酒精相关颅脑损伤研究进展

酒精暴露常见于颅脑损伤(traumatic brain injury,TBI)的发生过程中,与颅脑损伤死亡具有紧密联系。国内外此方面研究纷繁复杂。本文总结了近十年相关国内外实验研究,从临床实验研究、动物模型应用、脑损伤鉴别不同方面对不同血清酒精水平(blood alcohol concentration,BAC)对于颅脑损伤影响相关研究进展进行系统阐述。本综述为进一步相关研究提供参考,也对相关死亡案件鉴定具有借鉴意义。     

GFAP和VEGF在创伤性脑损伤中表达的研究进展

创伤性脑损伤是世界上导致死亡及残疾的主要原因之一。检测对中枢神经系统损伤有高度特异性和敏感性的生物标志物,可以在一定程度上反映损伤情况。胶质纤维酸性蛋白与血管内皮生长因子均可作为颅脑损伤的生物学标记物,其表达变化规律、峰值出现时间,与创伤性脑损伤的严重程度及损伤时间的推断密切相关,对于法医病理学具有重大意义。该文对胶质纤维酸性蛋白与血管内皮生长因子的分子生物学特性及其在创伤性脑损伤中的表达进行综述。     

国外期刊有关脑外伤后遗精神障碍文献

综述：创伤性脑损伤的后果探讨［英」／StrattonM．C，etal／／BrainInj1994；8（7）：631本文将从病因学、疾病特点及预后三方面对创伤性脑损伤（TraumaticBrainInjury以下简称TBI）进行讨论，重点是TBI对患者神经心理功能和人际交往的影响。自一国：脑损伤及其历响一、TBI的性质（一）TBI的神经病理学TBI可分为开放性颅脑损伤和闭合性颅脑损伤。开放性颅脑损伤的定位诊断比较容易，脑组织损伤一般集中于外物的进入路径上；闭合性颅脑损伤较开放性颅脑损伤更为常见，脑组织所受损伤一般为挫伤、裂伤，脑损伤往往不仅仅局限于受创…     

轻度创伤性脑损伤脑脊液及血液生物标记物研究进展CSCD

轻度创伤性脑损伤(mild traumatic brain injury,MTBI)被认为是轻度脑损伤导致的短暂意识丧失和精神改变,但有时也会导致持久性、进行性的临床症状。MTBI可引起神经系统结构损伤及相应的体液生物标记物改变,但有关其严重程度及个体易感性与意识障碍持续时间的关联程度研究不足,同时,一次打击后脑损伤程度也缺乏可靠的评估方法。本文综述了与TBI有关的脑脊液及血液生物标记物,探讨这些标记物在MTBI诊断中的应用现状及研究前景,为法医学及临床医学中脑损伤的诊断及评估提供参考依据。     

轻度创伤性脑损伤脑脊液及血液生物标记物研究进展

轻度创伤性脑损伤(mild traumatic brain injury,MTBI)被认为是轻度脑损伤导致的短暂意识丧失和精神改变,但有时也会导致持久性、进行性的临床症状。MTBI可引起神经系统结构损伤及相应的体液生物标记物改变,但有关其严重程度及个体易感性与意识障碍持续时间的关联程度研究不足,同时,一次打击后脑损伤程度也缺乏可靠的评估方法。本文综述了与TBI有关的脑脊液及血液生物标记物,探讨这些标记物在MTBI诊断中的应用现状及研究前景,为法医学及临床医学中脑损伤的诊断及评估提供参考依据。     

创伤性脑损伤动物模型研究进展

创伤性脑损伤(traumatic brain injury,TBI)是多因素作用的高度复杂过程,TBI动物实验研究有利于阐明TBI原发性、继发性损伤机制及病理生理学过程,为诊断及治疗提供依据.动物模型的选择依赖于研究目的,然而各种动物模型均具有局限性,仅能复制TBI关键的损伤机制或某一重要的病理生理学过程而无法全面反映...     

