Políticas activas de empleo en la UE en tiempos de crisis económica

Las políticas activas de empleo constituyen un campo complejo de estudio. Durante estos años de crisis económica se ha cuestionado su eficacia, abriéndose un debate académico, político y social acerca de cómo tratar mejor los problemas del mercado laboral en periodos de crisis económica. Tres dimensiones políticas son relevantes en términos de mantener un buen funcionamiento de los mercados de trabajo: la legislación de protección laboral, las políticas activas del mercado de trabajo y las medidas de apoyo a través de prestaciones por desempleo que dan una protección en forma de renta a los desempleados (políticas pasivas). Esta investigación tiene por objeto analizar la importancia y el diseño de las políticas activas de empleo que se han venido desarrollando en el difícil contexto económico actual de la Unión Europea. El funcionamiento adecuado de estas políticas, en sus vertientes de promoción y creación de empleo; intermediación y activación; educación y formación, se erigen como instrumentos claves para la dinamización de los mercados laborales en Europa. Para realizar este estudio se han identificado y agrupado las medidas fundamentales de las políticas activas de empleo de la UE durante estos años de crisis en 10 clústeres que han permitido llevar a cabo un análisis comparativo de las medidas implementadas. A su vez, se ha elaborado un mapa de las 579 medidas en políticas activas recogidas en los clústeres y se han clasificado sobre la base de tres criterios comunes (país de procedencia, objetivo y colectivo destinatario). Este mapa es el que nos ha servido para hacer las comparaciones entre las medidas de políticas activas sobre la base de un común denominador. A través del análisis comparativo, se han identificado aquellas medidas consideradas como “buenas prácticas” por la Unión Europea y que sirven como aprendizaje mutuo para la transferencia de información entre los Estados miembros. Estas buenas prácticas se han centrado en los desafíos comunes que ha planteado la crisis económica en los mercados laborales europeos: desempleo juvenil, desempleo de larga duración y segmentación laboral. Los principales resultados a los que se llega, ponen de manifiesto que existe una gran divergencia entre las medidas de políticas activas aplicadas por los países europeos durante estos años de crisis. La política comunitaria de empleo ha ido gestándose sin una verdadera coordinación de los Estados miembros respondiendo a la evolución económica y del desempleo lo que dificulta lograr una política de empleo común en la UE

Políticas activas de empleo en la UE: buenas prácticas para tiempos de crisis

Este artículo analiza las medidas de políticas activas de empleo utilizadas por los países de la UE para intentar combatir el desempleo que, de manera generalizada, ha aumentado como consecuencia de la crisis económica. Las políticas activas responden a múltiples propósitos que están interrelacionados y que persiguen un triple objetivo: preservar la motivación de los desempleados en la búsqueda activa de empleo, reforzar su empleabilidad a través de la formación y crear empleos sostenibles. Una de las principales conclusiones de este trabajo es que no existe una política de empleo como tal sino más bien un conjunto de recomendaciones y programas que intentan orientar y coordinar las 28 políticas de empleo de los respectivos países miembros. Para ayudar a esta coordinación de las medidas llevadas a cabo por cada uno de los países miembros destacando aquellas políticas que pueden considerarse como buenas prácticas que puedan servir de ejemplo para ser aplicadas en el resto de países europeos

Moderate Peep After Tracheal Lipopolysaccharide Instillation Prevents Inflammation and Modifies the Pattern of Brain Neuronal Activation

ABSTRACT Background: Ventilatory strategy and specifically positive end-expiratory pressure (PEEP) can modulate the inflammatory response and pulmonary-to-systemic translocation of lipopolysaccharide (LPS). Both inflammation and ventilatory pattern may modify brain activation, possibly worsening the patient's outcome and resulting in cognitive sequelae. Methods: We prospectively studied Sprague–Dawley rats randomly assigned to undergo 3 h mechanical ventilation with 7 mL/kg tidal ventilation and either 2 cmH2O or 7 cmH2O PEEP after intratracheal instillation of LPS or saline. Healthy nonventilated rats served as baseline. We analyzed lung mechanics, gas exchange, lung and plasma cytokine levels, lung apoptotic cells, and lung neutrophil infiltration. To evaluate brain neuronal activation, we counted c-Fos immunopositive cells in the retrosplenial cortex (RS), thalamus, supraoptic nucleus (SON), nucleus of the solitary tract (NTS), paraventricular nucleus (PVN), and central amygdala (CeA). Results: LPS increased lung neutrophilic infiltration, lung and systemic MCP-1 levels, and neuronal activation in the CeA and NTS. LPS-instilled rats receiving 7 cmH2O PEEP had less lung and systemic inflammation and more c-Fos-immunopositive cells in the RS, SON, and thalamus than those receiving 2 cmH2O PEEP. Applying 7 cmH2O PEEP increased neuronal activation in the CeA and NTS in saline-instilled rats, but not in LPS-instilled rats. Conclusions: Moderate PEEP prevented lung and systemic inflammation secondary to intratracheal LPS instillation. PEEP also modified the neuronal activation pattern in the RS, SON, and thalamus. The relevance of these differential brain c-Fos expression patterns in neurocognitive outcomes should be explored

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Deep-sequencing reveals broad subtype-specific HCV resistance mutations associated with treatment failure.

