223 research outputs found

    Anatome Corporis Humani

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    Copia digital. Madrid : Ministerio de Cultura. Subdirección General de Coordinación Bibliotecaria, 2009Sign.: a-c-\p6\s, A-Z\p6\s, 2A-2E\p8\sIl. xil. al comienzo del textoLetras capitales ornadasTexto con apostillas marginalesPort. calc. arquitectónicaLám. cal

    Relativistic particle dynamics in D=2+1

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    We propose a SUSY variant of the action for a massless spinning particles via the inclusion of twistor variables. The action is constructed to be invariant under SUSY transformations and τ\tau-reparametrizations even when an interaction field is including. The constraint analysis is achieved and the equations of motion are derived. The commutation relations obtained for the commuting spinor variables λ\lambda show that the particle states have fractional statistics and spin. At once we introduce a possible massive term for the non-interacting model.Comment: 11 page

    Autophagy resolves early retinal inflammation in Igf1-deficient mice

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    Insulin-like growth factor-1 (IGF-1) is a growth factor with differentiating, anti-apoptotic and metabolic functions in the periphery, and anti-inflammatory properties in the nervous system. Mice that have mutations in the Igf1 gene, rendering the gene product inactive (Igf1(-/-)), present with age-related visual loss accompanied by structural alterations in the first synapses of the retinal pathway. Recent advances have revealed a crucial role of autophagy in immunity and inflammation. Keeping in mind this close relationship, we aimed to decipher these processes in the context of the defects that occur during ageing in the retina of Igf1(-/-) mice. Tnfa and Il1b mRNAs, and phosphorylation of JNK and p38 MAPK were elevated in the retinas of 6- and 12-month old Igf1(-/-) mice compared to those in age-matched Igf1(+/+) controls. In 6-month-old Igf1(-/-) retinas, increased mRNA levels of the autophagy mediators Becn1, Atg9, Atg5 and Atg4, decreased p62 (also known as SQSTM1) protein expression together with an increased LC3-II:LC3-I ratio reflected active autophagic flux. However, in retinas from 12-month-old Igf1(-/-) mice, Nlrp3 mRNA, processing of the IL1β pro-form and immunostaining of active caspase-1 were elevated compared to those in age-matched Igf1(+/+) controls, suggesting activation of the inflammasome. This effect concurred with accumulation of autophagosomes and decreased autophagic flux in the retina. Microglia localization and status of activation in the retinas of 12-month-old Igf1(+/+) and Igf1(-/-) mice, analyzed by immunostaining of Cd11b and Iba-1, showed a specific distribution pattern in the outer plexiform layer (OPL), inner plexiform layer (IPL) and inner nuclear layer (INL), and revealed an increased number of activated microglia cells in the retina of 12-month-old blind Igf1(-/-) mice. Moreover, reactive gliosis was exclusively detected in the retinas from 12-month-old blind Igf1(-/-) mice. In conclusion, this study provides new evidence in a mouse model of IGF-1 deficiency that autophagy is an adaptive response that might confer protection against persistent inflammation in the retina during agein

    A DNA damage repair gene-associated signature predicts responses of patients with advanced soft-tissue sarcoma to treatment with trabectedin

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    Signatura genètica; Biomarcadors predictius; TrabectedinaFirma genética; Biomarcadores predictivos; TrabectedinaGene signature; Predictive biomarkers; TrabectedinPredictive biomarkers of trabectedin represent an unmet need in advanced soft-tissue sarcomas (STS). DNA damage repair (DDR) genes, involved in homologous recombination or nucleotide excision repair, had been previously described as biomarkers of trabectedin resistance or sensitivity, respectively. The majority of these studies only focused on specific factors (ERCC1, ERCC5, and BRCA1) and did not evaluate several other DDR-related genes that could have a relevant role for trabectedin efficacy. In this retrospective translational study, 118 genes involved in DDR were evaluated to determine, by transcriptomics, a predictive gene signature of trabectedin efficacy. A six-gene predictive signature of trabectedin efficacy was built in a series of 139 tumor samples from patients with advanced STS. Patients in the high-risk gene signature group showed a significantly worse progression-free survival compared with patients in the low-risk group (2.1 vs 6.0 months, respectively). Differential gene expression analysis defined new potential predictive biomarkers of trabectedin sensitivity (PARP3 and CCNH) or resistance (DNAJB11 and PARP1). Our study identified a new gene signature that significantly predicts patients with higher probability to respond to treatment with trabectedin. Targeting some genes of this signature emerges as a potential strategy to enhance trabectedin efficacy.This study was funded by the Spanish Group for Research on Sarcoma (GEIS) and partially by PharmaMar. The authors would like to thank the GEIS data center for data management. The authors also thank the donors and the Hospital Universitario Virgen del Rocío—Instituto de Biomedicina de Sevilla Biobank (Andalusian Public Health System Biobank and ISCIII-Red de Biobancos PT17/0015/0041) for part of the human specimens used in this study. David S. Moura is recipient of a Sara Borrell postdoctoral fellowship funded by the National Institute of Health Carlos III (ISCIII) (CD20/00155)

    Propuesta de optimizaci?n de procesos operativos para incrementar la productividad y reducir el nivel de inventario en la conversi?n vehicular

