130,951 research outputs found

    MeSH term explosion and author rank improve expert recommendations

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    Information overload is an often-cited phenomenon that reduces the productivity, efficiency and efficacy of scientists. One challenge for scientists is to find appropriate collaborators in their research. The literature describes various solutions to the problem of expertise location, but most current approaches do not appear to be very suitable for expert recommendations in biomedical research. In this study, we present the development and initial evaluation of a vector space model-based algorithm to calculate researcher similarity using four inputs: 1) MeSH terms of publications; 2) MeSH terms and author rank; 3) exploded MeSH terms; and 4) exploded MeSH terms and author rank. We developed and evaluated the algorithm using a data set of 17,525 authors and their 22,542 papers. On average, our algorithms correctly predicted 2.5 of the top 5/10 coauthors of individual scientists. Exploded MeSH and author rank outperformed all other algorithms in accuracy, followed closely by MeSH and author rank. Our results show that the accuracy of MeSH term-based matching can be enhanced with other metadata such as author rank

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    "Closing the R&D Gap, Evaluating the Sources of R&D Spending"

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    Both spending and tax policies have been implemented in the United States with the goal of stimulating private sector research and development (R&D). Karier questions whether current R&D policy, especially the research and experimentation tax credit, can contribute to closing the gap between nondefense expenditures on R&D in the United States and such expenditures in other countries, such as Japan and Germany. He also explores possible changes to our current R&D policy to make it more effective.

    A. D. Fricke, author

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    Black and white photograph of author, A. D. Fricke

    Dispelling the Myths Behind First-author Citation Counts

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    We conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more sophisticated methods

    Scholarly Communication and Publishing Lunch and Learn Talk #11: The ULS Open Access Author Fee Fund

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    At the May 2014 talk, you will learn about the ULS Open Access Author Fee Fund--what it is, why we do it, how it works, and how the program is going so far

    T cell mediated immunity in malaria and mycobacterial infection : a protective role for gd+ T cells

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    T cell mediated immunity is essential against intracellular infections. Studies of cell mediated immunity are important for the optimal design and development of effective vaccines. Identifying correlates of protective immunity will also enable measurement of vaccine efficiency. This thesis includes studies of T cell mediated immune protection against malaria and mycobacterial infections. A major focus of this work was the investigation of the role of [gamma][delta]+ T cell responses. In an initial study of lymphocyte subset compositions, a higher percentage of cytotoxic T cells were found in the peripheral blood of healthy adults from Ethiopia and Bangladesh than from Sweden. This suggested the involvement of environmental and/or genetic factors on the adaptation of the cellular immune system.During acute malaria illness there was a complex pattern of changes in lymphocyte subset distribution and activation that appeared to be different in P. falciparum infection compared to P. vivax. During acute P. falciparum illness an increase in level and activation of [gamma][delta]+ T cells, that was mostly due to increase in V[delta]1+ cells was found. However, during both infections increased numbers of CD4+, CD8+ and [gamma][delta]+ T cells in peripheral blood were expressing the proliferation marker Ki-67. These results suggest that all T cells are activated and that lymphocyte redistribution and /or activation driven apoptosis may be the cause of the altered phenotypic profiles in peripheral blood.An in vitro assay was developed to study the functional significance of [gamma][delta]+ T cells. Generally activated [gamma][delta]+ T cells of both V[delta]1+ and V[delta]2+ subsets but not similarly activated [alpha][beta] T cells from non-malaria exposed individuals inhibited the in vitro growth of asexual blood stages of P. falciparum parasite. The inhibition was correlated to the number of [gamma][delta]+ T cells and required cell-to-cell contact. Kinetic analysis suggested the likely targets to be the late infected erythrocyte (schizonts) or extracellular merozoites. These results suggest [gamma][delta]+ T cells may have a protective role during malaria infection independent of previous exposure to malaria.An in vitro assay was also developed to measure T cell mediated inhibition of mycobacterial growth. Both [alpha][beta]+ and [gamma][delta]+ T cells from PPD positive individuals inhibited intracellular growth of BCG, but only when activated by mycobacterial antigens. The mycobacterial growth inhibition capacity was up regulated by BCG vaccination and required cell-to-cell contact. These results suggest a role for [gamma][delta]+ T cells in the memory responses against mycobacteria.Expressions of proinflammatory cytokines and cytolytic molecules such as perforin, granzymes, granulysin and Fas/Fas ligand, were characteristic of both malaria and BCG growth inhibitory T cells. However, expression of these molecules in non-inhibitory activated cells were also seen, suggesting that growth inhibition requires restricted recognition of target cells by specific effectors. Our results indicate that [gamma][delta]+ T cells may represent an important component of the primary immune defense against P. falciparum infection and the memory immune defense against mycobacterial infection.List of scientific papersI. Worku S, Christensson B, Bjorkman A, Islam D (1997). "Higher proportion of CD8+ T cells in the blood in healthy adults from Ethiopia and Bangladesh compared with Sweden" Trans R Soc Trop Med Hyg 91(5): 618-22 https://pubmed.ncbi.nlm.nih.gov/98124846II. Worku S, Bjorkman A, Troye-Blomberg M, Jemaneh L, Farnert A, Christensson B (1997). "Lymphocyte activation and subset redistribution in the peripheral blood in acute malaria illness: distinct gammadelta+ T cell patterns in Plasmodium falciparum and P. vivax infections" Clin Exp Immunol 108(1): 34-41 https://pubmed.ncbi.nlm.nih.gov/97252339III. Worku S, Troye-Blomberg M, Christensson B, Bjorkman A, Fehniger T (2000). "Activation of T cells in the blood of patients with acute malaria, Proliferative activity as indicated by Ki 67 expression" Scand J Immunol (In Print)IV. Troye-Blomberg M, Worku S, Tangteerawatana P, Jamshaid R, Soderstrom K, Elghazali G, Moretta L, Hammarstrom M, Mincheva-Nilsson L (1999). "Human gamma delta T cells that inhibit the in vitro growth of the asexual blood stages of the Plasmodium falciparum parasite express cytolytic and proinflammatory molecules" Scand J Immunol 50(6): 642-50 https://pubmed.ncbi.nlm.nih.gov/20075382V. Worku S, Hoft DF (2000). "In vitro measurement of protective mycobacterial immunity: antigen-specific expansion of T cells capable of inhibiting intracellular growth of bacille Calmette-Guerin" Clin Infect Dis Suppl 3: S257-61 https://pubmed.ncbi.nlm.nih.gov/20336492VI. Worku S, Hoft DF (2000). "Differential effects of antigen specific and control T cells on intracellular mycobacterial growth, in vitro models of protective immunity and mycobacterial persistence" (Submitted)</p

