Traumatic axonal injury (TAI) is one of the most common pathological features of severe traumatic brain injury (TBI). Our previous study using proteomics suggested that peripherin (PRPH) should be a potential candidate as a biomarker for TAI diagnosis. This study is to further elucidate the role and association of PRPH with TAI. In the animal study, we performed immunohistochemistry, ELISA and morphological analysis to evaluate PRPH level and distribution following a severe impact. PRPH-positive regions were widely distributed in the axonal tract throughout the whole brain. Axonal injuries with PRPH inclusion were observed post-TBI. Besides, PRPH was significantly increased in both cerebral spinal fluid and plasma at the early phase post-TBI. Colocalization analysis based on microscopy revealed that PRPH represents an immunohistological biomarker in the neuropathological diagnosis of TAI. Brain samples from patients with TBI were included to further test whether PRPH is feasible in the real practice of neuropathology. Immunohistochemistry of PRPH, NFH, APP and NFL on human brain tissues further confirmed PRPH as an immunohistological biomarker that could be applied in practice. Collectively, we conclude that PRPH mirrors the cytoskeleton injury of axons and could represent a neuropathological biomarker for TAI.

Splenic angiosarcoma (SA) is a rare disease that can cause spontaneous splenic rupture leading to unexpected death. The rare incidence and non-specific clinical presentations made the early correct diagnosis of SA impossible in clinical practice. Even with medical intervention, 80% of patients died within 6 months after diagnosis. Here, we report a man who had complained of abdominal distension for 2 weeks and succumbed to the disease nine hours after admission. Diagnosis of hepatic and splenic angiosarcomas was based on post-mortem histopathological examination and immunohistochemistry, and the cause of death was hemorrhagic shock caused by spontaneous splenic rupture secondary to SA. This present case was the first forensic autopsy of spontaneous splenic rupture secondary to SA, which can highlight the diagnosis of rare diseases in forensic practice, and forensic pathologists should bear in mind these rare diseases even in routine practice.

主动脉食管瘘(AEF)是食道和主动脉之间的异常通道,是一种罕见且致命的疾病,通常由各种主动脉和食道疾病引起,可导致致命的上消化道出血 [1].本文报道1例因胃肠道出血死亡法医学鉴定中确诊为AEF的案例.

法医病理学是高校法医专业的通识必修课程,是培养创新人才的重要环节.文章分析了当前法医病理学基础教学的现状与不足,提出基于仿真技术的教学模式改革,强调知识内容的可视化和可交互,有助于学生理解计算机软硬件系统,更好地培养学生的法医病理学知识和实践动手操作能力.

水中尸体的检验是法医工作中的常见情形,也是法医病理学研究的重要课题之一.实践中在颈项部有索沟的水中尸体往往多被考虑为他杀后抛尸入水.但也有例外 , 笔者现报告一例颈部有索沟的水中尸体死亡方式被确定为自杀的案例.

Aluminum phosphide (ALP) has been extensively used as an economical and effective insecticide, rodenticide, and fumigant. The active ingredient of ALP is phosphine (PH3), the use of which can lead to accidental inhalation and mass poisoning with high mortality. Exposure to PH3 will give rise to global damage in the human body. This study reviewed 4 fatal accidents including 8 children with PH3 poisoning and aimed to determine the pathological changes that resulted from exposure to PH3 and, secondly, aimed to determine whether oxidative stress was involved in PH3-induced neurotoxicity using histopathological and immunohistochemistry (IHC) methods. After focusing on the pathological changes on the major organs, we found severe damage induced by PH3 in many systems, especially the neurological system, including neuronal, axonal, and vascular injuries as well as oxidative damage with increased expression of 4-hydroxy-2-trans-nonenal (4HNE), 8-hydroxy-2'-deoxyguanosine (8-OH-dG), and 3-nitrotyrosine (3-NT) in the brain, which indicated that oxidative stress was a crucial mechanism for neuronal death in PH3 toxicity. Moreover, we observed severe myocardial and hepatocellular fatty degeneration in the tissues of the heart and liver. We considered that these characteristic changes are a suggestive sign of PH3 poisoning and partly explained the toxic mechanism of PH3 (inhibition of mitochondrial oxidative phosphorylation). We hope that this research could improve the understanding of the toxicity of PH3 in both forensic and clinical practice.

