Biomedical subjects
Publications and source records attributed to J Lefort.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Allergies and allergic asthma are believed to be mediated by allergen-specific IgE antibodies. We have investigated the therapeutic potential of inhibiting endogenous IgE by a non-anaphylactogenic anti-mouse IgE antibody 1-5 with respect to its effects on antigen-induced skin reaction, lung function changes and lung inflammation in mice. METHODS: Mice were immunized with benzylpenicillinoyl-KLH or ovalbumin, and antigen-mediated skin reaction, bronchoconstriction, bronchopulmonary hyperresponsiveness (BHR) and lung eosinophilic inflammation determined in anti-IgE 1-5-treated versus untreated animals. RESULTS: Application of anti-IgE 1-5 inhibited (by 90%) the serum IgE and, 3-4 days after onset of treatment, blocked the antigen-induced skin reaction. Furthermore, the antibody also inhibited (by 90%) the antigen-induced infiltration of eosinophils into the lung. This latter effect seems to be mediated by blocking the IgE-CD23 interaction and indicates that lung eosinophilic inflammation also depends on IgE. Moreover, when applied to rats passively sensitized with mouse IgE, antibody 1-5 inhibited the antigen-induced bronchoconstriction. A similar effect could be seen in actively immunized mice, where antibody 1-5 was able to inhibit (by 70%) the ovalbumin-induced bronchoconstriction as well as BHR. CONCLUSIONS: In summary, non-anaphylactogenic anti-IgE antibodies can markedly inhibit IgE levels and IgE-mediated allergic reactions. Since bronchoconstriction, BHR and lung eosinophilic inflammation can be suppressed, such antibodies may be attractive principles for the treatment of allergic asthma.
Among the various lipid mediators, platelet-activating factor (PAF) is likely to participate in the development of inflammatory and allergic reactions. Indeed, PAF mimics the symptoms of anaphylactic shock and causes bronchial hyperreactivity in various species. The availability of specific PAF antagonists led to determination of the precise role of this mediator in experimental allergic situations. Here we provide evidence that the bronchopulmonary and inflammatory effects of PAF in the guinea-pig are different depending on the immunological status of the animals. Consequently, the search for novel PAF antagonists should take into account the experimental model developed for studying its implication in allergic reactions and in the accompanying airway inflammation.
Seventeen nonmenopausal women with symptomatic uterine myomas, diagnosed by clinical examination and confirmed by pelvic ultrasonography, were treated with a delayed-release microcapsule preparation of D-Trp-6-LH-RH (Decapeptyl) injected intramuscularly, every 28 days. The microcapsules were designed to release 100 micrograms/day for 30 days. The mean duration of treatment was 4.7 months (range, 1-11). In all patients, the pituitary-ovarian axis was suppressed after 1 month of treatment, and mean serum estradiol levels fell to 17.3 pg/mL (range, 5-80). There were no significant changes in serum LH and FSH levels. Fifteen patients (83%) experienced an improvement of such symptoms as abdominal pain and bleeding. Enlarged uteri decreased in 81% of patients during the treatment, and in 38% of them the decrease in uterine volume was more than 50%. Among the 12 myomas found in 10 women, 2 disappeared and 9 decreased in volume during the treatment; for 7 myomas the decrease was more than 50%. After Decapeptyl, eight patients did not require any additional therapy, four underwent surgery, and the others were treated with progestins. The side effects were mild, consisting mainly of hot flushes. Our findings suggest that Decapeptyl may be useful for the treatment of uterine myomas.
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A study of 35 cases of congenital fusion of the cervical vertebrae demonstrated the high incidence of its association with urinary anomalies (52 per cent). More than half of these cases concerned unilateral kidney defects. The urinary anomalies are normally asymptomatic, but there is always the risk of chronic renal failure, and preventive surgery may be necessary. It is therefore advisable to make a systematic practice of obtaining ultrasound examinations and intravenous urograms. There are many other possible associated anomalies, which are often the first to be noted and lead to the discovery of the vertebral and urinary malformations. The authors define Klippel-Feil syndrome as the synostosis of two or more cervical vertebrae.
A literature study has been written about each failure concerning a very particular mishaping linking an agenesy of the left lung and of the left diaphragm to an esophagal atresia (type III). None similar case has been discovered in the literature. Concerning the diaphragmatic agenesies, the authors report several familial cases and outline the possibility of a genetic pathogeny.