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[Trophoblastic gestational diseases. Triploid syndrome, perivillous trophoblastic hyperplasia, trophoblastic pseudotumor, trophoblastic microcarcinoma and carcinoma]. 滋养细胞妊娠疾病。三倍体综合征,绒毛周围滋养细胞增生,滋养细胞假瘤,滋养细胞微癌和癌]。
Pub Date : 1980-01-01
E Philippe, J Boue, A Boue

Comparing the cytogenetic and morphological data on cases of hyperplasia and neoplasia of the trophoblast allows some conditions to be better defined and separated. The term partial mole or embryonic mole should be replaced by the term triploid syndrome because of the especially strong correlation between the triploid caryotype and the special aspect of the placenta. Triploidy is usually the result of fecundation of a haploid ovule by two spermatozoids, probably due to the similarity of the haploids of the two parents, as is suggested by the study of HLA antigens. Classical hydatidiform mole, or perivillous trophoblastic hyperplasia, is usually discovered earlier, during an ultrasound examination or abortion and its histological diagnosis is easy. The caryotype of complete hydatidiform mole is diploid, nearly always XX, with the two sex chromosomes coming from the father (the maternal sex chromosome being eliminated). The caryotype of vesicular dystrophia without trophoblastic hyperplasia is, on the other hand, normal. Trophoblastic microcarcinomas have a better known presentation. And trophoblastic carcinomas are distinct from non-trophoblastic neoplasms which secrete HCG and from benign trophoblastic pseudo-tumors which are often non-secretory.

通过比较滋养细胞增生和瘤变病例的细胞遗传学和形态学资料,可以更好地界定和区分某些情况。由于三倍体核型与胎盘的特殊方面具有特别强的相关性,因此应将“部分痣”或“胚胎痣”一词替换为“三倍体综合征”。三倍体通常是一个单倍体胚珠由两个精子受精的结果,可能是由于双亲的单倍体相似,正如HLA抗原的研究所表明的那样。经典葡萄胎,或绒毛周围滋养细胞增生,通常在超声检查或流产时早期发现,其组织学诊断很容易。完整的葡萄胎的核型是二倍体,几乎总是XX,两条性染色体来自父亲(母亲的性染色体被消除)。另一方面,没有滋养层增生的水疱性营养不良的核型是正常的。滋养细胞微癌的表现更为人所知。滋养细胞癌不同于分泌HCG的非滋养细胞肿瘤,也不同于通常不分泌的良性滋养细胞假肿瘤。
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引用次数: 0
[Oculo-cutaneous tyrosinosis (Richner-Hanhart syndrome). Histo-pathological study of a case]. 皮肤酪氨酸病(Richner-Hanhart综合征)。1例组织病理学研究]。
Pub Date : 1980-01-01
M Larregue, P de Giacomoni, M Odievre, P Babin, G Lorette

The Richner-Hanhart syndrome corresponds to a tyrosine elevation in serum due to deficit in soluble tyrosine aminotransferase in liver cells. This new enzymopathy which is transmitted in an autosomal recessive mode is called oculocutaneous tyrosinosis. It is curable by a poor diet in tyrosine and its precursors. The diagnosis has been invoked in a 18 months old girl, on the association of punctuate palmar and plantar keratosis, dentritic ulcerated keratitis, and mental retardation. The diagnosis is confirmed by elevation of tyrosinemia to 52 mgs/100 mls associated with a high urinary elimination of tyrosine and plenylcetonic acid. Absences of anomaly in the metabolism of methionin and hepatorenal absence of disturbance of hepatorenal system is characteristic. The keratosis accompany orthokeratotic hyperkeratosis. The keratinocytes show 2 types of anomaly ranged in strates in the epiderm. Intracytoplasmic vacuoles which include or lead to pseudomyelinic formations extend progressively from the mitochondrial alterations in the epidemial basal layers. Bulky polyhedral electron dense particles are found in the cytoplasm of the superficial keratinocytes. Most of these aspects have been demonstrated anteriorly in the keratinocytes and the cornea; on the other hand, signs of mitochondrial sulferance had not been observed. The genesis of these cellular alterations based on the liberation of lysosomial enzymes by the action of crystals of tyrosine has been suggested by Goldsmith from experimental facts. However, it seems the mitochondrial defect occurs outside this mechanism.

