1,720,961 research outputs found
Gut barrier dysfunction after hemorrhagic shock
No full textIntroduction: Hemorrhagic shock is a frequent complication in trauma patients, after gastrointestinal
bleeding and major surgery. Hemorrhagic shock is associated with end organ damage, caused by
hypoperfusion and local and systemic inflammation. The intestine is one of the first organs affected by
hemorrhagic shock. An early event in intestinal damage is gut wall integrity loss, including the opening
or breakdown of tight junctions. In the first part of the study, the sequence of events in the gut after
hemorrhagic shock and the underlying mechanism causing tight junction loss were studied. In the
second part, the use of the transmembrane tight junction protein, claudin-3, as urinary marker for
intestinal tight junction loss was investigated.
Methods: Sprague-Dawley rats were subjected to hemorrhagic shock and sacrificed 15, 30, 60 and
90 minutes after shock. Control rats were sacrificed without intervention. Tight junction integrity was
studied by immunofluorescence (IF) and western blot analysis (WB) of tight junction proteins ZO-1 and
claudin-3 in the ileum. The underlying mechanism of tight junction loss was investigated by studying
ADF activation by WB and changes in actin cytoskeleton by IF. Epithelial cell injury was investigated
by ileal lipid binding protein (ILBP) detection in epithelial cells and plasma. Intestinal barrier function
was studied by investigating intestinal permeability to macromolecules and bacterial translocation.
Finally, local and systemic inflammation were studied by investigating neutrophil influx and by
measuring TNF- plasma concentration by ELISA respectively. For the second part of the study,
claudin-3 urine levels were semi-quantitatively analyzed by WB. To investigate whether claudin-3
detected in the urine is released by intestinal tight junction loss and not by tight junction loss in the
liver and kidney, tight junction integrity loss in the liver and kidney was studied by IF and WB.
Results: The first part of the study shows that hemorrhagic shock leads to neutrophil influx from 15
minutes after shock. From this time point, hemorrhagic shock causes a significant upregulation of
activated ADF and the turnover of F-actin (filamentous or polymeric actin) into G-actin (globular or
monomeric actin). This is followed by a significant loss of tight junction proteins claudin-3 from 30
minutes and ZO-1 from 60 minutes after shock. Epithelial ILBP content decreases from 60 minutes
after shock. Intestinal barrier function loss from 60 minutes after shock is represented by bacterial
translocation and from 90 minutes after shock by enhanced permeability to horseradish peroxidase
(HRP). Plasma TNF- levels are significantly elevated from 60 minutes after shock. The results of the
second part of the study show that claudin-3 urine levels are significantly increased 30, 60 and 90
minutes after hemorrhagic shock. Tight junction integrity in the liver and kidney is maintained 15, 30,
60 and 90 minutes after hemorrhagic shock.
Discussion: This study gives more insight into the sequence of events in the gut after hemorrhagic
shock. Hemorrhagic shock leads to neutrophil influx followed by intestinal tight junction integrity loss
after upregulation of activated ADF and consequent actin cytoskeleton degradation. This is followed
by bacterial translocation and systemic hyperinflammation. In addition, this study indicates that
intestinal claudin-3 loss is followed by an increase in claudin-3 urine levels and that claudin-3 integrity
in the liver and kidney is maintained, suggesting that claudin-3 can be used as urinary marker for
intestinal tight junction loss
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
Gut barrier dysfunction after hemorrhagic shock
No full textIntroduction: Hemorrhagic shock is a frequent complication in trauma patients, after gastrointestinal
bleeding and major surgery. Hemorrhagic shock is associated with end organ damage, caused by
hypoperfusion and local and systemic inflammation. The intestine is one of the first organs affected by
hemorrhagic shock. An early event in intestinal damage is gut wall integrity loss, including the opening
or breakdown of tight junctions. In the first part of the study, the sequence of events in the gut after
hemorrhagic shock and the underlying mechanism causing tight junction loss were studied. In the
second part, the use of the transmembrane tight junction protein, claudin-3, as urinary marker for
intestinal tight junction loss was investigated.
Methods: Sprague-Dawley rats were subjected to hemorrhagic shock and sacrificed 15, 30, 60 and
90 minutes after shock. Control rats were sacrificed without intervention. Tight junction integrity was
studied by immunofluorescence (IF) and western blot analysis (WB) of tight junction proteins ZO-1 and
claudin-3 in the ileum. The underlying mechanism of tight junction loss was investigated by studying
ADF activation by WB and changes in actin cytoskeleton by IF. Epithelial cell injury was investigated
by ileal lipid binding protein (ILBP) detection in epithelial cells and plasma. Intestinal barrier function
was studied by investigating intestinal permeability to macromolecules and bacterial translocation.
Finally, local and systemic inflammation were studied by investigating neutrophil influx and by
measuring TNF- plasma concentration by ELISA respectively. For the second part of the study,
claudin-3 urine levels were semi-quantitatively analyzed by WB. To investigate whether claudin-3
detected in the urine is released by intestinal tight junction loss and not by tight junction loss in the
liver and kidney, tight junction integrity loss in the liver and kidney was studied by IF and WB.
Results: The first part of the study shows that hemorrhagic shock leads to neutrophil influx from 15
minutes after shock. From this time point, hemorrhagic shock causes a significant upregulation of
activated ADF and the turnover of F-actin (filamentous or polymeric actin) into G-actin (globular or
monomeric actin). This is followed by a significant loss of tight junction proteins claudin-3 from 30
minutes and ZO-1 from 60 minutes after shock. Epithelial ILBP content decreases from 60 minutes
after shock. Intestinal barrier function loss from 60 minutes after shock is represented by bacterial
translocation and from 90 minutes after shock by enhanced permeability to horseradish peroxidase
(HRP). Plasma TNF- levels are significantly elevated from 60 minutes after shock. The results of the
second part of the study show that claudin-3 urine levels are significantly increased 30, 60 and 90
minutes after hemorrhagic shock. Tight junction integrity in the liver and kidney is maintained 15, 30,
60 and 90 minutes after hemorrhagic shock.
Discussion: This study gives more insight into the sequence of events in the gut after hemorrhagic
shock. Hemorrhagic shock leads to neutrophil influx followed by intestinal tight junction integrity loss
after upregulation of activated ADF and consequent actin cytoskeleton degradation. This is followed
by bacterial translocation and systemic hyperinflammation. In addition, this study indicates that
intestinal claudin-3 loss is followed by an increase in claudin-3 urine levels and that claudin-3 integrity
in the liver and kidney is maintained, suggesting that claudin-3 can be used as urinary marker for
intestinal tight junction loss
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
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
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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