Linked Life Data

17465388

Source:http://linkedlifedata.com/resource/pubmed/id/17465388

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Suppl
pubmed:dateCreated
2007-4-30
pubmed:abstractText
The devastating neurological deficit associated with myelomeningocele has previously been assumed to be a direct and inevitable consequence of the primary malformation-failure of neural tube closure. An alternative view is that secondary damage to the pathologically exposed spinal cord tissue in utero is responsible for the neurological deficiency. If the latter mechanism were shown to be correct, it would provide an objective rationale for the performance of in utero surgery for myelomeningocele, because coverage of the exposed spinal cord could be expected to alleviate or perhaps prevent neurodegeneration. To examine this question, the authors studied the development of neuronal connections and neurological function of mice during fetal and neonatal stages in a genetic model of exposed lumbosacral spina bifida.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3085
pubmed:author
pubmed:issnType
Print
pubmed:volume
106
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
213-21
pubmed:dateRevised
2007-8-13
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Fetal spina bifida in a mouse model: loss of neural function in utero.
pubmed:affiliation
Department of Pediatric Surgery, University Children's Hospital Zurich, Switzerland. stiefel_d@yahoo.co.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't