57 research outputs found

    Sequential Compatibility Effects and Cognitive Control: Does Conflict Really Matter?

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    International audienceAlthough it is widely accepted that control mechanisms are necessary for human behavior tobe adapted, very little is known about how such mechanisms are recruited. A suggestion tofill the gap was put forward by M. M. Botvinick, T. S. Braver, C. S. Carter, D. M. Barch, andJ. D. Cohen (2001), who proposed the conflict-loop theory. This theory has been successfulin accounting for the reduction of compatibility effects after an incompatible trial: The levelof conflict being, on average, higher during an incompatible trial, more control occurs aftersuch a trial. The authors have tested this prediction by sorting the trials on the basis of amountof conflict (quantified by the electromyographic activity) they presented. A reduction of thecompatibility effect was observed after incompatible trials, but it was independent of the levelof conflict on previous trials, suggesting that the conflict does not trigger changes in executivecontrol. Consequences for the conflict monitoring model are discussed

    Comunicación organizacional interna e identidad corporativa dentro de la institución educativa inicial N° 210 dulce Virgen de Fátima en la provincia de Trujillo en el año 2020

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    El objetivo de esta investigación es precisar la relación e impacto entre la comunicación interna y la identidad corporativa de los integrantes dentro de la Institución Educativa Inicial N.º 210 Dulce Virgen de Fátima, para lo cual se empleó un diseño transversal cualitativo no experimental con un rango de correlación causal. Uno de los métodos y capacidades en comunicación interna y ejecución laboral es buscar mejoras en la gestión del buen desempeño de los colaboradores desde la interacción entre gerentes y trabajadores. En ciertas entidades, la dirección de la comunicación interna es un compañero fundamental para perfeccionar el desenvolvimiento en el trabajo de la entidad. Para concretar la indagación, se encontró el problema: ¿Cómo influye la comunicación interna en el fortalecimiento de la identidad corporativa de la institución educativa inicial n.º 210 Dulce Virgen de Fátima?, Porque los diferentes procesos operativos y estratégicos de la entidad se comunican a través de los colaboradores “comunicación organizacional interna” por lo tanto tiene una relación directa en el ambiente de trabajo. De tal manera, la investigación se diseña utilizando métodos cualitativos, en los que el tipo de investigación es de diseño básico, no experimental y transversal, y tiene un nivel descriptivo explicativo. Para llevar a cabo esta investigación, realizamos dos cuestionarios por muestreo de todos los trabajadores de la institución, la cual incluyó en 2 variables, comunicación organizacional interna e identidad corporativa, con un total de 34 preguntas. Teniendo como base el cuestionario, podemos verificar si la institución aplica diversos métodos de comunicación interna asertivas para cubrir una amplia gama de públicos internos. La investigación ayuda a brindar sugerencias y soluciones para la comunicación interna dentro de la organización.Tesi

    Error Negativity Does Not Reflect Conflict: A Reappraisal of Conflict Monitoring and Anterior Cingulate Cortex Activity

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    Our ability to detect and correct errors is essential for our adaptive behavior. The conflict-loop theory states that the anterior cingulate cortex (ACC) plays a key role in detecting the need to increase control through conflict monitoring. Such monitoring is assumed to manifest itself in an electroencephalographic (EEG) component, the "error negativity" (Ne or "error-related negativity" [ERN]). We have directly tested the hypothesis that the ACC monitors conflict through simulation and experimental studies. Both the simulated and EEG traces were sorted, on a trial-by-trial basis, as a function of the degree of conflict, measured as the temporal overlap between incorrect and correct response activations. The simulations clearly show that conflict increases as temporal overlap between response activation increases, whereas the experimental results demonstrate that the amplitude of the Ne decreases as temporal overlap increases, suggesting that the ACC does not monitor conflict. At a functional level, the results show that the duration of the Ne depends on the time needed to correct (partial) errors, revealing an "on-line" modulation of control on a very short time scale

    Prognostic Value of Routinely Measured Inflammatory Biomarkers in Older Cancer Patients: Pooled Analysis of Three Cohorts

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    BACKGROUND: The prognostic assessment of older cancer patients is complicated by their heterogeneity. We aimed to assess the prognostic value of routine inflammatory biomarkers. METHODS: A pooled analysis of prospective multicenter cohorts of cancer patients aged >/=70 was performed. We measured CRP and albumin, and calculated Glasgow Prognostic Score (GPS) and CRP/albumin ratio. The GPS has three levels (0 = CRP /= 35 g/L, i.e., normal values; 1 = one abnormal value; 2 = two abnormal values). One-year mortality was assessed using Cox models. Discriminative power was assessed using Harrell's C index (C) and net reclassification improvement (NRI). RESULTS: Overall, 1800 patients were analyzed (mean age: 79 +/- 6; males: 62%; metastases: 38%). The GPS and CRP/albumin ratio were independently associated with mortality in patients not at risk of frailty (hazard ratio [95% confidence interval] = 4.48 [2.03-9.89] for GPS1, 11.64 [4.54-29.81] for GPS2, and 7.15 [3.22-15.90] for CRP/albumin ratio > 0.215) and in patients at risk of frailty (2.45 [1.79-3.34] for GPS1, 3.97 [2.93-5.37] for GPS2, and 2.81 [2.17-3.65] for CRP/albumin ratio > 0.215). The discriminative power of the baseline clinical model (C = 0.82 [0.80-0.83]) was increased by adding GPS (C = 0.84 [0.82-0.85]; NRI events (NRI+) = 10% [2-16]) and CRP/albumin ratio (C = 0.83 [0.82-0.85]; NRI+ = 14% [2-17]). CONCLUSIONS: Routine inflammatory biomarkers add prognostic value to clinical factors in older cancer patients

    A family of process-based models to simulate landscape use by multiple taxa

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    Context: Land-use change is a key driver of biodiversity loss. Models that accurately predict how biodiversity might be affected by land-use changes are urgently needed, to help avoid further negative impacts and inform landscape-scale restoration projects. To be effective, such models must balance model realism with computational tractability and must represent the different habitat and connectivity requirements of multiple species. Objectives: We explored the extent to which process-based modelling might fulfil this role, examining feasibility for different taxa and potential for informing real-world decision-making. Methods: We developed a family of process-based models (*4pop) that simulate landscape use by birds, bats, reptiles and amphibians, derived from the well-established poll4pop model (designed to simulate bee populations). Given landcover data, the models predict spatially-explicit relative abundance by simulating optimal home-range foraging, reproduction, dispersal of offspring and mortality. The models were co-developed by researchers, conservation NGOs and volunteer surveyors, parameterised using literature data and expert opinion, and validated against observational datasets collected across Great Britain. Results: The models were able to simulate habitat specialists, generalists, and species requiring access to multiple habitats for different types of resources (e.g. breeding vs foraging). We identified model refinements required for some taxa and considerations for modelling further species/groups. Conclusions: We suggest process-based models that integrate multiple forms of knowledge can assist biodiversity-inclusive decision-making by predicting habitat use throughout the year, expanding the range of species that can be modelled, and enabling decision-makers to better account for landscape context and habitat configuration effects on population persistence

    Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

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    Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation
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