| pubmed-article:16817642 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16817642 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:16817642 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:16817642 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
| pubmed-article:16817642 | lifeskim:mentions | umls-concept:C1272745 | lld:lifeskim |
| pubmed-article:16817642 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
| pubmed-article:16817642 | pubmed:dateCreated | 2006-7-4 | lld:pubmed |
| pubmed-article:16817642 | pubmed:abstractText | Experimental autoimmune encephalomyelitis (EAE) animal models is an autoimmune demyelinating disease of the central nervous system, which is widely accepted as an animal for human multiple sclerosis (MS). Ependymal cells line the spinal canal and cerebral ventricles and proliferate in response to damage. These cells have the potential to differentiate into neural support cells. However, there is controversy as whether the response of the ependymal cells is a result of injury or repair. This study demonstrates using the rat EAE model a proliferative response of the ependymal cells occurred as a result of the disease. Interestingly, a more pronounced ependymal proliferative effect was seen in animals being fed a phase 2 enzyme inducer. The data suggests ependymal cells play a role in the post-inflammatory response of the brain and also may be involved in the remyelination process. | lld:pubmed |
| pubmed-article:16817642 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16817642 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16817642 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16817642 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16817642 | pubmed:issn | 0067-8856 | lld:pubmed |
| pubmed-article:16817642 | pubmed:author | pubmed-author:BenghuzziHH | lld:pubmed |
| pubmed-article:16817642 | pubmed:author | pubmed-author:YunusMohammed... | lld:pubmed |
| pubmed-article:16817642 | pubmed:author | pubmed-author:HamadainElgen... | lld:pubmed |
| pubmed-article:16817642 | pubmed:author | pubmed-author:MohamedAdelA | lld:pubmed |
| pubmed-article:16817642 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16817642 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:16817642 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16817642 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16817642 | pubmed:pagination | 405-9 | lld:pubmed |
| pubmed-article:16817642 | pubmed:dateRevised | 2009-11-11 | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:meshHeading | pubmed-meshheading:16817642... | lld:pubmed |
| pubmed-article:16817642 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16817642 | pubmed:articleTitle | Possible role of ependymal proliferation in improving experimental allergic encephalomyelitis in Lewis rats. | lld:pubmed |
| pubmed-article:16817642 | pubmed:affiliation | Anatomy and Cell Biology, University of Saskatchewan, SK, Canada. | lld:pubmed |
| pubmed-article:16817642 | pubmed:publicationType | Journal Article | lld:pubmed |