    The R&D Tax Incentives

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    This article sets out some background information and reflections of the author on the R&amp;D tax incentive schemes included in the Common Corporate Tax Base (CCTB) Proposal. In particular the author analyzes the stimulus to private R&amp;D through ad hoc tax incentives included in the CCTB Proposal and dives into the actual provisions included in the Proposal highlighting the most relevant issues connected with their design and interpretation. Moreover, the author explores the interaction between the CCTB Proposal and the granting by Member States of domestic R&amp;D tax incentives

    Helicobacter infection in the surfactant protein D-deficient mouse

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    BACKGROUND: Surfactant protein D (SP-D), a component of innate immunity, is expressed in the gastric mucosa and is up-regulated in the presence of Helicobacter infection. SP-D binds to Helicobacter in vitro, suggesting the involvement of SP-D in Helicobacter-induced immune responses. The aim of this study was to determine the role of SP-D in gastric epithelial defense in vivo. METHODS: Specific pathogen-free SP-D-deficient mice (SP-D(-/-)) and C57BL/6 wild-type controls were challenged by gavage with different doses of Helicobacter felis, a mouse-adapted Helicobacter strain. Mice were assessed for colonization rates and density of infection. Inflammatory responses were measured by neutrophil counting and T-cell responses by proliferation assays on spleen cells stimulated with H. felis sonicate. The in vitro effect of SP-D on Helicobacter uptake by monocyte-derived dendritic cells was assessed by confocal microscopy and FACS analyses. RESULTS: SP-D(-/-) mice were more susceptible to low-dose infectious challenge than C57BL/6 controls (p = .02). The density of colonization was higher in the SP-D(-/-) infected mice. Neutrophil infiltrates were lower in the SP-D(-/-) mice, particularly in the acid-secreting regions of the stomach. T-cell proliferative responses to Helicobacter antigen were reduced in SP-D(-/-) mice (p = .001) after 12 weeks infection. In vitro uptake of Helicobacter by dendritic cells was significantly enhanced in the presence of SP-D (p = .001). CONCLUSION: In the absence of SP-D, Helicobacter uptake by dendritic cells is impaired. This provides an explanation for the diminished inflammation and immune responses in the SP-D(-/-) mice
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