1,721,034 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
Huntingtin: an iron-regulated protein essential for normal nuclear and perinuclear organelles
No full textHuntington's disease (HD), with its selective neuronal cell loss, is caused by an
elongated glutamine tract in the huntingtin protein. To discover the pathways
that are candidates for the protein's normal and/or abnormal function, we
surveyed 19 classes of organelle in Hdh(ex4/5)/Hdh(ex4/5) knock-out compared with
wild-type embryonic stem cells to identify any that might be affected by
huntingtin deficiency. Although the majority did not differ, dramatic changes in
six classes revealed that huntingtin's function is essential for the normal
nuclear (nucleoli, transcription factor-speckles) and perinuclear membrane
(mitochondria, endoplasmic reticulum, Golgi and recycling endosomes) organelles
and for proper regulation of the iron pathway. Moreover, upmodulation by
deferoxamine mesylate implicates huntingtin as an iron-response protein. However,
excess huntingtin produced abnormal organelles that resemble the deficiency
phenotype, suggesting the importance of huntingtin level to the protein's normal
pathway. Thus, organelles that require huntingtin to function suggest roles for
the protein in RNA biogenesis, trafficking and iron homeostasis to be explored in
HD pathogenesis
Mutant huntingtin forms in vivo complexes with distinct context-dependent conformations of the polyglutamine segment
No full textHuntington's disease (HD) is caused by an expanded glutamine tract, which confers
a novel aggregation-promoting property on the 350-kDa huntingtin protein. Using
specific antibodies, we have probed the structure of the polyglutamine segment in
mutant huntingtin complexes formed in cell culture from either truncated or
full-length protein. Complexes formed by a mutant amino terminal fragment most
frequently entail a change in conformation that eliminates reactivity with the
polyglutamine-specific mAb 1F8, coincident with production of insoluble
aggregate. By contrast, complexes formed by the full-length mutant protein remain
soluble and are invariably 1F8-reactive, indicating a soluble polyglutamine
conformation. Therefore, aggregates in HD may form by different biochemical
mechanisms that invoke different possibilities for the pathogenic process. If
pathogenesis is triggered by a truncated fragment, it probably involves the
formation of an insoluble aggregate. However, the observation of soluble
complexes in which an HD-specific pathogenic conformation of the glutamine tract
remains accessible suggests that pathogenesis could also be triggered at the
level of full-length huntingtin by abnormal aggregation with normal or abnormal
protein partners
Amyloid formation by mutant huntingtin: threshold, progressivity and recruitment of normal polyglutamine proteins
No full textHuntington's disease (HD) is caused by an expanded CAG trinucleotide repeat
encoding a tract of consecutive glutamines near the amino terminus of huntingtin,
a large protein of unknown function. It has been proposed that the expanded
polyglutamine stretch confers a new property on huntingtin and thereby causes
cell and region-specific neurodegeneration. Genotype-phenotype correlations
predict that this novel property appears above a threshold length (approximately
38 glutamines), becomes progressively more evident with increasing polyglutamine
length, is completely dominant over normal huntingtin and is not appreciably
worsened by a double genetic dose in HD homozygotes. Recently, an amino terminal
fragment of mutant huntingtin has been found to form self-initiated fibrillar
aggregates in vitro. We have tested the capacity for aggregation to assess
whether this property matches the criteria expected for a fundamental role in HD
pathogenesis. We find that that in vitro aggregation displays a threshold and
progressivity for polyglutamine length remarkably similar to the HD disease
process. Moreover, the mutant huntingtin amino terminus is capable of recruiting
into aggregates normal glutamine tract proteins, such as the amino terminal
segments of both normal huntingtin and of TATA-binding protein (TBP). Our
examination of in vivo aggregates from HD post-mortem brains indicates that they
contain an amino terminal segment of huntingtin of between 179 and 595 residues.
They also contain non-huntingtin protein, as evidenced by immunostaining for TBP.
Interestingly, like the in vitro aggregates, aggregates from HD brain display
Congo red staining with green birefringence characteristic of amyloid. Our data
support the view that the expanded polyglutamine segment confers on huntingtin a
new property that plays a determining role in HD pathogenesis and could be a
target for treatment. Moreover, the new property might have its toxic
consequences by interaction with one or more normal polyglutamine-containing
proteins essential for the survival of target neurons
Huntingtin immunoreactivity in the rat neostriatum: differential accumulation in projection and interneurons
No full textHuntington's disease is caused by a mutation of the gene encoding the protein
huntingtin. Features of the human disease, characterized by selective loss of
neurons from the neostriatum, can be replicated in rodents by administration of
excitotoxins. In both affected individuals and the rodent model, there is massive
loss of striatal projection neurons with selective sparing of interneurons.
Furthermore, in the human disease the earliest evidence of striatal injury is
found in striosomal regions of the striatum. The mRNA encoding huntingtin is
known to be expressed by neurons throughout the brain, a distribution which does
not account for the selective patterns of neuronal death which are observed.
Using fluorescence immunocytochemistry and confocal microscopy with an antibody
to huntingtin, we have observed that in rats a subset of striatal projection
neurons contains dense accumulations of huntingtin immunoreactivity (HT-ir),
while most neurons in the striatum contain much smaller amounts. The intensely
stained neurons are concentrated within the striatal striosomes, as defined by
calbindin-D28K staining. In the matrix regions, relatively few neurons contain
dense accumulations of HT-ir, and these cells always lack perikaryal staining for
calbindin-D28K. Striatal interneurons, identified by the presence of
immunoreactivity for choline acetyltransferase, parvalbumin, calretinin, or
neuronal nitric oxide synthase, exhibit little or no HT-ir. The paucity of HT-ir
in striatal interneurons, as well as the prominence of staining in a subset of
striosomal neurons, mirrors the selective vulnerability of these different types
of cells in early stages of human Huntington's disease and in rodent excitotoxic
models of the disorder. Our observations suggest that mechanisms which modulate
the accumulation of huntingtin may play a central role in the neuronal
degeneration of Huntington's disease
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
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