title: Evaluation of human brain damage in fatalities due to extreme environmental temperature by quantification of basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP), S100β and single-stranded DNA (ssDNA) immunoreactivities.
abstract: Fatalities due to extreme environmental temperatures involving hypothermia (cold exposure) and hyperthermia (heat stroke) might present with poor or nonspecific morphological pathologies, which are insufficient to establish the cause of death in forensic practice. The present study immunohistochemically investigated basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP), S100β and single-stranded DNA (ssDNA) in the parietal lobe and hippocampus of the brain in fatalities from hypothermia (n=15) and hyperthermia (n=18), and compared them to those of controls (n=39), including acute death due to ischemic heart disease, mechanical asphyxiation and drowning. In addition, S100β concentration in cerebrospinal fluid (CSF) was measured. Characteristic findings in hypothermia cases were higher glial bFGF immunopositivity in the cerebral cortex and white matter, and higher S100β immunopositivity in the cerebral cortex with a lower CSF S100β concentration. Hyperthermia showed lower glial GFAP and S100β immunopositivities in the white matter, and higher neuronal ssDNA immunopositivity in the cerebral cortex and hippocampus, accompanied by high glial bFGF and S100β immunopositivities in the cerebral cortex. These findings suggest neuroprotective glial responses without marked neuronal or glial damage in fatal hypothermia, and diffuse neuronal apoptosis despite initiation of neuroprotective cortical astrocyte responses, accompanied by glial damage in the white matter, in fatal hyperthermia. These markers may be useful for evaluating brain damage and responses in fatalities due to extreme environmental temperatures.
authors.affiliation: Department of Legal Medicine, Osaka City University Medical School, Abeno, Osaka, Japan. wangqi1980@live.com
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: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis; D016022:Case-Control Studies; D002467:Cell Nucleus / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D003080:Cold Temperature / Q000009:adverse effects; D004277:DNA, Single-Stranded / Q000378:metabolism; D005260:Female; D005334:Fever / Q000378:metabolism*; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D049429:Forensic Pathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D006358:Hot Temperature / Q000009:adverse effects; D006801:Humans; D007035:Hypothermia / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009414:Nerve Growth Factors / Q000378:metabolism; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000378:metabolism; D055815:Young Adult
chemical_list: D004277:DNA, Single-Stranded; D005904:Glial Fibrillary Acidic Protein; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D016222:Fibroblast Growth Factor 2