外伤性癫痫生物标志物的研究进展

外伤性癫痫(post traumatic epilepsy,PTE)是创伤性脑损伤的严重并发症,是法医学鉴定实践的疑难问题。近年来,许多生物标志物被应用于损伤和疾病的诊断、治疗及预后。在癫痫研究领域现有许多PTE生物标志物的研究。本文就近年来有关PTE生物标志物的研究进展进行综述,以期对PTE的法医学鉴定提供借鉴。     

衰老相关生物分子标志物在法医年龄推断中的研究进展

未知个体的年龄推断能够在案件侦破、灾害遇难者鉴别及失踪人员调查等法医工作中提供重要线索。随着衰老相关生物分子标志物研究的开展，多种生物标志物被证明与年龄密切相关，如DNA甲基化、端粒长度、非编码RNA等，基于生物分子标志物构建年龄推断模型成为法医遗传学的研究热点。本文就目前常见随龄变化的生物分子标志物在法医年龄推断领域中的应用现状进行综述。     

外伤性癫痫遗传标记物研究进展

外伤性癫痫(posttraumatic epilepsy, PTE)系由创伤性脑损伤(traumatic brain injury, TBI)所致,可导致严重的伤、残,甚至死亡,目前仍缺乏PTE评定的客观方法。近年来,已有很多关于PTE遗传标记物的研究报道,其中一些具有很好的应用前景。因此,遗传生物标记物可能是PTE评定的客观标志。本文综述了PTE相关遗传标记物的研究现状,为PTE的客观评定研究提供借鉴。     

CDK5的表达与脑损伤时间推断的相关性研究进展

细胞周期蛋白依赖激酶5(cyclin-dependent kinase 5,CDK5)是CDK家族中一类不直接调控细胞周期的蛋白。CDK5通过靶蛋白的磷酸化在神经细胞的发育、修复及退行性变等方面发挥着不可替代的作用。脑损伤是指暴力作用于头部造成的脑组织器质性损伤,由于损伤发生后机体启动应激及修复机制,脑组织中变化的多种蛋白及酶类物质可作为损伤时间判定的指标。本文就CDK5的分布、活性机制、生理作用及其脑损伤研究与其作为脑损伤标志物可能性的研究进展进行综述。     

大鼠脑外伤后溶酶体酶Cathepsin—B和D的表达

目的研究大鼠脑外伤后溶酶体酶cathepsin-B和-D是否被激活及其不同时段表达变化,阐述其与凋亡执行因子caspase-3表达的关系,并探讨对脑外伤诊断及形成时间的意义。方法采用自由落体打击法建立脑外伤动物模型,并对模型及对照样本进行免疫荧光、双标和激光共聚焦检测,结果用SPSS10.0软件处理。结果脑外伤后1hcathepsin-B表达即增加,4～8d达高峰,脑外伤后32d仍处于高表达水平;cathepsin-D的表达于脑外伤后12h增加,4～8d达高峰,32d的表达仍然高于12h的表达水平。脑外伤初期,cathepsin-B和-D阳性细胞与caspase-3阳性细胞重叠较少,脑外伤后6h开始增加,32d仍然有很多阳性细胞重叠。结论脑外伤后cathepsin-B和-D被激活,其激活在脑外伤早期可能抑制细胞凋亡执行因子caspase-3的激活,之后(6h后)则与caspase-3起协同作用,共同促进细胞死亡;cathepsin-B和-D表达的时程变化对于脑外伤的法医学诊断和中晚期的时间推断有参考意义。     

Could NF-kappaB and caspase-3 be markers for estimation of post-interval of human traumatic brain injury?

BACKGROUND: Previous studies in a rat model showed expressions of caspase-3 (p20) and NF-kappaB (p65) in different time after TBI. We test the activation changes of caspase-3 and NF-kappaB of human specimen after traumatic brain injury (TBI) in this study to see whether they could be markers to estimate post-intervals of TBI for forensic practice. MATERIAL AND METHODS: Caspase-3 (p20) and NF-kappaB (p65) immunohistochemical staining were performed on 39 TBI specimens (dead from TBI) and eight controls (dead from none TBI reasons) grouped 0, 12, 24, 48, 72, 168, 264 and 480 h. Positive cells were counted and image analysis techniques were used to determine the morphological changes in each group. RESULTS: Immunohistochemical analysis showed a marked induction of caspase-3 (p20) in every injured group compared with normal controls; each positive group has it's morphological character with variant positive cell count. NF-kappaB (p65) did not showed markedly change compared with normal controls until 168 h after TBI and almost all nerve cells were stained by NF-kappaB (p65) in 264 and 480 h groups. CONCLUSION: NF-kappaB (p65) could contribute to estimate delayed death cases after TBI for forensic applications. Caspase-3 (p20) estimating post-TBI intervals are dubious but could suggest TBI exists.     

