¿Trabajo decente o trabajo indecente?

El trabajo decente, tal como lo define la OIT, es una forma digna de trabajar en un contexto de políticas de generación de empleo, con la capacidad de exigir judicialmente los derechos de los trabajadores, en el marco de una política institucional de protección social y con el reconocimiento de una negociación colectiva autonormativa consolidada. A estos cuatro objetivos tradicionales debemos sumar el objetivo transversal de la igualdad de género. El desempleo, el subempleo y el empleo precario, en el marco de la ideología de la flexiseguridad, configuran el caldo de cultivo del empleo indecente o empleo precario.Decent work, as defined by the ILO, is a worthy way of working, in a context of employment generation policies, with the capacity to legally demand the rights of workers, within the framework of an institutional policy of social protection and with the recognition of a consolidated autonomous collective bargaining. To these four traditional objectives we must add the transversal objective of gender equality. Unemployment, underemployment and precarious employment, within the framework of the ideology of flexicurity, are the breeding grounds of indecent employment or precarious employment

Estrogen Receptor-Alpha (ESR1) Governs the Lower Female Reproductive Tract Vulnerability to Candida albicans

Estradiol-based therapies predispose women to vaginal infections. Moreover, it has long been known that neutrophils are absent from the vaginal lumen during the ovulatory phase (high estradiol). However, the mechanisms that regulate neutrophil influx to the vagina remain unknown. We investigated the neutrophil transepithelial migration (TEM) into the vaginal lumen. We revealed that estradiol reduces the CD44 and CD47 epithelial expression in the vaginal ectocervix and fornix, which retain neutrophils at the apical epithelium through the estradiol receptor-alpha. In contrast, luteal progesterone increases epithelial expression of CD44 and CD47 to promote neutrophil migration into the vaginal lumen and Candida albicans destruction. Distinctive to vaginal mucosa, neutrophil infiltration is contingent to sex hormones to prevent sperm from neutrophil attack; although it may compromise immunity during ovulation. Thus, sex hormones orchestrate tolerance and immunity in the vaginal lumen by regulating neutrophil TEM.The authors thank the units of flow cytometry, cell culture and statistical analysis. We are grateful to J. Villarejo, M. Fernandez-Garcia, and F. Sanchez-Cobos, for expert help and support. This work was partially supported by Fundacion Mutua Madrilena and the Ministry of Economy and Competitiveness ISCIII-FIS grants PI13/00269, PI16/00050, and PI17/01324, co-financed by ERDF (FEDER) Funds from the European Commission, ``A way of making Europe.´´ MR holds a Miguel Servet II contract (CPII14/00009). LS-M holds a IiSGM intramural contract.S

Philosophy, science, and cinema: Feminist perspectives

A lo largo del curso académico 2021-2022, el proyecto “Filosofía, Ciencia y Cine: perspectivas feministas” ha logrado coordinar el trabajo de un elevado número de personal docente y estudiantado que ha participado activamente en la organización de eventos académicos, algunos de ellos previstos en la propuesta original y otros muchos ideados a lo largo del curso. En total, se han llevado a cabo 11 actividades, incluyendo la grabación de dos podcasts, la realización de 8 cinefórums y la celebración de un simposio. Las actividades han obtenido un gran éxito de asistencia y participación y se han difundido ampliamente tanto en la Facultad de Filosofía como en las redes sociales de la Facultad y del proyecto.Depto. de Lógica y Filosofía TeóricaFac. de FilosofíaFALSEsubmitte

Chemokine receptor CCR7 induces intracellular signaling that inhibits apoptosis of mature dendritic cells

6 Figures. The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked ‘‘advertisement’’ in accordance with 18 U.S.C. section 1734.Acquisition of CCR7 expression is an important phenotype change during dendritic cell (DC) maturation that endows these cells with the capability to migrate to lymph nodes. We have analyzed the possible role of CCR7 on the regulation of the survival of DCs. Stimulation with CCR7 ligands CCL19 and CCL21 inhibits apoptotic hallmarks of serum-deprived DCs, including membrane phosphatidylserine exposure, loss of mitochondria membrane potential, increased membrane blebs, and nuclear changes. Both chemokines induced a rapid activation of phosphatidylinositol 3'-kinase/Akt1 (PI3K/Akt1), with a prolonged and persistent activation of Akt1. Interference with PI3K, Gi, or G protein γ subunits abrogated the effects of the chemokines on Akt1 activation and on survival. In contrast, inhibition of extracellular signal-related kinase 1/2 (Erk1/2), p38, or c-Jun N-terminal kinase (JNK) was ineffective. Nuclear factor–κB (NFκB) was involved in the antiapoptotic effects of chemokines because inhibition of NFκB blunted the effects of CCL19 and CCL21 on survival. Furthermore, chemokines induced down-regulation of the NFκB inhibitor IκB, an increase of NFκB DNA-binding capability, and translocation of the NFκB subunit p65 to the nucleus. In summary, in addition to its well-established role in chemotaxis, we show that CCR7 also induces antiapoptotic signaling in mature DCs.We acknowledge Julia Villarejo and Isabel Trevino for their help, Patricio Aller for advice on Hoechst 33342 staining, Eduardo Munoz for the p65-GFP construct, and Robert Lefkovitch for providing the dominant negative ARK-CT construct. From the Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Madrid; Laboratorio de Inmunología, Hospital General Universitario Gregorio Maranón, Madrid; Departamento de Bioquímica and Instituto de Investigaciones Biomédicas Alberto Sols, Facultad de Medicina, Universidad Autónoma de Madrid; and Instituto de Farmacología y Toxicología Consejo Superior de Investigaciones Científicas (CSIC)–Universidad Complutense de Madrid (UCM), Facultad de Medicina, Universidad Complutense, Madrid, Spain. Supported by grants BFI-2001-228, CAM08.3/0040/2001.1, and PI021058 (J.L.R.-F) and SAF2002-04615-C02-02 (P.S.-M.); Fondo de Investigación Sanitaria and Ramon y Cajal programs (J.L.R.-F.); and a scholarship associated to grant PI021058 (L.R.-B.). N.S.-S. is recipient of a fellowship, Formación del Profesorado Universitario (FPU), conferred by the Ministerio de Educación (Spain).Peer reviewe

Estrogen Receptor-Alpha (ESR1) Governs the Lower Female Reproductive Tract Vulnerability to Candida albicans

Estradiol-based therapies predispose women to vaginal infections. Moreover, it has long been known that neutrophils are absent from the vaginal lumen during the ovulatory phase (high estradiol). However, the mechanisms that regulate neutrophil influx to the vagina remain unknown. We investigated the neutrophil transepithelial migration (TEM) into the vaginal lumen. We revealed that estradiol reduces the CD44 and CD47 epithelial expression in the vaginal ectocervix and fornix, which retain neutrophils at the apical epithelium through the estradiol receptor-alpha. In contrast, luteal progesterone increases epithelial expression of CD44 and CD47 to promote neutrophil migration into the vaginal lumen and Candida albicans destruction. Distinctive to vaginal mucosa, neutrophil infiltration is contingent to sex hormones to prevent sperm from neutrophil attack; although it may compromise immunity during ovulation. Thus, sex hormones orchestrate tolerance and immunity in the vaginal lumen by regulating neutrophil TEM

Filosofía y Humor: el cine como recurso audiovisual para pensar desde la risa filosófica

Depto. de Lógica y Filosofía TeóricaFac. de FilosofíaFALSEsubmitte