Asunto(s)
Endocarditis Bacteriana/diagnóstico , Infecciones por Haemophilus/diagnóstico , Haemophilus parainfluenzae/aislamiento & purificación , Insuficiencia de la Válvula Mitral/microbiología , Adulto , Bacteriemia/complicaciones , Bacteriemia/microbiología , Diagnóstico Tardío , Ecocardiografía Transesofágica , Endocarditis Bacteriana/diagnóstico por imagen , Endocarditis Bacteriana/microbiología , Femenino , Fiebre/etiología , Infecciones por Haemophilus/sangre , Infecciones por Haemophilus/diagnóstico por imagen , Infecciones por Haemophilus/microbiología , Humanos , Insuficiencia de la Válvula Mitral/diagnóstico por imagen , Enfermedad Relacionada con los ViajesRESUMEN
BACKGROUND: Ticagrelor and prasugrel have shown superiority over clopidogrel. However, it remains unclear if one is superior to another regarding on-treatment platelet reactivity. OBJECTIVES: To compare the impact of ticagrelor and prasugrel on high on-treatment platelet reactivity (HTPR). METHODS: The PubMed and Cochrane databases were searched for eligible studies in December 2014. Studies were eligible if they compared ticagrelor and prasugrel regarding high on-treatment platelet reactivity (HTPR). Pooled estimates were calculated by using a random-effects model with 95% confidence intervals. RESULTS: We included 14 studies and 1822 patients: 805 and 1017 in the ticagrelor and prasugrel groups, respectively. The rate of HTPR was significantly lower in the ticagrelor group: 1.5% vs. 9.8% (RR = 0.27 [0.14-0.50]). The pre-specified analysis focusing on randomized trials (n = 10) showed consistent results (RR = 0.27 [0.12-0.60]). CONCLUSION: Our results suggest that ticagrelor allows a higher platelet reactivity inhibition as compared with prasugrel and leads to a further decrease in the rate of HTPR.
Asunto(s)
Adenosina/análogos & derivados , Plaquetas/efectos de los fármacos , Cardiopatías/terapia , Intervención Coronaria Percutánea , Inhibidores de Agregación Plaquetaria/uso terapéutico , Agregación Plaquetaria/efectos de los fármacos , Clorhidrato de Prasugrel/uso terapéutico , Adenosina/efectos adversos , Adenosina/uso terapéutico , Plaquetas/metabolismo , Distribución de Chi-Cuadrado , Resistencia a Medicamentos , Cardiopatías/sangre , Cardiopatías/diagnóstico , Humanos , Oportunidad Relativa , Intervención Coronaria Percutánea/efectos adversos , Inhibidores de Agregación Plaquetaria/efectos adversos , Pruebas de Función Plaquetaria , Clorhidrato de Prasugrel/efectos adversos , Valor Predictivo de las Pruebas , Factores de Riesgo , Ticagrelor , Resultado del TratamientoRESUMEN
Pseudomonas aeruginosa and Candida albicans are frequently coexisting opportunistic pathogens, responsible for colonization and infection in predisposed patients. They share a virulence specificity relying on auto-inducing, cell density-dependent molecules named quorum-sensing (QS). C. albicans virulence depends on its QS that influences morphological switch from yeast to filamentous form. Similarly, the production of P. aeruginosa virulence factors depends partly on QS molecules. Interactions have been investigated and demonstrated in vitro. P. aeruginosa may kill C. albicans either by producing toxins, such as pyocyanin, or by direct contact on its biofilm-dependent filamentous form. Cross-kingdom communication is a more subtle interaction: C. albicans can adapt its morphology in the presence of P. aeruginosa QS molecules, and inhibit P. aeruginosa QS-dependent virulence factor secretion, through farnesol, one of its QS molecule. But the in vivo relevance of these interactions is still controversial, as models of airway colonization/infection by C. albicans followed by subsequent P. aeruginosa pneumonia give contradictory results, suggesting the probable involvement of the immune system as a third party player. Finally, the authors of clinical studies performed in ventilated patients, indicate that C. albicans colonization could be a risk factor for P. aeruginosa pneumonia. The clinical outcome of C. albicans and P. aeruginosa interaction is uncertain, the virulence modulation demonstrated in these interactions opens new possibilities for future anti-infectious therapeutics.
Asunto(s)
Candida albicans/patogenicidad , Candidiasis/microbiología , Infecciones Oportunistas/microbiología , Infecciones por Pseudomonas/microbiología , Pseudomonas aeruginosa/patogenicidad , Biopelículas , Candida albicans/ultraestructura , Coinfección , Interacciones Huésped-Patógeno , Humanos , Percepción de Quorum/fisiología , Virulencia/fisiologíaRESUMEN
The capacity to launch a strong shock wave in a compressed target in the presence of large preplasma has been investigated experimentally and numerically in a planar geometry. The experiment was performed on the LULI 2000 laser facility using one laser beam to compress the target and a second to launch the strong shock simulating the intensity spike in the shock ignition scheme. Thanks to a large set of diagnostics, it has been possible to compare accurately experimental results with 2D numerical simulations. A good agreement has been observed even if a more detailed study of the laser-plasma interaction for the spike is necessary in order to confirm that this scheme is a possible alternative for inertial confinement fusion.
RESUMEN
Correct modeling of the electron-energy transport is essential for inertial confinement fusion target design. Various transport models have been proposed in order to extend the validity of a hydrodynamical description into weakly collisional regimes, taking into account the nonlocality of the electron transport combined with the effects of self-generated magnetic fields. We have carried out new experiments designed to be highly sensitive to the modeling of the heat flow on the Ligne d'Intégration Laser facility, the prototype of the Laser Megajoule. We show that two-dimensional hydrodynamic simulations correctly reproduce the experimental results only if they include both the nonlocal transport and magnetic fields.