肿瘤坏死因子及中性粒细胞在脊髓继发性损伤中的作用

目的 探讨炎性反应对脊髓损伤细胞凋亡的影响及其作用机制。方法 健康Wistar大鼠48只。随机分为2组，实验组与对照组。采用Allen法挫伤大鼠T10节段脊髓，于术后1、8h和1、2、3、7d取材。检测肿瘤坏死因子（TNF）与髓过氧化物酶水平的变化。结果 实验组肿瘤坏死因子与髓过氧化物酶水平均明显升高（P〈0．01）。结论 中性粒细胞及TNF-α参与了脊髓继发性损伤，并可能是触发迟发性神经元凋亡的重要因素之一。     

大鼠肝细胞凋亡和坏死动物模型的建立及评价

目的:通过大鼠肝右叶血供干预分别建立肝细胞凋亡和坏死动物模型,为进一步的磁共振成像实验奠定基础。方法:选取体重为250-300克的SD大鼠90只,随机分为A、B、C三组,每组30只,分别行肝右叶门静脉和肝动脉结扎术、门静脉结扎术及假手术,各组在术后3 h及1、3、7和14 d分别处死6只大鼠,取肝脏标本送病理及电镜检查。结果: A组30只大鼠肝右叶发生凝固性坏死,光镜及电镜下均呈典型的坏死改变,TUNEL染色呈阴性;B组30只大鼠肝右叶发生小灶性凋亡,光镜下可见肝细胞核固缩改变,电镜下见肝组织核边集和凋亡小体,TUNEL染色呈阳性改变。术后3 h 即可见凋亡细胞,24 h时凋亡细胞数最多,7 d后肝组织开始发生小灶性坏死;C组30只大鼠肝右叶未发生凋亡和坏死的病理改变。结论:大鼠肝右叶门静脉和肝动脉双结扎可建立胆脏凝固性坏死模型,单纯肝右叶门静脉结扎能构建肝细胞小灶性凋亡模型。     

带血管骨膜瓣移植修复烧伤坏死管状骨的实验研究

目的探讨带血管骨膜瓣移植修复烧伤坏死管状骨的可行性，试图为临床修复烧伤坏死骨提供一种有效的方法。方法8月龄成年新西兰家兔20只，设一侧肢体的桡骨为实验组，另一侧为对照组，采用同体对照法。实验组保留带血管的骨膜瓣，从桡骨中下段离断1．2cm桡骨，置沸水中煮沸30min冷却后原位回植，再行骨膜瓣移植包绕、固定。对照组按上述方法处理后不移植骨膜瓣。分别于术后2、4、6、8～10、12周摄X线平片，同时分别处死4～5只兔并取两侧桡骨行组织学切片检查。结果实验组：术后2～4周在骨坏死区见到明显的骨膜增生影像；术后6～8周见骨折断端连接征象，新生骨小梁形成并逐渐改建；术后8—10周可见网织骨普遍融合重建，形成板层，新的哈佛系统形成；术后12周新生骨结构更加成熟，骨折愈合。对照组：术后2周仍为死骨，骨坏死区无骨膜增生现象；术后4、6周未见骨折愈合征象；8周可见骨缺损；12周坏死骨完全溶解、吸收，骨缺损区清晰可见，骨缺损区被少许纤维组织充填。结论带血供的骨膜瓣能不断形成新生骨并爬行替代原坏死骨，使坏死骨获得再生，能很好地修复烧伤坏死的管状骨。     

股骨头缺血性坏死的CT诊断

本文报告了19例股骨头缺血性坏死的CT及多平面重建和三维CT成像表现,并探讨其对术前病变评估的价值,在显示Ⅱ期病变时CT明显优于平片,多平面重建有利于发现股骨头塌陷、关节间隙改变和髋臼改变,三维CT可作为一种补充检查手段。     

当归或三七对兔甘油致急性肾衰的保护作用及其机制研究

目的：用甘油复制兔急性肾小管坏死(ATN)模型，观察当归、三七对ATN的保护作用，并初步探讨其机制。方法：40只健康新西兰白色家兔，等分为四组：当归组、三七组、对照组、正常组。当归、三七、对照三组均用50％甘油等渗盐水15ml/kg注入兔双后肤皮下，复制ATN模型，当归组于注射甘油后即刻，第3小时，第6小时，肌注当归注射液50mg／kg，三七组于相同时点肌注三七皂甙50mg／kg，正常组则于兔双后肢皮下注射生理盐水15ml/kg，并于相同时点注射5％葡萄糖注射液。于实验第24小时取血液、尿液和肾脏，检测血清尿素氮、肌酐、尿液总渗透压、尿总氨基酸、肾组织MDA、SOD、GSH—PX、ATP酶、Ca2^ 、肾组织病理形态学检查。结果：各组与正常组比，肌酐、尿素氮明显升高，说明模型复制成功。当归、三七纪元l例死亡，对照组死士率为30％，血清肌酐、尿素氮、丙二醛、尿总氨基酸、滤过钠排泄分数和肾组织钙含量均明显低于对照组(P＜0．01)，而肾组织ATP酶、SOD、GSH-PX活性均高于对照组(P＜0.01)，病理形态学变化轻于对照组。以上指标，当归与三七组无显著差异(P＞0．05)。结论：当归、三七对甘油所致的ATN有明显保护作用，二者效果无差异，其机制可能与二者均有改善微循环、血液流变学、抑制脂质过氧化反应、保护肾脏抗氧化酶和ATP酶活性及减轻肾组织钙超载有关。     

