Alternativas de centralización de la función de tesorería en holdings de compañías internacionales

A través del proyecto se pretende buscar diferentes alternativas de centralización de la función de tesorería y el continuum de madurez para un holding internacional de compañías, lo que implica desde modelos de cash pooling, a modelos de centros de servicios compartidos (factorías de cobros y pagos), a modelos avanzados de bancos internos, analizando en qué casos puede ser aplicable cada uno. En términos generales, el proyecto se divide en cuatro bloques: -Repaso a los roles, responsabilidades y evolución de la función de tesorería, a nivel general -Repaso a las alternativas de centralización de la función de tesorería -Caso sobre un diseño de un modelo de centralización para un grupo internacional -Conclusiones---ABSTRACT---Through the project aims to find different alternatives of centralized treasury function and the continuum of maturity for an international holding company, which means from models of cash pooling, models of shared service centers (factories collections and payments ), to advanced models of domestic banks, analyzing in which cases may be applicable each. Overall, the project is divided into four main parts: -Review of the roles, responsibilities and evolution of the treasury function, in general --Review of the alternatives of centralization of the treasury function -Case study on a design of a centralized model for an international group -Conclusion

Evaluación formativa del TFG del Grado de Psicologia. Diseño de Rubricas para diferentes modalidades, fases y acciones

El Trabajo de Fin de Grado (TFG), es una asignatura novedosa y de elevada complejidad que ha necesitado el desarrollo de un marco normativo por las Universidades y sus Centros (Reglamentos y Guías Docentes específicas). Tras varios cursos de implantación en el Grado en Psicología de la Universidad de Málaga, este equipo docente consideró necesario revisar el sistema de evaluación de las competencias adquiridas por los alumnos. Para ello se eligió el sistema de evaluación por rúbricas por los beneficios que de ellas se derivan (Alsina, 2010; Del Pozo, 2012; Fernández, 2010; García y Terrón, 2010; Mertler, 2001), especialmente por su valor formativo y evaluador (Blanco, 2008; Cano, 2015; Fernández, 2010), tanto para los estudiantes como para el profesorado. Por tanto, el objetivo de este trabajo fue el diseño de rúbricas para facilitar a todos los implicados (estudiantes, tutores y tribunales) el desarrollo del TFG y la evaluación formativa de los resultados de aprendizaje vinculados a cada una de sus fases, para cada modalidad (Trabajo de Investigación, desarrollo y/o innovación; Análisis y propuesta de resolución de casos prácticos reales; Trabajo de revisión y actualización teórica y/o metodológica y Proyecto de emprendimiento). Para ello se eligió un tipo de rúbrica analítica (Blanco, 2008) y su diseño y elaboración se llevó a cabo según los pasos establecidos por Mertler (2005), de acuerdo al consenso del equipo docente, bajo la supervisión y guía de una profesora experta en evaluación. Fueron evaluadas cualitativamente por el equipo docente, estando prevista la validación de las mismas en cursos posteriores. Se presenta aquí la primera de las rúbricas realizadas para la evaluación de los Trabajos de Fin de Grado en Psicología de la Universidad de Málaga según la modalidad Trabajo de Investigación, desarrollo y/o innovación, sobre un tema determinado relacionado con la Psicología en cualquiera de sus ámbitos de aplicación. Palabras clave: Trabajo de fin de grado, rúbricas, evaluación formativa, enseñanza superior.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Loss of p53 Attenuates the Contribution of IL-6 Deletion on Suppressed Tumor Progression and Extended Survival in Kras-Driven Murine Lung Cancer

