Metabolically dependent blood-brain barrier breakdown in chronic relapsing experimental allergic encephalomyelitis
Acta Neuropathologica, ISSN: 0001-6322, Vol: 83, Issue: 6, Page: 630-635
1992
- 25Citations
- 9Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations25
- Citation Indexes25
- 25
- CrossRef15
- Captures9
- Readers9
Article Description
We have studied chronic relapsing experimental allergic encephalomyelitis (CREAE), a model of immune-mediated demyelination, using gadolinium (Gd)-enhanced magnetic resonance imaging in vivo and the bood-brain barrier (BBB) markers, lanthanum nitrate and Gd nitrate, histologically. In regions of the spinal cord showing Gd enhancement, there was evidence for vesicular transport as a mechanism of BBB breakdown in CREAE, shown by an increased number of endiothelial vesicles containing lanthanide (lanthanum or Gd, whichever had been perfused) and deposition of tracer in the perivascular space; tight interendothelial junctions remained intact. Prior perfusion with 2,4-dinitrophenol, a metabolic inhibitor, suppressed the appearance of endothelial vesicles containing lanthanide and tracer in the perivascular space. We conclude that an important contribution to BBB breakdown in CREAE is mediated by a metabolic change in the endothelial cells associated with increased vesicular transport. © 1992 Springer-Verlag.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0026752465&origin=inward; http://dx.doi.org/10.1007/bf00299413; http://www.ncbi.nlm.nih.gov/pubmed/1636379; http://link.springer.com/10.1007/BF00299413; http://www.springerlink.com/index/pdf/10.1007/BF00299413; http://www.springerlink.com/index/10.1007/BF00299413; https://dx.doi.org/10.1007/bf00299413; https://link.springer.com/article/10.1007/BF00299413
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