大鼠皮肤挫裂创细胞间粘附分子-1的表达

目的 观察大鼠皮肤钝器伤后细胞间粘附分子-1(ICAM-1)表达的变化规律。方法 应用免疫组化方法,观察大鼠皮肤钝器伤后1h、3h、6h、12h、1d、3d、5d、7d、9d ICAM-1的表达情况,并用MIAS图像分析系统进行图像分析。结果 正常对照组大鼠皮肤有低水平ICAM-1表达,钝器伤后ICAM-1表达增加,伤后7d达峰值,伤后9d开始下降。结论 皮肤钝器伤可诱导ICAM-1表达增加,其时序性变化可望作为一种客观指标用于法医学损伤时间的推断。     

The relevance of the detection of troponins to the forensic diagnosis of cardiac contusion

The forensic diagnosis of cardiac contusion has hitherto been based mainly on anamnesis, concomitant thoracic injuries and the detection of macroscopic changes to the heart. Parallel histological and serological investigations of the heart-specific troponins have been conducted with varying results. This paper aims to show whether heart-specific troponins are suitable as a means of securing the diagnosis in proven cases of cardiac contusion and of determining which of the three heart-specific troponins cTnT, cTnI and cTnC are most significant in serology and histology for postmortem diagnosis.In the study, 25 cases of known cardiac contusion and 11 controls without vital myocardial trauma taken from autopsy material were prospectively investigated. Investigation of the venous serum revealed significant differences in the concentrations of the case and control groups for troponin T (mean value 5.5056 versus 0.4982; p = 0.014), for troponin C (mean value 263.9280 versus 68.5640; p = 0.001) and for troponin I (mean value 1404.0560 versus 36.1650; p = 0.003). In histology there are also significantly different depletions between the groups investigated (cTnT: p = 0.002; cTnC: p = 0.003; cTnI: p < 0.001) taking into account the autolysis time.     

大鼠脑挫伤后脑组织COX-1/COX-2的表达

目的　观察脑损伤后COX 1和COX 2蛋白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　以自由落体撞击雄性SD大鼠右顶叶制备脑挫伤模型 ,用免疫组织化学SP法处理脑组织检材 ,观察不同时间 ( 1、 3、 5、 7、 14d)脑组织COX 1/COX 2蛋白的表达情况。结果　正常及手术对照组大鼠 ,脑组织内有低水平的COX 1/COX 2表达 ;脑挫伤后 1～ 5d ,大鼠脑组织内COX 1表达逐渐增加 ,14d时仍维持在高表达水平 ;脑挫伤后 1～ 3d ,大鼠脑组织皮质内COX 2表达逐渐增加 ,1d时海马COX 2表达达高峰。结论　脑挫伤后可诱导COX 1/COX 2蛋白在脑内表达 ,并呈现出时序性变化。     

大鼠皮肤挫伤修复过程中NF_κB P65表达的研究

目的探讨皮肤挫伤修复过程中,核转录因子(NFkB)P65在挫伤区不同时间表达的变化规律。方法 应用免疫组化技术对挫伤后0h、3h、6h、9h、12h、1d、3d、5d、7d、10d的大鼠皮肤挫伤组织中NFkB P65的表达进行研究。结果伤后3h,挫伤区内浸润的少量多核粒细胞的胞质中NFkB P65呈弱阳性表达,阳性率为(3.20％±0.15％);伤后6h,阳性表达增强,阳性率为(11.33％±0.88％);伤后12h,表达继续增强,阳性率(75.67％±0.82％);伤后1d,在浸润的几乎所有单核细胞和多核粒细胞的胞质和胞核中均可见NFkB P65呈强阳性表达,阳性率为(97.33％±0.88％),表达达高峰,以后逐渐下降。结论 大鼠皮肤挫伤修复过程中,NFkB P65在挫伤后的炎症反应中发挥重要作用;同时,NFkB P65在挫伤区内多核粒细胞,单核细胞及成纤维细胞中的表达呈规律性变化,可对挫伤时间的推断提供参考。     

