Cerebral hypoxia and ischemia: the forensic point of view: a review

In cases with suspected brain anoxia/ischemia and hypoxia/hypoxemia a neuropathological investigation should give additional information to elucidate the cause of death and its pathophysiological mechanisms. Primary ischemic brain damage is associated with morphological and biochemical alterations. While acute ischemic neuronal injury reveals axon sparing and selective neuronal lesions due to the release of large quantities of glutamate, late neuronal death is associated with antiapoptotic growth factors, and decreased expression of microtubule-associated proteins and tubulin. On the morphological level ischemia can be detected by necrosis of neurons, proliferation of microglia, and astrocytes in vulnerable regions of the brain. In cases of permanent ischemia the so-called pale nervous cell injury is observed, in cases of partial perfusion the so-called dark nerve cell injury and apoptosis are detectable. In spite of the considerable advantages of recent research, presently there is no reliable qualitative marker to ascertain death due to acute hypoxic or ischemic events.     

Psychological Distress of Children and Mothers in Domestic Violence Emergency Shelters

Abused mothers and their school-aged children who recently entered domestic violence emergency shelters were assessed by individual interview and psychometric measures. Children had positiveviews of the shelter residence. Mothers and children reported high-quality relationships with eachother. Children came from highly violent homes, and the majority had attempted to intervene in theinteradult violence. Hierarchical multiple regressions were conducted on child PTSD symptoms, child behavior problems, and maternal depression, anxiety, and anger. Child PTSD symptoms were associated with amount of physical violence. Child behavioral problems were related to mother anxiety andanger. The predictors of maternal emotional distress varied. Depression was associated with sexualabuse, child physical intervention, and quality of mother–child relationship; anxiety was related to witnessing child abuse, child age, and child internalizing behaviors; anger was associated with abuse-related injuries, violence frequency, and child internalizing behaviors. Augmentationof shelter-based interventions for children's trauma, maternal emotional distress, and parenting are discussed.     

Testing the Trauma Model of Violence

The present study sought to explore the relationship between trauma and violence, as measured by the Traumatic Events Questionnaire and the Conflict Tactics Scale. Using Multiple Regression Analysis, several types of traumatic experiences were studied as predictors to violent behavior in 55 graduate students. Results suggest that trauma as a set, as well as being the victim of a violent crime, are significantly related to future violent behavior. However, no other individual predictor variable, including being the victim of childhood physical abuse, significantly predicted future violence. Implications of the findings are discussed.     

大鼠液压冲击脑损伤后bFGF及其受体FGFR1的表达

目的观察脑损伤后碱性成纤维细胞生长因子(bFGF)及其受体FGFR1的表达及其时序性变化,探讨脑损伤的分子机制及法医学脑损伤时间推断。方法用免疫组织化学技术观察大鼠侧位中度液压冲击脑损伤后bFGF及FGFR1蛋白在伤后不同时间(30min,1,3,6,12h,1,3,7d)的表达情况,以正常大鼠及手术大鼠作为对照。结果正常对照组和手术对照组大鼠脑组织内有低水平的bFGF和FGFR1表达。脑冲击伤后6h,大脑皮层和脑干bFGF和FGFR1蛋白表达开始显著增加,1～3d达高峰,7d时已有所下降;海马冲击后3h即开始增加,1d达峰值,此后逐渐下降,7d时恢复正常。结论脑损伤可诱导bFGF/FGFR1的表达,提示机体对脑损伤存在自身保护机制,其表达的时序性改变可望用于法医学脑损伤时间推断。     

OTS-2．2S基因芯片对人脑挫伤后基因表达差异的初步研究

目的利用基因芯片技术,研究人挫伤脑组织中基因表达差异。方法从脑组织提取mRNA,通过OTS-2.2S基因芯片,研究脑挫伤组织与对照脑组织细胞原癌及抑癌相关基因特异性表达差异。结果发现在挫伤脑组织中,HoJ-1和KIAAOO65基因表达水平显著下降,而p107mRNA表达水平显著升高。结论在脑挫伤中仅发现3条基因的表达有显著性差异;本研究是对脑损伤后基因表达水平及其法医学意义进行的探索性研究。     