颅脑损伤后血液中S100β含量与损伤程度的关系

目的探讨血清中S100β蛋白含量与创伤性脑损伤程度的关系及法医学意义。方法选取健康体检者、颅脑损伤患者和其他创伤患者各30名作为研究对象,再根据入院时的GCS评分,将颅脑损伤患者分为轻中型组（GCS≥8分）和重型组（GCS〈8分）。用ELISA法对上述研究对象血清中S100β蛋白含量进行检测。结果在脑外伤6h内,颅脑损伤组血清S100β蛋白含量较正常对照组和创伤对照组升高,差异有统计学意义（P〈0.05）;重型组与轻中型组相比,差异有统计学意义（P〈0.05）。血清中S100β蛋白含量越高,患者颅脑损伤程度越严重。结论S100β蛋白可作为早期检测创伤性颅脑损伤的指标之一,其含量越高,颅脑损伤程度越重。     

实验性脑挫伤后caspase-3表达的免疫组织化学研究

目的 观察大鼠在不同程度及不同时间脑挫伤后caspase-3表达的变化。方法 对48例实验性脑挫伤大鼠的脑组织进行检验,同时以10例非脑挫伤的脑组织做对照。结果 伤后1h,caspase-3即有表达;24～48h达高峰,2周时仍有阳性细胞存在。阳性细胞多集中于挫伤区及周围带皮质和脑实质内海马区;不同程度脑挫伤组之间于伤后1h,12h,24h,72h,1周和2周caspase-3表达有差异。结论 不同程度脑损伤后caspase-3表达量不同;在脑损伤后caspase-3的表达有时间变化规律,对探讨脑挫伤后二次损害原因和研究脑挫伤程度有一定意义。     

脑外伤者血浆NSE含量与损伤程度的相关性

目的探讨血浆中神经元特异性烯醇化酶（NSE）含量与创伤性脑损伤程度的关系及法医学意义。方法选取25名健康体检者、34名颅脑损伤患者作为研究对象,根据入院时的GCS评分,将颅脑损伤患者分为轻中型组（GCS≥8分）和重型组（GCS〈8分）。用酶联免疫法对上述研究对象血浆中神经元特异性烯醇化酶含量进行检测。结果在脑外伤24h内,颅脑损伤组血浆中神经元特异性烯醇化酶含量较正常对照组升高,差异有统计学意义（P〈0.05）,重型组与轻中型组相比,差异有统计学意义（P〈0.05）,血清中血浆中神经元特异性烯醇化酶含量越高,患者颅脑损伤程度越严重。结论神经元特异性烯醇化酶可作为早期检测创伤性颅脑损伤的特异性指标,其含量越高,颅脑损伤程度越重。     

实验性脑挫伤后caspase—1表达的研究

目的阐明不同程度及不同时间脑挫伤后caspase-1表达的变化。方法应用免疫组织化学染色、Western-blotting和RT-PCR方法对48例实验性脑挫伤大鼠的脑组织进行了检验,同时以3例非脑挫伤和3例假手术的脑组织做对照。结果脑挫伤后1h caspase-1即有表达,24-48h达高峰,挫伤后两周caspase-1阳性细胞仍维持较高水平。阳性细胞多集中于挫伤区及周围带皮质和脑实质内海马区,不同程度脑挫伤各组之间阳性细胞面积存在差异;损伤组caspase-1酶原裂解增加;损伤组caspase-1mRNA表达量明显高于对照组;不同程度脑挫伤组之间于各个时间段caspase-1mRNA表达未见差异。 结论 Caspase-1表达增加,可辅助诊断1h-14d的脑挫伤,并可根据caspase-1阳性细胞面积的变化来确定脑挫伤程度,同时对判断挫伤时间方面也有一定的价值。caspase-1参与脑挫伤后的神经细胞凋亡。     

