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10.1177/0271678X15617172

http://scihub22266oqcxt.onion/10.1177/0271678X15617172
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C4776312!4776312 !26661240
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suck abstract from ncbi

pmid26661240
      J+Cereb+Blood+Flow+Metab 2016 ; 36 (3 ): 513-38
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  • Molecular pathophysiology of cerebral edema #MMPMID26661240
  • Stokum JA ; Gerzanich V ; Simard JM
  • J Cereb Blood Flow Metab 2016[Mar]; 36 (3 ): 513-38 PMID26661240 show ga
  • Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the study of cerebral edema is the study of maladaptive ion transport. Following acute CNS injury, cells of the neurovascular unit, particularly brain endothelial cells and astrocytes, undergo a program of pre- and post-transcriptional changes in the activity of ion channels and transporters. These changes can result in maladaptive ion transport and the generation of abnormal osmotic forces that, ultimately, manifest as cerebral edema. This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of cerebral edema.
  • |Animals [MESH]
  • |Aquaporins/metabolism [MESH]
  • |Blood-Brain Barrier/metabolism/pathology/physiopathology [MESH]
  • |Brain Edema/metabolism/pathology/*physiopathology [MESH]
  • |Brain/blood supply/metabolism/pathology/*physiopathology [MESH]
  • |Humans [MESH]
  • |Ion Transport [MESH]
  • |Ions/metabolism [MESH]
  • |Permeability [MESH]


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