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    En el presente trabajo de investigaci?n no experimental se expondr? el an?lisis, diagn?stico y propuesta de soluci?n para optimizar el proceso de preparaci?n veh?cular de una de las empresas con mayor participaci?n de mercado en el sector automotriz en el Per?. El objetivo principal de esta investigaci?n es dise?ar una propuesta de mejora de procesos bajo el marco metodol?gico de Business Process Management (BPM) que busca incrementar la productividad con la cual se tendr?a un impacto directo en el nivel de inventario de veh?culos en el Centro de Distribuci?n. Se realiz? un an?lisis de todos los procesos que forman parte del ?rea de producci?n, el cual incluye la preparaci?n de veh?culos (inspecciones de calidad, conversiones a gas, etc) antes de ser despachados al cliente final (directo o por concesionario). Se estableci? un redise?o de procesos como propuesta de soluci?n que pretende aumentar la productividad. Para comprobar el nivel de impacto de la propuesta de soluci?n se ha empleado el software de simulaci?n Arena. Finalmente, se menciona la variaci?n de los indicadores determinados del modelo actual (AS IS) y despu?s de la simulaci?n obtenida con el dise?o de la propuesta de soluci?n (TO BE) obteniendo un impacto te?rico significativo

    Dachshund acts with Abdominal-B to trigger programmed cell death in the Drosophila central nervous system at the frontiers of Abd-B expression

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    A striking feature of the nervous system pertains to the appearance of different neural cell subtypes at different axial levels. Studies in the Drosophila central nervous system reveal that one mechanism underlying such segmental differences pertains to the segment-specific removal of cells by programmed cell death (PCD). One group of genes involved in segment-specific PCD is the Hox homeotic genes. However, while segment-specific PCD is highly precise, Hox gene expression is evident in gradients, raising the issue of how the Hox gene function is precisely gated to trigger PCD in specific segments at the outer limits of Hox expression. The Drosophila Va neurons are initially generated in all nerve cord segments but removed by PCD in posterior segments. Va PCD is triggered by the posteriorly expressed Hox gene Abdominal-B (Abd-B). However, Va PCD is highly reproducible despite exceedingly weak Abd-B expression in the anterior frontiers of its expression. Here, we found that the transcriptional cofactor Dachshund supports Abd-B-mediated PCD in its anterior domain. In vivo bimolecular fluorescence complementation analysis lends support to the idea that the Dachshund/Abd-B interplay may involve physical interactions. These findings provide an example of how combinatorial codes of transcription factors ensure precision in Hox-mediated PCD in specific segments at the outer limits of Hox expressionMinisterio de Ciencia y Educación, Grant/Award Number: PID2019-110952GB-I0

    A DNA damage repair gene-associated signature predicts responses of patients with advanced soft-tissue sarcoma to treatment with trabectedin

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    Predictive biomarkers of trabectedin represent an unmet need in advanced soft-tissue sarcomas (STS). DNA damage repair (DDR) genes, involved in homologous recombination or nucleotide excision repair, had been previously described as biomarkers of trabectedin resistance or sensitivity, respectively. The majority of these studies only focused on specific factors (ERCC1, ERCC5, and BRCA1) and did not evaluate several other DDR-related genes that could have a relevant role for trabectedin efficacy. In this retrospective translational study, 118 genes involved in DDR were evaluated to determine, by transcriptomics, a predictive gene signature of trabectedin efficacy. A six-gene predictive signature of trabectedin efficacy was built in a series of 139 tumor samples from patients with advanced STS. Patients in the high-risk gene signature group showed a significantly worse progression-free survival compared with patients in the low-risk group (2.1 vs 6.0 months, respectively). Differential gene expression analysis defined new potential predictive biomarkers of trabectedin sensitivity (PARP3 and CCNH) or resistance (DNAJB11 and PARP1). Our study identified a new gene signature that significantly predicts patients with higher probability to respond to treatment with trabectedin. Targeting some genes of this signature emerges as a potential strategy to enhance trabectedin efficacy.This study was funded by the Spanish Group for Research on Sarcoma (GEIS) and partially by PharmaMar. The authors would like to thank the GEIS data center for data management. The authors also thank the donors and the Hospital Universitario Virgen del Rocío—Instituto de Biomedicina de Sevilla Biobank (Andalusian Public Health System Biobank and ISCIII-Red de Biobancos PT17/0015/0041) for part of the human specimens used in this study. David S. Moura is recipient of a Sara Borrell postdoctoral fellowship funded by the National Institute of Health Carlos III (ISCIII) (CD20/00155)

    Innovative Educational Approach in Healthcare-Associated Infection Prevention and Control. Results of a European Study

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    Prevent and control healthcare-associated infections (HAIs) is a priority in healthcare assistance, not only due to present COVID-19 pandemic. Annually, around 3.2 million patients are affected by one of these infections and it is estimated that without controlling them, by 2050, 10 million more people could die every year, with especial relevance among elderly with infectious situations representing a third of mortality in people over 65 years old. Higher Education Institutions (HEI) in healthcare area have an important role in this panorama, by preparing students to be future professionals, stimulating them to have an innovative and entrepreneurial approach to today’s real-life challenges. A mixed-methods research was conducted, at European level (in Portugal, Finland, Poland and Spain), to facilitate learning of good practices on HAIs prevention and control while developing innovative solutions. 1475 participants were enrolled, from all partner HEI: 79 professors and mentors were interviewed (individual or focus group), 1326 final year nursing students made a self-report inventory (application of InovSafeCare Scale) and 70 students participated on focus group (agile piloting of the Model). The result of this research is a pedagogical model that mixes dimensions and methods that take nursing students closer to the demands of HAIs prevention and control and capacitates them to transfer knowledge to work settings with an innovative and entrepreneurial perspective – the InovSafeCare Model.info:eu-repo/semantics/publishedVersio
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