本文選題：電損傷 + 電擊傷　； 參考：《重慶醫(yī)科大學(xué)》2007年碩士論文

【摘要】： 目的:電擊傷(electrical injury)和電擊死(electrouction)是法醫(yī)實(shí)踐工作中常遇的案例,但其診斷有一定的困難,因此對電擊傷和電擊死的研究具有重要意義。盡管已經(jīng)有很多學(xué)者對其進(jìn)行了大量的相關(guān)研究,但是在沒有典型的電擊損傷標(biāo)志(如皮膚電流斑、金屬化)出現(xiàn)時(shí)仍然沒有哪一個(gè)指標(biāo)可以直接對電擊傷和電擊死進(jìn)行診斷。在實(shí)際工作中,研究發(fā)現(xiàn)只有約1/3的案例出現(xiàn)典型的電擊標(biāo)志,故對未出現(xiàn)典型電擊標(biāo)志的疑似電擊傷和電擊死的診斷尤為重要。有文獻(xiàn)報(bào)道在對電擊傷進(jìn)行心臟組織基因芯片研究時(shí)發(fā)現(xiàn)PEG-3在電擊傷案例中有顯著增高,本實(shí)驗(yàn)采用了免疫組織化學(xué)和原位雜交的方法,旨在觀察: 1. PEG-3在電擊傷和電擊死中的診斷價(jià)值; 2. PEG-3在電擊傷后的時(shí)間表達(dá)相關(guān)性; 3. PEG-3在死后電擊和電擊死中的表達(dá)情況。 方法:將250-300g的Wister大鼠分成隨機(jī)分成兩大組:陰性對照組和實(shí)驗(yàn)組,陰性對照組又按照斷頸處死后取材時(shí)間的不同分為6個(gè)亞組(0 h, 0.5h, 1h, 3h, 6h, 12h)實(shí)驗(yàn)組又分為3個(gè)小組,即:電擊傷組(0h, 3h, 6h, 12h, 24h, 3d, 6d, 12d)、電擊死組(0h, 1h, 3h, 6h, 12h )和死后電擊組(0 h, 0.5h, 1h, 3h),共計(jì)23組(n=3)。建模的方法分別是: 1.陰性對照組采用斷頸處死; 2.電擊傷組是將老鼠電擊30秒;電擊死組則是將老鼠直接電死;死后電擊組是在斷頸處死后分別于相應(yīng)的時(shí)間進(jìn)行電擊,電擊時(shí)間60s;模型建立后分別在相應(yīng)的時(shí)間取心臟組織(取材的部位均為左心室前壁中央部)。進(jìn)行HE、免疫組織化學(xué)和原位雜交染色,然后進(jìn)行半定量分析。 結(jié)果:1.HE染色可見電擊傷組在3-6h期間,心肌多灶性壞死,廣泛心肌斷裂、缺血,部分心肌細(xì)胞呈波紋狀排列及收縮帶壞死;心肌胞漿凝聚、均質(zhì)變和嗜酸變,部分心肌橫紋不清,胞核固縮、深染、扭曲,部分核伸長,部分核染色質(zhì)邊集、核膜增厚、呈空泡狀;心肌間隙增寬,水腫,部分區(qū)域散在出血;細(xì)小血管擴(kuò)張,紅細(xì)胞聚集,血管內(nèi)皮細(xì)胞細(xì)胞核固縮、深染,平滑肌變性。12h-3d期間,心肌變性壞死的范圍擴(kuò)大,心肌細(xì)胞渾濁腫脹更加明顯,心肌細(xì)胞內(nèi)小肌束間隙增寬使心肌橫斷面呈篩狀;心肌細(xì)胞橫紋不清,部分心肌細(xì)胞呈肌溶解、肌漿淡染,部分心肌細(xì)胞核消失;心肌間細(xì)小血管擴(kuò)張,內(nèi)皮細(xì)胞腫脹、壞死、脫落,平滑肌層疏松腫脹,大量紅細(xì)胞黏附于血管壁,管腔內(nèi)嗜中性粒細(xì)胞聚集,僅個(gè)別炎癥細(xì)胞游出血管外。6d-12d期間,心肌變性壞死范圍仍在擴(kuò)大,大片心肌溶解壞死,肌間隙明顯增寬。電擊死組也可以看到心肌細(xì)胞的變性壞死,死后電擊組只在死后即刻電擊可以看到心肌的缺血性改變,而陰性對照組則未見異常。 2.免疫組織化學(xué)染色和原位雜交染色可見直接電擊死組和電擊傷組心肌細(xì)胞內(nèi)有很強(qiáng)的陽性染色,位于肌漿內(nèi),在電擊傷后即刻即開始增加,在12h時(shí)達(dá)到高峰,而后逐漸減少,在12d時(shí)其值仍高于對照組,但與對照組接近;電擊致死組也呈強(qiáng)陽性表達(dá),在電擊致死后即刻表達(dá)就開始增加,3h時(shí)達(dá)到高峰,而后逐漸減少,12h時(shí)其值仍高于對照組,但與對照組接近;而陰性對照組和死后電擊組只有極其微弱的陽性染色。以上這一變化規(guī)律可推斷心肌電損傷所經(jīng)過的時(shí)間。 