Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1988-11-23
pubmed:abstractText
The optic nerves from a goat fetus affected with beta-mannosidosis and a control fetus were analysed morphologically in order to investigate developmental aspects of beta-mannosidosis-associated myelin deficits. In the affected fetus, the number of myelinated axons per unit area was about 25% of the control values. Histograms of axonal diameter indicated that a greater percentage of the myelinated and unmyelinated axons were of larger caliber in the affected fetus than in the control fetus and that very few small axons were myelinated in the affected animal. The mean values of myelin sheath thickness in the affected and control animals did not differ significantly. Ultrastructural analysis revealed a decreased proportion of oligodendrocytes and an increased proportion of astrocytes in the affected fetus. These results indicate that the pathogenetic process leading to cellular abnormalities and myelin deficits in beta-mannosidosis has been initiated prior to 124 days gestation, during an early stage of myelination in the goat optic nerve. The decrease in number of oligodendrocytes suggests that early cell death and/or change in oligodendrocyte proliferation contribute to the myelin deficit. Analysis of the prenatal development of lesions will help clarify the pathogenesis of dysmyelinogenesis in beta-mannosidosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0736-5748
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
243-53
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Dysmyelinogenesis in caprine beta-mannosidosis: ultrastructural and morphometric studies in fetal optic nerve.
pubmed:affiliation
Department of Pathology, Michigan State University, East Lansing 48824.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.