病毒性心肌炎和扩张性心肌病心肌中β-sarcoglycan的免疫组化染色观察

目的探讨病毒性心肌炎(viralmyocarditis,VCM)和扩张型心肌病(dilatedcardiomyopathy,DCM)的发病机制及相互关系,从而提高心性猝死法医学鉴定的可靠性和准确性。方法对17例对照组(包括冠心病、高血压性心脏病和正常心脏等),25例VCM和28例DCM的心肌组织进行改良的β-sarcoglycan免疫组织化学染色观察,并对其阳性反应率进行χ2检验及相关分析。结果β-SG蛋白在对照组,VCM组和DCM组中阳性反应率分别为100%,80%,46.4%。经χ2检验,3组阳性反应率差异有显著性意义(P<0.05);用χ2分割法分析,VCM和DCM组间差异有显著意义(P<0.05),且Spearman等级相关分析呈显著负相关(rs=-0.605)。结论病毒性心肌炎和扩张性心肌病病变与β-SG的被破坏有关;随着VCM病变程度的加重,其可能发展为DCM。     

大鼠急性早期心肌梗死细胞膜PNA受体表达

探测急性心肌缺血早期细胞膜PNA受体的表达特点。应用免疫组化法(S-P法)对32只SD大鼠急性心肌缺血早期不同时间心肌细胞膜凝集素受体的表达进行研究。结果发现:心肌缺血15min时,心肌局部可出现PNA染色阳性,且随着缺血时间的延长,其阳性表达面积明显增加;缺血2h;其表达水平达到高峰,呈弥漫性染色阳性,明显高于对照组;2h后,心肌缺血区域PNA受体的表达开始出现下降趋势。实验结果稳定,敏感性强,可为心肌缺血早期诊断提供客观的依据。     

心肌早期缺血再灌流损伤免疫组化观察

探询原癌基因c fos蛋白产物在心肌早期缺血再灌流损伤中的病理形态学改变。用SD大白鼠建立心肌早期缺血再灌流损伤模型 ,3 2只大鼠分为正常、缺血对照组与缺血再灌流组。心脏标本经HE染色及免疫组化观察。结果发现 :在缺血 3 0min再灌流 3 0min后 ,再灌流区心肌细胞有部分细胞核 ( 3 7 76%± 9 66% )呈弱阳性着色 ,而在缺血 60min再灌流 3 0min后 ,心肌细胞核 ( 4 0 3 4 %± 3 3 2 % )呈棕褐色阳性染色 ,但正常和单纯缺血组心肌细胞核未见有阳性反应 ;HE染色无明显改变。提示c fos蛋白免疫组化对显示实验性心肌早期缺血再灌流损伤有重要的价值     

Immunohistochemical detection of CCR2 and CX3CR1 in sepsis-induced lung injury

Sepsis is a systemic inflammatory disease with high mortality. In the present study, we immunohistochemically examined CCR2 and CX3CR1 expression in sepsis-induced lung injury, and discussed its availability for the postmortem diagnosis of sepsis. Lung samples were obtained from different lung lobes of nine sepsis and eight control cases with postmortem intervals between 12 and 48 h. Immunohistochemically, mononuclear cells recruited into the lungs expressed CCR2 and CX3CR1 in both sepsis and non-septic groups. In double-color immunofluorescence analysis, CCR2- or CX3CR1-positive cells could be identified as CD68-positive macrophages. Moreover, most of CD68-positive macrophages expressed both CCR2 and CX3CR1. Morphometrically, the average of CCR2- and CX3CR1-positive macrophages was significantly increased in sepsis group, compared with control group (sepsis vs. control: 41.6 ± 1.3% vs. 8.0 ± 0.4% in CCR2; 36.2 ± 1.3% vs. 9.2 ± 0.4% in CX3CR1). These observations implied that CCR2- or CX3CR1-positive macrophages were recruited into the lungs under several pathological conditions. In particular, their recruitment might be more evident in sepsis. Moreover, from the forensic aspects, immunohistochemical detection of CCR2 and CX3CR1 expression in the lungs can be considered as valuable diagnostic tools for the postmortem diagnosis of sepsis.     

挤压伤——挤压综合征的实验病理学研究

观察挤压伤后挤压综合征的发生发展过程及肾脏病理改变特点。以家兔制造挤压伤—挤压综合征的动物模型 ,取血和尿进行生化检验并应用光镜、电镜及免疫组化等方法 ,观察肾脏的形态学改变。结果显示 :(1)挤压伤后血K+和血BUN明显升高 ,血CO2 CP明显下降 (P <0 0 5 ) ;(2 )在挤压综合征时 ,肾脏肾小球肿胀 ,肾小管上皮细胞不同程度的变性坏死 ,管腔内有以肌红蛋白为主要成分的管型 ,血BUN持续下降 ,血K+改变不明显。肾小管上皮细胞的变性坏死及肾小管内肌红蛋白管型形成可作为挤压综合征的法医病理学诊断依据之一 ,血K+升高是挤压伤后急性死亡的原因之一