Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ependyma reacts to injury with a few stereotypical responses and does not regenerate at any age. Non-neoplastic ependymal cells do not undergo mitotic proliferation and do not re-express fetal cytoskeletal or secretory proteins. Atrophy of ependymal cells accompanies generalized cerebral atrophy. The ependyma may be damaged by stretching during ventricular dilatation, by infarcts of the ventricular wall or by infection and inflammation. Tearing of the epithelium leaves discontinuities that become filled with processes of subventricular astrocytes. In some cases reactive gliosis is minimal, but in most it is extensive and gliotic nodules form beneath intact ependyma and within gaps between ependymal islands. Ependymal rosettes may form in several ways: sequestration of diverticuli from the surface; curling of a torn edge or penetration of an edge into the parenchyma; reactive gliosis overgrowing an ependymal edge; in situ differentiation of ependymal cells from deep neuroepithelial cells. Migration and metaplasia are unlikely mechanisms. Bacterial and fungal ependymitis are highly destructive. Several viruses, especially mumps, selectively infect ependymal cells and are an important cause of acquired aqueductal stenosis without inflammation. Damaged ependyma may not be able to perform its function in the regulation of transport of fluid, ions and small molecules between cerebral parenchyma and ventricular fluid and thus may contribute to hydrocephalus. Damage to the fetal ependyma may result in secondary focal dysplasias of the developing brain.
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PMID:Ependymal reactions to injury. A review. 774 40

Experimental production of congenital hydrocephalus was undertaken by inoculating mumps virus into pregnant hamsters intravenously or intraplacentally. When the mumps virus was inoculated intravenously on the 8th, 10th, 12th, or 14th day of gestation, some fetuses were aborted and those which could come to term did not develop hydrocephalus after birth. Offsprings from the mothers, which had had intraplacental inoculation on the 14th day of gestation, showed ventricular dilatation in about 28%. Histological examination revealed inflammatory infiltration on the surface of ependymal layers, subependymal edema and microglial activation in the underlying ependyma of the aqueduct. These findings were thought to have resulted from ependymitis caused by mumps virus. The transplacental infection of mumps virus is considered to be extremely rare. However, in such conditions as the placental barrier is impaired, mumps virus will possibly pass through the placenta, and will cause hydrocephalus to the infant.
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PMID:[Experimental hydrocephalus induced by intraplacental mumps virus inoculation]. 818 78

To elucidate the pathogenesis of early ventricular dilatation in hydrocephalus, we examined early morphological changes in ependymal layers at the lateral ventricles in suckling hamsters without aqueductal stenosis 5 days after the intracerebral inoculation of mumps virus. Mumps virus antigen was detectable in all ependymal cells. The ependymal cilia had almost disappeared and only the microvilli remained. A number of supraependymal cells were also observed on the surface of the lateral ventricles. Transmission electron microscopy revealed intracytoplasmic viral-like inclusions in the infected ependymal cells. These results suggest that functional and morphological disturbances in infected ependymal cells may cause early ventricular dilatation before aqueductal stenosis occurs.
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PMID:Early ependymal changes in experimental hydrocephalus after mumps virus inoculation in hamsters. 849 59