急性心功能不全时大脑皮质超微结构的变化

用电子显微镜对10例死于急性左心功能不全的患者大脑额叶、顶叶和颞叶皮质进行了研究.发现毛细血管周围星形胶质细胞的突起水肿,基膜破坏,内皮细胞质空泡化,线粒体变性,溶酶体堆积,毛细血管腔缩窄,紧密连接变性.神经元核内出现膜性包含物.神经细胞及胶质细胞内有纤维性包含物,线粒体变性,胞质空泡化以及脂褐素体沉积.突触的变性表现为突触前末梢肿胀,突触小泡集聚、融合、破坏.     

老年痴呆症大脑皮质超微结构的研究

用电子显微镜对１０例老年痴呆症和１０例正常老年人大脑额叶、顶叶和颞叶皮质进行对比研究。发现两组间神经元、胶质细胞和突触等超微结构的一致性变化。它们包括：核内包含物的出现，神经细胞和胶质细胞内出现多形态的神经原纤维缠结，胞质内脂褐素体的堆积以及衰老斑的出现等。突触的变性表现为突触前、后末梢的肿胀，空泡化等。统计学资料表明，这些变化从量上来看，老年痴呆症明显高于正常人。     

大鼠脑缺血后突触超微结构的变化

目的：探讨脑缺血损伤对突触的影响。方法：采用大鼠，制成脑缺血模型，应用透射电镜观察大脑顶叶皮质突触的变化。结果：随着缺血时间的延长，神经毡内突触数目逐渐减少；突触结构中突触小泡、线粒体也发生改变。缺血48h，突触小泡减少，甚至消失；线粒体变性、减少乃至消失，嵴减少或消失呈空泡状。突触前后膜被破坏，典型的突触结构已不存在。结论：脑缺血后，随缺血时间延长，突触结构异常，突触密度下降。     

流行性出血热病人肝穿组织的光镜与电镜观察

用光镜和电镜研究12例流行性出血热(EHF)患者肝穿组织病变。见肝细胞普遍有变性、单个细胞坏死或成片梗死,再生肝细胞少;肝窦内皮细胞变性、增生、窦腔狭窄、闭合或淤滞扩张,可见微出血。光镜还看到肝细胞内有与经典描述不同的脂褐素颗粒。超微结构首次发现枯否细胞吞噬血小板,观察到肝细胞线粒体内存在有微管样丝状物。本研究为EHF病人出现肝功能障碍提供了形态学基础。     

帕金森病患者丘脑腹外侧核超微结构观察

利用透射电镜对１６例帕金森病患者丘脑腹外侧核活检组织进行了超微结构观察，结果发现：神经细胞数量减少，胞体变小，核呈浓缩变形，线粒体肿胀变性，嵴突短小或消失。突触末梢水肿，扩大呈空泡样，突触小泡数量减少或消失。星形胶质细胞水肿，膜性细胞器破坏。毛细血管内皮细胞肿胀，管腔狭窄，线粒体肿胀变性。病变随患者病情加重而变化明显。结果提示丘脑腹外侧核超微结构上的改变有可能成为临床判断病变程度的辅助诊断指标。     

人胎海马发育的研究 Ⅱ、电镜观察

在电镜下观察了4-10个月人胎儿海马CA_2亚区多形细胞层突触复合体的发育。结果,4个月胎儿即见到含少量、分散的圆形无芯小泡的对称型轴-树突触。数量不多但结构非常典型。突触前成分内还可见到结构不发达的线粒体。此时,在数量上占优势的突触前身结构构成突触样接触,即膜的相接近部分发生特化的增厚,间隙清楚可辨,但无突触小泡。随着胎龄的增大,出现下述一系列变化:(1) 突触前身结构的数量优势逐渐被典型突触所代替;(2) Ⅰ型突触出现,并逐渐增多;(3) 突触形式由低胎龄时的简单突触逐渐出现并联突触和突触群;(4) 突触小泡数量增加,并向突触前膜靠拢,在10个月材料还见到扁平小泡和圆形小泡共存;(5) 线粒体的数量和结构也日趋增多和典型。基于上述发现,作者认为(1)人胎海马CA_2亚区内突触的个体发育经历了突触前身结构和典型突触两个连续过程;(2) 该部的突触具有简单突触、并联突触和突触群等多种形式;(3) 参与海马活动的神经递质至少应具有兴奋和抑制两类。     

血管性痴呆大鼠海马超微结构的变化及药物干预

目的：探讨血管性痴呆病理机制及黄精口服液的作用机制。方法：结扎双侧颈总动脉建立血管性痴呆模型,黄精口服液灌胃,应用透射电镜观测神经细胞、胶质细胞、微血管病理变化和突触结构参数的变化。结果：血管性痴呆大鼠海马CAI区神经组织线粒体肿胀、嵴断裂、模糊或消失,微管断裂、排列紊乱,神经毡中突起肿胀、变性,突触结构参数明显改变;毛细血管内皮细胞局部基膜和星形胶质细胞也有病理改变。黄精口服液干预的大鼠海马组织病理变化明显减轻;海马CAI突触界面曲率增大、突触后致密物增厚、突触活性区增长。结论：(1)突触结构变化是血管性痴呆的病理机制之一;(2)黄精口服液促进突触重建、改善血管性痴呆大鼠学习记忆能力。     