Richner-Hanhart综合征对应于由于肝细胞中可溶性酪氨酸转氨酶缺乏而引起的血清酪氨酸升高。这种以常染色体隐性遗传方式传播的新酶病被称为眼皮肤酪氨酸病。它可以通过摄入酪氨酸及其前体的不良饮食来治愈。诊断已被引述在一个18个月大的女孩,在关联点掌和足底角化病,树突状溃疡性角膜炎,和智力低下。诊断为酪氨酸血症升高至52毫克/100毫升,伴有尿中酪氨酸和全酪氨酸酸的高清除。蛋氨酸代谢无异常,肝肾无肝肾系统紊乱为特征性表现。角化伴塑形角化过度。表皮角化细胞呈2种不同类型的异常。包括或导致假髓鞘形成的胞浆内液泡从线粒体的改变逐渐延伸至流行基底层。在浅表角质形成细胞的细胞质中发现体积庞大的多面体电子致密颗粒。这些方面的大多数已经在以前的角质形成细胞和角膜中得到证实;另一方面,没有观察到线粒体硫的迹象。这些细胞变化的起源是基于酪氨酸晶体作用下溶酶体酶的释放,戈德史密斯根据实验事实提出的。然而,线粒体缺陷似乎发生在这一机制之外。
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引用次数: 0
[Diabetic glomerulosclerosis in the DBM mouse. Correlated study of quantitative morphology, immunofluorescence and electronic microscopy]. DBM小鼠糖尿病性肾小球硬化。定量形态学、免疫荧光和电镜的相关研究]。
Pub Date : 1980-01-01
G Chomette, J Sterne, M Auriol, P Tranbaloc, J L Junien

Using an experimental model of genetic diabetes (DBM mouse) a comparison was made of the results of quantitative data obtained by light and electron microscopy (measurement of glomerular and mesangial surface areas, assessment of the thickness of the basal membrane and its irregularities) and was used to demonstrate the actual presence of glomerulosclerosis in the renal parenchyma of 31 diabetic animals. In addition, immunofluorescent investigations in these same animals demonstrated the presence of serum proteins (in particular immunoglobulins and albumin) in the glomerulus and the tubular basal membrane. These substances transude through the vessels as a result of increased vascular permeability. In this area, membrane abnormalities are not a consequence of hyperglycaemia. In the group, one batch of animals in which hyperglycaemia was partially reduced by glycoregulatory therapy showed the same glomerular changes. Amongst other factors, the possible role of hyperinsulinaemia constantly present in these animals, regardless of their blood glucose level, is worthy of considération.

采用遗传性糖尿病(DBM小鼠)实验模型,比较了光镜和电子显微镜所获得的定量数据(肾小球和系膜表面积的测量,基膜厚度及其不规则性的评估),并用于证实31只糖尿病动物肾实质中肾小球硬化的实际存在。此外,这些动物的免疫荧光研究表明,肾小球和肾小管基膜中存在血清蛋白(特别是免疫球蛋白和白蛋白)。由于血管渗透性增加,这些物质穿过血管。在这个区域,膜异常不是高血糖的结果。在该组中,通过糖调节治疗部分降低高血糖的一批动物显示出相同的肾小球变化。除其他因素外,高胰岛素血症在这些动物中持续存在的可能作用,无论其血糖水平如何,都值得考虑。
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引用次数: 0
[White sponge nevus-type familial leucodysplasia of the oral cavity. Electron microscopic study of a case]. 口腔白色海绵痣型家族性白质发育不良。一个病例的电子显微镜研究]。
Pub Date : 1980-01-01
G Chomette, M Auriol, C Plocieniak, J M Vaillant

In a case of white sponge naevus type congenital buccal keratosis, electron microscopic study revealed severe disturbances in filamentogenesis which was insufficient (pale cells) or on the contrary excessive and anarchic (dark cells) and, to a lesser degree, corneal maturation. This was accompanied by slight abnormalities of the cellular junctions, rarely described in such a condition up to the present time. With regard to the delayed epithelial exfoliation typical of this condition, the manner and causes of its development are discussed in the light of ultrastructural findings.

