1,721,012 research outputs found
The Size-Life Span Trade-Off Decomposed: Why Large Dogs Die Young
No full textLarge body size is one of the best predictors of long life span across species of mammals. In marked contrast, there is considerable evidence that, within species, larger individuals are actually shorter lived. This apparent cost of larger size is especially evident in the domestic dog, where artificial selection has led to breeds that vary in body size by almost two orders of magnitude and in average life expectancy by a factor of two. Survival costs of large size might be paid at different stages of the life cycle: a higher early mortality, an early onset of senescence, an elevated baseline mortality, or an increased rate of aging. After fitting different mortality hazard models to death data from 74 breeds of dogs, we describe the relationship between size and several mortality components. We did not find a clear correlation between body size and the onset of senescence. The baseline hazard is slightly higher in large dogs, but the driving force behind the trade-off between size and life span is apparently a strong positive relationship between size and aging rate. We conclude that large dogs die young mainly because they age quickly.American Federation of Aging Researc
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
An integrative approach to understanding variation in the form, pattern and pace of ageing
No full textVariation in the form, pattern and pace of ageing is studied by scientists in multiple disciplines and there is much to be gained from more cross-disciplinary communication. This chapter suggests here that the framework provided by Tinbergen’s ‘Four Questions’ is useful in integrating ageing research. It emphasizes the need to separate biological and chronological age and describe several markers of age-related deterioration that could be used more widely to measure biological age, with a focus on those that can be deployed outside of the standard laboratory setting and be used repeatedly in individuals to enable longitudinal studies. Whole organism frailty measures are currently little used by evolutionary ecologists and this chapter describes how these could be used more extensively. Telomere attrition and mitochondrial function are highly conserved processes and have been studied in an increasingly wide range of taxa in recent years. The chapter also discusses other markers, including those related to immune function, oxidative damage, inflammation and DNA methylation. Great progress is currently being made in the use of epigenetic alterations to provide information on chronological and biological age in a range of (predominantly) vertebrate taxa. The chapter outlines how this integrative approach could be developed further and highlight future directions
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
Cancer et sénescence : une approche éco-évolutive multi-échelle
No full textSelon les théories dominantes de l'oncogenèse, le cancer résulte d'un processus d'accumulation d'altérations (épi)génétiques transmises le long de lignages cellulaires somatiques. Si des observations moléculaires empiriques valident partiellement ces modèles multistades, ceux-ci ne permettent pas de prédire les patrons d'incidence du cancer i) aux grands âges et ii) entre les espèces (Paradoxe de Peto). En effet, ces modèles prédisent que l'incidence du cancer devrait être une fonction croissante de l'âge. Or, chez l'humain, le taux d'incidence du cancer décélère voire décroît aux grands âges. L'existence de ce patron dans d'autres espèces est à confirmer. Partant de cette observation, cette thèse étudie la relation évolutive entre le cancer et la sénescence : nous supposons qu'il existe, à l'échelle de l'organisme, un compromis évolutif entre ces composantes de la mortalité. Ce compromis serait arbitré par l'accumulation de cellules sénescentes dans les tissus. En effet, la sénescence cellulaire est largement considérée, en biologie cellulaire, comme un mécanisme de défense contre la cancérogenèse. Mais, la sénescence n'est pas la seule option pour une cellule mutée : l'apoptose, un programme de mort cellulaire, en est une autre. De plus, chaque destin cellulaire a un coût. L'accumulation de cellules sénescentes est liée aux maladies du vieillissement alors que l'apoptose induit une prolifération compensatoire qui pourrait, sur le long terme, augmenter l'accumulation de mutations dans les tissus. Ainsi, nous faisons l'hypothèse que le compromis évolutif à l'échelle de l'organisme serait le reflet d'un équilibre entre les coûts de ces mécanismes cellulaires. Cette thèse explore donc le rôle de la sénescence cellulaire dans la sénescence de l'organisme et la cancérogenèse : 1) À l'échelle de l'organisme, nous cherchons si une probabilité optimale d'entrer en sénescence pour une cellule endommagée permet à l'individu de maximiser sa survie et sa reproduction. Pour ce faire, nous utilisons un modèle théorique partant des dynamiques cellulaires pour ensuite se tourner vers leurs conséquences pour l'organisme : la sénescence de l'organisme et la mortalité par cancer. De plus, nous examinons l'influence de différents traits d'histoire de vie sur cet équilibre. 