Diffuse axonal injury (DAI) is one of the most common and severe pathological consequences of traumatic brain injury (TBI). The molecular mechanism of DAI is highly complicated and still elusive, yet a clear understanding is crucial for the diagnosis, treatment, and prognosis of DAL In our study, we used rats to establish a DAI model and applied isobaric tags for relative and absolute quantitation (iTRAQ) coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis to identify differentially expressed proteins (DEPs) in the corpus callosum. As a result, a total of 514 proteins showed differential expression between the injury groups and the control. Among these DEPs, 14 common DEPs were present at all seven time points postinjury (1, 3, 6, 12, 24, 48, and 72 h). Next, bioinformatic analysis was performed to elucidate the pathogenesis of DAI, which was found to possibly involve calcium ion-regulatory proteins (e.g., calsenilin and ryanodine receptor 2), cytoskeleton organization (e.g., peripherin, NFL, NFM, and NFH), apoptotic processes (e.g., calsenilin and protein kinase C delta type), and inflammatory response proteins (e.g., complement C3 and C-reactive protein). Moreover, peripherin and calsenilin were successfully confirmed by western blotting to be significantly upregulated during DAI, and immunohistochemical (IHC) analysis revealed that their expression increased and could be observed in axons after injury, thus indicating their potential as DAI biomarkers. Our experiments not only provide insight into the molecular mechanisms of axonal injury in rats during DAI but also give clinicians and pathologists important reference data for the diagnosis of DAI. Our findings may expand the list of DAI biomarkers and improve the postmortem diagnostic rate of DAI.

In clinical and forensic practice, the cause of death is often attributed to acute myocardial infarction, among which the coronary atherosclerosis being the Captain of the Men of Death. However, other reasons such as coronary septic embolization with neutrophilic granulocyte myocarditis although rare, can also cause sudden unexpected death. This paper reports a case with this rare cause-a 21-year-old woman diagnosed with "acute gastroenteritis" who died 4 days later. A forensic autopsy revealed an inflammatory polypous embolic located at 1.0 cm from the left anterior descending branch (LAD) with serve neutrophilic granulocyte myocarditis, which resulted in embolic at the opening of the left main coronary artery, acute myocardial infarction and eventually leading to her death. Histopathological examination showed large amounts of neutrophilic granulocyte infiltration in the arterial layer forming the septic embolic and eventually resulting in coronary occlusion. To find the real cause of septic embolic, myocarditis, bacterial, fungal, protozoan and virus detection was performed through RT-PCR, with negative findings. Septic embolic leading coronary occlusion in left main coronary artery and LAD is rarely reported in forensic practice, we hope this report can pave the way on understanding this rare disease to make correct diagnosis in medical practice.

外周蛋白(peripherin,PRPH)广泛分布于外周神经系统(PNS),也可较小程度表达于中枢神经系统(CNS)内少数直接向外周有投射纤维的神经元群.研究发现,CNS损伤后,PRPH表达可出现上调,且可表达于正常状态下不表达的部位.此外,PRPH有多种不同亚型,各亚型在CNS中发挥着不同的作用,某些亚型系在某些病理条件下产生或出现上调.然而,PRPH及其各亚型在CNS损伤中的确切生物学功能尚不明确.本文综述了PRPH在中枢神经系统损伤中的研究进展,提示了其在法医学领域中的应用及研究前景.

法医病理学和法医毒理学是法医学主干课程,课程均要求学生观察大量的组织切片,学习病变或损伤组织的显微结构变化特征,为将来从事法医病理鉴定奠定基础.随着病理切片数字化技术的出现和日渐成熟,给法医组织病理学的实践教学带来了新的契机和挑战.文章对法医组织病理学实践教学的现状进行剖析,对基于数字化资源的法医组织病理学实践教学改革的具体实施内容进行叙述,并对实施过程中存在的具体问题进行了探讨.

扼颈致机械性窒息的死亡机制通常是颈部血管阻塞、迷走神经抑制或刺激颈动脉窦导致心电紊乱、阻塞呼吸道等综合因素导致的全脑缺氧,其中前二种因素在死亡机制中起更重要的作用且是扼颈急速死亡的原因 [1,2].本文报道 2 例罕见扼颈后迟发死亡,并结合文献探讨其机制及法医学鉴定注意事项.