1,721,035 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
Burn-Derived Stem Cells - A Promising New Cell Source For Skin Regeneration
No full textIntroduction: Burns affect millions of people worldwide. Available wound coverage materials are insufficient due to a lack of cells. Mesenchymal stem cells (MSCs) promote wound healing but are limited by lack of availability. We hypothesise that burned skin contains functioning MSCs (burn derived MSCs; BD-MSCs) that promote wound healing.
Methods: BD-MSCs were compared to umbilical cord MSCs in terms of key biological characteristics. Then, skin-scaffolds were cellularized with BD-MSCs, applied onto excisional porcine wounds and observed over 30d.
Results: We found no difference between BD- and UC-MSCs in mitochondrial function, proliferation, colony formation, cell cycle stage distribution, reactive oxygen species, and MHC I/II expression. BD-MSCs are safe and improved wound healing in mice and pigs.
Conclusion: Burned skin contains healthy MSCs that promote wound healing. Key biological functions are not altered by burn trauma. Further studies are needed to evaluate the role of BD-MSCs in wound healing.M.Sc
Persistent Hypermetabolism after Severe Burn Injury: Effects of Hepatic Stress and Regeneration
Get PDFBurn injury represents one of the most severe forms of trauma. Persistent hypermetabolism and inflammatory response are common in major burned patients, contributing to morbidity and mortality. The underlying mechanisms are largely unknown and therefore novel and effective treatments are lacking. Liver is the fundamental mediator of post-burn immunologic and metabolic derangement and significant hepatomegaly is universally present and associated with the persistent hypermetabolism and inflammatory response in severely burned patients. We sought to understand if such a hepatomegaly is the consequence of 1) increased hepatic fat infiltration due to intensified lipolysis in white adipose tissue (WAT) and inter-organ cross-talk between liver and WAT, or 2)aberrant liver regeneration induced by stress response and liver damage which carries on hypermetabolic and pro-inflammatory signaling, contributing to persistent hypermetabolism and inflammatory response after major burn injury.
Rodent models of burn plus LPS administration, high fat diet (HFD) plus burn, and 30% TBSA burn of Sox9-cre/ERT2:ROSA26-EYFP mice were used for the studies.
In the rat model of burn plus LPS, we demonstrated 1) increased ER stress, inflammasome activation, apoptosis and lipolysis in WAT,contributing to liver steatosis (Chapter 2);2) hepatic ER stress and inflammasome activation, contributing to liver damage and organ dysfunction(Chapter 3). In the mouse model of HFD plus burn, we showed that hepatic fat infiltration and meta-flammation augment the liver damage and metabolic dysfunction post-burn(Chapter 4). We lineage-traced the facultative liver progenitor cells after burn injury and demonstrated that liver regeneration by this group of cells peaked around 2 weeks post-burn. Significant activation of multiple inflammatory and metabolic signaling pathways was indicated by transcriptomic analysis and verified by further analysis in the liver stem cells and their progeny post-burn as compared with both sham and self-renewal mature hepatocytes. Concomitant down-regulation of LXR signaling in the liver stem cells post-burn implicated the therapeutic potential of LXR agonist in ameliorating pro-inflammatory response and restoring lipid homeostasis after major burn injury (Chapter 5).
In conclusion, severe burn injury leads to hepatic stress response, liver damage and steatosis, stimulating liver regeneration from facultative stem cells which contributes to persistent hypermetabolism and pro-inflammatory response.Ph.D
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
The Role of NLPR3 Inflammasome in Response to Thermal Injury and Sepsis
No full textAlthough the induction of acute-phase inflammation after burn injury is essential, if prolonged it can induce increased risk of infection and sepsis. The NLRP3 inflammasome has established itself as an integral mediator of the acute phase response, however there is a current lack of understanding how it is involved in the inflammatory response after burn injury.
In this study we investigated the role of the NLRP3 inflammasome in burn and septic patients and further aimed to determine if its components can be used to predict sepsis. In Chapter 2 we established the hyperinflammatory response in adult burn and septic burn patients. We also showed that there is increased NLRP3 inflammasome activation and expression in white adipose tissue (WAT) of burn patients and that its pro-inflammatory by-products increase with increasing injury severity.
In Chapter 3, we studied the effect that NLRP3 knockout would have on survival and the immune response in rodents. Interestingly, knocking out NLRP3 inflammasome resulted in increased bacterial clearance and survival in rodents. However, it also induced greater acute responsiveness at the site of injury and WAT characterized by greater macrophage and
neutrophil infiltration, ER stress, apoptosis/pyroptosis, and increased systemic inflammation.
Differential effects were found in other organs with an overall faster return to baseline in inflammatory mediators. In septic burn patients, we found peaks in WAT NLRP3 gene expression occurring later than non-septic’s.
Extending these findings in Chapter 4, we used the major source of NLRP3 inflammasome (macrophages) and its by-product (IL-1β) to generate the Septic Predictor Index to identify burn patients susceptible to sepsis. Patients with Index ratios greater than 0.5 had reduced macrophages proportions in WAT that were producing excess amounts of pro-inflammatory IL- 1β, and subsequently developed sepsis. Collectively, these results suggest that the NLRP3 inflammasome is a critical acute-phase mediator in septic burn patients and despite its utility to identify patient susceptible to sepsis, its mechanism is complex yet protective of sepsis development.Ph.D
The Role of NLPR3 Inflammasome in Response to Thermal Injury and Sepsis
No full textAlthough the induction of acute-phase inflammation after burn injury is essential, if prolonged it can induce increased risk of infection and sepsis. The NLRP3 inflammasome has established itself as an integral mediator of the acute phase response, however there is a current lack of understanding how it is involved in the inflammatory response after burn injury.
