1,721,059 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe 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
Get PDF“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
Get PDFWe 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
Programmed cell death in Legionella infection
No full textLegionella ssp. are the causative agents of severe inflammatory pneumonia, known as Legionnaires’ Disease, which is fatal in up to 30 % of cases. Legionella replicate within alveolar macrophages by hijacking host cell pathways to establish a unique vacuolar niche. This includes the regulation of programmed host cell death factors, as Legionella must first prevent, and then induce, host cell death to promote bacterial growth and egress, respectively. However, the molecular mechanisms involved in toggling “off” and “on” host cell death signalling pathways remain undetermined. The major focus of the work described in this thesis was the delineation of the role that programmed host cell death pathways play in Legionella infection. To do this, a novel live-cell imaging technique was employed to visualise the intracellular life-cycle of Legionella and to monitor macrophage health in real-time. Using this method, I was able to confirm that wild-type Legionella induce a rapid form of cell death, termed pyroptosis, which is dependent on bacterial flagellin and the host protease, caspase-1. While flagellin/caspase-1-mediated pyroptosis prevents bacterial replication, I have identified that aflagellated Legionella also induce caspase-11-dependent pyroptosis. In contrast to caspase-1, caspase-11-mediated pyroptosis is induced in the late stages of infection, concomitant with Legionella egress, and does not interfere with intracellular bacterial replication. Legionella are also thought to induce other forms of host cell death, however, genetic ablation of mitochondrial apoptosis (BAX and BAK deletion), caspase-independent necroptotic cell death (RIPK3 and MLKL deletion), or BNIP3 and BCL-RAMBO, the putative targets of the effector protein SidF, did not affect Legionella replication or the killing of host macrophages. Legionella must prevent the activation of host cell death signalling to allow for efficient replication. While down-regulation of flagellin enables intracellular growth in the presence of caspase-1, little is known about how Legionella might evade apoptotic cell death. Using live-cell imaging, I have now shown that Legionella-infected macrophages depend critically upon the anti-apoptotic activity of host cell BCL-XL, but not other BCL-2 family members, for viability. In the absence of BCL-XL, Legionella-infected cells underwent apoptosis, which abolished bacterial replication and dissemination. Legionella infection could be fully restored by inhibiting mitochondrial apoptosis, either via BAX/BAK deletion or caspase inhibition. A single dose of BCL-XL-targeted BH3-mimetic therapy significantly reduced Legionella burden in the lungs of mice and prevented lethal bacterial infection. Mechanistically, I identified that Legionella infection inhibits host protein synthesis, which sensitises macrophages to BCL-XL loss or inhibition, via depletion of another anti-apoptotic BCL-2 family protein, MCL-1. Together, these results demonstrate that Legionella- infected macrophages are specifically and acutely sensitive to apoptotic cell death following the loss, or inhibition, of BCL-XL. Thus, the re-purposing of existing drugs, such as chemotherapeutic BH3-mimetics, to target host, rather than bacterial, pathways represents a novel and promising strategy for the treatment of intracellular pathogens that show increased, and often rapidly acquired, antibiotic resistance
Dispelling the Myths Behind First-author Citation Counts
Get PDFWe 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
The role of Staphylococcus aureus Panton-Valentine leukocidin (PVL) in mammalian macrophages
No full textMethicillin-resistant Staphylococcus aureus (MRSA) causes skin infections and life-threatening necrotizing pneumonia in otherwise healthy individuals. Nearly all of these community-acquired MRSA (CA-MRSA) strains express the secreted pore-forming leukotoxin Panton-Valentine leukocidin (PVL). However, its role in pathogenesis remains controversial, as it fails to kill mice and its immune cells. Recently, PVL was shown to bind human, but not mouse, complement receptor 5a (C5aR). While this explained species and cell specificity, the underlying mechanism that leads to PVL pore formation and cell death remains poorly described. Thus, the major focus of the work described in this thesis was to characterize PVL cytotoxicity and identify host factors that mediate cell death. To further probe its function, I generated recombinant PVL, its subunits, LukS-PV and LukF-PV and utilized S. aureus culture supernatants from wild type, ∆pvl and complemented ∆pvl strains. Notably, both native and recombinant PVL were highly cytotoxic to PMA-differentiated human THP-1 macrophages in vitro whereas the subunits LukS-PV or LukF-PV showed no effect (Chapter Two). Intriguingly, human THP-1 monocytes, HeLa epithelial cells and RAW264.7 mouse macrophages remained refractory to PVL toxicity, consistent with the absence of human C5a receptor (hC5aR) expression. While binding to hC5aR is essential for PVL-induced killing of macrophages, I have now shown for the first time that PVL specifically interacts with several anionic phospholipids, including phosphatidylserine (PS), phosphatidic acid (PA) and cardiolipin (CL) (Chapter Three). Surprisingly, these lipids are enriched on different organellar membranes in host cells, suggesting that PVL kills macrophages by targeting intracellular membranes. To gain a spatial-temporal view on the PVL-macrophage interaction, single-cell analysis by live-cell imaging was established. This showed that PVL caused mitochondrial and lysosomal damage prior to cell death, which can be partially prevented by lysosomal cathepsin B inhibitors (Ca-074Me) (Chapter Three). Intriguingly, PVL cytotoxicity was blocked by inhibiting osmotic lysis and potassium efflux (using glycine and potassium chloride enriched media, respectively), and NLRP3 inflammasome activity (glyburide and MCC950) in mammalian macrophages (Chapter Four). In addition, PVL triggered caspase-1 activation and subsequently induced inflammatory responses in mammalian macrophages. Surprisingly, loss of caspase-1 activity did not affect PVL-mediated cell death, but genetic deletion of other inflammatory caspases, such as caspase-4 or caspase-5, in THP-1 macrophages reduced PVL cytotoxicity compared to wild type and caspase-8 deficient cells (Chapter Four). Furthermore, pharmacological inhibition of apoptotic caspases (using pan-caspase inhibitors such as Q-VD-OPh) and RIPK1 (using necrostatin-1s, nec-1s) did not protect mammalian macrophages from PVL-mediated cell death. These observations suggest that PVL kill macrophages by targeting different intracellular membranes and activating several host cell death factors. Collectively, I have identified important host factors that are targeted by PVL to induce macrophage cell death and inflammation. This may lead to host-directed compounds to prevent MRSA-induced immune evasion during infections and the development of new therapeutic treatment options
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
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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