脑缺氧损伤后线粒体途径神经元凋亡

脑缺氧后神经元线粒体损伤不单使细胞发生能量缺失和功能丧失,还可以介导凋亡调节信号,是缺氧损伤后神经元凋亡的一个中心环节。线粒体膜通透性转变,释放细胞色素C活化特定的caspase蛋白酶,使细胞进入不可逆的凋亡程序中;Bcl-2家族促凋亡和抑制凋亡成员之间相互作用,调控细胞色素C释放,调节线粒体介导的凋亡过程。     

实验性大鼠脑震荡后C—FOS蛋白表达的研究

目的探讨原癌基因c-fos的表达和脑震荡性损伤的关系,同时寻找脑震荡后法医病理学的诊断依据。方法55只实验大鼠随机分为脑震荡组和对照组。用免疫组织化学SABC法观察大鼠脑震荡后脑内C-FOS蛋白表达的变化规律。结果对照组大鼠未见C-FOS蛋白的表达。然而脑震荡组损伤后15min即可在神经细胞观察到C-FOS蛋白的表达,随着损伤后经过时间的延长,表达C-FOS蛋白的细胞数及范围逐渐扩大,损伤后6h表达达高峰,直至损伤后96h均有大量C-FOS蛋白表达。结论 c-fos原癌基因的检测可成为诊断脑震荡和推断脑震荡后经过时间的一项敏感指标。     

交通事故颅脑损伤233例法医学鉴定分析

通过对233例交通事故颅脑损伤案例的分析,对受伤者的性别、年龄及损伤程度进行了统计。并对其颅脑外伤后遗症和伤残等级的关系、评定时间及脑外伤后神经功能障碍的认定进行了探讨。     

脑死亡脑外器官病理变化的实验性研究

选用34只家猫研究脑死亡后脑外器官（心、肺、肝、肾）的病理学变化。经任内持续加压造成脑死亡模型,根据人工维持心跳和呼吸的时间分3组。结果脑死亡后出现：（1）缺血性心肌病变,心内膜下出血,心肌局灶性坏死及线粒体、微丝破坏;（2）肺淤血,水肿,间质炎症;（3）肝小叶中央带、中间带缺血性病变;（4）肾近曲小管缺血性病变。     

Evaluation of Agonal Cardiac Function for Sudden Cardiac Death in Forensic Medicine with Postmortem Brain Natriuretic Peptide (BNP) and NT-proBNP: A Meta-analysis

Sudden cardiac death (SCD) is an unexpected death caused by a sudden loss of cardiac function, which is currently a global public health problem. Evaluation of the agonal cardiac function of the deceased is a quite important task for the diagnosis of SCD in forensic medicine. Brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) are currently considered as significant biomarkers for the diagnosis of heart failure in both clinical and forensic practices. To investigate the postmortem evaluation roles of postmortem BNP and NT-proBNP levels for SCD, the present study meta-analyzed eight related studies from Embase, Cochrane Library, PubMed, China Biomedical Literature Database, China National Knowledge Infrastructure, and Wanfang Data. Newcastle–Ottawa Quality Assessment Scale was used to assess the quality of the included literature, and the meta-analysis was performed by RevMan 5.3.5 software. Postmortem NT-proBNP in pericardial fluid showed higher levels in the SCD group than that of the non-SCD group with the weighted mean difference = 3665.74, 95% confidence interval: 1812.89–5518.59, and p = 0.0001. However, postmortem levels of BNP in pericardial fluid and NT-proBNP in serum revealed no statistical difference between SCD and non-SCD subjects. The results of present meta-analysis demonstrated that postmortem NT-proBNP in the pericardial fluid could be used as an ancillary indicator for evaluation of agonal cardiac function in forensic medicine.