COSMO: Corrientes Marinas y Seguridad en el Medio Marino

Ejercicio internacional de salvamento y lucha contra la contaminación marina "Polex 24-17" organizado por la Dirección General de Marina Mercante y Salvamento Marítimo del 14 al 16 de junio de 2017 en SantanderDisponer en tiempo real de información sobre las corrientes oceánicas es clave para algunos de los servicios encomendados a la Sociedad de Salvamento y Seguridad Marítima y al Cuerpo Nacional de Policía (CNP). Un alto porcentaje de las emergencias de búsqueda de personas y náufragos, y de los incidentes de contaminación gestionados por Salvamento Marítimo, tienen lugar en zonas cercanas a la costa. Asimismo, el 71% de los casos de restos humanos no identificados (CSI) acontecidos en España durante el período 1968-2015 se da en zonas costeras. El proyecto COSMO busca mejorar la eficacia de las operaciones de búsqueda y de predicción de derivas, y mejorar la proporción de identificaciones positivas acelerando la resolución de casos de recuperación de restos humanosProyecto cofinanciado por el Ministerio de Economía Industria y Competitividad y Fondos FEDER de la UE (COSMO-CTM2016-79474-R, UE)Peer Reviewe

Modulating mitophagy in mitochondrial disease

Mitochondrial diseases may result from mutations in the maternally-inherited mitochondrial DNA (mtDNA) or from mutations in nuclear genes encoding mitochondrial proteins. Their bi-genomic nature makes mitochondrial diseases a very heterogeneous group of disorders that can present at any age and can affect any type of tissue. The autophagic-lysosomal degradation pathway plays an important role in clearing dysfunctional and redundant mitochondria through a specific quality control mechanism termed mitophagy. Mitochondria could be targeted for autophagic degradation for a variety of reasons including basal turnover for recycling, starvation induced degradation, and degradation due to damage. While the core autophagic machinery is highly conserved and common to most pathways, the signaling pathways leading to the selective degradation of damaged mitochondria are still not completely understood. Type 1 mitophagy due to nutrient starvation is dependent on PI3K (phosphoinositide 3-kinase) for autophagosome formation but independent of mitophagy proteins, PINK1 (PTEN-induced putative kinase 1) and Parkin. Whereas type 2 mitophagy that occurs due to damage is dependent on PINK1 and Parkin but does not require PI3K. Autophagy and mitophagy play an important role in human disease and hence could serve as therapeutic targets for the treatment of mitochondrial as well as neurodegenerative disorders. Therefore, we reviewed drugs that are known modulators of autophagy (AICAR and metformin) and may effect this by activating the AMP-activated protein kinase signaling pathways. Furthermore, we reviewed data available on supplements, such as Coenzyme Q and the quinone idebenone, that we assert rescue increased mitophagy in mitochondrial disease by benefiting mitochondrial function