Interleukin-6 (IL-6) is involved in lung cancer tumorigenesis, tumor progression, metastasis, and drug resistance. Previous studies show that blockade of IL-6 signaling can inhibit tumor growth and increase drug sensitivity in mouse models. Clinical trials in non-small cell lung cancer (NSCLC) reveal that IL-6 targeted therapy relieves NSCLC-related anemia and cachexia, although other clinical effects require further study. We crossed IL-6-/- mice with KrasG12D mutant mice, which develop lung tumors after activation of mutant KrasG12D, to investigate whether IL-6 inhibition contributes to tumor progression and survival time in vivo. KrasG12D; IL-6-/- mice exhibited increased tumorigenesis, but slower tumor growth and longer survival, than KrasG12D mice. Further, in order to investigate whether IL-6 deletion contributes to suppression of lung cancer metastasis, we generated KrasG12D; p53flox/flox; IL-6-/- mice, which developed lung cancer with a trend for reduced metastases and longer survival than KrasG12D; p53flox/flox mice. Tumors from KrasG12D; IL-6-/- mice showed increased expression of TNFα and decreased expression of CCL-19, CCL-20 and phosphorylated STAT3 (pSTAT3) than KrasG12D mice; however, these changes were not present between tumors from KrasG12D; p53flox/flox; IL-6-/- and KrasG12D; p53flox/flox mice. Upregulation of pSTAT3 and phosphorylated AKT (pAKT) were observed in KrasG12D tumors with p53 deletion. Taken together, these results indicate that IL-6 deletion accelerates tumorigenesis but delays tumor progression and prolongs survival time in a Kras-driven mouse model of lung cancer. However, these effects can be attenuated by p53 deletion

Efficacy of BET bromodomain inhibition in Kras-mutant non-small cell lung cancer

PurposeAmplification of MYC is one of the most common genetic alterations in lung cancer, contributing to a myriad of phenotypes associated with growth, invasion and drug resistance. Murine genetics has established both the centrality of somatic alterations of Kras in lung cancer, as well as the dependency of mutant Kras tumors on MYC function. Unfortunately, drug-like small-molecule inhibitors of KRAS and MYC have yet to be realized. The recent discovery, in hematologic malignancies, that BET bromodomain inhibition impairs MYC expression and MYC transcriptional function established the rationale of targeting KRAS-driven NSCLC with BET inhibition.Experimental DesignWe performed functional assays to evaluate the effects of JQ1 in genetically defined NSCLC cells lines harboring KRAS and/or LKB1 mutations. Furthermore, we evaluated JQ1 in transgenic mouse lung cancer models expressing mutant kras or concurrent mutant kras and lkb1. Effects of bromodomain inhibition on transcriptional pathways were explored and validated by expression analysis.ResultsWhile JQ1 is broadly active in NSCLC cells, activity of JQ1 in mutant KRAS NSCLC is abrogated by concurrent alteration or genetic knock-down of LKB1. In sensitive NSCLC models, JQ1 treatment results in the coordinate downregulation of the MYC-dependent transcriptional program. We found that JQ1 treatment produces significant tumor regression in mutant kras mice. As predicted, tumors from mutant kras and lkb1 mice did not respond to JQ1.ConclusionBromodomain inhibition comprises a promising therapeutic strategy for KRAS mutant NSCLC with wild-type LKB1, via inhibition of MYC function. Clinical studies of BET bromodomain inhibitors in aggressive NSCLC will be actively pursued

Evaluación formativa del TFG del Grado en Psicología: diseño de rúbricas para la modalidad Proyecto de Emprendimiento

En el contexto de la Facultad de Psicología de la Universidad de Málaga, un Trabajo de Fin de Grado (TFG) en la modalidad Proyecto de emprendimiento debe plantear una solución a un problema real de una determinada organización, institución, empresa o tipo de empresas relacionadas con cualquiera de sus ramas de conocimiento. Esta modalidad implica conocer los objetivos y la metodología a utilizar, ya que la definición de un plan de empresa o un planning de actuaciones no es una tarea sencilla para alguien que no sea experto en el tema. Para que el desarrollo y la evaluación de las competencias de los alumnos fuese la más adecuada, se consideró necesario utilizar instrumentos de evaluación que orientaran a todos los implicados, tanto en el aprendizaje, como en la evaluación formativa y de la producción compleja final realizada (Fernández, 2010). Se eligió la rúbrica como herramienta didáctica, porque permite la descripción de las características específicas del TFG en varios niveles de rendimiento, y por su capacidad para contribuir significativamente a la mejora de los procesos de aprendizaje-enseñanza en su conjunto (Andrade, 2005). El objetivo de este trabajo fue la elaboración de rúbricas específicas para esta modalidad de TFG que guiaran tanto a profesores como a alumnos en el desempeño de sus tareas y competencias de manera satisfactoria, definiendo unos criterios claros. Se diseñaron rúbricas analíticas (Blanco, 2008) según la metodología de Mertler (2005), alineando la evaluación con los resultados y las actividades de aprendizaje-enseñanza a realizar (Biggs, 2005). Para ello se describieron los atributos del mejor desempeño de los diferentes componentes del TFG, se diseñó la escala para valorar el nivel de desempeño en cada categoría-dimensión y se redactaron los descriptores de cada nivel. Se evaluaron cualitativamente por el equipo docente, estando prevista su validación externa en cursos posteriores.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech. Proyecto de Innovación Educativa (PIE15-108

