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What Remains on Your Mind After You Are Done?: Flexible Regulation of Knowledge Accessibility.

ABSTRACT: The accessibility of stored knowledge has been found to decline over time after activation without further stimulation. A special case is goal pursuit; goal-related knowledge remains accessible until goal completion, and then its accessibility declines rapidly. We hypothesized that after goal completion the decline in accessibility of goal-related knowledge would be especially rapid for strong promotion-focused individuals because their motivation to eagerly advance beyond the status quo would make accessibility of this knowledge an irrelevant detriment. We hypothesized an opposite effect for strongly prevention-predominant individuals because their motivation to vigilantly maintain a satisfactory state would make accessibility of this knowledge continually relevant. The results of two studies supported both these predicted moderators of accessibility change. Indeed, we found that for strongly prevention-predominant participants, knowledge accessibility actually increased over time after goal completion. We discuss how even basic cognitive mechanisms, like changes in accessibility, can be affected by general motivational concerns.

SUBMITTER: Hedberg PH

PROVIDER: S-EPMC3134315 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature

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What Remains on Your Mind After You Are Done?: Flexible Regulation of Knowledge Accessibility.

Hedberg Per H PH Higgins E Tory ET

Journal of experimental social psychology 20110901 5

The accessibility of stored knowledge has been found to decline over time after activation without further stimulation. A special case is goal pursuit; goal-related knowledge remains accessible until goal completion, and then its accessibility declines rapidly. We hypothesized that after goal completion the decline in accessibility of goal-related knowledge would be especially rapid for strong promotion-focused individuals because their motivation to eagerly advance beyond the status quo would m ...[more]

PMID: 21765541

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Project description:ObjectiveIn this review, we aim to collect and discuss available data about the role and composition of tumor microenvironment (TME) in oligometastatic (OMD) and oligoprogressive (OPD) non-small cell lung cancer (NSCLC). Furthermore, we aim to summarize the ongoing clinical trials evaluating as exploratory objective the TME composition, through tissue and/or blood samples, in order to clarify whether TME and its components could explain, at least partially, the oligometastatic/oligoprogressive process and could unravel the existence of predictive and/or prognostic factors for local ablative therapy (LAT).BackgroundOMD/OPD NSCLC represent a heterogeneous group of diseases. Several data have shown that TME plays an important role in tumor progression and therefore in treatment response. The crucial role of several types of cells and molecules such as immune cells, cytokines, integrins, protease and adhesion molecules, tumor-associated macrophages (TAMs) and mesenchymal stem cells (MSCs) has been widely established. Due to the peculiar activation of specific pathways and expression of adhesion molecules, metastatic cells seem to show a tropism for specific anatomic sites (the so-called "seed and soil" hypothesis). Based on this theory, metastases appear as a biologically driven process rather than a random release of cancer cells. Although the role and the function of TME at the time of progression in patients with NSCLC treated with tyrosine-kinase inhibitors and immune checkpoint inhibitors (ICIs) have been investigated, limited data about the role and the biological meaning of TME are available in the specific OMD/OPD setting.MethodsThrough a comprehensive PubMed and ClinicalTrials.gov search, we identified available and ongoing studies exploring the role of TME in oligometastatic/oligoprogressive NSCLC.ConclusionsDeepening the knowledge on TME composition and function in OMD/OPD may provide innovative implications in terms of both prognosis and prediction of outcome in particular from local treatments, paving the way for future investigations of personalized approaches in both advanced and early disease settings.

Project description:BackgroundEndothelial cells are constantly exposed to mechanical forces in the form of fluid shear stress, extracellular stiffness, and cyclic strain. The mechanoresponsive activity of YAP (Yes-associated protein) and its role in vascular development are well described; however, whether changes to transcription or epigenetic regulation of YAP are involved in these processes remains unanswered. Furthermore, how mechanical forces are transduced to the nucleus to drive transcriptional reprogramming in endothelial cells is poorly understood. The YAP target gene, AmotL2 (angiomotin-like 2), is a junctional mechanotransducer that connects cell-cell junctions to the nuclear membrane via the actin cytoskeleton.MethodsWe applied mechanical manipulations including shear flow, stretching, and substrate stiffness to endothelial cells to investigate the role of mechanical forces in modulating YAP transcription. Using in vitro and in vivo endothelial depletion of AmotL2, we assess nuclear morphology, chromatin organization (using transposase-accessible chromatin sequencing), and whole-mount immunofluorescent staining of the aorta to determine the regulation and functionality of YAP. Finally, we use genetic and chemical inhibition to uncouple the nuclear-cytoskeletal connection to investigate the role of this pathway on YAP transcription.ResultsOur results reveal that mechanical forces sensed at cell-cell junctions by the YAP target gene AmotL2 are directly involved in changes in global chromatin accessibility and activity of the histone methyltransferase EZH2, leading to modulation of YAP promotor activity. Functionally, shear stress-induced proliferation of endothelial cells in vivo was reliant on AmotL2 and YAP/TAZ (transcriptional coactivator with PDZ-binding motif) expression. Mechanistically, uncoupling of the nuclear-cytoskeletal connection from junctions and focal adhesions led to altered nuclear morphology, chromatin accessibility, and YAP promotor activity.ConclusionsOur findings reveal a role for AmotL2 and nuclear-cytoskeletal force transmission in modulating the epigenetic and transcriptional regulation of YAP to maintain a mechano-enforced positive feedback loop of vascular homeostasis. These findings may offer an explanation as to the proinflammatory phenotype that leads to aneurysm formation observed in AmotL2 endothelial deletion models.

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What Remains on Your Mind After You Are Done?: Flexible Regulation of Knowledge Accessibility.

Publications

What Remains on Your Mind After You Are Done?: Flexible Regulation of Knowledge Accessibility.

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