在一例白色海绵痣型先天性颊角化病中,电镜检查显示丝状细胞发生严重紊乱(苍白细胞)或相反,丝状细胞过多且无秩序(暗细胞),角膜成熟程度较轻。这伴随着细胞连接的轻微异常,很少在这种情况下描述到目前为止。关于这种情况的典型延迟上皮脱落,其发展的方式和原因在超微结构的发现进行了讨论。
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引用次数: 0
[Chronology of breast cancer using Gompertz' growth model]. [使用Gompertz生长模型的乳腺癌年表]。
Pub Date : 1980-01-01
W Bauer, J P Igot, Y Le Gal

The chronology of carcinoma of the breast based upon the size of the primary tumour and of its metastatic nodes in a simple exponential growth model leads to anomalies. The Gompertz model may be substituted for it in order to date the primary tumour and its metastases at the price of a hypothesis: the asymptotic size of the carcinoma. Its value has little influence on the initial doubling times chosen as a new time unit. 337 radical mastectomy specimens out of 500 examined fulfilled the necessary conditions for a precise quantitative study. If the age of the lesion expressed by taking the initial doubling time as a time unit is called K, the mean age of the primary carcinoma at the time of the first metastasis (FM) is K = 35. Its size is 15 mm3 and its diameter 3 mm. 90% of lymph node metastases occurred at K = 43 (size of primary carcinoma 125 mm3; diameter 6 mm). These results are in agreement with others obtained on theoretical or experimental bases. They tend to show that the earliest diagnosis, taking technical possibilities into account, cannot be early enough to precede lymphatic spread.

乳腺癌的年表基于原发肿瘤的大小和它的转移淋巴结在一个简单的指数增长模型导致异常。Gompertz模型可以代替它,以便确定原发肿瘤及其转移的日期,但代价是假设:肿瘤的渐近大小。它的值对选择作为新时间单位的初始倍增次数影响不大。500例根治性乳房切除术标本中有337例符合精确定量研究的必要条件。若以初始倍增时间为时间单位表示病变的年龄为K,则原发性癌首次转移时的平均年龄(FM)为K = 35。其大小为15 mm3,直径为3 mm, 90%的淋巴结转移发生在K = 43(原发癌大小为125 mm3;直径6毫米)。这些结果与其他在理论或实验基础上得到的结果一致。它们往往表明,考虑到技术上的可能性,最早的诊断不能早到足以先于淋巴传播。
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引用次数: 0
[Anatomo-pathologic lesions of kidneys in mice subjected to chronic stress]. [慢性应激小鼠肾脏的解剖病理损伤]。
Pub Date : 1980-01-01
P Garzonis, S Manta, J S Papadopoulos

Three groups of white mice were used. The experiment took place over 138 days. The first Group was used as a control group. The second group was exposed to continuous stress (Population Stress). The third Group was exposed to chronic Stress by electroshock with 22-45 volts for a duration of 4 seconds each minute for one hour each day. The blood vessels are the first to be affected quickly followed by degenerative changes of the glomeruli, which are possible due to hemodynamic disturbances, results in progressive destruction of the kidneys. The following pathanatomical changes were found in the stressed kidneys. (1) Spasm of the arterioles and dilation of the veins. (2) Excavation of hemolysed RBC into Bowmans Capsule. (3) Retraction of the glomerula apparatus with degenerative changes of the cells which to a great extent reached total necrosis or even total destruction of the whole glomerulus. (4) Injury to the renal tubules : the cells of the renal tubules were found edematous with unclear borders between cells in the renal cortex and protoplasmic atrophy medullary cells. The observations derived from this work clearly show that stress causes functional disturbances and histologic changes in the kidneys of white mice.

