362 research outputs found

    Aspects of Cooling at the TRIμ\muP Facility

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    The Triμ\muP facility at KVI is dedicated to provide short lived radioactive isotopes at low kinetic energies to users. It comprised different cooling schemes for a variety of energy ranges, from GeV down to the neV scale. The isotopes are produced using beam of the AGOR cyclotron at KVI. They are separated from the primary beam by a magnetic separator. A crucial part of such a facility is the ability to stop and extract isotopes into a low energy beamline which guides them to the experiment. In particular we are investigating stopping in matter and buffer gases. After the extraction the isotopes can be stored in neutral atoms or ion traps for experiments. Our research includes precision studies of nuclear β\beta-decay through β\beta-ν\nu momentum correlations as well as searches for permanent electric dipole moments in heavy atomic systems like radium. Such experiments offer a large potential for discovering new physics.Comment: COOL05 Workshop, Galena, Il, USA, 18-23. Sept. 2005, 5 pages, 3 figure

    Tourism and the city: the impact on residents' quality of life

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    The present work investigates the relationship between tourism presence and perceptions of urban quality of life of resident populations (UQOL). Nowadays, this topic is at the forefront since many European cities have started raising their voice against mass tourism. An ad hoc questionnaire was designed and submitted to resident population of two Mediterranean destinations. Following an integrative approach à la Sen, UQOL is analysed using the presence of the services/amenities (capabilities) as well as their accessibility (functionings). Findings indicate that both presence and mainly accessibility of services/amenities matter for UQOL and that a negative effect of tourism prevails

    Leaping and dancing with digitality : Exploring human-smartphone-entanglements in classrooms

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    This chapter explores digitality as part of young people’s everyday lives in the Arctic. It is based on two ethnographic studies situated in the political context of the “digital leap”, the governmental and curricular emphasis on digitality in education in Finland. With the more formal “digital leap”, informal engagements and attachments with digitality intertwine, in which students’ own smartphones play an increasingly significant role. The analyses use the notion of entanglement (Barad) to examine how primary school and upper secondary school students emerge in their situated and specific encounters with smartphones in school. The starting points of things, bodies, affect, time and space open up insights to connectivity between young people’s digital activities and global economic networks as well as to the multidirectionality between humans and technologies: while the students access their digital devices, the digitalities also access their users. We suggest that this wilder form of “digital leap” requires reconsidering materiality, affect, and instability of space and time.Peer reviewe

    A novel class of microRNA-recognition elements that function only within open reading frames.

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    MicroRNAs (miRNAs) are well known to target 3' untranslated regions (3' UTRs) in mRNAs, thereby silencing gene expression at the post-transcriptional level. Multiple reports have also indicated the ability of miRNAs to target protein-coding sequences (CDS); however, miRNAs have been generally believed to function through similar mechanisms regardless of the locations of their sites of action. Here, we report a class of miRNA-recognition elements (MREs) that function exclusively in CDS regions. Through functional and mechanistic characterization of these 'unusual' MREs, we demonstrate that CDS-targeted miRNAs require extensive base-pairing at the 3' side rather than the 5' seed; cause gene silencing in an Argonaute-dependent but GW182-independent manner; and repress translation by inducing transient ribosome stalling instead of mRNA destabilization. These findings reveal distinct mechanisms and functional consequences of miRNAs that target CDS versus the 3' UTR and suggest that CDS-targeted miRNAs may use a translational quality-control-related mechanism to regulate translation in mammalian cells

    Identification and Differential Expression of MicroRNAs during Metamorphosis of the Japanese Flounder (Paralichthys olivaceus)

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    BACKGROUND: MicroRNAs (miRNAs) are a class of endogenous small non-coding RNAs of 20-25 nucleotides that play a key role in diverse biological processes. Japanese flounder undergo dramatic metamorphosis in their early development. The metamorphosis is characterized by morphological transformation from a bilaterally symmetrical to an asymmetrical body shape concomitant with extensive morphological and physiological remodeling of organs. So far, only a few miRNAs have been identified in fish and there are very few reports about the Japanese flounder miRNA. METHODOLOGY/PRINCIPAL FINDINGS: Solexa sequencing technology was used to perform high throughput sequencing of the small RNA library from the metamorphic period of Japanese flounder. Subsequently, aligning these sequencing data with metazoan known miRNAs, we characterized 140 conserved miRNAs and 57 miRNA: miRNA* pairs from the small RNA library. Among these 57 miRNA: miRNA* pairs, twenty flounder miRNA precursors were amplified from genomic DNA. We also demonstrated evolutionary conservation of Japanese flounder miRNAs and miRNA* in the animal evolution process. Using miRNA microarrays, we identified 66 differentially expressed miRNAs at two metamorphic stages (17 and 29 days post hatching) of Japanese flounder. The results show that miRNAs might play a key role in regulating gene expression during Japanese flounder metamorphosis. CONCLUSIONS/SIGNIFICANCE: We identified a large number of miRNAs during flounder metamorphosis, some of which are differentially expressed at two different metamorphic stages. The study provides an opportunity for further understanding of miRNA function in the regulation of flounder metamorphosis and gives us clues for further studies of the mechanisms of metamorphosis in Japanese flounder

    MiR-107 and MiR-185 Can Induce Cell Cycle Arrest in Human Non Small Cell Lung Cancer Cell Lines

