28 research outputs found
Human and animal epidemic of Yersinia enterocolitica O:9, 1989-1997, Auvergne, France.
Yersinia enterocolitica O:9 infections were reported in Auvergne in 1988 to 1989, while brucellosis due to Brucella abortus was almost eliminated. The serologic cross-reactions between the two bacteria complicated the diagnosis of brucellosis cases. In 1996, human cases of Yersinia enterocolitica O:9 infection were detected, with a peak incidence of 12 cases. Veterinary surveillance could have predicted the emergence of this disease in humans
CP-120 Comparison of antibiotic consumption and bacterial resistance in two teaching hospitals: impact of a multidisciplinary antibiotic management program
Formes neurologiques des infections à Mycoplasma pneumoniae : à propos de neuf cas pédiatriques
S-01 Amélioration de la qualité des échantillons d’expectoration à visée bactériologique après optimisation de la méthode de recueil
Utilisation de la gélose VCA3 (bioMérieux) pour l'isolement sélectif des Enterococci résistants à la vancomycine à partir de prélèvements fécaux
International audienc
AMP deaminase 1 gene polymorphism and heart disease-A genetic association that highlights new treatment
Nucleotide metabolism and signalling is directly linked to myocardial function. Therefore analysis how diversity of genes coding nucleotide metabolism related proteins affects clinical progress of heart disease could provide valuable information for development of new treatments. Several studies identified that polymorphism of AMP deaminase 1 gene (AMPD1), in particular the common C34T variant of this gene was found to benefit patients with heart failure and ischemic heart disease. However, these findings were inconsistent in subsequent studies. This prompted our detailed analysis of heart transplant recipients that revealed diverse effect: improved early postoperative cardiac function associated with C34T mutation in donors, but worse 1-year survival. Our other studies on the metabolic impact of AMPD1 C34T mutation revealed decrease in AMPD activity, increased production of adenosine and de-inhibition of AMP regulated protein kinase. Thus, genetic, clinical and biochemical studies revealed that while long term attenuation of AMPD activity could be deleterious, transient inhibition of AMPD activity before acute cardiac injury is protective. We suggest therefore that pharmacological inhibition of AMP deaminase before transient ischemic event such as during ischemic heart disease or cardiac surgery could provide therapeutic benefit
