Linked Life Data

8902730

Source:http://linkedlifedata.com/resource/pubmed/id/8902730

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1997-2-7
pubmed:abstractText
Nitric oxide (NO) may be involved in myelin and oligodendrocyte injury associated with multiple sclerosis (MS), a demyelinating disease of unknown etiology. The cerebrospinal fluid (CSF) from MS patients may provide an important signal inducing a pathologic process within the central nervous system (CNS). To investigate this question, CSF-induced NO production by glial cells was studied in 38 patients with multiple sclerosis (MS), 30 patients with other CNS inflammatory diseases (ID) and 20 with tension headache (TH) as control. Neuron damage was estimated by release of lactate dehydrogenase (LDH), whereas oligodendrocyte damage was estimated by a percentage of viable cells in primary oligodendrocyte cultures. Here we show that CSFs from 13/38 (34%) patients with MS stimulate glial cells to produce NO, compared to 2/20 (10%) of patients with ID and 1/30 (3%) with tension headache. The levels of NO production correlated positively with the amounts of LDH released and negatively with percentage of viable oligodendrocytes, suggesting that NO may represent a mechanism for oligodendrocyte losses in affected tissues and play a role in lesion formation in MS and its animal model experimental allergic encephalomyelitis (EAE).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-510X
pubmed:author
pubmed:issnType
Print
pubmed:volume
142
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
114-20
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
The cerebrospinal fluid from patients with multiple sclerosis promotes neuronal and oligodendrocyte damage by delayed production of nitric oxide in vitro.
pubmed:affiliation
Division of Neurology, Karolinska Institute, Huddinge Hospital, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't