Programa de vigilància de les infeccions nosocomials als hospitals de Catalunya (Programa VINCat)

Infeccions nosocomials; Hospitals; Vigilància epidemiològicaNosocomial infections; Hospitals; Epidemiological surveillanceInfecciones nosocomiales; Hospitales; Vigilancia epidemiológicaVINCat és un programa del Servei Català de la Salut que estableix un sistema de vigilància unificat de les infeccions nosocomials als hospitals de Catalunya. La seva missió és contribuir a reduir les taxes d’aquestes infeccions mitjançant la vigilància epidemiològica activa i continuada. El programa es fonamenta en la tasca que porten a terme els professionals dels equips multidisciplinaris de control d’infecció dels hospitals catalans.VINCat is a program of the Catalan Health Service that establishes a unified surveillance system for nosocomial infections in hospitals in Catalonia. Its mission is to help reduce the rates of these infections through active and ongoing epidemiological surveillance. The program is based on the work carried out by the multidisciplinary teams of infection control of Catalan hospitals.VINCat es un programa del Servicio Catalán de la Salud que establece un sistema de vigilancia unificado de las infecciones nosocomiales en los hospitales de Cataluña. Su misión es contribuir a reducir las tasas de estas infecciones mediante la vigilancia epidemiológica activa y continuada. El programa se fundamenta en la tarea que llevan a cabo los profesionales de los equipos multidisciplinares de control de infección de los hospitales catalanes

The endocytic adaptor Numb regulates thymus size by modulating pre-TCR signaling during asymmetric division

Stem cells must proliferate and differentiate to generate the lineages that shape mature organs; understanding these 2 processes and their interaction is one of the central themes in current biomedicine. An intriguing aspect is asymmetric division, by which 2 daughter cells with different fates are generated. Several cell fate determinants participate in asymmetric division, with the endocytic adaptor Numb as the best-known example. Here, we have explored the role of asymmetric division in thymocyte development, visualizing the differential segregation of Numb and pre-TCR in thymic precursors. Analysis of mice where Numb had been inhibited by expressing a dominant negative revealed enhanced pre-T-cell receptor (TCR) signaling and a smaller thymus. Conversely, Numb overexpression resulted in loss of asymmetric division and a larger thymus. The conclusion is that Numb determines the levels of pre-TCR signaling in dividing thymocytes and, ultimately, the size of the pool from which mature T lymphocytes are selected. © 2010 by The American Society of Hematology.Peer Reviewe

Regulation of c-Myc and Max in Megakaryocytic and Monocytic-Macrophagic Differentiation of K562 Cells Induced by Protein Kinase C Modifiers: c-Myc Is Down-Regulated but Does Not Inhibit Differentiation

16 pages, 12 figures, 1 table.We have studied the regulation and role of c-Myc and Max in the differentiation pathways induced in K562 cells by 12-O-tetradecanoyl phorbol-13 acetate (TPA) and staurosporine, an activator and inhibitor, respectively, of protein kinase C (PKC). We found that staurosporine induced megakaryocytic differentiation, as revealed by the cellular ultrastructure, platelet formation, and DNA endoreduplication. In contrast, TPA induced a differentiated phenotype that more closely resembled that of the monocyte-macrophage lineage. c-myc expression was down-regulated in K562 differentiated by both TPA and staurosporine, whereas max expression did not change in either case. Although PKC enzymatic activity was low in cells terminally differentiated with TPA and staurosporine, inhibition of PKC activity by itself did not induce c-myc down-regulation. We conclude that the c-myc gene is switched off as a consequence of the differentiation process triggered by these drugs in a manner independent from PKC. Ectopic overexpression of c-Myc in K562 cells did not affect the monocytic-macrophagic and megakaryocytic differentiation, indicating that c-Myc suppression is not required for these processes in K562. Similarly, both differentiation pathways were not affected by Max overexpression or by concomitant overexpression of c-Myc and Max. This result is in contrast with the inhibition of erythroid differentiation of K562 exerted by c-Myc, suggesting divergent roles for c-Myc/Max, depending on the differentiation pathway.Supported by Grant CICYT-SAF96–0083 from the Spanish government and Biomed 96-3532 from the European Community. A. L. and P. G. are recipients of fellowships of the Spanish Ministerio de Educación y Cultura, and M. C. is the recipient of a fellowship from Gobierno Vasco.Peer reviewe