肝豆状核变性肝组织的超微结构观察

目的 报道1例肝豆状核变性肝组织超微结构特征.方法 经皮穿刺活检肝豆状核变性患者的肝组织,进行组织学、组织化学和超微结构观察.结果 患者为青年男性, 临床表现脾脏肿大;组织学示肝细胞有脂肪变,未见纤维组织增生;电镜检查显示肝细胞内出现多量形态不一的异常或畸形线粒体和脂褐素颗粒;其中特征性变化是线粒体内出现线条状结晶体和脂褐素颗粒内形成透明小体.结论 肝细胞内出现线条状结晶体的线粒体和形成透明小体的脂褐素颗粒,对肝豆状核变性的诊断具有价值.     

视神经损伤后视神经及其内毛细血管的早期超微结构的变化

目的观察视神经损伤后视神经和神经内毛细血管的超微结构变化,探讨视神经损伤的机制。方法建立家兔视神经损伤的动物模型,利用透射电子显微镜观察视神经及神经内毛细血管超微结构的变化。结果视神经损伤0.5h后,轴突部分肿胀,髓鞘疏松,微管、微丝排列出现紊乱,线粒体肿胀,毛细血管内皮细胞中的吞饮小泡和微绒毛明显减少;损伤6h后,线粒体出现髓样变和空泡样变性,血管内皮细胞肿胀,管腔变窄;损伤12h后,轴突空泡样变性,髓鞘脱失,毛细血管周围间隙增宽;损伤48h后,轴质密度增加,部分髓鞘板层完全分离,微管、微丝及线粒体发生颗粒性溶解,内皮细胞中的线粒体出现广泛变性;损伤96h时,轴索崩解呈空泡状变性,髓鞘更广泛崩解,毛细血管扩张破裂,红细胞外溢。结论视神经损伤早期轴突肿胀、空泡样变性,线粒体水肿变性,微管、微丝数量减少;视神经内毛细血管扩张,通透性增加。     

人参皂甙对老龄大鼠海马CA3区神经元超微结构影响的定性、定量研究

应用透射电镜技术结合图像分析观察了老龄大鼠海马CA_3区神经元超微结构的改变,并对比观察了人参皂甙对超微结构的影响.结果表明:老龄组神经元脂褐素数量比青年组增加6倍(P<0.01),面积增加9倍(P<0.01);而给药组脂褐素数量比老龄组减少18%(P<0.05),面积减少31%(P<0.05).此外,老龄组神经元内线粒体等细胞器出现明显变性、坏死、突触变性,神经毡内出现髓样体,膜性结构等异常改变;而给药组上述改变均见明显减轻或不出现.     

Focal cytomegaly of the adult adrenal cortex. A rare variant of black adenoma

A pigmented adrenocortical nodule was found incidentally in an adrenal gland resected for endocrine manipulation of breast carcinoma. The sharply circumscribed, nonencapsulated nodule was composed of cells with diameters as large as 95 micron. The cells had ample eosinophilic cytoplasm and contained much lipofuscin pigment. Electron microscopy disclosed tubulovesicular mitochondria, lipofuscin pigment, cytoplasmic vacuolization, and lipid without degenerative changes or intranuclear inclusions. This unusual lesion of adult adrenal glands is best considered as a rare variant of adrenocortical black adenoma.     

Ultrastructural Alterations in Canine Lung Allografts

Morphologic alterations in transplanted dog lungs undergoing acute rejection were studied with the electron microscope. Earliest changes were swelling of the type I alveolar cells and cytoplasmic vacuolization in the capillary endothelial cells. Later, there was progressive infiltration of macrophages which contained large osmiophilic inclusions. Type II alveolar cells increased in number and showed vacuolization, fraying and membrane disruption of their lamellar inclusions. A decrease in the relative number of type II cell inclusions and extensive endothelial damage were observed in preterminal biopsies. The significance of these cellular changes in relation to pulmonary rejection requires further investigation.     

Schwannian crystalline-like inclusions bodies (Fardeau-Engel bodies) revisited in peripheral neuropathies

In 1969, Fardeau and Engel described polygonal organelles containing crystalline-like structures located in the Schwann cell cytoplasm of unmyelinated fibers. Such inclusions were reported in various conditions, mainly with axonal lesions. They were also reported in a few cases of peripheral neuropathy associated with primary mitochondriopathy. Although they are surrounded by a double membrane, their mitochondrial origin is not definitely proven. Their significance remains obscure but they deserve to be better known as Fardeau-Engel bodies, so as not to be mistaken with mitochondrial crystalline inclusions, which are frequently observed in patients with ragged-red fibers in muscle.     