钙依赖性蛋白激酶Ⅱδ在脑外伤后皮质中的表达变化

目的：观察钙-钙调素依赖性蛋白激酶Ⅱδ（calcium-calmodulin dependent protein kinaseⅡδ,CaMKⅡδ）在脑损伤后皮质中不同时段的表达变化。方法建立大鼠脑外伤模型,通过Western印迹法和免疫组织化学染色法检测损伤区周围皮质CaMKⅡδ的表达变化。结果 Western印迹法显示,CaMKⅡδ在正常皮质中有表达,损伤后表达上调,在损伤3d达到高峰,并随着损伤时间延长逐渐恢复到正常水平。免疫组织化学结果与Western印迹法结果一致。结论 CaMKⅡδ在脑组织损伤灶及其周围呈现先增高后降低的表达变化,为法医学推断脑外伤后损伤经过时间提供了新的参考指标。     

Traumatic brain injury in a forensic intellectual disability population

Traumatic brain injury (TBI) screening in forensic populations has been recommended, due to a high prevalence, links to specific offence profiles and poorer outcomes, such as higher rates of psychiatric disturbance, longer stays in prison, and reoffending. Research focusing on TBI among offenders with intellectual disability (ID) is lacking. This study therefore describes the implementation of TBI screening using the Brain Injury Screening Index (BISI©), TBI prevalence and correlates in a forensic ID service. TBI appeared under recorded in case notes, with considerably more patients self-reporting TBI. Reported causes of TBI differed somewhat to the general population, including childhood physical abuse, self-harming behaviour, and assault. Approximately one-third of injuries did not receive any treatment. Though further adaptations may be required on current screening measures for TBI in offenders with ID, screening can provide valuable information, contributing positively to individual patient therapeutic and risk formulations.     

The expression of excitatory amino acid transporter 2 in traumatic brain injury

It is well recognized that glutamate is the major excitatory neurotransmitter, which is removed from the synaptic cleft by excitatory amino acid transporter 2 (EAAT2) located on the perisynaptic astrocytes and that neuronal death has been associated with an increased extracellular glutamate concentration. In this study, we have immunohistochemically demonstrated the expression of EAAT2 protein in the human brain after traumatic brain injury (TBI). The EAAT2 expression patterns can be divided into three types: continuous and highly extensive staining (E); continuous but sporadic staining (M); and sporadic pattern staining (S). In six of the nine short survival cases studied (1 h to 1 day), continuous and highly extensive staining for EAAT2 (E type) was observed in the ipsilateral cerebral cortex. On the other hand, we were able to demonstrate weak staining (S and M types) in 5 of the 7 long survival cases (≥1 day) and in 12 of the 14 very short survival cases (<1 h) studied. Similar findings were obtained in the contralateral cerebral cortex and also in the ipsilateral hippocampus. In addition, positive staining for glial fibrillary acidic protein was detected around the cerebral contusion, but the EAAT2-positive expression was not observed in the same region for all of the six short and long survival cases (≥1 h) after TBI. These findings clearly showed the differences in EAAT2 expression in the cerebral cortex according to the survival time and severity of cerebral contusion after TBI. Therefore, we emphasized that EAAT2 might play an important role in contributing to extracellular glutamate concentrations and secondary brain injury after TBI.     

Chronic Traumatic Encephalopathy Pathology After Shotgun Injury to the Brain

Chronic traumatic encephalopathy (CTE) was initially conceptualized in boxers, but has extended to other athletes in recent years, albeit with limited clinical correlations. It is often asserted that CTE pathology represents the substrate for progressive neurodegenerative disease. We report the case of a shotgun injury to the brain with 42‐year survival and no neurological disease progression until shortly before death. The decedent had no other traumatic brain injury (TBI) exposure and did not play football or other high energy collision sport. Neuropathological examination confirmed tissue damage, but additionally demonstrated localized patterns of phosphorylated tau (p‐tau) meeting criteria for CTE pathology. P‐tau and TDP‐43 deposits within marginal tissue of damaged brain were also present focally. No amyloid‐β (Aβ) deposits were present. These findings indicate that CTE pathology may occur following a single, severe TBI.