title: Quantitative immunohistochemical analysis of human brain basic fibroblast growth factor, glial fibrillary acidic protein and single-stranded DNA expressions following traumatic brain injury.
abstract: Previous studies demonstrated the healing process after traumatic brain injury (TBI), usually at the site or in the area adjacent to the injury, in connection with wound timing. However, the whole brain condition after TBI has not been elucidated clearly. In the present study, we investigated immunohistochemistry of the basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP) and single-stranded DNA (ssDNA) in the parietal lobe and hippocampus distant from the primary injury site in forensic autopsy cases of TBI (n=174). Characteristic findings were detected with regard to brain compression signs and survival time (ST). Peracute deaths (n=22) had a lower GFAP positivity in the parietal white matter. Fatalities without a brain compression sign (parahippocampal herniation/Duret hemorrhage; n=53) had a lower brain weight without glial loss; however, GFAP positivity in the parietal white matter was decreased during ST of <12h, and glial bFGF positivity was increased at each site in deaths after 12h to 3 days, followed by a delayed neuronal loss after 3 days. Fatalities with a brain compression sign (n=78) showed a higher brain weight, and gradual glial and neuronal losses with an early increase of glial bFGF positivity in the parietal cerebral cortex (ST <0.5h). This was followed by an increase of glial bFGF positivity in other sites (ST, 6-24h), and final decreases of glial bFGF and GFAP positivities with increased neuronal ssDNA positivity in the parietal lobe and hippocampus (ST >3 days), which were detected in earlier deaths despite decompressive craniectomy (ST, 12-60h; n=21). These observations suggest that the combined use of bFGF, GFAP and ssDNA immunohistochemistry can be used to evaluate the severity of damage and response of brain after TBI.
authors.affiliation: Department of Legal Medicine, Osaka City University Medical School, Osaka, Japan. m2041106@med.osaka-cu.ac.jp
authors.forename: Qi
authors.initials: Q
authors.lastname: Wang
authors.forename: Takaki
authors.initials: T
authors.lastname: Ishikawa
authors.forename: Tomomi
authors.initials: T
authors.lastname: Michiue
authors.forename: Bao-Li
authors.initials: BL
authors.lastname: Zhu
authors.forename: Da-Wei
authors.initials: DW
authors.lastname: Guan
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Maeda
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001921:Brain / Q000473:pathology; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D004277:DNA, Single-Stranded / Q000378:metabolism*; D056424:Decompressive Craniectomy; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism*; D049429:Forensic Pathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D020300:Intracranial Hemorrhages; D008297:Male; D008875:Middle Aged; D009457:Neuroglia / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D009929:Organ Size; D013997:Time Factors; D055815:Young Adult
chemical_list: D004277:DNA, Single-Stranded; D005904:Glial Fibrillary Acidic Protein; D016222:Fibroblast Growth Factor 2