The nature and timing of excitotoxic neuronal necrosis in the cerebral cortex,hippocampus and thalamus due to flurothyl-induced status epilepticus

Summary Flurothyl-induced status epilepticus was studied by light and electron microscopy (LM, EM) to determine the time course and structural features of neuronal necrosis in the vulnerable brain regions in epilepsy. The cerebral cortex, hippocampus and thalamus were examined after closely spaced recovery periods of up to 1 week. The results showed that acidophilic neurons appeared simultaneously in neurons of the neocortex, hippocampus and thalamus, and that this occurred within 1 h following the end of the epilepsy. The corresponding features of acidophilic neurons by EM were mitochondrial flocculent densities and large discontinuities in cell and nuclear membranes. Dark neurons were ubiquitous during the epilepsy, but recovered almost universally. A few dark neuronal forms persisted and underwent cytorrhexis after 12-h recovery or longer. Axon-sparing dendritic lesions characteristic of excitotoxic neuronal death were found in the neuropil of the neocortex, and in both vulnerable CA1 and resistant CA3 neurons of the hippocampus. Other than acute edema, glial changes were absent. The findings support an excitotoxic mechanism in epilepsy-induced selective neuronal necrosis also in brain regions outside the hippocampus, and contrast with previous reports in ischemia and hypoglycemia in that neuronal necrosis occurs virtually immediately after an epileptic insult. No maturation of cell damage, as described in ischemia, was seen. Furthermore, even exceedingly dark neuronal forms and massive dendritic swelling must be considered sub-lethal or prelethal cellular changes. Lethal cellular changes include acidophilia by LM, cell membrane breaks, and mitochondrial flocculent densities by EM.Supported by the Alberta Hertage Foundation for Medical Research, the Swedish Society of Medicine, the Swedish Medical Research Council, the Magnus Bergvall Foundation, and the Research Funds of the Karolinska Institute.     

CYTOMEGALOVIRUS OOPHORITIS WITH CORTICAL NECROSIS DURING REMISSION OF ACUTE LYMPHOCYTIC LEUKEMIA

Ovarian involvement of cytomegalovirus (CMV) is rarely observed in autopsy and biopsy materials. Cortical necrosis of the ovaries was found in an autopsy case with generalized CMV infection. The patient was an 11-year-old girl in a remission state of acute lymphocytic leukemia. Autopsy revealed several areas showing necrotic change up to 2 mm in size in the cortex of both ovaries. Many cytomegalic cells were found in both the necrotic and intact areas of the cortex. CMV had infected the granulosa, thecal and stromal cells as well as vascular endothelial cells. Oocytes of neither primary nor graafian follicles showed cytomegalic changes, although they were destroyed due to the necrosis. CMV antigen was immunohistologically detected in these cytomegalic cells. Ultrastructurally, herpesvirus-type particles were revealed in the nuclei and cytoplasm of the cytomegalic cells. This case demonstrated that ovarian infection with CMV can potentially induce cortical necrosis and decrease the number of oocytes. ACTA PATHOL JPN 38 : 1069 ∼ 1076, 1988.     

骨髓坏死

引起骨髓坏死的原因是多种多样的,但最主要的原因是由恶性赘生性疾病引起,该症诊断上有一定难度,常常尸解时才被发现;主要的症状有骨痛、发热;骨髓抽吸及活检有特征性改变,有时在骨髓检查中可发现癌细胞,该症主要的治疗是对原发病的治疗。     

Ultrastructural confirmation of neuronal protection by melatonin against the neurotoxin 6-hydroxydopamine cell damage

6-Hydroxydopamine (6-OHDA) is a neurotoxin used in the induction of experimental Parkinson's disease in both animals and cultured neuronal cells. Biochemical and molecular approaches showed previously that low doses of 6-OHDA induced apoptosis in PC12 cells, while high doses of this neurotoxin induced necrosis. Melatonin has been shown to protect against the neuronal programmed cell death induced by 6-OHDA, although it was not able to prevent the massive necrotic cellular death occurring after the addition of high doses of the neurotoxin. In the present work, we demonstrate by ultrastructural analysis that although low doses of 6-OHDA induced apoptosis in PC12 cells, it also damaged the non-apoptotic cells, morphologically corresponding this damage to incipient and reversible necrotic lesions. When the doses of the neurotoxin increase, there are still apoptotic cells, although most of the cells show necrotic irreversible lesions. We also found that melatonin partially prevents the incipient necrotic lesions caused by low doses of 6-OHDA. The fact that melatonin was shown in previous work to prevent apoptosis caused by low doses of 6-OHDA, but not necrosis induced by high doses of the neurotoxin, seemed to indicate that this agent is only able to protect against apoptosis. However, our present results, melatonin preventing also the incipient necrotic neuronal lesions, suggest that this hormone may provide a general protection against cell death, suggesting that higher doses should be tried in order to prevent the necrotic cell death induced by high doses of the neurotoxin.