Biomedical subjects
Publications and source records attributed to S Rousset.
Membrane bound monkey antigens can be localized in different clones of somatic monkey-mouse hybrid cells. These antigens are detected, using peroxidase labelled anti-monkey sera, in thin sections observed in the electron microscope. The different clones contain a small number of simian chromosomes (9 to 25) and a complete set of murin chromosomes.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
The model of IFN receptor system which we initially proposed in 1973 is now better documented. The receptor system seems to consist of an IFN species specific glycoprotein, which could be the high affinity receptor (30) to which IFN has to bind in order to act. The glycoprotein is thus the activator site. Furthermore, IFN can bind to gangliosides in a non-specific manner. Cooperation between these membrane elements requires the free mobility of the membrane constituents in the plane of the membrane and the integrity of the cytoskeleton. Decay of these constituents during some virus-induced or malignant transformation processes could result in a defect in the synthesis of one of these constituents, causing in parallel a loss of IFN sensitivity. Sodium butyrate, which restores the cytoskeleton, enhances simultaneously the response to IFN. The modulatory effect of IFN on the cell membrane is thus a major step in the regulatory action of IFN on the different phenotypic expressions of the cell. This property of IFN could be one of its principal physiological roles.
An anatomo-clinical observation of toxoplasmic pneumonia with generalization in a six-year old child is reported. The serology of toxoplasmosis is positive. The histopathological examination revealed an interstitial pneumonia with toxoplasma located in the tumified alveolar lining cells and in the intra-alveolar macrophages. Parasitic lesions were also observed in the myocardium, peripheral striated muscle, liver, spleen, adrenal gland, lymph nodes, digestive tract and bone marrow. In the absence of the isolation of a toxoplasma strain, the diagnosis was based on the examination of a bone marrow smear performed the day before death. The proliferating forms of Toxoplasma gondii were abundant and characteristic. These data were confirmed by an ultrastructural study of toxoplasma in the lung and myocardium of the patient. In rapidly evolutive generalized toxoplasmosis of this type, the existence of a particular site is obvious but difficult to define. However, this study points out the usefulness of a bone marrow study in the hope of determining an etiological diagnosis with little delay which would thus increase the chances of an effective therapy.
To elucidate the reasons for glycolytic deviation commonly found in brain tumors, hexokinase (HK) activity, mitochondria-HK binding, oxidative phosphorylation and mitochondrial ultrastructure were studied in 4 human xenografted gliomas. Lactate/pyruvate ratios were increased 3-4 fold and HK activity was of 2-4 fold lower than that of normal rat brain tissue, used as the control. The mitochondria-bound HK (mHK) fraction varied considerably and represented 9 to 69% of the total HK of that normal rat brain. The respiratory activity of glioma mitochondria, assessed by polarography and spectrophotometry, was within the normal range. However, the mitochondrial content of gliomas was lower than in the rat brain tissue, as revealed by the markedly decreased, activities of two unrelated mitochondrial enzymes, cytochrome c oxidase and citrate synthase in glioma homogenates. Electron microscopical studies confirmed the reduced number of mitochondria in 3 out of the 4 gliomas. Profound alterations of mitochondrial ultrastructure, namely of cristae and matrix densities, were observed in the 4 gliomas. The intercrista space was wider in all gliomas and the crista area was larger in 3 out of the 4 gliomas than in normal rat brain. Finally, the outer membrane of glioma mitochondria interacted intimately and extensively with the rough endoplasmic reticulum (RER) and/or nuclear membrane. These results suggest that, because of the very low content of normally functioning mitochondria, gliomas shift their energy metabolism towards a high-level glycolysis to generate their cellular ATP supply, probably through RER-mitochondria interactions and transformation-dependent redistribution of particulate HK from non-mitochondrial to mitochondrial receptors.