| pubmed-article:16186357 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16186357 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:16186357 | lifeskim:mentions | umls-concept:C0027745 | lld:lifeskim |
| pubmed-article:16186357 | lifeskim:mentions | umls-concept:C1882801 | lld:lifeskim |
| pubmed-article:16186357 | lifeskim:mentions | umls-concept:C0301630 | lld:lifeskim |
| pubmed-article:16186357 | lifeskim:mentions | umls-concept:C0815279 | lld:lifeskim |
| pubmed-article:16186357 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:16186357 | pubmed:dateCreated | 2005-9-27 | lld:pubmed |
| pubmed-article:16186357 | pubmed:abstractText | The signaling of retinal ganglion cell (RGC) death after axotomy is partly dependent on the generation of reactive oxygen species. Shifting the RGC redox state toward reduction is protective in a dissociated mixed retinal culture model of axotomy. The hypothesis for the current study was that tris(2-carboxyethyl)phosphine (TCEP), a sulfhydryl reductant, would protect RGCs in a rat optic nerve crush model of axotomy. | lld:pubmed |
| pubmed-article:16186357 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16186357 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16186357 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16186357 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16186357 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16186357 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16186357 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:16186357 | pubmed:issn | 0146-0404 | lld:pubmed |
| pubmed-article:16186357 | pubmed:author | pubmed-author:LevinLeonard... | lld:pubmed |
| pubmed-article:16186357 | pubmed:author | pubmed-author:LievenChristo... | lld:pubmed |
| pubmed-article:16186357 | pubmed:author | pubmed-author:SchlieveChris... | lld:pubmed |
| pubmed-article:16186357 | pubmed:author | pubmed-author:SwansonKyle... | lld:pubmed |
| pubmed-article:16186357 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16186357 | pubmed:volume | 46 | lld:pubmed |
| pubmed-article:16186357 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16186357 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16186357 | pubmed:pagination | 3737-41 | lld:pubmed |
| pubmed-article:16186357 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:16186357 | pubmed:meshHeading | pubmed-meshheading:16186357... | lld:pubmed |
| pubmed-article:16186357 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16186357 | pubmed:articleTitle | Neuroprotective effect of sulfhydryl reduction in a rat optic nerve crush model. | lld:pubmed |
| pubmed-article:16186357 | pubmed:affiliation | Department of Ophthalmology and Visual Science, University of Wisconsin Medical School, Madison, 53792, USA. | lld:pubmed |
| pubmed-article:16186357 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16186357 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:16186357 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16186357 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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