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Biomedical subjects

M Boutet

Publications and source records attributed to M Boutet.

51 records · Page 3Linked to original sources
PubMed1975

Light and electron microscopic study of cellular proliferation in carcinoid heart disease.

An ultrastructural and histochemical study of the subendocardial lesion in carcinoid heart disease showed six different cell types within a myxoid matrix. The matrix, composed of a mucopolysaccharidic ground substance, collagen, and reticluin fibers, contained stem cells, four types of fusiform cells (fibrocytes, fibroblasts, myofibroblasts, and smooth muscle cells), and intermediary cell type. Our observations suggest that the humoral mediators of the carcinoid syndrome may induce the differentiation of a subendocardial stem cell into contractile elements.

Bradykinin↗
PubMedDate not supplied

Airway inflammation and structural changes in airway hyper-responsiveness and asthma: an overview.

Asthma treatment has moved from bronchodilator therapy to an emphasis on anti-inflammatory therapy. Airway inflammation is believed to induce airway hyper-responsiveness (AHR) through the release of mediators that increase the airway response to agonists. However, the exact contribution of airway inflammation in the physiology of airway hyper-responsiveness remains undefined. Structural modifications in airways resulting from inflammation may contribute to the development and persistence of AHR and the development of asthma. This paper reviews some of the main components of airway inflammation and structural changes in asthma, and discusses how these processes may interact to modify airway function and induce respiratory symptoms.

Airway Resistance↗
PubMedDate not supplied

Production of tissue-engineered three-dimensional human bronchial models.

We have reported morphological and functional features of cells isolated from human bronchial biopsies. Both epithelial and fibroblastic cells were isolated from the same biopsies using collagenase. A few models have been established to study normal bronchial response to various agents and to understand the mechanisms responsible for some disorders, such as asthma. We produced three-dimensional bronchial equivalents in culture, using human epithelial and fibroblastic cells. We previously showed that peripheral anchorage can prevent the dramatic collagen contraction in gels seeded with fibroblasts when properly adapted to the size and type of cultured tissues. Our bilayered bronchial constructs were anchored and cultured under submerged conditions and at the air-liquid interface. Three culture media were compared. Serum-free medium supplemented with retinoic acid (5 x 10(-8) M) was found to be the best for maintenance of bronchial cell properties in the reconstructed bronchial tissue. Immunohistological and ultrastructural analyses showed that these equivalents present good structural organization, allowing ciliogenesis to occur in culture. Moreover, human bronchial goblet cells could differentiate and secrete mucus with culture time. Laminin, a major constituent of the basement membrane and basal cells, was also detected at the mesenchymoepithelial interface. Such models will be useful for studying human bronchial properties in vitro.

Bronchi↗
PubMedDate not supplied

Coronary microcirculatory factors and cardiac muscle cell injury.

Coronary artery ligation with or without reperfusion was carried out in Wistar rats to study the role of coronary microcirculatory factors and membrane permeability alteration of cardiac muscle cell in the evolution of cardiac muscle cell injury by using the fine structural extracellular protein tracer, horseradish peroxidase (HRP). The findings were compared with those obtained in noncoronarogenic myocardial injury models following administration of norepinephrine, a pressor, and isoproterenol, a depressor catecholamine. Following left coronary artery ligation lastingfor 10 and 20 minutes, some of the collaterals in the ischemic zone were perused by the tracer, but the numer of patent capillaries decreased during 60-min ligation. The inhomogeneous involvement of cardiac muscle cells in ischemic injury correlated well with these microcirculatory findings. In comparison to permanent ischemia, an abrupt deterioration of the cardiac muscle cell alteration occured after reperfusion with influx of HRP into the damaged cells. The binding of tracer to myofilaments was, however, a later event as compared to that seen in the catecholamine models. The latter observation implies that, in addition to microcirculatory factors, direct cardiac muscle cell stimulation should also be considered in the evolution of noncoronarogenic myocardial injury.

Animals↗
PubMedDate not supplied

[Ultrastructural and histochemical study of Hamasaki-Wesenberg bodies in lymph node sarcoidosis].

Report of a histochemical and ultrastructural study of the Hamasaki-Wesenberg Bodies in ganglionic sarcoidosis. These peculiar bodies have variable form and size and are located in the ganglionic sinuses as free elements or in the histiocytes; they are found most often in cases with sarcoidosis but are not specific of this disease. The results of this study suggest that their origin is probably lysosomial and that their nature is not unlike that of ceroid or lipofuscinic pigments. The exact signification of the presence of these bodies in the lymph nodes would need deeper investigation.

Humans↗