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
2017 ◽  
Vol 38 (6) ◽  
pp. 1047-1059 ◽  
Author(s):  
Joanne O Davidson ◽  
Vittoria Draghi ◽  
Sean Whitham ◽  
Simerdeep K Dhillon ◽  
Guido Wassink ◽  
...  

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.


2000 ◽  
Vol 41 (1) ◽  
pp. 111 ◽  
Author(s):  
C.E. Young ◽  
P. Falkai ◽  
W.G. Honer

1995 ◽  
Vol 42 (1) ◽  
pp. 41-53 ◽  
Author(s):  
M. R. M. Ursell ◽  
J. McLaurin ◽  
D. D. Wood ◽  
C. A. Ackerley ◽  
M. A. Moscarello ◽  
...  

2021 ◽  
pp. 1-6
Author(s):  
Camilla Omann ◽  
Kendall M. Lawrence ◽  
Mallory L. Hunt ◽  
James K. Moon ◽  
Jamuna Buchanan ◽  
...  

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.


1981 ◽  
Vol 27 (5) ◽  
pp. 742-744 ◽  
Author(s):  
W B Macklin ◽  
M B Lees ◽  
S R Cohen ◽  
S B Ayella

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.


Data in Brief ◽  
2017 ◽  
Vol 10 ◽  
pp. 438-443 ◽  
Author(s):  
Eric H. Chang ◽  
Miklos Argyelan ◽  
Manisha Aggarwal ◽  
Toni-Shay S. Chandon ◽  
Katherine H. Karlsgodt ◽  
...  

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