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L Orcel

Publications and source records attributed to L Orcel.

104 records · Page 6Linked to original sources
PubMedDate not supplied

[Physical state of lipids accumulated in atherosclerotic lesions (author's transl)].

The work of Small and al. concerning the physical state of lipids accumulated in atherosclerotic plaques, is analysed. This team of biophysicists studies the composition in cholesterol, cholesterol esters and phospholipids, of each type of lesion and reports it on a phase diagram, while identifying the physical state of these lipids by polarizing microscope and by X-ray diffraction. In such a way, they show that the ordinary fatty streak has a composition which situates it in the 2 phases-zone, and actually demonstrate liquid crystals of phospholipids (+ cholesterol + cholesterol esters) and oily droplets of cholesterol esters, but never cholesterol crystals. In the other types of lesions (intermediary lesions, fibrous plaques and atheromatous plaques) they find, in addition to liquid crystals and oily droplets previously mentioned, crystals of cholesterol monohydrate, which leads to 3 phases. These findings are in accord with experimental models studied by the authors, for whom the physical state of lipids plays a very important role in the formation as well as the regression of atherosclerotic plaques.

Arteriosclerosis↗
PubMedDate not supplied

Diffuse intimal thickening in chronic obliterating disease of arteries of the lower extremities in humans.

The concept of atherosclerosis is essentially applicable to the arteries of the elastic type. Lesions in the arteries of the muscular type have a different character. They show an association of fibrosis of the media with a diffuse intimal thickening and the presence of stratified fibro-hyaline plaques, representing organized parietal thrombi. Deposition of lipids is weak or moderate and apparently a secondary event. Intimal thickening of peripheral arteries exceeds largely the limits of the thrombotic zone. It is covered by normal endothelium and populated by myocytes with a few fibroblasts. The intercellular substance shows all stages of formation of elastic structures, a process which is probably related to the activity of myocytes. It leads to the formation of one or several fairly distinct elastic membranes. Concomitantly the lamina elastica interna undergoes considerable degradation. We are, thus, confronted with a lesion of considerable age which, nevertheless, remains active and shows continuing structural changes. The origin of cells in intimal thickening and its significance in terms of general pathology are discussed with respect to the experimental results.

Adult↗
PubMedDate not supplied

[Morphological studies of intraepithelial carcinomas of the cervix uteri (author's transl)].

A morphological study at light and electron microscopy, of 61 cases of intraepithelial epithelioma allowed the authors to distinguish two types of carcinoma: undifferentiated intraepithelial epithelioma arising from the exo-endocervical junction, probably by proliferation of vestigial cells which derived from persistent sinusal remnants; differentiated intraepithelial epithelioma developing upon the mature exocervical epithelium modified by inflammatory processes. These two types of "in situ" epitheliomas have different evolution. The undifferentiated form, supported by an uninterrupted membrane consisting of imbricated reticulin fibres has a slow evolution. The differentiated form, often multifocal, supported by a basal membrane frequently disrupted, has a rapid evolution. These morphological studies allowed the authors to refuse the theory of metaplasia from subcylindrical reserve cells in the genesis of intraepithelial epitheliomas of the cervix.

Adult↗
PubMedDate not supplied

[Intimate mechanism of premature separation of the normally inserted placenta].

Retro-placental haemorrhage comes from rupture of patent utero-placental arteries which are neither sclerosed nor thrombosed. This applies whether the form of haemorrhage is minor (simple depression found when the placenta is examined) or grave with utero-placental apoplexy (with complete detachment of the placenta and syndrome of shock). The method by which the arteries rupture depend on the intensity and excessive duration of uterine contractions: --moderate; normal uterine contractions give rise to a prolonged blockage of the return circulation, whereas the arterial flow has not stopped. Rupture occurs because the distended utero-placental arterial wall bursts under the insult of raised pressure during the uterine contraction; --intense; these anomalies come from total blockage, both veinous and arterial, and the arterial rupture is due to anoxaemic necrosis of the utero-placental arterial wall. The rupture of the utero-placental arterial wall, which is normally very fragile because it has no elasticity in its musculature, gives the explanation for the histogenesis of retro-placental haemorrhages.

Abruptio Placentae↗