126,356 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
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
FIGURE 4. Bromus husainii. A. Nodes. B. Collar. C in Bromus husainii (Poaceae:Bromeae), a new species from Valley of Flowers National Park, Uttarakhand, India
No full textFIGURE 4. Bromus husainii. A. Nodes. B. Collar. C. Ligule.Published as part of Yadav, Rekha, Prasad, Dileshwar, Tripathi, Shailja, Jaiswal, Shubham & Agnihotri, Priyanka, 2021, Bromus husainii (Poaceae:Bromeae), a new species from Valley of Flowers National Park, Uttarakhand, India, pp. 73-82 in Phytotaxa 516 (1) on page 78, DOI: 10.11646/phytotaxa.516.1.5, http://zenodo.org/record/531678
FIGURE 3. Bromus husainii. A. Normal Spikelet. B. Lower glume. C. Upper glume. D. Lower Lemma. E. Palea. F. Anther. G. Gynoecium. H in Bromus husainii (Poaceae:Bromeae), a new species from Valley of Flowers National Park, Uttarakhand, India
No full textFIGURE 3. Bromus husainii. A. Normal Spikelet. B. Lower glume. C. Upper glume. D. Lower Lemma. E. Palea. F. Anther. G. Gynoecium. H. Lodicules.Published as part of Yadav, Rekha, Prasad, Dileshwar, Tripathi, Shailja, Jaiswal, Shubham & Agnihotri, Priyanka, 2021, Bromus husainii (Poaceae:Bromeae), a new species from Valley of Flowers National Park, Uttarakhand, India, pp. 73-82 in Phytotaxa 516 (1) on page 77, DOI: 10.11646/phytotaxa.516.1.5, http://zenodo.org/record/531678
FIGURE 2. Bromus husainii. A. Inflorescence. B. Robust spikelet. C. Lower glume. D. Upper glume. E–K. Lemma. L. Palea. M. Anthers. N in Bromus husainii (Poaceae:Bromeae), a new species from Valley of Flowers National Park, Uttarakhand, India
No full textFIGURE 2. Bromus husainii. A. Inflorescence. B. Robust spikelet. C. Lower glume. D. Upper glume. E–K. Lemma. L. Palea. M. Anthers. N. Gynoecium.Published as part of Yadav, Rekha, Prasad, Dileshwar, Tripathi, Shailja, Jaiswal, Shubham & Agnihotri, Priyanka, 2021, Bromus husainii (Poaceae:Bromeae), a new species from Valley of Flowers National Park, Uttarakhand, India, pp. 73-82 in Phytotaxa 516 (1) on page 76, DOI: 10.11646/phytotaxa.516.1.5, http://zenodo.org/record/531678
Pragmatic Case Studies as a Source of Unity in Applied Psychology
No full textTo unify or not to unify applied psychology: that is the question. In this article we review pendulum swings in the historical efforts to answer this question—from a comprehensive, positivist, “top-down,” deductive yes between the 1930s and the early 60s, to a postmodern no since then. A rationale and proposal for a limited, “bottom-up,” inductive yes in applied psychology is then presented, employing a case-based paradigm that integrates both positivist and postmodern themes and components. This paradigm is labeled “pragmatic psychology” and, its specific use of case studies, the “Pragmatic Case Study Method” (“PCS Method”). We call for the creation of peer-reviewed journal-databases of pragmatic case studies as a foundational source of unifying applied knowledge in our discipline. As one example, the potential of the PCS Method for unifying different angles of theoretical regard is illustrated in an area of applied psychology, psychotherapy, via the case of Mrs. B. The article then turns to the broader historical and epistemological arguments for the unifying nature of the PCS Method in both applied and basic psychology.Peer reviewe
Dopamine and dopamine-quinones toxicity in Parkinson's disease: cellular models revealing a possible role for superoxide dismutases
Get PDFParkinson’s disease is a widespread neurodegenerative disorder that affect 2% of the population above the age of 60. The hallmark of the pathology is the preferential degeneration of the dopaminergic neurons in the substantia nigra pars compacta of the midbrain, and the presence of proteinaceous inclusions called Lewy bodies in the surviving neurons (Braak 2004). In 10% of the cases, the disease is linked to mutation on several genes, among them α-synuclein, DJ-1, PARKIN, PINK1 and LRRK2, but in the vast majority of the cases the aetiology is still unknown (sporadic PD) (Gwinn-Hardy 2002). Post mortem studies and in vitro and in vivo PD model have revealed a possible interconnection between genetic and sporadic PD, which involves both mitochondrial dysfunction and oxidative stress as central players in the pathogenesis of the disease (Gilgun-Sherki Y. et al. 2001, Mythri R. B. et al. 2011). Oxidative stress is a condition characterized by the inability of the cellular antioxidant defences to cope with the production of reactive oxygen species (ROS). This condition of unbalance between the production and the clearance of ROS causes irreversible damage to cellular components such as lipids, proteins and DNA, leading eventually to cell death (Lotharius et al. 2002). Among the enzymes implicated in the detoxification of ROS, are superoxide dismutases (SODs) that catalyze the dismutation of superoxide anion into molecular oxygen and hydrogen peroxide (Fridovich 1995). Since oxidative stress does not explain alone the selectivity death of dopaminergic neurons, the main working hypothesis is that dopamine itself could have a central role. Under physiological conditions, dopamine is synthesized in the cytosol and stored in synaptic vesicles by the action of Vesicular Monoamine Transporter (VMAT2) where it is stabilized by the low pH (Erickson, J. D 1992). If the amount of cytosolic DA exceeds the physiological concentration, DA is metabolized to the non-toxic metabolite 3,4-dihydroxyphenylacetic acid and hydrogen peroxide by the action of monoamine oxidase (MAO) and aldehyde dehydrogenase, or sequestered into lysosomes where it can auto-oxidize to form neuromelanin (NM). If not buffered by these pathways, cytosolic DA can be oxidized to DA-quinone (DAQs) (spontaneously or enzymatically), (Sulzer, D., 2000, Elsworth, J. D. 1997), a reaction that also leads to the formation of ROS. On these premise, we evaluated two line of research using a cellular model for PD (SH SY5Y cell line): one concerning about the effect of dopamine and its oxidized forms on cellular viability, the second one on the potential role of superoxide dismutases (1 and 2) over expression.
