1,720,961 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe 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
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Dispelling the Myths Behind First-author Citation Counts
Full text linkWe 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
Monoacylglycerol Lipase Regulates Fever Response.
No full textCyclooxygenase inhibitors such as ibuprofen have been used for decades to control fever through reducing the levels of the pyrogenic lipid transmitter prostaglandin E2 (PGE2). Historically, phospholipases have been considered to be the primary generator of the arachidonic acid (AA) precursor pool for generating PGE2 and other eicosanoids. However, recent studies have demonstrated that monoacyglycerol lipase (MAGL), through hydrolysis of the endocannabinoid 2-arachidonoylglycerol, provides a major source of AA for PGE2 synthesis in the mammalian brain under basal and neuroinflammatory states. We show here that either genetic or pharmacological ablation of MAGL leads to significantly reduced fever responses in both centrally or peripherally-administered lipopolysaccharide or interleukin-1β-induced fever models in mice. We also show that a cannabinoid CB1 receptor antagonist does not attenuate these anti-pyrogenic effects of MAGL inhibitors. Thus, much like traditional nonsteroidal anti-inflammatory drugs, MAGL inhibitors can control fever, but appear to do so through restricted control over prostaglandin production in the nervous system
koamabayili/VECTRON-author-checklist: VECTRON author checklist
No full textWe have done our best to complete the author checklist relating to the use of animals in the hut study. Note that the objective for the hut study was to evaluate the IRS treatment applications for residual efficacy against Anopheles mosquitoes, including the local An. coluzzii mosquito population. Cows were only used to attract mosquitoes into the huts and no tests were carried out directly on the cows. The author checklist is intended for use with studies where experiments are carried out on animals, which is why we have had such difficulty in completing this for the hut study, as many of the questions do not relate to how the cows were used
The Role of Schwann Cell Mitochondrial Metabolism in Schwann Cell Biology and Axonal Survival
Full text linkMitochondrial dysfunction has emerged as a common cause of peripheral neuropathies. While the role of neuronal and axonal mitochondria in peripheral nerve disease is well appreciated, whether Schwann cell: SC) mitochondrial deficits contribute to peripheral neuropathies is unclear. Greater insight into the biology and pathology of SC mitochondrial metabolism could be relevant to the treatment of peripheral neuropathies, particularly because SCs critically support axonal stability and function as well as promote peripheral nerve regeneration. The present thesis investigates the contribution of SC mitochondrial deficits to disease progression in peripheral neuropathies as well as the gene regulatory network that drives the SC regenerative response after injury and in disease states. We describe the generation and characterization of the first mouse model useful in directly interrogating the contribution of SC mitochondrial dysfunction to peripheral neuropathy. These mice: Tfam-SCKOs) were produced through the tissue-specific deletion of the mitochondrial transcription factor A gene: Tfam), which is required for mtDNA transcription and replication. Interestingly, induction of SC-specific mitochondrial dysfunction did not affect SC survival; instead, these deficits resulted in a severe, progressive peripheral neuropathy characterized by extensive axonal degeneration that recapitulated critical features of human neuropathy. Mechanistically, we demonstrated that SC mitochondrial dysfunction activates a maladaptive integrated stress response and causes a shift in lipid metabolism away from new lipid biosynthesis towards increased lipid oxidation. These alterations in lipid metabolism caused the early depletion of key myelin lipid components as well as a dramatic accumulation of acylcarnitine lipid intermediates. Importantly, release of acylcarnitines from SCs was toxic to axons and induced their degeneration. Our results show that normal mitochondrial function in SCs is essential for maintenance of axonal survival and normal peripheral nerve function, suggesting that SC mitochondrial dysfunction contributes to human peripheral neuropathies. Moreover, our work identifies alterations in SC lipid metabolism and the accumulation of toxic lipid intermediates as novel mechanisms driving some of the pathology in peripheral neuropathies associated with mitochondrial dysfunction. Tfam-SCKO mice showed a severe deficiency in their ability to remyelinate peripheral nerve axons after injury. To gain insight into the highly orchestrated process of SC-mediated support of axonal regeneration, we also investigated the transcriptional and post-transcriptional gene regulatory program that drives the SC regenerative response. We profiled the expression of SC microRNAs: miRNAs) after peripheral nerve lesions as well as characterized the injury response of SCs with disrupted miRNA processing and showed that SC miRNAs modulated the injury response largely by targeting positive regulators of SC dedifferentiation/proliferation. SC miRNAs cooperated with transcriptional regulators to promote rapid and robust transitions between the distinct differentiation states necessary to support nerve regeneration. Moreover, we identified miR-34a and miR-140 as regulators of SC proliferation and myelination. We then used a novel computational approach to infer the gene regulatory network involved in this SC injury response and gain insight on cooperative regulation of this process by transcription factors and miRNAs. Together, the results described in the present thesis represent a significant increase in our understanding of how mitochondrial abnormalities specifically in SCs contribute to clinical impairment in patients with peripheral neuropathy. Moreover, the mechanistic characterization of lipid metabolism abnormalities in SCs following mitochondrial dysfunction elucidates potentially important therapeutic targets. Finally, our analysis of the transcriptional and post-transcriptional gene regulatory network involved in the SC regenerative response also provides valuable insight that could be harnessed to help restore normal nerve function in patients with peripheral neuropathy
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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