O legado de Stuart Hall para os estudos de recepção no Brasil

The text evokes the itinerary of Hall’s contributions to the field of communication in the country, in particular to reception studies. It discusses how his reflections were used by theses and dissertations in the field, defended in the Brazilian graduate programs between 2000 and 2009. The analysis reveals Hall’s importance for consolidating them in Brazil for offering theoretical and methodological inputs within a context of expansion of research centers and of problematics addressed. His ideas are adopted according to the demands of the objects of research, which have a multiplicity that denotes the amplitude of the the author’s contribution to Brazilian reception studies.O texto resgata o itinerário das contribuições de Hall ao campo da comunicação no país, em especial aos estudos de recepção. Discute como suas reflexões foram apropriadas pelas teses e dissertações da área defendidas nos programas de pós-graduação brasileiros entre 2000 e 2009. A análise revela a importância de Hall para consolidá-los no Brasil ao oferecer o insumo teórico e também metodológico em um contexto de expansão dos centros de pesquisa e de problemáticas abordadas. Suas ideias são adotadas de acordo com as demandas dos objetos de pesquisa, cuja multiplicidade denota a amplitude da contribuição do autor aos estudos de recepção brasileiros

Työn fyysisen kuormittavuuden yhteys fyysiseen toimintakykyyn alle 40-vuotiailla kunta-alan työntekijöillä

Vertaisarvioitu. English summary.Peer reviewe

A Large Intergenic Noncoding RNA Induced by p53 Mediates Global Gene Repression in the p53 Response

Recently, more than 1000 large intergenic noncoding RNAs (lincRNAs) have been reported. These RNAs are evolutionarily conserved in mammalian genomes and thus presumably function in diverse biological processes. Here, we report the identification of lincRNAs that are regulated by p53. One of these lincRNAs (lincRNA-p21) serves as a repressor in p53-dependent transcriptional responses. Inhibition of lincRNA-p21 affects the expression of hundreds of gene targets enriched for genes normally repressed by p53. The observed transcriptional repression by lincRNA-p21 is mediated through the physical association with hnRNP-K. This interaction is required for proper genomic localization of hnRNP-K at repressed genes and regulation of p53 mediates apoptosis. We propose a model whereby transcription factors activate lincRNAs that serve as key repressors by physically associating with repressive complexes and modulate their localization to sets of previously active genes.National Institutes of Health (U.S.) (New Innovator Award)Smith Family FoundationDamon Runyon Cancer Research FoundationSearle Scholars ProgramNational Institutes of Health (U.S.) (1R01CA119176-01

Pequeno Relato de um Grande Esforço: “Jovem e consumo midiático em tempos de convergência” // Short Report of a Great Effort: "Young and media consumption in convergence times"

O texto trata das principais estratégias e procedimentos de uma pesquisa nacional comparativa, desenvolvida por 27 equipes estaduais, sobre as práticas e consumo midiático de jovens brasileiros, em tempos de convergência midiática. Apresenta também alguns aspectos conceituais referentes ao âmbito do método, da metodologia e dos procedimentos técnicos. Sumary The text deals with the main strategies and procedures of a National Comparative Research, develop by 27 states teams about media practices and consumption of brazilian youth in times of media convergence. It also introduces some conceptual aspects about the framework of the method, methodology and technical procedures

Tissue of origin dictates branched-chain amino acid metabolism in mutant Kras-driven cancers

Tumor genetics guides patient selection for many new therapies, and cell culture studies have demonstrated that specific mutations can promote metabolic phenotypes. However, whether tissue context defines cancer dependence on specific metabolic pathways is unknown. Kras activation and Trp53 deletion in the pancreas or the lung result in pancreatic ductal adenocarinoma (PDAC) or non-small cell lung carcinoma (NSCLC), respectively, but despite the same initiating events, these tumors use branched-chain amino acids (BCAAs) differently. NSCLC tumors incorporate free BCAAs into tissue protein and use BCAAs as a nitrogen source, whereas PDAC tumors have decreased BCAA uptake. These differences are reflected in expression levels of BCAA catabolic enzymes in both mice and humans. Loss of Bcat1 and Bcat2, the enzymes responsible for BCAA use, impairs NSCLC tumor formation, but these enzymes are not required for PDAC tumor formation, arguing that tissue of origin is an important determinant of how cancers satisfy their metabolic requirements.National Institutes of Health (U.S.) (Grant F30CA183474)National Institutes of Health (U.S.) (Grant T32GM007753

Dissecting cell-type-specific metabolism in pancreatic ductal adenocarcinoma.

