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  • Articles: DFG German National Licenses  (2)
  • 1985-1989  (2)
  • Granular layer  (1)
  • Myofibrillar degeneration  (1)
Source
  • Articles: DFG German National Licenses  (2)
Material
Years
  • 1985-1989  (2)
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 78 (1989), S. 484-491 
    ISSN: 1432-0533
    Keywords: Nemaline myopathy ; Lysosomal enzymes ; Acid phosphatase ; Cathepsins ; Myofibrillar degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Four of seven patients with nemaline myopathy had severe, rapidly progressing symptoms. These four showed an increase in acid phosphatase activity in muscle fibers demonstrated by histochemistry and cathepsin B&L activity by biochemical measurement. On electron microscopy, nemaline bodies, occasionally disorganized myofibrils and autophagic vacuoles containing sarcoplasmic debris and glycogen particles were seen. Focal myofibrillar degeneration, through an unknown pathogenetic mechanism, induces an increase in lysosomal enzymes in the skeletal muscles which may be closely correlated with a rapid aggravation of muscle weakness in nemaline myopathy.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    ISSN: 1432-0533
    Keywords: Cerebellum ; Granular layer ; Autolysis ; Brain death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a study of duration of brain death, granular layer autolysis (GLA) of the cerebellar cortex was analyzed in 45 patients who died of acute cerebrovascular diseases (CVDs). Twelve patients who died of causes other than intracranial disease served as controls. Tonsillar herniation occurred in all who died of acute CVDs. More advanced GLA was seen in the central folia adjacent to the central white medullary body of the cerebellum as compared with the peripheral folia. Widespread GLA involving the most of the peripheral folia was found solely in patients in whom brain death had been present over 18 h. Of the 12 control patients, 4 showed GLA only in the central folia. Although GLA of the central folia might develop during immersion fixation of the brain, the alteration of the peripheral folia is assumed to develop in the period of brain death. Widespread GLA extending to the peripheral folia could be a pathological finding characteristic of brain death, where intracranial blood flow could be absent or significantly reduced. Brain death for little less than 1 day would be necessary for GLA to develop.
    Type of Medium: Electronic Resource
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