急性乙醇中毒和外伤在蛛网膜下腔出血致死机制中的作用

目的研究人脑在急性乙醇中毒状态下tPA、MMP-2、MMP-9及AEG-1表达水平与乙醇浓度的关系,分析乙醇与外伤在蛛网膜下腔出血死亡机制中的作用。方法选取15例实际案例,提取脑组织进行组织病理学检查、心血进行乙醇浓度检测,用免疫组织化学法观察人脑干、大脑、小脑tPA、MMP-2、MMP-9及AEG-1表达水平。结果急性乙醇中毒外伤组和急性乙醇中毒组的脑组织肿胀。除小脑tPA外,tPA、MMP-2、MMP-9及AEG-1表达水平在饮酒者较未饮酒者在脑干、大脑、小脑均有升高(P0.05),MMP-2、MMP-9和AEG-1表达水平与心血乙醇浓度存在正相关(P0.05,r0.6)。结论急性乙醇中毒状态下人脑tPA、MMP-2、MMP-9、AEG-1表达较未饮酒者均显著增强,MMP-2、MMP-9及AEG-1表达水平与乙醇浓度存在相关性,乙醇对脑细胞有毒性作用。     

Sudden Death due to Brainstem Leukemic Hemorrhage:A Case Report

Introduction Leukemia is a hematologic neoplasm character- ized by potential infectious and hemorrhagic com- plications. In adult patients with acute leukemia, in- fection is the most common complication. Intracra- nial hemorrhage （ICH） is the second most common complication. However, ICH has been identified as the major cause of morbidity and mortality in pa- tients with leukemia[1-6].     

Identifying Fatal Head Injuries on Postmortem Computed Tomography Using Convolutional Neural Network/Deep Learning: A Feasibility Study

Postmortem computed tomography (PMCT) is a relatively recent advancement in forensic pathology practice that has been increasingly used as an ancillary investigation and screening tool. One area of clinical CT imaging that has garnered a lot of research interest recently is the area of “artificial intelligence” (AI), such as in screening and computer-assisted diagnostics. This feasibility study investigated the application of convolutional neural network, a form of deep learning AI, to PMCT head imaging in differentiating fatal head injury from controls. PMCT images of a transverse section of the head at the level of the frontal sinus from 25 cases of fatal head injury were combined with 25 nonhead-injury controls and divided into training and testing datasets. A convolutional neural network was constructed using Keras and was trained against the training data before being assessed against the testing dataset. The results of this study demonstrated an accuracy of between 70% and 92.5%, with difficulties in recognizing subarachnoid hemorrhage and in distinguishing congested vessels and prominent falx from head injury. These results are promising for potential applications as a screening tool or in computer-assisted diagnostics in the future.     

等速肌力检测在辨别伪肢体瘫中的应用

目的：探讨等速肌力检测在法医学鉴定中辨别伪肢体瘫的应用价值,为建立规范、统一的法医学肌力评价方法提供科学依据。方法选取骨折或神经损伤者57例（损伤组）和伪装者128例（伪装组）,应用等速肌力测试系统对损伤组两侧膝关节与伪装组膝关节进行检测,对双侧膝关节屈、伸肌的峰力矩（peak torque,PT）、峰力矩角度（peak torque angle,PTA）进行比较,归纳两组膝关节的力矩-时间图特征。结果损伤组膝关节屈、伸肌的双侧PT的比较差异有统计学意义（P＜0.05）,PTA的比较差异无统计学意义（P＞0.05）;伪装组膝关节屈、伸肌的双侧PT、PTA的比较差异均有统计学意义（P＜0.05）。损伤组两侧膝关节力矩-时间图主要为单峰前置型,伪装组膝关节力矩-时间图主要为多峰型。结论在法医学鉴定中,等速肌力检测在辨别伪肢体瘫方面可以通过力矩-时间图的相关特点进行评价。     