結(jié)論:在電擊傷和直接電擊死早期即可見大量的心肌纖維斷裂,胞漿凝聚以及嗜酸性變;細(xì)胞核的固縮、深染、扭曲以及部分核伸長和空泡樣變化,這些改變與急性心肌梗死及其他心肌疾病、損傷的病理改變不盡相同,說明這些損傷是電流作用的結(jié)果。免疫組化和原位雜交的強(qiáng)陽性染色也說明電流對心肌造成了損傷. PEG-3是與細(xì)胞核損傷相關(guān)的基因,在心肌電損傷和電擊致死的早期即表達(dá)增高,而在其他心肌損傷及非腫瘤性心肌疾病中很少在早期出現(xiàn)高表達(dá),這提示PEG-3有助于診斷心肌電損傷,可將其作為一個(gè)診斷早期心肌電損傷的指標(biāo)。此外,還發(fā)現(xiàn)其在電擊傷和直接電擊死后不同時(shí)間的表達(dá)有一定的規(guī)律,根據(jù)這一規(guī)律的變化可推斷心肌電擊傷(死)的時(shí)間。而在死后電擊則只有弱表達(dá),根據(jù)這點(diǎn)可以將死后電擊和電擊致死進(jìn)行區(qū)分。
[Abstract]:Objective: electrical injury (electrical injury) and electric shock (electrouction) are common cases in forensic practice, but their diagnosis is difficult. Therefore, it is of great significance for the study of electrical injury and electric shock death. No one index, such as skin current spots, metallization, can be used to diagnose electrical injury and shock death. In actual work, only about 1/3 cases are found to have typical electric shock signs, so it is particularly important for the diagnosis of suspected electrical injury and shock death without typical electric shock signs. It was found that PEG-3 was significantly increased in the case of electrical injury when the cardiac tissue microarray was studied. This experiment was conducted by immunohistochemistry and in situ hybridization.
1. the diagnostic value of PEG-3 in electrical injury and electrocution.
2. PEG-3 was associated with the time after electrical injury.
3. the expression of PEG-3 in electrocution and electrocution after death.
Methods: the Wister rats of 250-300g were divided into two groups randomly: negative control group and experimental group. The negative control group was divided into 6 subgroups (0 h, 0.5h, 1H, 3h, 6h, 12h) and divided into 3 groups according to the difference of the time after the death of the neck. The experimental group was divided into 3 groups, namely, the electrical injury group (0h, 3h, 6h, 12h, 12h, 12h, 6h, etc.) 6h (12h) and postmortem shock group (0 h, 0.5h, 1H, 3H), a total of 23 groups (n=3).
