[Early coronary recanalization followed by revascularization surgery in the acute phase of myocardial infarction].
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Biomedical subjects
Publications and source records attributed to M Franco.
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We studied a case of long-standing chondrocalcinosis that after 40 years affected almost all fibrocartilages, hyaline cartilages, and articular cavities within the subject. Massive deposits of dihydrocalcium pyrophosphate (CPP) were also found in nonfissured nucleus pulposus of the vertebral disks. To our knowledge, this is the first report of CPP deposits in these disks.
A person exposed to trimellitic anhydride (TMA) an epoxy resin widely used in industry, experienced respiratory failure, anemia, and gastrointestinal bleeding. A lung biopsy specimen demonstrated intra-alveolar hemorrhage and damage to alveolar lining cells. The patient and six co-workers were examined. Results indicated the presence of hemolytic antibodies directed against TMA-haptenized erythrocytes, IgG, IgA, and IgM antibodies directed against TMA-erythrocyte complexes, and antibodies against TMA-human serum albumin. Antibody levels in the patient were greater than in the co-workers. The elevated antibody levels demonstrate the antigenic potential of TMA. However, the cause of the pulmonary and hematologic damage remains uncertain and may represent either immunologic or direct toxic effects of TMA. In patients with multisystem failure of this nature, occupational hazards should be added to the differential diagnosis.
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An in vitro assay system was developed to test the propensity of "old" and sialidase-treated rat erythrocytes to be bound and phagocytosed by rat peritoneal macrophages. Cells considered to be old were phagocytosed to a greater degree than those considered to be young. When erythrocytes were treated with immobilized Vibrio cholerae sialidase, higher amounts of sialic acids had to be removed (25--30%) to induce binding and phagocytosis of the cells, than if the cells had been treated with soluble enzyme (9--15%).
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Inflammatory cell populations from synovial effusions or synovial villi in rheumatoid arthritis have been cultured in vitro. Prostaglandin productive capacity, measured by radioimmunoassay, showed the polymorphonuclear leucocyte rich populations from synovial effusions to be poor sources of PGE production whereas the synovial fragments produced substantial amounts of PGE activity. It is suggested that the macrophage is the major source of local prostaglandin formation both in gout and rheumatoid arthritis.
The prostaglandins PGE1, E2, F2alpha, and A1, had no significant cell migration inhibitory or chemotactic activity for guinea pig peritoneal exudate cells when tested in vitro using respectively the capillary tube cell migration test and the Boyden chamber test for chemotaxis. PGE1 and PGE2 also did not affect the positive chemotactic action of lymphokine. The proposed role of prostaglandins as chemotactic agents in inflammatory responses therefore should be treated with some caution.
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