A percentage of hepatitis C virus (HCV)-infected patients fail direct acting antiviral (DAA)-based treatment regimens, often because of drug resistance-associated substitutions (RAS). The aim of this study was to characterize the resistance profile of a large cohort of patients failing DAA-based treatments, and investigate the relationship between HCV subtype and failure, as an aid to optimizing management of these patients. A new, standardized HCV-RAS testing protocol based on deep sequencing was designed and applied to 220 previously subtyped samples from patients failing DAA treatment, collected in 39 Spanish hospitals. The majority had received DAA-based interferon (IFN) α-free regimens; 79% had failed sofosbuvir-containing therapy. Genomic regions encoding the nonstructural protein (NS) 3, NS5A, and NS5B (DAA target regions) were analyzed using subtype-specific primers. Viral subtype distribution was as follows: genotype (G) 1, 62.7%; G3a, 21.4%; G4d, 12.3%; G2, 1.8%; and mixed infections 1.8%. Overall, 88.6% of patients carried at least 1 RAS, and 19% carried RAS at frequencies below 20% in the mutant spectrum. There were no differences in RAS selection between treatments with and without ribavirin. Regardless of the treatment received, each HCV subtype showed specific types of RAS. Of note, no RAS were detected in the target proteins of 18.6% of patients failing treatment, and 30.4% of patients had RAS in proteins that were not targets of the inhibitors they received. HCV patients failing DAA therapy showed a high diversity of RAS. Ribavirin use did not influence the type or number of RAS at failure. The subtype-specific pattern of RAS emergence underscores the importance of accurate HCV subtyping. The frequency of "extra-target" RAS suggests the need for RAS screening in all three DAA target regions

Overall survival in the OlympiA phase III trial of adjuvant olaparib in patients with germline pathogenic variants in BRCA1/2 and high-risk, early breast cancer

International audienc

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

International audienceSignificance There is growing evidence that preexisting autoantibodies neutralizing type I interferons (IFNs) are strong determinants of life-threatening COVID-19 pneumonia. It is important to estimate their quantitative impact on COVID-19 mortality upon SARS-CoV-2 infection, by age and sex, as both the prevalence of these autoantibodies and the risk of COVID-19 death increase with age and are higher in men. Using an unvaccinated sample of 1,261 deceased patients and 34,159 individuals from the general population, we found that autoantibodies against type I IFNs strongly increased the SARS-CoV-2 infection fatality rate at all ages, in both men and women. Autoantibodies against type I IFNs are strong and common predictors of life-threatening COVID-19. Testing for these autoantibodies should be considered in the general population

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

International audienceSignificance There is growing evidence that preexisting autoantibodies neutralizing type I interferons (IFNs) are strong determinants of life-threatening COVID-19 pneumonia. It is important to estimate their quantitative impact on COVID-19 mortality upon SARS-CoV-2 infection, by age and sex, as both the prevalence of these autoantibodies and the risk of COVID-19 death increase with age and are higher in men. Using an unvaccinated sample of 1,261 deceased patients and 34,159 individuals from the general population, we found that autoantibodies against type I IFNs strongly increased the SARS-CoV-2 infection fatality rate at all ages, in both men and women. Autoantibodies against type I IFNs are strong and common predictors of life-threatening COVID-19. Testing for these autoantibodies should be considered in the general population

Rare predicted loss-of-function variants of type I IFN immunity genes are associated with life-threatening COVID-19

BackgroundWe previously reported that impaired type I IFN activity, due to inborn errors of TLR3- and TLR7-dependent type I interferon (IFN) immunity or to autoantibodies against type I IFN, account for 15-20% of cases of life-threatening COVID-19 in unvaccinated patients. Therefore, the determinants of life-threatening COVID-19 remain to be identified in similar to 80% of cases.MethodsWe report here a genome-wide rare variant burden association analysis in 3269 unvaccinated patients with life-threatening COVID-19, and 1373 unvaccinated SARS-CoV-2-infected individuals without pneumonia. Among the 928 patients tested for autoantibodies against type I IFN, a quarter (234) were positive and were excluded.ResultsNo gene reached genome-wide significance. Under a recessive model, the most significant gene with at-risk variants was TLR7, with an OR of 27.68 (95%CI 1.5-528.7, P=1.1x10(-4)) for biochemically loss-of-function (bLOF) variants. We replicated the enrichment in rare predicted LOF (pLOF) variants at 13 influenza susceptibility loci involved in TLR3-dependent type I IFN immunity (OR=3.70[95%CI 1.3-8.2], P=2.1x10(-4)). This enrichment was further strengthened by (1) adding the recently reported TYK2 and TLR7 COVID-19 loci, particularly under a recessive model (OR=19.65[95%CI 2.1-2635.4], P=3.4x10(-3)), and (2) considering as pLOF branchpoint variants with potentially strong impacts on splicing among the 15 loci (OR=4.40[9%CI 2.3-8.4], P=7.7x10(-8)). Finally, the patients with pLOF/bLOF variants at these 15 loci were significantly younger (mean age [SD]=43.3 [20.3] years) than the other patients (56.0 [17.3] years; P=1.68x10(-5)).ConclusionsRare variants of TLR3- and TLR7-dependent type I IFN immunity genes can underlie life-threatening COVID-19, particularly with recessive inheritance, in patients under 60 years old