利多卡因在蛛网膜下腔和静脉注射致死犬体内的死后分布

目的比较利多卡因在蛛网膜下腔和静脉注射致死犬体内的死后分布特点。方法犬12只,其中6只经蛛网膜下腔,另6只经股静脉匀速注入利多卡因(5×15mg/kg)致死,迅速解剖动物,取大脑、侧脑室脑脊液、腰段脊髓腔脑脊液、不同脊髓节段(颈髓、胸髓、腰髓、骶髓),心、肺、肝、脾、肾、胆汁、尿、心血、周围血、注射部位肌肉和注射部位20 cm以外肌肉等脏器组织和体液,用气质联用法定性,气相色谱法定量检测其中利多卡因含量。结果蛛网膜下腔注射致死犬体内利多卡因的含量由高到低顺序依次为腰段脊髓腔脑脊液、骶段脊髓、胸段脊髓、侧脑室脑脊液、腰段脊髓、颈段脊髓、肺、肾、注射部位肌肉、心、大脑、脾、心血、肝、周围血、胆汁、注射部位20 cm以外的肌肉、尿;静脉注射致死犬体内利多卡因的含量由高到低顺序依次为肾、心、肺、脾、大脑、肝、周围血、胆汁、心血、颈段脊髓、胸段脑脊液、注射部位肌肉、腰段脊髓、注射部位20 cm以外的肌肉、侧脑室脑脊液、尿、腰段脊髓腔脑脊液、骶段脊髓。结论蛛网膜下腔注射致死犬背侧脊髓液中利多卡因含量最高,静脉注射致死犬肾脏利多卡因含量最高,此分布特征可为利多卡因麻醉意外法医学鉴定中入体途径的判定提供参考。     

酗酒后外伤性蛛网膜下腔出血及其死因分析

酗酒后外伤性蛛网膜下腔出血及其死因分析于晓军，吴家Ａｎａｌｙｓｉｓｏｆｃａｕｓｅｏｆｄｅａｔｈｆｏｌｌｏｗｉｎｇｔｒａｕｍａｔｉｃｓｕｂａｒａｃｈｎｏｉｄｈａｅｍｏｒｒｈａｇｅａｆｔｅｒｄｒｕｎｋ￥ＹｕＸｉａｏｊｕｎ；ＷｕＪｉａｗｅｎ（Ｄｅｐａｒｔｍ...     

头颈外伤致椎动脉破裂伴颅底蛛网膜下腔出血1例尸检分析

头颈外伤致椎动脉破裂伴颅底蛛网膜下腔出血１例尸检分析易旭夫，刘敏，吴家Ｓｕｂａｒａｃｈｎｏｉｄｈａｅｍｏｒｒｈａｇｅｄｕｅｔｏｒｕｐｔｕｒｅｏｆｔｈｅｖｅｒｔｅｂｒａｌａｒｔｅｒｙａｓｓｏｃｉａｔｅｄｗｉｔｈｈｅａｄｔｒａｕｍａ：ｒｅｐｏｒｔｏｆｏｎ...     

慢性乙醇中毒脑β-淀粉样前体蛋白与外伤性蛛网膜下腔出血死亡的关系

目的观察大鼠慢性乙醇中毒下脑组织轻微伤后β-淀粉样前体蛋白(β-amyloid precursor protein,β-APP)的表达,探讨乙醇中毒与外伤性蛛网膜下腔出血(traumatic subarachnoid haemorrhage,TSAH)死亡的相关性。方法雄性SD大鼠60只,随机分为灌水组、灌水打击组、灌酒组、灌酒打击组。灌酒组以食用酒连续灌胃4周,打击组予脑震荡打击,各组大鼠脑组织行HE、免疫组织化学染色,组织病理图像系统量化分析检测结果。结果灌水组脑无异常;灌水打击组全脑神经元轻度水样变性;灌酒组脑表面可见血管纹理,神经纤维排列稍疏松、间隙增大;灌酒打击组脑表面弥漫性淤血,脑干周围多见厚层斑片状TSAH,轴索不规则断裂。灌酒组额叶、海马、小脑、脑干β-APP IOD值高于灌水打击组及灌酒打击组。结论慢性乙醇中毒脑组织的耐受性明显下降,轻微损伤情况下即可引起致死性TSAH和神经病理学变化。     

Subarachnoid Hemorrhage and Carbon Monoxide Exposure: Accidental Association or Fatal Link?

This case study reports a fatal subarachnoid hemorrhage (SAH) with concomitant accidental carbon monoxide (CO) exposure in 32‐year‐old man. Autopsy results indicated an antemortem aspiration of smoke, and a massive SAH was identified as the cause of death. Intriguingly, the carboxyhemoglobin level was 30%, suggesting that CO could have played a specific role. Intracranial hemorrhages following CO exposure in brain areas and tissues such as the basal ganglia, globus pallidus, or white matter are rare, but well characterized, whereas SAH related to CO exposure has not been previously described. In this case report, the possible role of CO, either as a primary cause or as a facilitating factor, in the pathogenesis of SAH is discussed. In particular, we propose the hypothesis that the excessive vasodilating effects produced by CO on the cerebral endothelium results in consequential loss of microvascular integrity.