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• W2183597551 abstract "It has been known for a long time that hepatic encephalopathy (HE) and other cerebral disorders related to hyperammonemia (HA) are manifested by pronounced neuropathological changes that primarily affect astrocytes, leaving the other cell types of the CNS relatively intact. In 1912, von Hösslin and Alzheimer (1) were the first to note the occurrence in the brain of a patient with pseudosclerosis, of large, pale astrocytes with enlarged, lobulated nuclei. These cells, later consistently defined as Alzheimer type II cells, were convincingly associated with HE by Adams and Foley (2). Since then the literature has become flooded with reports of HE— induced astroglial changes, which beside the appearance of degenerated forms of these cells include diffuse proliferation of protoplasmic astrocytes: for excellent reviews on this subject the reader is referred to the articles of Diemer (3) and Norenberg (4). However, until recently, these glial changes have been considered as unrelated to the neurological symptoms of HE. This was not unexpected, as at that time astrocytes were considered to perform only static, supportive functions." @default.
• W2183597551 created "2016-06-24" @default.
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• W2183597551 creator A5063700491 @default.
• W2183597551 date "1994-01-01" @default.
• W2183597551 modified "2023-09-26" @default.
• W2183597551 title "Astrocyte-Neuron Interactions in Hyperammonemia and Hepatic Encephalopathy" @default.
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• W2183597551 doi "https://doi.org/10.1007/978-1-4615-1989-8_5" @default.
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