In this study we investigated the role of the NLRP3 inflammasome in burn and septic patients and further aimed to determine if its components can be used to predict sepsis. In Chapter 2 we established the hyperinflammatory response in adult burn and septic burn patients. We also showed that there is increased NLRP3 inflammasome activation and expression in white adipose tissue (WAT) of burn patients and that its pro-inflammatory by-products increase with increasing injury severity.
In Chapter 3, we studied the effect that NLRP3 knockout would have on survival and the immune response in rodents. Interestingly, knocking out NLRP3 inflammasome resulted in increased bacterial clearance and survival in rodents. However, it also induced greater acute responsiveness at the site of injury and WAT characterized by greater macrophage and
neutrophil infiltration, ER stress, apoptosis/pyroptosis, and increased systemic inflammation.
Differential effects were found in other organs with an overall faster return to baseline in inflammatory mediators. In septic burn patients, we found peaks in WAT NLRP3 gene expression occurring later than non-septic’s.
Extending these findings in Chapter 4, we used the major source of NLRP3 inflammasome (macrophages) and its by-product (IL-1β) to generate the Septic Predictor Index to identify burn patients susceptible to sepsis. Patients with Index ratios greater than 0.5 had reduced macrophages proportions in WAT that were producing excess amounts of pro-inflammatory IL- 1β, and subsequently developed sepsis. Collectively, these results suggest that the NLRP3 inflammasome is a critical acute-phase mediator in septic burn patients and despite its utility to identify patient susceptible to sepsis, its mechanism is complex yet protective of sepsis development.Ph.D
The Reprogramming of White Adipose Tissue to Brown Adipose Tissue Mediates Adverse Metabolic Dysfunction After A Burn Injury
No full textA burn injury represents one of the most severe forms of trauma and affects more than two million people in North America annually. Of all cases, nearly 4000 people die of complications related to the injury. A hallmark of severely burned patients is the activation of a hypermetabolic stress response, which is characterized by hyperglycemia, lipolysis, and protein catabolism. Perhaps the most serious gap in our understanding of the hypermetabolic response in burns is the role of the adipose tissue. Humans harbour two distinct adipose depots, white adipose tissue (WAT) and brown adipose tissue (BAT) that carry out essentially opposite functions. WAT is primarily involved in storing excess energy, whereas BAT burns excess energy in the form heat. This fat burning aspect of BAT has emerged as a powerful tool in combating the metabolic syndrome (hyperglycemia, excess body fat, hypertension). Additionally, it has been discovered that our WAT can be reprogrammed to become BAT, however, whether or not such reprogramming (white to brown fat) occurs after a burn injury is unknown. We therefore investigated the adipose tissue, and its role in post-burn hypermetabolism, by using an animal model of burn injury and tissue from clinical burn patients. In our first study, we report the reprogramming of WAT to BAT in both burn patients and post-burn mice indicated by increased expression of the brown adipocyte marker, uncoupling protein 1 (UCP-1). This reprogramming of WAT post-burn injury required both IL-6 and catecholamine secretion from alternatively activated macrophages. In our second study, we demonstrated that WAT browning with its associated lipolysis increased plasma levels of free fatty acids, leading to the accelerated development of hepatic steatosis and dysfunction after a burn injury. The last study of this thesis was geared towards clinical applications, and centered on the inhibition of the WAT to BAT switch via the use of an IL-6R blocker and propranolol to improve post-burn hypermetabolism and organ steatosis. In summary, our findings highlight an essential role of the adipose tissue in contributing to post-burn hypermetabolism and pathology.Ph.D
The Reprogramming of White Adipose Tissue to Brown Adipose Tissue Mediates Adverse Metabolic Dysfunction After A Burn Injury
No full textA burn injury represents one of the most severe forms of trauma and affects more than two million people in North America annually. Of all cases, nearly 4000 people die of complications related to the injury. A hallmark of severely burned patients is the activation of a hypermetabolic stress response, which is characterized by hyperglycemia, lipolysis, and protein catabolism. Perhaps the most serious gap in our understanding of the hypermetabolic response in burns is the role of the adipose tissue. Humans harbour two distinct adipose depots, white adipose tissue (WAT) and brown adipose tissue (BAT) that carry out essentially opposite functions. WAT is primarily involved in storing excess energy, whereas BAT burns excess energy in the form heat. This fat burning aspect of BAT has emerged as a powerful tool in combating the metabolic syndrome (hyperglycemia, excess body fat, hypertension). Additionally, it has been discovered that our WAT can be reprogrammed to become BAT, however, whether or not such reprogramming (white to brown fat) occurs after a burn injury is unknown. We therefore investigated the adipose tissue, and its role in post-burn hypermetabolism, by using an animal model of burn injury and tissue from clinical burn patients. In our first study, we report the reprogramming of WAT to BAT in both burn patients and post-burn mice indicated by increased expression of the brown adipocyte marker, uncoupling protein 1 (UCP-1). This reprogramming of WAT post-burn injury required both IL-6 and catecholamine secretion from alternatively activated macrophages. In our second study, we demonstrated that WAT browning with its associated lipolysis increased plasma levels of free fatty acids, leading to the accelerated development of hepatic steatosis and dysfunction after a burn injury. The last study of this thesis was geared towards clinical applications, and centered on the inhibition of the WAT to BAT switch via the use of an IL-6R blocker and propranolol to improve post-burn hypermetabolism and organ steatosis. In summary, our findings highlight an essential role of the adipose tissue in contributing to post-burn hypermetabolism and pathology.Ph.D
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