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      Cellular accumulation of extravasated serum protein and DNA fragmentation following vasogenic edema.

      Journal of Neurotrauma
      Animals, Apoptosis, physiology, Blood Proteins, analysis, Blood-Brain Barrier, Brain Edema, etiology, pathology, physiopathology, Brain Injuries, Brain Ischemia, complications, Capillary Permeability, Cold Temperature, adverse effects, DNA Fragmentation, Evans Blue, diagnostic use, Extravasation of Diagnostic and Therapeutic Materials, In Situ Nick-End Labeling, Male, Mice, Mice, Inbred Strains, Reperfusion Injury, Vascular Diseases

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          Abstract

          Accumulation of serum protein has been demonstrated in injured brain cells following vasogenic brain edema. The present study was conducted to test whether this phenomenon is also observed in apoptotic cells as well as in necrotic cells. Apoptotic cell death has been implicated in a variety of brain injuries, including ischemia and trauma. Cold injury and focal cerebral ischemia-reperfusion were used to induce both vasogenic edema and apoptotic cell death. Evans blue extravasation was used to determine the cellular accumulation of serum albumin. Apoptotic cell death was evaluated by both morphological alterations and by terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling (TUNEL) staining. Evans blue accumulation in cells was observed not only in the surrounding zone of the lesion after cold injury and in the entire ischemic area after focal ischemia, but was also detected in the regions remote from the primary injury site. Some of these cells demonstrated nuclei fragmentation. TUNEL staining confirmed that apoptosis was induced in the region where apoptotic cells were morphologically detected. These observations suggest that accumulation of the extravasated serum component is accompanied by apoptotic cell death following vasogenic brain edema.

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