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  • Electronic Resource  (3)
  • 1985-1989  (3)
  • Ependymal cell  (2)
  • CT scan  (1)
Material
  • Electronic Resource  (3)
Years
  • 1985-1989  (3)
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 70 (1986), S. 227-234 
    ISSN: 1432-0533
    Keywords: Medulloblastoma ; CT scan ; Embryonal neoplasm ; Kinetics ; Growth rate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Growth analysis of medulloblastomas was performed in two children. They initially manifested symptoms at the age of 3 years and 9 months and at the age of 2 months respectively. Computerized tomography (CT) scans were obtained at different points in each case. The growth curves were drawn on a semilogarithmic graph by calculating the tumor volume on CT on the assumptions that the tumor started from a single tumor cell and that the growth rate was constant. By extrapolating the curves back, tumor inception was estimated to have occurred respectively at the 14–23rd week and at the 16–17th week of gestation. Additional cell kinetic data were obtained from DNA analysis of surgical pathology specimens. Calculated cell-cycle times were 22–32 h for both cases. The S phases comprised 26.3% and 27% and the G0G1 phases 66.8% and 62% of the cell cycle, respectively, for case 1 and 2. Assuming a labelling index of 14%, the cell loss factors were estimated to be 97% and 74% (case 1 and case 2 respectively). The seventeenth week of gestation in humans corresponds to the timing of events occurring postnatally at days 3–18 in the developing cerebella of rodents, i.e., at the time of maximal activity in the migration and differentiation of the cells of the fetal external granular layer. Medulloblastomas have been experimentally induced in rodents by the injection of oncogenic viruses during the neonatal period, and statistical data on the epidemiology of human medulloblastomas have suggested a possible association with the contamination of polio vaccine by the SV 40 virus. Therefore, it seems reasonable to assume that these medulloblastomas originated in the cerebellum during the period of active development of the cerebellum.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 70 (1986), S. 71-74 
    ISSN: 1432-0533
    Keywords: 6-Aminonicotinamide ; Ependymal cell ; Mitosis ; Suckling mice ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mitotic ependymal cells were encountered in 10-day-old mice treated with 6-aminonicotinamide, an antagonist of niacin. These occurred along the medial surface of the lateral ventricle and the ventral portion of the aqueduct. Electron microscopy revealed that both mitotic ependymal cells had eccentrically placed chromosomes without a nuclear membrane and well-formed gap junctions in contact with adjacent ependymal cells. Microtubules from a centriole radiated to the chromosomes. These data show that cell division occurs in morphologically matured ependymal cells in the postnatal brain under pathological conditions. We believe this to be the first ultrastructural demonstration of this phenomenon.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 71 (1986), S. 243-250 
    ISSN: 1432-0533
    Keywords: 6-Aminonicotinamide ; Aqueduct “agenesis” ; Ependymal cell ; Hydrocephalus ; Suckling mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Suckling mice which received a single intraperitoneal injection of 6-aminonicotinamide on the 5th postnatal day, consistently developed hydrocephalus. During the early stages of hydrocephalus (7–9 days after injection), aqueductal lesions were characterized by edematous ependymal and subependymal cells, and spongy changes in the periaqueductal area, which resulted in aqueduct stenosis. Later stages (after 20 days post-injection) showed that these edematous changes totally subsided, leaving an obliterated aqueduct which was similar to that of human congenital hydrocephalus. At the completely obliterated area, ultrastructural investigation disclosed a normal-looking neuropil but no aqueductal lumen. In the remaining ependymal cell, increased intermediate filaments and lipid droplets occurred. These data suggest that acute ependymal cell degeneration during the perinatal period may result in the profile of aqueduct “agenesis” in human congenital hydrocephalus.
    Type of Medium: Electronic Resource
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