首页> 外文期刊>Forensic science international >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
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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

机译:通过定量碱性成纤维细胞生长因子(bFGF),神经胶质原纤维酸性蛋白(GFAP),S100β和单链DNA(ssDNA)免疫反应性评估极端环境温度导致的人脑死亡伤害

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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.
机译:由于极端环境温度(包括低温(冷暴露)和高温(中暑))导致的死亡可能表现为不良或非特定的形态病理,不足以在法医实践中确定死亡原因。本研究通过免疫组织化学方法研究了在低温(n = 15)和体温过高致死中脑的顶叶和海马中的碱性成纤维细胞生长因子(bFGF),神经胶质纤维酸性蛋白(GFAP),S100β和单链DNA(ssDNA) (n = 18),并与对照组(n = 39)进行比较,包括因缺血性心脏病,机械性窒息和溺水而导致的急性死亡。另外,测量了脑脊液(CSF)中的S100β浓度。体温过低病例的特征发现是脑皮质和白质中神经胶质bFGF免疫阳性,脑脊液S100β浓度较低时,大脑皮层S100β免疫阳性。热疗在白质中显示出较低的神经胶质GFAP和S100β免疫阳性,在大脑皮层和海马体中神经元ssDNA免疫阳性较高,同时在大脑皮层中还具有较高的神经胶质bFGF和S100β免疫阳性。这些发现表明,在致命的体温过高的情况下,在致命的体温过低的情况下,神经保护性神经胶质反应没有明显的神经元或神经胶质损害;尽管在致命的体温过高,尽管启动了神经保护性皮层星形胶质细胞反应并伴有白质的神经胶质破坏,但弥漫性神经元凋亡。这些标记物可用于评估由于极端环境温度引起的脑部损伤和死亡反应。

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