Figura del periodista en la ficción televisiva: un análisis mixto de los rasgos distintivos profesionales

TFG defendido en el área de Periodismo.La profesión periodística siempre ha estado muy representada en la cultura popular, convirtiendo al periodista en un reiterativo personaje dramático y a las redacciones en el escenario perfecto para congregar toda clase de sentimientos y conflictos. Tanta es la fascinación por la disciplina periodística, que la ficción televisiva tampoco ha sido indiferente a este encantamiento, y lo ha hecho con una particularidad narrativa que la distingue por completo del medio fílmico. La amplia extensión del formato serial permite incidir en la naturaleza diaria de una redacción, deteniéndose en algunos de los elementos propios de la profesión: la relación de confianza con las fuentes, el enfrentamiento del periodista con los impedimentos deontológicos, la recopilación de detalles o la lucha entre directivos y empleados. La imagen que ofrece la pequeña pantalla de los periodistas influye de manera considerable en la idea que los espectadores y la sociedad guardan de estos profesionales. Parece que la labor de búsqueda, creación y difusión de la información, que habitualmente viene acompañada de ciertas dosis de drama y suspense, resulta muy atrayente para el público. Sin embargo, en la ficción televisiva, la figura del periodista se muestra, en ocasiones, de forma simplificada y transformada.Ciencias de la Comunicació

La presencia de criados particulares en la Casa de Dementes de Santa Isabel

Sin resumen

Editorial. Sobre la necesidad de crear la especialidad de psiquiatría infantil en España.

Sin resumen

Identification of novel candidate target genes in amplicons of Glioblastoma multiforme tumors detected by expression and CGH microarray profiling

BACKGROUND: Conventional cytogenetic and comparative genomic hybridization (CGH) studies in brain malignancies have shown that glioblastoma multiforme (GBM) is characterized by complex structural and numerical alterations. However, the limited resolution of these techniques has precluded the precise identification of detailed specific gene copy number alterations. RESULTS: We performed a genome-wide survey of gene copy number changes in 20 primary GBMs by CGH on cDNA microarrays. A novel amplicon at 4p15, and previously uncharacterized amplicons at 13q32-34 and 1q32 were detected and are analyzed here. These amplicons contained amplified genes not previously reported. Other amplified regions containg well-known oncogenes in GBMs were also detected at 7p12 (EGFR), 7q21 (CDK6), 4q12 (PDGFRA), and 12q13-15 (MDM2 and CDK4). In order to identify the putative target genes of the amplifications, and to determine the changes in gene expression levels associated with copy number change events, we carried out parallel gene expression profiling analyses using the same cDNA microarrays. We detected overexpression of the novel amplified genes SLA/LP and STIM2 (4p15), and TNFSF13B and COL4A2 (13q32-34). Some of the candidate target genes of amplification (EGFR, CDK6, MDM2, CDK4, and TNFSF13B) were tested in an independent set of 111 primary GBMs by using FISH and immunohistological assays. The novel candidate 13q-amplification target TNFSF13B was amplified in 8% of the tumors, and showed protein expression in 20% of the GBMs. CONCLUSION: This high-resolution analysis allowed us to propose novel candidate target genes such as STIM2 at 4p15, and TNFSF13B or COL4A2 at 13q32-34 that could potentially contribute to the pathogenesis of these tumors and which would require futher investigations. We showed that overexpression of the amplified genes could be attributable to gene dosage and speculate that deregulation of those genes could be important in the development and progression of GBM. Our findings highlight the important influence in GBM of signaling pathways such as the PI3K/AKT, consistent with the invasive features of this tumor

Current state of biology and diagnosis of clonal mast cell diseases in adults

[EN] Mastocytosis comprises a heterogeneous group of disorders characterized by the presence of clonal mast cells (MC) in organs such as skin, bone marrow (BM), and gastrointestinal tract, among other tissues. The clonal nature of the disease can be established in most adult patients by the demonstration of activating KIT mutations in their BM MC. When highly sensitive techniques capable of identifying cells present at very low frequencies in a sample are applied, BM MC from virtually all systemic mastocytosis patients display unique immunophenotypical features, particularly the aberrant expression of CD25. By contrast, large, multifocal BM MC aggregates (the only World Health Organization major criterion for systemic mastocytosis) are absent in a significant proportion of patients fulfilling at least three minor criteria for systemic mastocytosis, particularly in subjects studied at early stages of the disease with very low MC burden. Moreover, recent molecular and immunophenotypical investigations of BM MC from patients with indolent systemic mastocytosis have revealed a close association of some biological features (e.g., multilineage involvement of hematopoiesis by the KIT mutation and an immature mast cell immunophenotype) with an increased risk for disease progression. These observations support the fact that, although the current consensus diagnostic criteria for systemic mastocytosis have been a major advance for the diagnosis and classification of the disease, rationale usage of the most sensitive diagnostic techniques available nowadays is needed to improve the diagnosis, refine the classification, and reach objective prognostic stratification of adult mastocytosis