1. the negative control group was executed with broken neck.
The 2. electric injury group was a mouse electric shock for 30 seconds; the electric shock group was killed directly by the mouse; after the death, the electric shock group was struck at the corresponding time after the death of the neck, and the electric shock time was 60s. After the model was established, the heart tissue was taken at the corresponding time (the central part of the left ventricle was in the central part of the left ventricle). In situ hybridization, and then semi quantitative analysis.
Results: 1.HE staining showed multifocal necrosis of myocardium in the electrical injury group during 3-6h, extensive myocardial rupture, ischemia, partial myocardial cells with ripple arrangement and contraction zone necrosis, myocardial cytoplasm condensation, homogenization and eosinophilia, partial myocardial transmutation, nuclear condensation, deep staining, distortion, partial nucleus elongation, partial nucleus chromatin set and thickening of nuclear membrane. The myocytes were vacuolated; the interventricular space was broadened, edema, and partial areas were scattered; the small vessels dilated, the red blood cells gathered, the vascular endothelial cell nuclear condensation, the deep staining and the smooth muscle degeneration.12h-3d, the range of myocardial degeneration and necrosis expanded, the turbid swelling of the cardiac myocytes was more obvious, and the widening of the small myoplastic space within the myocardial cells made the transverse section of the myocardium present the cross section of the myocardium. Sieves; myocardial cells were indistinct, some of the myocytes were myolysis, myoplasm was pale, and some of the nucleus of the myocardium disappeared; the small blood vessels were dilated, the endothelial cells swelled, necrotic, exfoliated, the smooth muscle layer was loose and swollen, a large number of red cells adhered to the vascular wall, the neutrophils gathered in the lumen, and only a few inflammatory cells swam out of the extravascular.6d-1 During the period of 2D, the extent of myocardial degeneration and necrosis was still enlarged, large myocardial infarction was dissolved and necrotic, and the muscle space was broadened obviously. The necrosis of myocardial cells could be seen in the death group of electric shock. The ischemic changes of myocardium could be seen in the post death electric shock group only after death, but the negative control group had no abnormal.
2. immuno histochemical staining and in situ hybridization showed that there was a strong positive staining in the cardiac myocytes of the direct electric shock group and the electric injury group. It was located in the muscular plasma and increased immediately after the electrical injury. It reached the peak at 12h and then decreased gradually. At 12D, its value was still higher than that of the control group, but it was close to the control group; and the death group in the electric shock was also present. The expression of strong positive expression began to increase immediately after the death of electric shock, and reached the peak at the time of 3H, and then decreased gradually. The value of 12h was still higher than that of the control group, but it was close to the control group, while the negative control group and the post death electric shock group had only a very weak positive staining. The above change rules could deduce the time of myocardial electrical injury.
Conclusions: in the early stages of electrical injury and direct shock death, a large number of myocardial fibers, cytoplasm agglomerates and eosinophilic changes are visible, nuclear condensation, deep staining, distortion, and partial nuclear elongation and vacuolating change are different from the pathological changes of acute myocardial infarction and other myocardial diseases and injury, indicating that these injuries are current. The strong positive staining of immunohistochemistry and in situ hybridization also showed that the current caused damage to the myocardium.
PEG-3 is a gene associated with nuclear damage, which is increased in the early stage of myocardial electrical injury and death by electric shock, and is rarely expressed in the early stages of other myocardial injury and non tumor myocardium diseases. This suggests that PEG-3 can help diagnose electrical injury of the myocardium, and can be used as an indicator for the diagnosis of early myocardial damage. It is found that there is a certain regularity in the expression of electric shock and direct electric shock at different time after death. The time of myocardial electrical injury (death) can be deducted according to the change of the law. And the electric shock is only weak after death. According to this, the electric shock and the death of electric shock can be distinguished.
【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2007
【分類號】：D919

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