使用了三组小白鼠。实验持续了138天。第一组为对照组。第二组连续应激(种群应激)。第三组以22-45伏特电流慢性电击,每分钟4秒,每天1小时。血管首先受到影响,其次是肾小球的退行性变化,这可能是由于血液动力学紊乱,导致肾脏的进行性破坏。应激肾的病理变化如下:(1)小动脉痉挛,静脉扩张。(2)溶血红细胞进入Bowmans囊。(3)肾小球内缩,细胞发生退行性改变,在很大程度上达到肾小球全坏死甚至全破坏。(4)肾小管损伤:肾小管细胞水肿,肾皮质细胞与原浆性萎缩髓质细胞边界不清。从这项工作中得出的观察结果清楚地表明,应激会引起小白鼠肾脏的功能紊乱和组织学改变。
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引用次数: 0
[Histochemistry of mucosubstances. Technical considerations]. 黏液物质的组织化学。技术因素)。
Pub Date : 1980-01-01
C A Pagnini, L Bozzola

A report concerning the histochemical methods used to differentiate mucosubstances and certain technical modifications made with the aim of obtaining better results : 1) rapid passage in a solution at pH1 after alcian blue reaction in order to ensure staining of sulfate mucosubstances only ; 20 plunging of sections first in FeCl for 10 minutes by the H.I.D. method ; 3) in the methylation reaction the optimum time is 12 hours.

关于用于区分黏液物质的组织化学方法和为获得更好结果而进行的某些技术修改的报告:1)在阿利新蓝反应后在ph为1的溶液中快速通过,以确保仅染色硫酸盐黏液物质;采用h.i.d法,先在FeCl中下切20段,持续10分钟;3)甲基化反应最佳时间为12 h。
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引用次数: 0
[Benign mesotheliomas of different coelomic cavities. Apropos of 5 cases]. 不同体腔的良性间皮瘤。约5例]。
Pub Date : 1980-01-01
M Peffault de Latour, Y Fonck
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引用次数: 0
[Hepatocyte changes in experimental iron overloading. An ultrastructural and microanalytic study]. 实验铁超载时肝细胞的变化。超微结构和显微分析研究]。
Pub Date : 1980-01-01
A Lopez, J Vilches, L Bardet, S Vazquez, J Gomez

In this paper the ultrastructural changes in hepatocytes which were experimentally induced by oral and parenteral iron overloading in Sprague-Dawley rats fed on a steatogenous U.A.R. 2-13 diet are analysed. The changes in the mitochondria consisted of flocculation, vesiculation and crystolysis. The R.E.G. showed marked phenomena of dilatation degranulation and fragmentation. The lysosomes became more numerous and increased their content of ferric macromolecules. Degenerative nuclear phenomena were also seen. A microanalytic study of the cellular organelles and nucleus was done relating the cellular lesion and the intracellular distribution of the iron.

本文对Sprague-Dawley大鼠饲喂高脂性ua.r.2 -13日粮后,口服和肠外铁超载诱导肝细胞超微结构的变化进行了分析。线粒体的变化主要表现为絮凝、囊泡和晶体溶解。reeg显示明显的扩张、脱粒和碎裂现象。溶酶体数量增多,铁大分子含量增加。核变性现象也可见。细胞器和细胞核的微分析研究与细胞损伤和铁在细胞内的分布有关。
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引用次数: 0
[Degos' malignant atrophic papulosis. Ultrastructural study of a new case]. Degos氏恶性萎缩性丘疹病。一个新病例的超微结构研究]。
Pub Date : 1980-01-01
P Bioulac, M S Doutre, C Beylot

The authors report a case of Degos' malignant atrophic papulosis (MAP) with typical skin lesions from a clinical and histological standpoint. They stress in particular the ultrastructural study of skin biopsies which revealed numerous "paramyxovirus-like" tubulo-reticular structures in the endothelial cells, lymphocytes of the perivascular infiltrate, fibroblasts and keratinocytes. Although the significance of these inclusions remains open to discussion and is probably non-specific, their frequency in MAP is worthy of emphasis.

作者报告了一例Degos的恶性萎缩性丘疹病(MAP)与典型的皮肤病变从临床和组织学的观点。他们特别强调了皮肤活检的超微结构研究,发现内皮细胞、血管周围浸润的淋巴细胞、成纤维细胞和角化细胞中有许多“副粘病毒样”的小管网状结构。虽然这些夹杂物的意义仍有待讨论,而且可能是非特异性的,但它们在MAP中的频率值得强调。
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引用次数: 0
期刊
Annales d'anatomie pathologique
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