1,055 research outputs found

    A Conceptual Model for Scholarly Research Activity

    Get PDF
    This paper presents a conceptual model for scholarly research activity, developed as part of the conceptual modelling work within the ???Preparing DARIAH??? European e-Infrastructures project. It is inspired by cultural-historical activity theory, and is expressed in terms of the CIDOC Conceptual Reference Model, extending its notion of activity so as to also account, apart from historical practice, for scholarly research planning. It is intended as a framework for structuring and analyzing the results of empirical research on scholarly practice and information requirements, encompassing the full research lifecycle of information work and involving both primary evidence and scholarly objects; also, as a framework for producing clear and pertinent information requirements, and specifications of digital infrastructures, tools and services for scholarly research. We plan to use the model to tag interview transcripts from an empirical study on scholarly information work, and thus validate its soundness and fitness for purpose

    Long-Term Oxygen Therapy in COPD: Factors Affecting and Ways of Improving Patient Compliance

    Get PDF
    Long-term oxygen therapy (LTOT) is the cornerstone mode of treatment in patients with severe chronic obstructive pulmonary disease (COPD) associated with resting hypoxaemia. When appropriately prescribed and correctly used, LTOT has clearly been shown to improve survival in hypoxemic COPD patients. Adherence to LTOT ranges from 45% to 70% and utilization for more than 15 hours per day is widely accepted as efficacious. Although several studies have addressed the level of patients' adherence to LTOT, few have suggested or evaluated interventions that conduce to compliance enhancement. The lack of sufficient data regarding COPD patients following oxygen prescription is an enormous void that must be duly confronted to augment clinical effectiveness and cost containment for the long term use. The present review article highlights factors influencing the compliance of patients using LTOT and emphasizes novel strategies and interventions that may prove to be of significant benefit given the remarkably little current research appraising this issue. Therefore, additional research should be promptly performed to verify the efficacy of newly designed approaches in improving the outcomes of patients receiving LTOT

    Meneco, a Topology-Based Gap-Filling Tool Applicable to Degraded Genome-Wide Metabolic Networks

    Get PDF
    International audienceIncreasing amounts of sequence data are becoming available for a wide range of non-model organisms. Investigating and modelling the metabolic behaviour of those organisms is highly relevant to understand their biology and ecology. As sequences are often incomplete and poorly annotated, draft networks of their metabolism largely suffer from incompleteness. Appropriate gap-filling methods to identify and add missing reactions are therefore required to address this issue. However, current tools rely on phenotypic or taxonomic information, or are very sensitive to the stoichiometric balance of metabolic reactions, especially concerning the co-factors. This type of information is often not available or at least prone to errors for newly-explored organisms. Here we introduce Meneco, a tool dedicated to the topological gap-filling of genome-scale draft metabolic networks. Meneco reformulates gap-filling as a qualitative combinatorial optimization problem, omitting constraints raised by the stoichiometry of a metabolic network considered in other methods, and solves this problem using Answer Set Programming. Run on several artificial test sets gathering 10,800 degraded Escherichia coli networks Meneco was able to efficiently identify essential reactions missing in networks at high degradation rates, outperforming the stoichiometry-based tools in scalability. To demonstrate the utility of Meneco we applied it to two case studies. Its application to recent metabolic networks reconstructed for the brown algal model Ectocarpus siliculosus and an associated bacterium Candidatus Phaeomarinobacter ectocarpi revealed several candidate metabolic pathways for algal-bacterial interactions. Then Meneco was used to reconstruct, from transcriptomic and metabolomic data, the first metabolic network for the microalga Euglena mutabilis. These two case studies show that Meneco is a versatile tool to complete draft genome-scale metabolic networks produced from heterogeneous data, and to suggest relevant reactions that explain the metabolic capacity of a biological system

    Pay Inequality and Gender Pay Gap

    Full text link
    The topic of this thesis paper is pay inequality and gender pay gap, specifically within the United States while occasionally comparing Europe and other parts of the world. The research questions that are brought up while starting this thesis process were how the topic started and developed with the last 10 years. Plus, the potential strides to eliminate the thesis topics issues within the United States. The method of analysis for this thesis paper includes an integrative desktop literature review while analyzing various online and prior academic research articles. The result of studying the numerous amounts of research helped gather three primary resolutions to remove the pay inequality and gender pay gap in the United States. This academic research was only conducted analyzing only male and female genders. Future research should include or attempt to interview and find data regarding the LGBTQ2+ community and those affected such as transgenders, non-binary, etc

    Inherited Cardiomyopathies: From Genotype to Phenotype

    Get PDF
    The heart undergoes extensive morphological, metabolic, and energetic remodeling in response to inherited, or familial, hypertrophic cardiomyopathies (FHC). Myocyte contractile perturbations downstream of Ca2+, the so-called sarcomere-controlled mechanisms, may represent the earliest indicators of this remodeling. We can now state that the dynamics of cardiac contraction and relaxation during the progression of FHC are governed by downstream mechanisms, particularly the kinetics and energetics of actin and myosin interaction to drive the trajectory of pathological cardiac remodeling. This notion is unambiguously supported by elegant studies above linking inheritable FHC-causing mutations to cardiomyopathies, known to disturb contractile function and alter the energy landscape of the heart. Although studies examining the biophysical properties of cardiac myocytes with FHC-causing mutations have yielded a cellular and molecular understanding of myofilament function, this knowledge has had limited translational success. This is driven by a critical failure in elucidating an integrated and sequential link among the changing energy landscape, myofilament function, and initiated signaling pathways in response to FHC. Similarly, there continues to be a major gap in understanding the cellular and molecular mechanisms contributing to sex differences in FHC development and progression. The primary reason for this gap is a lack of a “unifying” or “central” hypothesis that integrates signaling cascades, energetics, sex and FHC
    corecore