and peroxidatic reactions of commercial horseradish peroxidase with myelin basic protein

1978 ◽  
Vol 169 (3) ◽  
pp. 567-575 ◽  
Author(s):  
Wendy Cammer ◽  
Lesley Z. Bieler ◽  
William T. Norton
Keyword(s):  
Horseradish Peroxidase ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Protein A ◽  
Low Molecular Weight ◽  
Basic Proteins ◽  
Molecular Weights ◽  
Low Concentrations ◽  
High Concentrations ◽  
A Minor

Degradation of myelin basic protein during incubations with high concentrations of horseradish peroxidase has been demonstrated [Johnson & Cammer (1977) J. Histochem. Cytochem.25, 329–336]. Possible mechanisms for the interaction of the basic protein with peroxidase were investigated in the present study. Because the peroxidase samples previously observed to degrade basic protein were mixtures of isoenzymes, commercial preparations of the separated isoenzymes were tested, and all three degraded basic protein, but to various extents. Three other basic proteins, P2 protein from peripheral nerve myelin, lysozyme and cytochrome c, were not degraded by horseradish peroxidase under the same conditions. Inhibitor studies suggested a minor peroxidatic component in the reaction. Therefore the peroxidatic reaction with basic protein was studied by using low concentrations of peroxidase along with H2O2. Horseradish peroxidase plus H2O2 caused the destruction of basic protein, a reaction inhibited by cyanide, azide, ferrocyanide, tyrosine, di-iodotyrosine and catalase. Lactoperoxidase plus H2O2 and myoglobin plus H2O2 were also effective in destroying the myelin basic protein. Low concentrations of horseradish peroxidase plus H2O2 were not active against other basic proteins, but did destroy casein and fibrinogen. Although high concentrations of peroxidase alone degraded basic protein to low-molecular-weight products, suggesting the operation of a proteolytic enzyme contaminant in the absence of H2O2, incubations with catalytic concentrations of peroxidase in the presence of H2O2 converted basic protein into products with high molecular weights. Our data suggest a mechanism for the latter, peroxidatic, reaction where polymers would form by linking the tyrosine side chains in basic-protein molecules. These data show that the myelin basic protein is unusually susceptible to peroxidatic reactions.

scholarly journals How long is sufficient for optimal neuroprotection with cerebral cooling after ischemia in fetal sheep?

2017 ◽  
Vol 38 (6) ◽  
pp. 1047-1059 ◽  
Author(s):  
Joanne O Davidson ◽  
Vittoria Draghi ◽  
Sean Whitham ◽  
Simerdeep K Dhillon ◽  
Guido Wassink ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Ischemia ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Close Association ◽  
Global Cerebral Ischemia ◽  
Fetal Sheep ◽  
Head Cooling ◽  
Improved Outcomes ◽  
Eeg Power

The optimal duration of mild “therapeutic” hypothermia for neonates with hypoxic-ischemic encephalopathy is surprisingly unclear. This study assessed the relative efficacy of cooling for 48 h versus 72 h. Fetal sheep (0.85 gestation) received sham ischemia (n = 9) or 30 min global cerebral ischemia followed by normothermia (n = 8) or delayed hypothermia from 3 h to 48 h (n = 8) or 72 h (n = 8). Ischemia was associated with profound loss of electroencephalogram (EEG) power, neurons in the cortex and hippocampus, and oligodendrocytes and myelin basic protein expression in the white matter, with increased Iba-1-positive microglia and proliferation. Hypothermia for 48 h was associated with improved outcomes compared to normothermia, but a progressive deterioration of EEG power after rewarming compared to 72 h of hypothermia, with impaired neuronal survival and myelin basic protein, and more microglia in the white matter and cortex. These findings show that head cooling for 48 h is partially neuroprotective, but is inferior to cooling for 72 h after cerebral ischemia in fetal sheep. The close association between rewarming at 48 h, subsequent deterioration in EEG power and increased cortical inflammation strongly suggests that deleterious inflammation can be reactivated by premature rewarming.

Increased myelin basic protein in BA 10 white matter in schizophrenia

2000 ◽  
Vol 41 (1) ◽  
pp. 111 ◽  
Author(s):  
C.E. Young ◽  
P. Falkai ◽  
W.G. Honer
Keyword(s):  
White Matter ◽  
Myelin Basic Protein ◽  
Basic Protein

scholarly journals Myelin basic protein autoantibodies, white matter disease and stroke outcome

2012 ◽  
Vol 252 (1-2) ◽  
pp. 106-112 ◽  
Author(s):  
Dean Shibata ◽  
Kevin Cain ◽  
Patricia Tanzi ◽  
Dannielle Zierath ◽  
Kyra Becker
Keyword(s):  
White Matter ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
White Matter Disease ◽  
Stroke Outcome

N.M.R. Studies of Myelin Basic Protein. III. Interactions of the Protein with Lipid Micelles by 1H and 31P N.M.R.

