Gonadoliberin-promoted release of gonadotropins and increased sensitivity of the pituitary by oestradiol-17beta.
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Biomedical subjects
Publications and source records attributed to J Duval.
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We studied 64 cases of bacterial endocarditis which required heart surgery for hemodynamic defects and/or failure of the antibiotic therapy. We performed a bacteriologic and histologic investigation of the removed valves. The organisms were evidenced through culture and specific stainings. According to the different organisms we evaluated the best duration of antibiotic therapy to achieved sterilization, and suggest a helpful medical and surgical treatment for the bacterial endocarditis.
A single dose (1 microgram) of oestradiol sub-cutaneously injected to an immature male rat promotes a transitory increase of the pituitary mitotic activity, the maximum of which is reached between 32 and 48 hours ; the observed fluctuations are similar to those previously described for the thymidine kinase activity. In these conditions, the concentration of blood prolactin remains unaltered, as were those of LH and FSH. It follows that hyperplasy of the pituitary can be quickly induced by doses of oestrogen that do not affect significantly the hormone release. Using Moxestrol, a synthetic oestrogen not bound by the oestradiol plasma binding protein, we show that in the very young rat, the in vivo responsiveness of the pituitary increases and reaches its maximum by day 17. This results can be tentatively related to the ontogeny of the oestradiol receptors in the pituitary described by others ; all our attempts to induce the thymidine kinase in cultured glands remained unsuccessful.
A wild-type strain of Staphylococcus aureus that inactivates the 4,6-glycosidically linked deoxystreptamine aminoglycoside antibiotics by a plasmid-mediated process was found to harbor two enzymes: an acetyltransferase of the AAC(6') type and a new phosphotranferase specific to the gentamicin components. The target of this last enzyme is the 2''-hydroxyl function of these antibiotics, since one inactivated compound is 2''-(O)-phosphorylsisomicin.
A wild strain of Staphylococcus aureus which inactivates a wide variety of antibiotics has been found to inactivate pristinamycin IIA, an antistaphylococcal antibiotic. This phenomenon has been demonstrated to be plasmid mediated. The plasmid directs the biosynthesis of an acetyltransferase which is able to O-acetylate the drug. We propose to call the new enzyme PAC (IIA): Pristinamycin acetyltransferase.
Pristinamycin and virginiamycin, two antibiotics belonging to the streptogramin group, are widely used in France against staphylococcal infections. They are mixtures of two different active compounds, pristinamycin I and II, virginiamycine S and M. The present study describes five clinical isolates of Staphylococcus aureus with unusual resistance to these antibiotics. This resistance, whose level is variable according to the strains, concerns both compounds of these antibiotics. It is lost at high frequency spontaneoulsy or after treatment by curing agents, suggesting that the resistance is plasmid mediated. The drug inactivation by the resistant strains supports the hypothesis of an enzymatic mechanism of resistance. Furthermore, this new resistance seems to be linked, in some strains, to either of the two aminoglycoside resistance patterns recently described in S. aureus.
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A wild-type strain of Staphylococcus aureus, which inactivates a wide variety of aminoglycosides (except the gentamicin components), has been found to harbor a plasmid (RAp01) that mediates the biosynthesis of a nucleotidyltransferase. This enzyme modifies the 4'-hydroxy function of these antibiotics. The plasmid has been studied, the enzyme responsible for this resistance pattern has been isolated by affinity chromatography, and its kinetics and physicochemistry have been characterized. The target of this enzyme has also been located by demonstrating the structure of one inactivated compound, 4'-(O)-adenylyltobramycin.
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A new nucleotidyltransferase has been obtained from clinical isolates of kanamycin, amikacin, tobramycin, neomycin and lividomycin resistant strains of Staphylococcus aureus. The enzyme has been purified by affinity chromatography then characterized in a kinetic and physicochemical point of view. The results obtained support that the target of this enzyme is the 4'-hydroxyl group of a number of aminoglycosides. We propose to call it ANT(4')I.
Recently, strains of Staphylococcus aureus resistant to gentamicin, tobramycin and amikacin have been discovered in several hospitals in France. These new resistances, of two different types, are of plasmid origin and of enzyme mechanism. This study describes their current incidence.
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A successfull bone marrow transplant was achieved in a case of post hepatitic aplastic anemia after cyclophosphamide immunosuppression. Caryotype analysis, erythrocytic phenotype and IgG Gm allotype demonstrated evidence of complete chimerism. Anti-thymocyte serum undoubtly was able to suppress a life threatening episode of graft versus host reaction. Severe long lasting skin lesions are now persisting 2 years after the graft.