[Clinical and epidemiological evaluation of preventive antibiotherapy in scheduled digestive surgery. Results apropos of 121 cases].
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Biomedical subjects
Publications and source records attributed to M Torres.
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The pulmonary effects of NO2 were investigated in two animal species. Rats and guinea pigs aged from 5 to 60 days or more were exposed for 3 days either to 2 ppm or to 10 ppm NO2. Lung histology or superoxide dismutase (SOD) determination in alveolar macrophages was assessed in air and NO2-exposed animals. Results demonstrated that the lung histological alterations are different for both NO2-exposed species. Rats were more tolerant than guinea pigs, but rat and guinea pig newborns were less affected than adults. The enzyme response to NO2 exposure was similar in both species and a decrease in SOD activity was noted in animals of all ages. These observations support the conclusion that NO2 exposure leads to increased lung damage during the life span, but on the contrary, exposure to oxygen does not involve SOD induction. This suggests that the defense mechanisms against NO2 are different from those of O2.
Forty-four patients with severe systemic bacterial infection were treated with azlocillin (20) or gentamicin (24). The commonest sites of infection were skin and soft tissue, lungs and bone. Thirty-eight patients had received previous antimicrobial therapy. The commonest infecting organism was Pseudomonas aeruginosa. The overall response rate in the azlocillin group was cure or partial cure in 18 patients and failure in one patient, and in the gentamicin group 15 cures or partial cures and six failures. Four patients, one on azlocillin and three on gentamicin, could not be evaluated. Azlocillin was an effective and safe therapy for the treatment of Ps. aeruginosa infections.
Polymorphonuclear functions were studied in 3 patients of the same brotherhood with Papillon-Lefèvre disease (hyperkeratosis palmaris and plantaris and acute periodontosis resulting in loss of teeth) who developed severe and recurrent infections. Chemotaxis, oxygen consumption and production of H2 O2 were investigated by polarography, O2 production by quantitative reduction of nitroblue tetrazolium and iodination by the Pinus and Klebanoff technique. functional anomalies of polymorphonuclears involving chemotaxis, induced O2 consumption and H2 O2 production were detected in all three patients. This study confirms the presence of polymorphonuclear functional anomalies in patients with Papillon-Lefèvre disease. Analysis of the family tree of the patients, which went back to 1761, showed that this was probably not a chance association.
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It is well known that phenobarbital treatment increases the production of superoxide anion by liver microsomes. Since the toxicity of superoxide anion and of its product, hydrogen peroxide, is well documented we measured the activities of the liver enzymes which protect the cell against the reduced forms of oxygen and the microsomal content of lipoperoxides in phenobarbital-treated rats. It was found that no lipoperoxides accumulate in the microsomes and that glutathione peroxidase, glutathione reductase activities, and the peroxidative activity of cytochrome P-450 were increased while catalase and superoxide dismutase activities were not modified.
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A 38-year-old male with proven Takayasu's arteritis presented, in a routine investigation, with thrombocytopenia, prolonged whole blood clotting time and activated partial thromboplastin time. Further studies demonstrated low levels of factor IX caused by a circulating anticoagulant. Immunological studies revealed an IgG (with kappa chains predominance) nature of this. Corticoid therapy decreased but did not suppress the anticoagulant activity. Since similar coagulation abnormalities have been described in collagen diseases, this observation is in support of this etiology to be considered in Takayasu's arteritis.