89 research outputs found

    The factor structure and psychometric properties of the Clinical Outcomes in Routine Evaluation - Outcome Measure (CORE-OM) in Norwegian clinical and non-clinical samples

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    Background The Clinical Outcomes in Routine Evaluation - Outcome Measure (CORE-OM) is a 34-item instrument developed to monitor clinically significant change in out-patients. The CORE-OM covers four domains: well-being, problems/symptoms, functioning and risk, and sums up in two total scores: the mean of All items, and the mean of All non-risk items. The aim of this study was to examine the psychometric properties of the Norwegian translation of the CORE-OM. Methods A clinical sample of 527 out-patients from North Norwegian specialist psychiatric services, and a non-clinical sample of 464 persons were obtained. The non-clinical sample was a convenience sample consisting of friends and family of health personnel, and of students of medicine and clinical psychology. Students also reported psychological stress. Exploratory factor analysis (EFA) was employed in half the clinical sample. Confirmatory (CFA) factor analyses modelling the theoretical sub-domains were performed in the remaining half of the clinical sample. Internal consistency, means, and gender and age differences were studied by comparing the clinical and non-clinical samples. Stability, effect of language (Norwegian versus English), and of psychological stress was studied in the sub-sample of students. Finally, cut-off scores were calculated, and distributions of scores were compared between clinical and non-clinical samples, and between students reporting stress or no stress. Results The results indicate that the CORE-OM both measures general (g) psychological distress and sub-domains, of which risk of harm separates most clearly from the g factor. Internal consistency, stability and cut-off scores compared well with the original English version. No, or only negligible, language effects were found. Gender differences were only found for the well-being domain in the non-clinical sample and for the risk domain in the clinical sample. Current patient status explained differences between clinical and non-clinical samples, also when gender and age were controlled for. Students reporting psychological distress during last week scored significantly higher than students reporting no stress. These results further validate the recommended cut-off point of 1 between clinical and non-clinical populations. Conclusions The CORE-OM in Norwegian has psychometric properties at the same level as the English original, and could be recommended for general clinical use. A cut-off point of 1 is recommended for both genders

    Co-evolutionary dynamics of collective action with signaling for a quorum

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    Collective signaling for a quorum is found in a wide range of organisms that face collective action problems whose successful solution requires the participation of some quorum of the individuals present. These range from humans, to social insects, to bacteria. The mechanisms involved, the quorum required, and the size of the group may vary. Here we address the general question of the evolution of collective signaling at a high level of abstraction. We investigate the evolutionary dynamics of a population engaging in a signaling N-person game theoretic model. Parameter settings allow for loners and cheaters, and for costly or costless signals. We find a rich dynamics, showing how natural selection, operating on a population of individuals endowed with the simplest strategies, is able to evolve a costly signaling system that allows individuals to respond appropriately to different states of Nature. Signaling robustly promotes cooperative collective action, in particular when coordinated action is most needed and difficult to achieve. Two different signaling systems may emerge depending on Nature's most prevalent states.Funding: This research was supported by FEDER through POFC - COMPETE, FCT-Portugal through grants SFRH/BD/86465/2012, PTDC/MAT/122897/2010, EXPL/EEI-SII/2556/2013, and by multi-annual funding of CMAF-UL, CBMA-UM and INESC-ID (under the projects PEst-OE/BIA/UI4050/2014 and UID/CEC/50021/2013) provided by FCT-Portugal, and by Fundacao Calouste Gulbenkian through the "Stimulus to Research" program for young researchers. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.info:eu-repo/semantics/publishedVersio

    New roles for renin and prorenin in heart failure and cardiorenal crosstalk

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    The renin-angiotensin-aldosterone-system (RAAS) plays a central role in the pathophysiology of heart failure and cardiorenal interaction. Drugs interfering in the RAAS form the pillars in treatment of heart failure and cardiorenal syndrome. Although RAAS inhibitors improve prognosis, heart failure–associated morbidity and mortality remain high, especially in the presence of kidney disease. The effect of RAAS blockade may be limited due to the loss of an inhibitory feedback of angiotensin II on renin production. The subsequent increase in prorenin and renin may activate several alternative pathways. These include the recently discovered (pro-) renin receptor, angiotensin II escape via chymase and cathepsin, and the formation of various angiotensin subforms upstream from the blockade, including angiotensin 1–7, angiotensin III, and angiotensin IV. Recently, the direct renin inhibitor aliskiren has been proven effective in reducing plasma renin activity (PRA) and appears to provide additional (tissue) RAAS blockade on top of angiotensin-converting enzyme and angiotensin receptor blockers, underscoring the important role of renin, even (or more so) under adequate RAAS blockade. Reducing PRA however occurs at the expense of an increase plasma renin concentration (PRC). PRC may exert direct effects independent of PRA through the recently discovered (pro-) renin receptor. Additional novel possibilities to interfere in the RAAS, for instance using vitamin D receptor activation, as well as the increased knowledge on alternative pathways, have revived the question on how ideal RAAS-guided therapy should be implemented. Renin and prorenin are pivotal since these are at the base of all of these pathways

    Comprehensive molecular characterization of the hippo signaling pathway in cancer

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    Hippo signaling has been recognized as a key tumor suppressor pathway. Here, we perform a comprehensive molecular characterization of 19 Hippo core genes in 9,125 tumor samples across 33 cancer types using multidimensional “omic” data from The Cancer Genome Atlas. We identify somatic drivers among Hippo genes and the related microRNA (miRNA) regulators, and using functional genomic approaches, we experimentally characterize YAP and TAZ mutation effects and miR-590 and miR-200a regulation for TAZ. Hippo pathway activity is best characterized by a YAP/TAZ transcriptional target signature of 22 genes, which shows robust prognostic power across cancer types. Our elastic-net integrated modeling further reveals cancer-type-specific pathway regulators and associated cancer drivers. Our results highlight the importance of Hippo signaling in squamous cell cancers, characterized by frequent amplification of YAP/TAZ, high expression heterogeneity, and significant prognostic patterns. This study represents a systems-biology approach to characterizing key cancer signaling pathways in the post-genomic era

    Tumor necrosis factor-α inhibits renin gene expression

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    How Is the Brain Renin–Angiotensin System Regulated?

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