Integrative genomic and proteomic analyses identify targets for Lkb1 deficient metastatic lung tumors

SummaryIn mice, Lkb1 deletion and activation of KrasG12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1 deficient primary and metastatic lung tumors and that the combined inhibition of SRC, PI3K and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathways that may be targeted for treatment

Cosmic CARNage II: the evolution of the galaxy stellar mass function in observations and galaxy formation models

We present a comparison of the observed evolving galaxy stellar mass functions with the predictions of eight semi-analytic models and one halo occupation distribution model. While most models are able to fit the data at low redshift, some of them struggle to simultaneously fit observations at high redshift. We separate the galaxies into 'passive' and 'star-forming' classes and find that several of the models produce too many low-mass star-forming galaxies at high redshift compared to observations, in some cases by nearly a factor of 10 in the redshift range 2.5 < z < 3.0. We also find important differences in the implied mass of the dark matter haloes the galaxies inhabit, by comparing with halo masses inferred from observations. Galaxies at high redshift in the models are in lower mass haloes than suggested by observations, and the star formation efficiency in low-mass haloes is higher than observed. We conclude that many of the models require a physical prescription that acts to dissociate the growth of low-mass galaxies from the growth of their dark matter haloes at high redshift.Facultad de Ciencias Astronómicas y GeofísicasInstituto de Astrofísica de La Plat

Cosmic CARNage II: the evolution of the galaxy stellar mass function in observations and galaxy formation models

We present a comparison of the observed evolving galaxy stellar mass functions with the predictions of eight semi-analytic models and one halo occupation distribution model. While most models are able to fit the data at low redshift, some of them struggle to simultaneously fit observations at high redshift. We separate the galaxies into 'passive' and 'star-forming' classes and find that several of the models produce too many low-mass star-forming galaxies at high redshift compared to observations, in some cases by nearly a factor of 10 in the redshift range 2.5 < z < 3.0. We also find important differences in the implied mass of the dark matter haloes the galaxies inhabit, by comparing with halo masses inferred from observations. Galaxies at high redshift in the models are in lower mass haloes than suggested by observations, and the star formation efficiency in low-mass haloes is higher than observed. We conclude that many of the models require a physical prescription that acts to dissociate the growth of low-mass galaxies from the growth of their dark matter haloes at high redshift.Facultad de Ciencias Astronómicas y GeofísicasInstituto de Astrofísica de La Plat

Cosmic CARNage II: the evolution of the galaxy stellar mass functionin observations and galaxy formation models

We present a comparison of the observed evolving galaxy stellar mass functions with the predictions of eight semi-analytic models and one halo occupation distribution model. While most models are able to fit the data at low redshift, some of them struggle to simultaneously fit observations at high redshift. We separate the galaxies into ‘passive’ and ‘star-forming’ classes and find that several of the models produce too many low-mass star-forming galaxies at high redshift compared to observations, in some cases by nearly a factor of 10 in the redshift range 2.5 < z < 3.0. We also find important differences in the implied mass of the dark matter haloes the galaxies inhabit, by comparing with halo masses inferred from observations. Galaxies at high redshift in the models are in lower mass haloes than suggested by observations, and the star formation efficiency in low-mass haloes is higher than observed. We conclude that many of the models require a physical prescription that acts to dissociate the growth of low-mass galaxies from the growth of their dark matter haloes at high redshift

Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer

As a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non-small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically-engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways leading to epigenetic transformation independent from canonical growth factor pathway activation. As such, tumors feature a transcriptional program distinct from KRAS- and EGFR-mutant mouse lung cancers, but shared with human lung adenocarcinomas exhibiting high EZH2 expression. To target EZH2-dependent cancers, we developed a novel and potent EZH2 inhibitor JQEZ5 that promoted the regression of EZH2-driven tumors in vivo, confirming oncogenic addiction to EZH2 in established tumors and providing the rationale for epigenetic therapy in a subset of lung cancer