2) À l'échelle cellulaire, des modèles individus-centrés sont utilisés pour explorer différents aspects de l'accumulation de mutations dans les tissus. Premièrement, les mutations sont transmises d'une cellule mère à une cellule fille, posant ainsi la question du rôle de la structuration spatiale en lignages somatiques. Deuxièmement, l'apoptose entraîne une prolifération compensatoire mais son coût est hypothétique. Nous testons donc si cette prolifération joue un rôle substantiel dans l'accumulation de mutations. Enfin, les cellules sénescentes sont caractérisées par un sécrétome (le SASP) dont les effets paracrines sont associés à la cancérogenèse et aux pathologies de la sénescence. Nous évaluons donc comment l'équilibre entre sénescence cellulaire et apoptose est modifié par le SASP. 3) À l'échelle des espèces, des données empiriques provenant d'espèces mammifères en captivité sont utilisées pour répondre à deux questions. D'une part, tester si la décélération du taux d'incidence est observable dans d'autres espèces. D'autre part, en distinguant la mortalité par cancer de la mortalité due à d'autres causes intrinsèques, nous comparons les patrons d'incidence empiriques aux attendus découlant de l'hypothèse du compromis évolutif. En conclusion, notre travail lie des connaissances en biologie cellulaire avec des concepts de la biologie évolutive afin de mieux comprendre la relation entre sénescence et cancérogenèse. Nous montrons que le cancer n'est peut-être pas qu'un processus sénescent et qu'il est important de considérer l'hypothèse que l'évolution de la sénescence a été (au moins partiellement) façonnée par le cancer.Dominant theories of oncogenesis state that cancer is a multistage process fueled by the accumulation of (epi)genetic alterations along somatic lineages of mitotically active cells. While this model finds some empirical support at the molecular level, it fails to accurately predict cancer incidence patterns i) at old ages and ii) between species. Indeed, the Doll-Armitage and further models predict that cancer incidence should be an increasing function of age. However, in Humans, cancer incidence rate has been shown to decelerate and even decrease at old ages. Evidence in other species is mostly lacking. Starting from this puzzling observation, the PhD work investigates the evolutionary relationship between cancer and senescence: we hypothesize that there is, at the organism scale, an evolutionary tradeoff between those mortality components. This trade-off between cancer and senescence would be mediated at the cellular scale by the accumulation of senescent cells. Indeed, mutated cells can turn senescent, a mechanism widely thought of as a defense against carcinogenesis in cellular biology. Still, at the cellular scale, senescence is not the only path a damaged cell can take: apoptosis, a cell death program, is another option. In our framework, both cellular senescence and apoptosis come at a cost. Accumulated senescent cells lead to ageing-related disorders and it is hypothesized that apoptosis leads to compensatory proliferation that could, in return, lead to even more damage accumulation. Hence, the organismal trade-off could also result from a cellular trade-off: senescence and apoptosis should be balanced to lessen their respective costs. Therefore, this thesis explores the role of cellular senescence in both organismal senescence and carcinogenesis at different scales: i) At the organism scale, we investigate whether the probability for a damaged cell to enter senescence can reach an optimum allowing to maximize the lifetime reproductive success of an individual. We do this by modeling theoretical cellular dynamics and their consequences at the organism scale : cellular senescence is associated with organismal senescence and apoptosis with cancer mortality. Additionally, we look at how different life-history traits influence this balance. ii) At the cellular scale, we investigate different aspects of mutation accumulation within tissues using agent-based models. First, damaged cells transmit their mutational burden to their daughters. Therefore, we first address whether spatial structuring in lineages influences damage accumulation. Second, apoptosis does lead to compensatory proliferation but its cost is hypothetical. Thus, we assess whether compensatory divisions can significantly increase damage accumulation. Third, senescent cells display a specific secretome (the SASP) that has auto- and paracrine effects thought to be associated with both ageing-related disorders and carcinogenesis. Hence, we determine how a mechanistic balance between cellular senescence and apoptosis is changed under the influence of the SASP. iii) At the species scale, we use empirical data from mammal species in captivity to answer two questions. First, we assess whether other species display the same pattern of late-life deceleration of cancer. Second, discriminating between cancer mortality and mortality from other intrinsic causes, we test whether empirical incidence patterns are congruent with expectations derived from the hypothesis that senescence trades against cancer. In conclusion, this PhD work bridges knowledge from cellular biology and evolutionary biology in order to better understand the relationship between senescence and carcinogenesis. It shows that cancer might not only be only a proximal senescent process, but that senescence evolution might be (partially) shaped by cancer mortality
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
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