Tumors are composed of many different cell types including cancer cells, fibroblasts, and immune cells. Dissecting functional metabolic differences between cell types within a mixed population can be challenging due to the rapid turnover of metabolites relative to the time needed to isolate cells. To overcome this challenge, we traced isotope-labeled nutrients into macromolecules that turn over more slowly than metabolites. This approach was used to assess differences between cancer cell and fibroblast metabolism in murine pancreatic cancer organoid-fibroblast co-cultures and tumors. Pancreatic cancer cells exhibited increased pyruvate carboxylation relative to fibroblasts, and this flux depended on both pyruvate carboxylase and malic enzyme 1 activity. Consequently, expression of both enzymes in cancer cells was necessary for organoid and tumor growth, demonstrating that dissecting the metabolism of specific cell populations within heterogeneous systems can identify dependencies that may not be evident from studying isolated cells in culture or bulk tissue

Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human cancers and shows resistance to any therapeutic strategy used. Here we tested small-molecule inhibitors targeting chromatin regulators as possible therapeutic agents in PDAC. We show that JQ1, an inhibitor of the bromodomain and extraterminal (BET) family of proteins, suppresses PDAC development in mice by inhibiting both MYC activity and inflammatory signals. The histone deacetylase (HDAC) inhibitor SAHA synergizes with JQ1 to augment cell death and more potently suppress advanced PDAC. Finally, using a CRISPR-Cas9–based method for gene editing directly in the mouse adult pancreas, we show that de-repression of p57 (also known as KIP2 or CDKN1C) upon combined BET and HDAC inhibition is required for the induction of combination therapy–induced cell death in PDAC. SAHA is approved for human use, and molecules similar to JQ1 are being tested in clinical trials. Thus, these studies identify a promising epigenetic-based therapeutic strategy that may be rapidly implemented in fatal human tumors

Activation of NF-kB Pathway by Virus Infection Requires Rb Expression

The retinoblastoma protein Rb is a tumor suppressor involved in cell cycle control, differentiation, and inhibition of oncogenic transformation. Besides these roles, additional functions in the control of immune response have been suggested. In the present study we investigated the consequences of loss of Rb in viral infection. Here we show that virus replication is increased by the absence of Rb, and that Rb is required for the activation of the NF-kB pathway in response to virus infection. These results reveal a novel role for tumor suppressor Rb in viral infection surveillance and further extend the concept of a link between tumor suppressors and antiviral activity

Economic Globalization, Nutrition and Health: a review of quantitative evidence

BACKGROUND: Unhealthy dietary patterns have in recent decades contributed to an endemic-level burden from non-communicable disease (NCDs) in high-income countries. In low- and middle-income countries rapid changes in diets are also increasingly linked to malnutrition in all its forms as persistent undernutrition and micronutrient deficiencies continue to coexist with a rising prevalence of obesity and associated NCDs. Economic globalization and trade liberalization have been identified as potentially important factors driving these trends, but the mechanisms, pathways and actual impact are subject to continued debate. METHODS: We use a ‘rigorous review’ to synthesize evidence from empirical quantitative studies analysing the links between economic globalization processes and nutritional outcomes, with a focus on impact as well as improving the understanding of the main underlying mechanisms and their interactions. FINDINGS: While the literature remains mixed regarding the impacts of overall globalization, trade liberalization or economic globalization on nutritional outcomes, it is possible to identify different patterns of association and impact across specific sub-components of globalization processes. Although results depend on the context and methods of analysis, foreign direct investment (FDI) appears to be more clearly associated with increases in overnutrition and NCD prevalence than to changes in undernutrition. Existing evidence does not clearly show associations between trade liberalization and NCD prevalence, but there is some evidence of a broad association with improved dietary quality and reductions in undernutrition. Socio-cultural aspects of globalization appear to play an important yet under-studied role, with potential associations with increased prevalence of overweight and obesity. The limited evidence available also suggests that the association between trade liberalization or globalization and nutritional outcomes might differ substantially across population sub-groups. Overall, our findings suggest that policymakers do not necessarily face a trade-off when considering the implications of trade or economic liberalization for malnutrition in all its forms. On the contrary, a combination of nutrition-sensitive trade policy and adequate regulation of FDI could help reduce all forms of malnutrition. In the context of trade negotiations and agreements it is fundamental, therefore, to protect the policy space for governments to adopt nutrition-sensitive interventions