Source:http://linkedlifedata.com/resource/pubmed/id/19949279
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2009-12-1
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| pubmed:abstractText |
A mouse model of spinal muscular atrophy with respiratory distress (SMARD1) was used to study the consequences of neuromuscular degenerative disease on bone quantity and morphology. Histomorphometry and micro-computed tomography were used to assess the cortical and cancellous bone in the tibia, femur and humerus of adult neuromuscular degeneration (nmd) mice (up to 21w) and age-matched wild-type controls (WT). At 21w, the average lengths of the humerus, tibia and femur were 15%, 10%, and 10% shorter in the nmd mice, respectively. The midshaft of the humerus, tibia and femur of nmd mice had 41%, 47% and 34% less cortical bone than the WT. In the humeral, tibial, and femoral metaphyses of the nmd mice, there was 50%, 78%, and 85% less trabecular bone volume, and 58%, 92%, and 94% less trabecular connectivity than the WT. NMD cortical bone had less than half of the 42% active surface measured in the WT, yet the mineral apposition rate of those surfaces were similar between strains (nmd: 1.80 microm x day(-1); WT: 2.05 microm x day(-1)). Osteoclast number and activity levels did not differ across strains. These data emphasize that neuromuscular degeneration as a result of immunoglobulin S-mu binding protein-2 (Ighmbp2) mutation will compromise several critical parameters of bone quantity and architecture, the most severe occurring in the trabecular compartment.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
1108-7161
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
9
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
215-24
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| pubmed:meshHeading |
pubmed-meshheading:19949279-Analysis of Variance,
pubmed-meshheading:19949279-Animals,
pubmed-meshheading:19949279-Behavior, Animal,
pubmed-meshheading:19949279-Bone Density,
pubmed-meshheading:19949279-Bone Remodeling,
pubmed-meshheading:19949279-Bone and Bones,
pubmed-meshheading:19949279-DNA-Binding Proteins,
pubmed-meshheading:19949279-Disease Models, Animal,
pubmed-meshheading:19949279-Disease Progression,
pubmed-meshheading:19949279-Mice,
pubmed-meshheading:19949279-Mutation,
pubmed-meshheading:19949279-Organ Size,
pubmed-meshheading:19949279-Osteoporosis,
pubmed-meshheading:19949279-Paralysis,
pubmed-meshheading:19949279-Spinal Muscular Atrophies of Childhood,
pubmed-meshheading:19949279-Statistics, Nonparametric,
pubmed-meshheading:19949279-Transcription Factors,
pubmed-meshheading:19949279-X-Ray Microtomography
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| pubmed:articleTitle |
Devastation of bone tissue in the appendicular skeleton parallels the progression of neuromuscular disease.
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| pubmed:affiliation |
Department of Biomedical Engineering, State University of New York, Stony Brook, New York 11794-2580, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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