1,721,139 research outputs found
Ampk activation reduces hepatic lipid content by increasing fat oxidation in vivo
No full textThe energy sensor AMP-activated protein kinase (AMPK) is a key player in the control of energy metabolism. AMPK regulates hepatic lipid metabolism through the phosphorylation of its well-recognized downstream target acetyl CoA carboxylase (ACC). Although AMPK activation is proposed to lower hepatic triglyceride (TG) content via the inhibition of ACC to cause inhibition of de novo lipogenesis and stimulation of fatty acid oxidation (FAO), its contribution to the inhibition of FAO in vivo has been recently questioned. We generated a mouse model of AMPK activation specifically in the liver, achieved by expression of a constitutively active AMPK using adenoviral delivery. Indirect calorimetry studies revealed that liver-specific AMPK activation is sufficient to induce a reduction in the respiratory exchange ratio and an increase in FAO rates in vivo. This led to a more rapid metabolic switch from carbohydrate to lipid oxidation during the transition from fed to fasting. Finally, mice with chronic AMPK activation in the liver display high fat oxidation capacity evidenced by increased [C-14]-palmitate oxidation and ketone body production leading to reduced hepatic TG content and body adiposity. Our findings suggest a role for hepatic AMPK in the remodeling of lipid metabolism between the liver and adipose tissue
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
Regulation of hepatic lipid metabolism by AMPK : implications in the development and the treatment of fatty liver
No full textLa stéatose hépatique affecte 20 à 40% de la population et progresse de façon constante. Il s’agit d’une pathologie chronique fortement associée au syndrome métabolique. Sa pathogenèse est mal comprise. Une altération du métabolisme des lipides dans le foie entraînant une accumulation intra-hépatique de lipides est probablement la cause majeure de la stéatose hépatique. A ce jour, il n’existe pas de traitement spécifique de la stéatose hépatique. La protéine kinase activée par l’AMP (AMPK) est un régulateur clé du métabolisme énergétique. Notamment, l’AMPK contrôle le métabolisme des lipides en inhibant la synthèse des acides gras et du cholestérol, et en stimulant l'oxydation des acides gras. Plusieurs études ont montré l’existence d’une association entre l’accumulation intracellulaire de lipides et une perte d’activité de l’AMPK dans le foie. Ces observations suggèrent que l’AMPK pourrait être un facteur impliqué dans la physiopathologie de la stéatose hépatique. Pour étudier cette hypothèse, nous avons généré un nouveau modèle de souris knockout dépourvu des sous-unités catalytiques α1 et α2 de l’AMPK spécifiquement dans le foie. Nous avons analysé les conséquences de cette délétion sur le métabolisme lipidique dans différentes situations nutritionnelles. La délétion de l’AMPK dans le foie ne modifie pas le contenu hépatique en triglycérides et en cholestérol au cours d’un jeûne ou après une réalimentation riche en glucides. Egalement, l’expression des gènes de la lipogenèse n’est pas modifiée dans le foie de ces animaux. De plus, l’oxydation des acides gras n’est pas altérée même après un jeûne de 24h. Etonnamment, l’absence de l’AMPK dans le foie n’amplifie pas la stéatose hépatique, ni l’hyperglycémie ou l’intolérance au glucose lorsque les souris sont nourries avec un régime riche en lipides. Cependant, l’activation de l’AMPK in vivo avec l'activateur direct, A-769662, normalise la stéatose hépatique chez des souris lipodystrophiques aP2-SREBP-1c et chez des souris obèses nourries avec un régime riche en lipides. Cet effet est dépendant de l’AMPK car il est totalement perdu chez des souris dépourvues d’AMPK dans le foie. Dans des hépatocytes de souris en culture primaire, l’activation de l'AMPK par un activateur direct (A-769662) ou par des activateurs indirects (metformine et AICAR) réduit le flux lipogénique et augmente l’oxydation des acides gras. Ces effets sont totalement abolis dans des hépatocytes AMPK KO, démontrant l’action spécifique de l'AMPK sur le métabolisme lipidique en réponse à ces composés. Ces résultats obtenus chez la souris sont extrapolables à l'homme puisque nous avons montré que l'activation de l'AMPK dans des hépatocytes humains en culture primaire inhibe de manière efficace la synthèse des acides gras et du cholestérol. En conclusion, nos résultats démontrent que l’inactivation de l’AMPK dans le foie n’est pas un facteur déclenchant ou aggravant dans la physiopathologie de la stéatose hépatique. En revanche, l’activation pharmacologique de l’AMPK améliore efficacement la stéatose hépatique. Ainsi, l’AMPK est une cible potentielle pour le développement d'activateurs dans le but de traiter la stéatose hépatique chez l’homme.Fatty liver disease affects between 20-40% of the population. This pathology is usually associated with metabolic disease. Its pathogenesis is poorly understood. Altered lipids metabolism in the liver resulting on hepatic fat accumulation is probably due to fatty liver. There is no specific treatment for fatty liver disease. AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism. In particular, AMPK regulates lipid metabolism by inhibiting fatty acids and cholesterol synthesis, and stimulating fatty acids oxidation. Several studies have shown an association between intracellular lipid accumulation and loss of AMPK activity in the liver. These observations suggest that AMPK may be a factor involved in the pathogenesis of hepatic steatosis. To investigate this hypothesis, we generated a new model of knockout mice lacking the catalytic subunits of AMPK α1 and α2 specifically in the liver. We analyzed the consequences of this deletion on lipid metabolism in different nutritional conditions. Deletion of AMPK in the liver does not affect hepatic triglyceride and cholesterol content in fasted or in refed conditions with a high carbohydrate diet. Also, lipogenic genes expression is not altered in the liver of these animals. Moreover, the oxidation of fatty acids is not impaired after 24 hour of fasting. Surprisingly, lacking AMPK specifically in the liver does not aggraving fatty liver, hyperglycemia, or impaired glucose tolerance when the mice are on high fat diet condition. However, the activation of AMPK in vivo with a direct activator, A-769662, normalizes hepatic steatosis in lipodystrophyc aP2-SREBP-1c mice and in obese mice placed on high-fat diet. This effect is AMPK dependent because it is completely abolished in mice lacking AMPK specifically in liver. In primary mice hepatocytes, AMPK activation by a direct activator (A-769662) or by indirect activators (metformin and AICAR) reduces lipogenesis rates and increases fatty acids oxidation rates. These effects were completely abolished in hepatocytes lacking AMPK, showing the specific action of AMPK on lipid metabolism in response to these compounds. These results obtained in mice can be extrapolated to humans. Indeed, we have shown that AMPK activation in primary humain hepatocytes inhibits effectively fatty acid and cholesterol synthesis rates. In conclusion, our results showed that inactivation of AMPK in the liver is not a triggering or an aggraving factor in the pathogenesis of hepatic steatosis. Nevertheless, AMPK re-activation has a therapeutic benefit for the treatment of fatty liver disease. Thus, AMPK is a potential target to treat fatty liver disease in human
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
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
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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