[Favorable development of 2 pregnancies in hypereosinophilic syndrome].
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Biomedical subjects
Publications and source records attributed to Y Pacheco.
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Methylation of phospholipids seems to be an essential step in the recognition and transduction of regulatory signals by eukaryotic cells. Phosphatidylethanolamine methylation was compared in alveolar macrophage membrane from patients presenting with pulmonary sarcoidosis or hypersensitivity pneumonitis and control subjects. Phosphatidylethanolamine methyltransferase (PMT1) activity was determined by various measures of incorporation of tritiated methyl group from (3H) S-adenosyl-L-methionine in membrane phospholipids. Tritiated methyl group incorporation in macrophage membrane was higher in some patients presenting with sarcoidosis or hypersensitivity pneumonitis, than in controls. PMT1 activity was found to be higher in sarcoidosis patients with a positive gallium lung scan. As lipids play an important role during macrophage activation and cell interaction, although a wide heterogeneity was observed in PMT1 activity, increased membrane phospholipid methylation seems to be an important feature in pulmonary diseases where macrophages are involved.
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Angiotensin converting enzyme activity (ACE), albumin, potassium, and alpha1-antitrypsin were measured in the serum and in the bronchoalveolar lavage fluid (BAL) of 10 normal control subjects and of 19 cases of extrinsic allergic alveolitis (EAA). Among these 19 patients, 6 had a acute form of extrinsic alveolitis, 8 a subacute or chronic form, and 5 received a steroid therapy. Serum ACE is not increased in the acute forms of extrinsic alveolitis, but is significantly lower than control values in the subacute and chronic forms (p less than 0.04) and in patients under steroid therapy (p less than 0.002). The ACE/albumin, ACE/potassium, ACE/IgG and ACE/alpha1-antitrypsin ratios were measured in sera and BAL fluids. The results suggest that ACE is selectively transported across the alveolar capillary septum into the alveolar space. This transport, very important in control subjects, decreases in the subacute and chronic forms and in patients under steroid therapy. In the acute forms, the high level of ACE in BAL fluid is not due to an increased secretion of ACE, but is the result of an increased passive transudation of ACE from the vascular compartment across the inflammatory alveolar capillary septum.