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为了探讨抗肌动蛋白单克隆抗体(HHF35)在早期心肌梗死死后诊断的特异性,作者用免疫组织化学S-P法检测梗死心肌和其它非梗死性的直接或间接心肌损害的心肌HHF35染色的变化。结果:梗死心肌均可见不同程度的HHF35缺染,其它非梗死性的直接或间接心肌损害的心肌中,如心脏挫伤、心肌炎、出血性休克、电击死、机械性窒息等,也有不同程度的HHF35缺染。因此用HHF35免疫组织化学方法诊断早期心肌梗死需慎重 相似文献
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纤维连接蛋白在诊断心肌梗死的特异性研究 总被引:6,自引:1,他引:5
探讨纤维连接蛋白 (Fn)对心肌梗死死后诊断的特异性。应用免疫组织化学和图像分析技术 ,对正常心脏、心肌梗死及其它非梗死性因素 ,如心肌炎、窒息、电击死、出血性休克、心挫伤、有机磷中毒等 ,直接或间接引起心脏损害时心肌细胞内Fn的变化进行研究。结果发现 :Fn仅在心肌梗死与心肌炎病例出现阳性反应 ,其阳性反应面积同正常对照组存在显著性差异 ,在窒息、电击死、出血性休克、心挫伤、有机磷中毒等病例未见明显阳性反应。Fn作为心肌梗死死后诊断指标仅受心肌炎的影响 ,对诊断心肌梗死具有较好的特异性 相似文献
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目的 研究cTnI免疫组织化学法诊断人体急性心肌梗死的法医病理学意义.方法 应用免疫组织化学法检测人体冠心病心肌组织cTnI的变化,进行图像分析,与HE染色法进行比较.结果 人体冠心病心肌组织急性心肌梗死区域心肌细胞内cTnI免疫组化染色缺染、分布失规律性;梗死修复区域纤维间质cTnI免疫组化染色弱阳性:陈旧性心肌梗死瘢痕区域纤维间质cTnI免疫组化染色阴性.失血性休克组近心内膜心肌细胞内cTnI免疫组化染色轻度增强,并见点灶状心肌细胞内cTnI免疫组化染色缺染.结论 cTnI免疫组织化学检测可以应用于人体急性心肌梗死的诊断. 相似文献
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为了探讨补体 C5在心肌梗死死后诊断的特异性,应用免疫组织化学和图像分析技术 ,对正常心脏、心肌梗死及其它非梗死性的引起直接或间接心脏损害的情况如心肌炎、窒息、电击死、出血性休克、心挫伤、有机磷中毒等心肌细胞内 C5的变化进行研究。结果发现: C5仅在心肌梗死与心肌炎病例出现阳性反应,其阳性反应面积同正常对照组存在显著性差异,在窒息、电击死、出血性休克、心挫伤、有机磷中毒等病例未见明显阳性反应。因此 C5作为心肌梗死死后诊断指标仅受心肌炎的影响,对诊断心肌梗死具有较好的特异性。 相似文献
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为探讨纤维蛋白原(Fg)在心肌梗死死后诊断的特异性,应用免疫组织化学和图像分析技术,对正常心脏、心肌梗死及其它非梗死性的引起直接或间接心脏损害的情况如心肌炎、窒息、电击死、出血性休克、心挫伤、有机磷中毒等心肌细胞内Fg的变化进行研究。结果发现:正常对照组心肌细胞内未见Fg阳性反应,而心肌梗死、心肌炎、窒息、电击、休克、心挫伤、有机磷中毒等组均可见Fg阳性反应,且各组Fg阳性反应面积与正常对照组存在显著性差异。因此Fg作为心肌梗死死后诊断指标,易受心肌炎、窒息、电击、休克、心挫伤、有机磷中毒等的影响,对诊断心肌梗死的特异性较差。 相似文献
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In order to explore the specificity of anti-muscle actin monoclonal antibody HHF35 in the postmortem diagnosis of early myocardial infarction, the changes of HHF35 staining in the infarcted myocardia and other non-infarcted myocardia with direct or indirect myocardial injury were studied with immunohistochemical S-P method. The results showed that the loss of HHF35 staining of different degrees was found in the infarcted myocardia, but also in the other non-infarcted myocardia with direct or indirect myocardial injury, such as cardiac contusion, myocarditis, hemorrhagic shock, electrocution, mechanical asphyxia. So it should be cautious in diagnosing early myocardial infarction with HHF35 immunohistochemistry. 相似文献
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Rodríguez-Calvo MS Tourret MN Concheiro L Muñoz JI Suárez-Peñaranda JM 《The American journal of forensic medicine and pathology》2001,22(3):278-284
Myocardial samples of hearts with histologic findings of acute myocardial infarction (group A), sudden coronary deaths without histologic changes (group B), and chronic ischemic heart disease (group C) were analyzed to investigate the appearance of apoptosis in acute and chronic ischemic cardiac disorders. This analysis involved the morphologic detection of DNA strand breaks in myocyte nuclei by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay and the biochemical determination of DNA laddering in the myocardium using archival formalin-fixed, paraffin-embedded tissue sections of human myocardium. The authors demonstrated that apoptosis of myocardial cells could occur after ischemic myocardial cell injury. In all documented cases of acute myocardial infarction (group A), the infarcted area included extensive presence of both apoptosis and necrosis. In the tissue bordering on and away from the obviously infarcted areas, positive nuclei were intermingled with nonstained normal myocytes. The number of positive nuclei decreased with the distance from the infarction foci. In group B, myocardial samples showed focal or diffuse nuclear positivity of varying degrees for apoptosis, confirming the presence of myocardial ischemic cell death, whereas the histologic diagnosis remained inconclusive. This finding suggests that apoptosis could be used as a marker for acute ischemic injury. In group C, stained nuclei were dispersed with intermingled normal cardiomyocytes. 相似文献
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Shashi Kiran Jasra Ph.D. Cherryl Badian B.F.Sc. Iain Macri B.F.Sc. Paul Ra M.D. 《Journal of forensic sciences》2012,57(6):1595-1600
Abstract: The diagnosis of early myocardial infarction (MI) after death, especially in the first few hours (c. 6 h) after the onset of MI, poses a challenge to the forensic pathologists. During this time, the damaged myocardium does not show grossly identifiable morphological changes and may not be recognized even with routine histological microscopic examination. However, the infarcted cardiac tissue releases certain chemicals that can be detected microscopically, two of these being cardiac troponin‐I (CT‐I) and complement C9 (C9). This study utilizes the importance of these two biomarkers immunohistochemically in an attempt to identify this early phase of MI. This study reveals that the early phase of MI of <6 h duration may be detected through immunohistochemical staining with CT‐I and C9. The ischemic/infarcted cardiac myofibers in the <6 h group display reduced/absent CT‐I staining as well as positive C9 staining. 相似文献