1979 ◽  
Vol 32 (12) ◽  
pp. 2631 ◽  
Author(s):  
LAT Littlemore ◽  
RW Ledeen
Keyword(s):  
Myelin Basic Protein ◽  
Conformational Changes ◽  
Basic Protein ◽  
Polypeptide Chain ◽  
Lipid Binding ◽  
Bovine Brain ◽  
Gm1 Ganglioside ◽  
Spectral Changes ◽  
Central Regions ◽  
Lipid Micelles

The interactions of bovine myelin basic protein with bovine brain GM1 ganglioside and with lysophosphatidylcholine have been followed by 1H and 31P N.M.R. The effect of the binding of lipid on the protein spectrum could be followed in methyl peaks due to methionine and NG-methylarginine and in peaks from aromatic side chains. Both lipids caused broadening of methyl resonances from methionine-20, the unique NG-methylarginine and phenylalanines. The N.M.R. spectral changes on interaction of peptides derived from N-terminal and C-terminal halves of the protein with lysolecithin indicated that the lipid binding was associated with conformational changes involving the central regions of the polypeptide chain and the methylarginine residue. The 31P spectra suggest that the average phosphate group in lysophosphatidylcholine becomes more mobile as a result of binding of basic protein to the lipid micelle.

Localization and partial characterization of a 60 kDa citrulline-containing transport form of myelin basic protein from MO3-13 cells and human white matter

1995 ◽  
Vol 42 (1) ◽  
pp. 41-53 ◽  
Author(s):  
M. R. M. Ursell ◽  
J. McLaurin ◽  
D. D. Wood ◽  
C. A. Ackerley ◽  
M. A. Moscarello ◽  
...  
Keyword(s):  
White Matter ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Partial Characterization ◽  
Transport Form

Chronic foetal hypoxaemia does not cause elevation of serum markers of brain injury

2021 ◽  
pp. 1-6
Author(s):  
Camilla Omann ◽  
Kendall M. Lawrence ◽  
Mallory L. Hunt ◽  
James K. Moon ◽  
Jamuna Buchanan ◽  
...  
Keyword(s):  
Brain Injury ◽  
White Matter ◽  
Glial Fibrillary Acidic Protein ◽  
Myelin Basic Protein ◽  
Oxygen Delivery ◽  
Basic Protein ◽  
Elevated Serum ◽  
Serum Levels ◽  
Acidic Protein ◽  
Protein Serum

Abstract Objectives: The objective of this study was to investigate changes in serum biomarkers of acute brain injury, including white matter and astrocyte injury during chronic foetal hypoxaemia. We have previously shown histopathological changes in myelination and neuronal density in fetuses with chronic foetal hypoxaemia at a level consistent with CHD. Methods: Mid-gestation foetal sheep (110 ± 3 days gestation) were cannulated and attached to a pumpless, low-resistance oxygenator circuit, and incubated in a sterile fluid environment mimicking the intrauterine environment. Fetuses were maintained with an oxygen delivery of 20–25 ml/kg/min (normoxemia) or 14–16 ml/kg/min (hypoxaemia). Myelin Basic Protein and Glial Fibrillary Acidic Protein serum levels in the two groups were assessed by ELISA at baseline and at 7, 14, and 21 days of support. Results: Based on overlapping 95% confidence intervals, there were no statistically significant differences in either Myelin Basic Protein or Glial Fibrillary Acidic Protein serum levels between the normoxemic and hypoxemic groups, at any time point. No statistically significant correlations were observed between oxygen delivery and levels of Myelin Basic Protein and Glial Fibrillary Acidic Protein. Conclusion: Chronic foetal hypoxaemia during mid-gestation is not associated with elevated serum levels of acute white matter (Myelin Basic Protein) or astrocyte injury (Glial Fibrillary Acidic Protein), in this model. In conjunction with our previously reported findings, our data support the hypothesis that the brain dysmaturity with impaired myelination found in fetuses with chronic hypoxaemia is caused by disruption of normal developmental pathways rather than by direct cellular injury.

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