Beneficial Effect of Caffeic Acid Phenethyl Ester (CAPE) on Hepatocyte Damage Induced by Bile Duct Ligation: An Electron Microscopic Examination

Recently the authors have reported the potent beneficial effect of caffeic acid phenethyl ester (CAPE) on cholestatic oxidative liver injury induced by acute bile ligation in Swiss albino rats. Herein, they report the ultrastructural hepatocellular alterations induced by acute bile duct ligation and the effect of CAPE administration on these alterations. Bile duct ligation resulted in many degenerative changes, such as vacuolization, mitochondrial degeneration, endoplasmic reticulum dilatation, and lysosome accumulation within the cytoplasm of hepatocytes. Mitochondrial degeneration was also observed within the cytoplasm of the cells of biliary ductular epithelium. CAPE potentially protected the hepatocytes from the cholestasis-induced cellular injury.     

Ultrastructure of the jejunal mucosa in human immunodeficiency virus infection

The ultrastructural changes in the jejunal mucosa of 11 male patients, three with clinical AIDS, five with AIDS related complex-progressive generalized lymphadenopathy (ARC-PGL), and three who were only HIV antibody positive, were studied. In the enterocytes, major abnormalities were proliferation of smooth endoplasmic reticulum mitochondrial changes, vacuolization of cells, and fat hold up. In the lamina propria, degeneration of enteric nerve axons and smooth muscle were seen. Microvasculature showed both endothelial cell degeneration and hyperplasia. The presence of tubuloreticular inclusions in endothelial cells paralleled the stage of the disease. Since none of the 11 patients had any opportunistic infection, these changes are likely to be the effect of HIV infection.     

Ultrastructural and immunohistochemical characteristics of the mechanism of cardiomyocytic death in arrhythmogenic dysplasia of the right ventricle

Right ventricular endomyocardial biopsy specimens from patients clinically diagnosed as having arrhythmogenic dysplasia of the right ventricle underwent electron microscopic and immunohistochemical studies. Myocardial fibrous fatty dysplasia was found in the semi-thin sections. The TUNEL immunohistochemic test revealed apoptotic nuclei in the cardiomyocytes. In the binucleated and trinuclated cardiomyocytes, one or two nuclei might be apoptotic, one or two others nuclei being intact. Electron microscopy identified the stages of movement of cardiomyocytic nuclei to the cell periphery as well as nuclear extrusion outside the cardiomyocytes. The cardiomyocytes themselves displayed pronounced vacuolization, mitochondrial destruction, accumulation of lipid inclusions and lysosome-like masses, and myofibrillar destruction.     

Extensive myocytolysis as a marker of sudden cardiac death

Colliquative myocytolysis, an intracellular vacuolization of myocardial cells, is considered an indicator of acute myocardial ischemia. Although often present in ischemic cardiac death, this lesion is often either overlooked, or not utilized as a criterion for diagnosing ischemia. This study reports light microscopic and ultrastructural studies of six autopsied patients who died suddenly and showed extensive myocytolysis as the only pathologic finding. In two of these patients, the clinical history and electrocardiogram findings documented an acute ischemic episode 1 to 3 hours antemortem. Six control patients with matched age and postmortem intervals did not show the intracellular vacuolization characteristic of myocytolysis. The postmortem intervals ranged from 2 to 12 hours. Ultrastructurally, myocytolysis was seen as a well-defined large intracellular vacuole without any lining membrane and associated with disrupted myofibrils, prominent Z band degeneration, and a few fat droplets. The mitochondria showed swelling and disruption, as well as electron dense amorphous inclusions. The swelling and disruption of mitochondria are well-known postmortem artefacts, and the mitochondrial amorphous inclusions, large intracellular vacuoles, prominent Z band degeneration, and fat droplets are not seen with autolysis. We conclude that myocytolysis, especially if extensive and restricted to an area supplied by a major coronary artery, can be a helpful pathologic marker of myocardial ischemia, particularly in sudden deaths without any other histologic findings.     

Fabry disease: a morphologic study of 11 cases.

Fabry disease is a metabolic disorder caused by the genetic deficiency of alpha-galactosidase A. Deposition of glycosphingolipids in podocytes, endothelial cells, and other cell types leads to formation of myelin-like inclusions, which are the hallmark of the disease. In most untreated males, the disorder progresses to end-stage kidney disease. Fabry disease is rare, and no renal biopsy series focusing on pathologic findings has been published in the past 25 years. We retrieved kidney biopsies diagnosed with Fabry disease from our files, and reviewed clinical data as well as the light and electron microscopy. In total, 11 patients were identified: six male subjects aged 17-43 years and five female subjects aged 30-73 years. On average, male patients presented more than 10 years earlier then female patients. A total of 10 patients had proteinuria, two with the nephrotic syndrome. Four male and three female patients had decreased renal function. Light microscopy showed vacuolization of the podocyte cytoplasm and variable glomerular sclerosis. Older patients and males had more advanced glomerular and interstitial sclerosis, but three of the five female patients also had advanced renal disease. Electron microscopy showed the characteristic myelin-like inclusions most prominently in the podocyte cytoplasm. Seven patients also had podocyte foot process effacement. A second type of deposit, unexpected and conspicuous, was identified in three males, and found to be associated with glomerular basement membrane duplications. These deposits were composed of layered membrane-like material, and therefore morphologically distinct from myelin-like inclusions. They probably represent remnants of damaged endothelial cells.