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    BACKGROUND: MicroRNAs (miRNAs) are short single stranded noncoding RNAs that suppress gene expression through either translational repression or degradation of target mRNAs. The annealing between messenger RNAs and 5' seed region of miRNAs is believed to be essential for the specific suppression of target gene expression. One miRNA can have several hundred different targets in a cell. Rapidly accumulating evidence suggests that many miRNAs are involved in cell cycle regulation and consequentially play critical roles in carcinogenesis. METHODOLOGY/PRINCIPAL FINDINGS: Introduction of synthetic miR-107 or miR-185 suppressed growth of the human non-small cell lung cancer cell lines. Flow cytometry analysis revealed these miRNAs induce a G1 cell cycle arrest in H1299 cells and the suppression of cell cycle progression is stronger than that by Let-7 miRNA. By the gene expression analyses with oligonucleotide microarrays, we find hundreds of genes are affected by transfection of these miRNAs. Using miRNA-target prediction analyses and the array data, we listed up a set of likely targets of miR-107 and miR-185 for G1 cell cycle arrest and validate a subset of them using real-time RT-PCR and immunoblotting for CDK6. CONCLUSIONS/SIGNIFICANCE: We identified new cell cycle regulating miRNAs, miR-107 and miR-185, localized in frequently altered chromosomal regions in human lung cancers. Especially for miR-107, a large number of down-regulated genes are annotated with the gene ontology term 'cell cycle'. Our results suggest that these miRNAs may contribute to regulate cell cycle in human malignant tumors

    Parvovirus B19 DNA CpG Dinucleotide Methylation and Epigenetic Regulation of Viral Expression

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    CpG DNA methylation is one of the main epigenetic modifications playing a role in the control of gene expression. For DNA viruses whose genome has the ability to integrate in the host genome or to maintain as a latent episome, a correlation has been found between the extent of DNA methylation and viral quiescence. No information is available for Parvovirus B19, a human pathogenic virus, which is capable of both lytic and persistent infections. Within Parvovirus B19 genome, the inverted terminal regions display all the characteristic signatures of a genomic CpG island; therefore we hypothesised a role of CpG dinucleotide methylation in the regulation of viral genome expression

    The role of microRNA-155/liver X receptor pathway in experimental and idiopathic pulmonary fibrosis

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    Background: Idiopathic Pulmonary Fibrosis (IPF) is progressive and rapidly fatal. Improved understanding of pathogenesis is required to prosper novel therapeutics. Epigenetic changes contribute to IPF therefore microRNAs may reveal novel pathogenic pathways. Objectives: To determine the regulatory role of microRNA(miR)-155 in the pro-fibrotic function of murine lung macrophages and fibroblasts, IPF lung fibroblasts and its contribution to experimental pulmonary fibrosis. Methods: Bleomycin-induced lung fibrosis in wild-type and miR-155-/- mice was analyzed by histology, collagen and pro-fibrotic gene expression. Mechanisms were identified by in silico and molecular approaches; validated in mouse lung fibroblasts and macrophages, and in IPF lung fibroblasts, using loss-and-gain of function assays, and in vivo using specific inhibitors. Results: miR-155-/- mice developed exacerbated lung fibrosis, increased collagen deposition, collagen 1 and 3 mRNA expression, TGFβ production, and activation of alternatively-activated macrophages, contributed by deregulation of the microRNA-155 target gene the liver X receptor (LXR)α in lung fibroblasts and macrophages. Inhibition of LXRα in experimental lung fibrosis and in IPF lung fibroblasts reduced the exacerbated fibrotic response. Similarly, enforced expression of miR-155 reduced the pro-fibrotic phenotype of IPF and miR-155-/- fibroblasts. Conclusion: We describe herein a molecular pathway comprising miR-155 and its epigenetic LXRα target that when deregulated enables pathogenic pulmonary fibrosis. Manipulation of the miR-155/LXR pathway may have therapeutic potential for IPF

    The learning styles neuromyth:when the same term means different things to different teachers

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    Alexia Barrable - ORCID: 0000-0002-5352-8330 https://orcid.org/0000-0002-5352-8330Although learning styles (LS) have been recognised as a neuromyth, they remain a virtual truism within education. A point of concern is that the term LS has been used within theories that describe them using completely different notions and categorisations. This is the first empirical study to investigate education professionals’ conceptualisation, as well as means of identifying and implementing LS in their classroom. A sample of 123 education professionals were administered a questionnaire consisting both closed- and open-ended questions. Responses were analysed using thematic analysis. LS were found to be mainly conceptualised within the Visual-Auditory-(Reading)-Kinaesthetic (VAK/VARK) framework, as well as Gardner’s multiple intelligences. Moreover, a lot of education professionals confused theories of learning (e.g., behavioural or cognitive theories) with LS. In terms of identifying LS, educators reported using a variety of methods, spanning from observation and everyday contact to the use of tests. The ways LS were implemented in the classroom were numerous, comprising various teaching aids, participatory techniques and motor activities. Overall, we argue that the extended use of the term LS gives the illusion of a consensus amongst educators, when a closer examination reveals that the term LS is conceptualised, identified and implemented idiosyncratically by different individuals. This study aims to be of use to pre-service and in-service teacher educators in their effort to debunk the neuromyth of LS and replace it with evidence-based practices.https://doi.org/10.1007/s10212-020-00485-236pubpub
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