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R Pariente

Publications and source records attributed to R Pariente.

At least 145 records · Page 8Linked to original sources
PubMed1976

[Bronchial lympho-epithelial nodules in the rat. Definition and morphological characteristics in optical and electron microscopy (author's transl)].

Among the bronchial lymphoid tissue, lympho-epithelial nodules are an original component, easily distinguished from other structures, particularly from lymphoid cell infiltrates. Such structures are encountered in many species and may be characterized by a flattened epithelium, containing a few ciliated cells, devoid of mucus producing cells, and infiltrated with lymphocytes. Inter and intracellular vacuoles are described in the lympho-epithelium and the underlying mucosa. Electron microscope studies support the view that lymphoepithelium has a "trapping" function of particulate matter, more direct evidence is however attempted. Peripheral lymphatic vessels and high endothelium veins contribute to the important lymphocyte transfer. An hypothesis of capacity for antigenic recognition of the lymphoepithelial nodule is discussed.

Animals↗
PubMed1976

Pulmonary mineral dust. A study of ninety patients by electron microscopy, electron microanalysis, and electron microdiffraction.

The results of a study of 90 patients are presented. Intrapulmonary mineral deposits were characterized by electron diffraction and electron probe microanalysis. Using this method, pneumoconioses may be distinguidhed from other pneumopathies. In cases of pneumoconiosis, there exists a specific relationship between the etiology of the dust exposure and the crystallographic characteristics of the intrapulmonary deposits. The nature of the deposits may be indicative of a specific type of pneumoconiosis. This method is particularly useful in differentiating between asbestos bodies and ferruginous bodies. The value of the method in general and its importance in the study of pneumoconiosis are discussed.

Asbestos↗
PubMed1975

[Tuberculosis].

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Antibiotics, Antitubercular↗
PubMed1975

[Asthma].

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Asthma↗
PubMed1975

[Normal ultrastructure of the small bronchi and bronchioli in man].

Ultrastructural topographic and morphological analysis of the small bronchi and bronchioli was carried out on selected biopsy specimens obtained from 6 operative specimens. The small bronchi had a ciliated cylindrical epithelium identical to that in the large bronchi, apart from a smaller number of goblet cells. Their reticulin layer was thin (1 to 3 microns). The glands in the submucosa were rare whereas there was a rich submucosal vascular network. The lobular bronchioli had a ciliated cylindrical epithelium without goblet cells but possessing rare Clara cells. The epithelium of the terminal bromchioli was characterized by: 1 - The presence of numerous Clara cells, generally grouped in groups of 2 or 3. 2 - The appearance on the opposite side of a satellite artery (this side shows alveoli first) of cells which we interpreted as pre-ciliated cells. These cells possess a range of basal corpuscles under the luminal membrane but do not have cilia. 3 - The appearance of small membranous pneumocytes in islets. The epithelium covering the smooth wall of the respiratory bronchioles still have a gutter of ciliated cells and Clara cells which become thinner towards the periphery. After the secondary respiratory bronchioli, there appears in this gutter a new cell type, the cubical cells. These cells which have poorly differentiated cytoplasmic characteristics, seem to us to be immature bronchial cells, precursors of the Clara cells rather than of the ciliated cells. The remainder of the smooth wall of the respiratory bronchioli is covered with membranous pneumocytes and, in the case of the 3rd order of bronchioli, also by granular pneumocytes. The sub-basal reticulin layer is lacking in the terminal and respiratory bronchioli. The total thickness of the wall becomes considerably thinner, the muscular layer becoming proportionally very thick.

Bronchi↗
PubMed1975

[Pulmonary edemas. Anatomic study].

Whatever the etiology of pulmonary edema, i.e. increase in intrapulmonary water, edema passes through three, moreover intricate phases: 1- intracellular edema clearly visible in the type 1 pneumocyte. This intracellular edema appears at the same time as: 2- interstitial edema; that which appears when: 3- numerous vesicules of pinocytosis and separation of the capillary endothelial cells account for it; 4- intra-alveolar edema itself appears later and corresponds to the major clinical phase of pulmonary edema. There is nothing surprising about this as the cellular functions of pneumocytes are impervious as can be shown for example by studies carried out with tracers. This intracellular alveolar edema seems to have two different aspects depending on whether the experimental conditions create an acute or sub-acute pathology. In the acute form, the edema is poor in lipids and in proteins. In the sub-acute of chronic forms, it is on the contrary very rich in them. 5-In the last phase, a veritable desquamation of the pneumocytes then of the endothelial cells is produced which is very frequently lethal. If survival occurs, two sorts of lesions are found: -colonisation of the alveolar surface with type II pneumocytes; - occurrence of possible intersitial fibrosis. The remarkable fact is that such lesions are visible in a more or less identical manner in all cases of pulmonary edema, whether they be hemodynamic or lesional. The morphology does not confirm this physiopathological distinction which is moreover questionable as all pulmonary edema become lesional sooner or later.

Humans↗