CD3 epsilon recruits Numb to promote TCR degradation

Modulation of TCR signaling upon ligand binding is achieved by changes in the equilibrium between TCR degradation, recycling and synthesis; surprisingly, the molecular mechanism of such an important process is not fully understood. Here, we describe the role of a new player in the mediation of TCR degradation: the endocytic adaptor Numb. Our data show that Numb inhibition leads to abnormal intracellular distribution and defective TCR degradation in mature T lymphocytes. In addition, we find that Numb simultaneously binds to both Cbl and a site within CD3 epsilon that overlaps with the Nck binding site. As a result, Cbl couples specifically to the CD3 epsilon chain to mediate TCR degradation. The present study unveils a novel role of Numb that lies at the heart of TCR signaling initiation and termination.The work was funded by grants BFU2004-01771, BFU2007-67476 and BFU2010-21634 from the Spanish Science and Education Ministry, a Special Intramural CSIC (Spanish Science Council) grant and the Excellence grant P06-CTS-02112 from the Department of Science and Innovation of the Regional Government of Andalucia, Spain (M.C.), and grants SAF08-01581 and RD06/0020/0017 (J.L.).Peer reviewe

NUMB inactivation confers resistance to imatinib in chronic myeloid leukemia cells

Chronic myeloid leukemia (CML) progresses from a chronic to a blastic phase, where the leukemic cells are proliferative and undifferentiated. The CML is nowadays successfully treated with BCR-ABL kinase inhibitors as imatinib and its derivatives. NUMB is an evolutionary well-conserved protein initially described as a functional antagonist of NOTCH function. NUMB is an endocytic protein associated with receptor internalization, involved in multiple cellular functions. It has been reported that MSI2 protein, a NUMB inhibitor, is upregulated in CML blast crisis, whereas NUMB itself is downregulated. This suggest that NUMB plays a role in the malignant progression of CML. Here we have generated K562 cells (derived from CML in blast crisis) constitutively expressing a dominant negative form of NUMB (dnNUMB). We show that dnNUMB expression confers a high proliferative phenotype to the cells. Importantly, dnNUMB triggers a partial resistance to imatinib in these cells, antagonizing the apoptosis mediated by the drug. Interestingly, imatinib resistance is not linked to p53 status or NOTCH signaling, as K562 lack p53 and imatinib resistance is reproduced in the presence of NOTCH inhibitors. Taken together, our data support the hypothesis that NUMB activation could be a new therapeutic target in CML.The work was supported by grants SAF2014-53526 (to JL), BFU2007-67476 and BFU2010-21634 (to MC) from Spanish Ministry of Economy and Competitiveness (MINECO), and RD12/0036/0033 (to JL), RD12/0036/0054 (to AB) and RD12/0019/0006 and PI12/01097 (to FM) from Instituto Carlos III, and grant PI-57069 from CICE, FEDER/Fondo de Cohesion Europeo (FSE) de Andalucía 2007–2013 (to FM). The funding from MINECO and Instituto Carlos III was co-sponsored by the European Union FEDER program. EGA was supported with a JAE-doc contract form CSIC, MCL-N was supported by the FPU program from MINECO and LG-G. We thank Rosa Blanco for excellent technical advice by the FPI program from MINECO.Peer Reviewe

MADCOVID-CSIC: Research and design of scientific dissemination activities on COVID-19 aimed at the Spanish youth

MADCOVID-CSIC is an outreach project aimed at young people concentrating on the most interesting aspects about the pandemic. These ranged from contagion to emotional impact. It is financed by the Recovery Fund and belongs to the Social Forum of the PTI+ Global Health.Objectives: • Disseminate, inform and promote knowledge about the pandemic among young people. • Promote greater awareness of young people about the risks of COVID-19. • Encourage young people to be the link of information and dissemination with their immediate family and friends. • Help young people emotionally manage the pandemic.Methods: First we sent a questionnaire to the teacher in order to determine the topics that interest the most: disease,contagion, vaccine, duration of the pandemic, misinformation, fake news and emotional management. The content of the talks is adapted to priorities. Then, an assessment of the experience is made between speakers and teachers to detect changes in behavior and perception of the pandemic among the students.Results and conclusions: To date, more than 25 talks have been given in educational centers, 11 of them in collaboration with secondary schools associated with the CSIC’s Science dissemination Project “Ciencia en el Barrio”, orientated to socially and vulnerable neighborhood in Madrid and the surrounded metropolitan area. In the talks, emotional management is treated preferentially, through collaboration with a cabinet of psychologists that is receiving great interest from teachers and students. They learn to recognize and name emotions, normalizing them and discarding emotional garbage, favoring more emotionally proactive, tolerant and healthy attitudes.Peer reviewe