From the use of different techniques we started to evaluate which kind of cell death pathway was activated by dopamine and DAQs. Looking for the presence of nuclear fragmentation, that is one of the later stages of apoptosis, we determined that both dopamine and DAQs induce cell death via apoptosis but the dopamine toxicity depends on its internalization by the action of the dopamine transporter (DAT), since the pre-treatment of cells with GBR 12909 (a DAT inhibitor) had a rescue effect. To confirm the apoptotic pathway we also evaluated another hallmark of apoptosis (one of the former stages of the apoptotic cascade): phosphatidil-serine externalization (PS) using ANNEXIN-V-FLUOS; a specific probe for PS. Using flow cytometry we confirm that both dopamine and DAQs induce cell death via apoptosis. Next we wanted to evaluate if dopamine and DAQs exert their toxicity from extracellular environment or they are required to enter in the cells. Treating cells with GBR12909, we demonstrate that dopamine needs to enter cells to exert its toxicity (since the treatment with the DAT inhibitor rescues cells from DA toxicity) while DAQs toxicity was not affected by this treatment leading to cell death. Since oxidative stress is one of the mechanisms that have been implicated in the pathogenesis of PD, and the chemistry of dopamine (auto-oxidation and enzyme-mediated oxidation) leads to the production of ROS, we evaluate the production of mitochondrial superoxide anion using a specific probe. The data demonstrate that only the auto oxidation of dopamine leads to the production of superoxide anion and dopamine is required to enter cell to exert its effect. To dissect more in depth the toxicity mechanism of both dopamine and DAQs, and since only cytosolic dopamine led to the production of mitochondrial superoxide anion, we asked if this two different oxidation processes activated different cell death pathways (the major are the mitochondrial one and the one mediated by death receptor) or not. From preliminary data we observed a marked difference in the activation of caspase 3 and the subsequent cleavage and inactivation of Poly (ADP) ribose polymerase (PARP) due to DAQs treatment convincing us to proceed in the investigation of the possible differences between this different oxidation processes. The second part of the work was focused on the role for superoxide dismutases 1 and 2 against dopamine and DAQs cytotoxicity since previous data demonstrated a role in superoxide anion production and induction of cell death in the case of cytosolic dopamine. Over expression of both SOD1 and SOD2 revealed a protective effect against dopamine cytotoxity, while they were not able to counteract DAQs-induced cell death. In the present work the main working hypothesis was that oxidative stress induced by dopamine and its oxidized forms accumulation could have a central role in the specific dopaminergic cell loss in Parkinson’s disease. The data obtained so far seems to highlights that dopamine and DAQs activates different apoptotic pathway that are superoxide anion-dependent for DA and superoxide anion-independent for DAQs. Since oxidative stress is considered one of the mechanism that interconnect genetic form and sporadic forms of the pathology and dopamine, in its oxidative chemistry, leads to the production of ROS, understanding which cell death pathways are activated and to which extent, is crucial to develop a therapy to counteract the start and the progression of the pathology. Data from the over expression of SODs demonstrate that compounds that counteract the production of superoxide anion (like SOD-mimetics that are currently used for other diseases) could have a protective role against the oxidative stress and the subsequent cell death condition induced by dopamine. Also compounds that block the activation of the apoptotic cascade induced by dopamine and DAQs could rescue cells from dying in this neurodegenerative diseas
Dr. Edwin Wright Collection: Author Unknown
Get PDFNotes - The author relates several short stories about his neighbours including Alex McDonell, homesteading and life around Meanook and Athabasca (1 page
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
Measurement of the ratio of branching fractions B(B0→K∗0γ )/B(B0s→φγ ) and the directCP asymmetry inB 0→K∗0γ
Get PDFThe ratio of branching fractions of the radiative B decays B0→K⁎0γ and B0s→ϕγ has been measured using an integrated luminosity of 1.0 fb−1 of pp collision data collected by the LHCb experiment at a centre-of-mass energy of s√=7TeV. The value obtained is
B(B0→K⁎0γ)B(B0s→ϕγ)=1.23±0.06(stat.)±0.04(syst.)±0.10(fs/fd),
where the first uncertainty is statistical, the second is the experimental systematic uncertainty and the third is associated with the ratio of fragmentation fractions fs/fd. Using the world average value for B(B0→K⁎0γ), the branching fraction B(B0s→ϕγ) is measured to be (3.5±0.4)×10−5.
The direct CP asymmetry in B0→K⁎0γ decays has also been measured with the same data and found to be
ACP(B0→K⁎0γ)=(0.8±1.7(stat.)±0.9(syst.))%.
Both measurements are the most precise to date and are in agreement with the previous experimental results and theoretical expectations
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