Foreign aid donors increasingly demand that aid is used efficiently and effectively. This study examines the effect of corruption levels, measured by the Corruption Perceptions Index, within a recipient country on the levels of economic growth. A growing literature outlines the mechanisms through which corruption impedes economic growth and is summarized within. Additionally, as longevity gains may result from foreign aid but are not captured in economic growth, this study computes a variable called the Life Quality Indicator (LQI) that combines such gains with economic growth and examines corruption’s effect on LQI growth. As any windfall, foreign aid has been argued to exacerbate problems within corrupt countries—causing economic decline. This study develops an interaction of corruption levels and the ratio of aid receipts to GDP to examine the effects of this interaction on economic growth and LQI growth. Conducting a regression analysis shows the relationships between the interaction term and economic growth and the interaction term and LQI growth are negative, leading to policy recommendations that corrupt countries not receive foreign aid. Using game theory, this study predicts the outcomes of interactions between aid recipients and donors during the Cold War, post-Cold War, and in the present. The present predicted outcomes suggest that recipients will be the winners because they are able to choose between receiving aid from emerging donors and from the Development Assistant Committee (DAC). Policy guidance to the aid community includes understanding that emerging donors may exert influence on aid recipients and programs to monitor this influence ensuring that it does not become exploitation may be necessary. Finally, a case study of Russia is presented, highlighting its corruption and foreign aid receipts in the post-Soviet timeframe. A separate analysis is conducted on the Former Soviet Union (FSU) countries to determine whether Russia’s corruption and foreign aid receipts caused lower levels of economic and LQI growth than that experienced by other FSU countries. While results do not show this, the negative relationship between the interaction term and economic and LQI growth is also found in this subset.

This thesis aims at contributing to the study of the valuation of insurance liabilities and the management of the assets backing these liabilities. It consists of four parts, each devoted to a specific topic. In the first part, we study the pricing of a classical single premium life insurance contract with profit, in terms of a guaranteed rate on the premium and a participation rate on the (terminal) financial surplus. We argue that, given the asset allocation of the insurer, these technical parameters should be determined by taking explicitly into account the risk management policy of the insurance company, in terms of a risk measure such as the value-at-risk or the conditional value-at-risk. We then design a methodology that allows us to fix both parameters in such a way that the contract is fairly priced and simultaneously exhibits a risk consistent with the risk management policy. In the second part, we focus on the management of the surrender option embedded in most life insurance contracts. In Chapter 2, we argue that we should model the surrender time as a random time not adapted to the filtration generated by the financial assets prices, instead of assuming that the surrender time is an optimal stopping time as it is usual in the actuarial literature. We then study the valuation of insurance contracts with a surrender option in such a model. We here follow the financial literature on the default risk and in particular, the reduced-form models. In Chapter 3 and 4, we study the hedging strategies of such insurance contracts. In Chapter 3, we study their risk-minimizing strategies and in Chapter 4, we focus on their ``locally risk-minimizing' strategies. As a by-product, we study the impact of a progressive enlargement of filtration on the so-called ``minimal martingale measure'. The third part is devoted to the systematic mortality risk. Due to its systematic nature, this risk cannot be diversified through increasing the size of the portfolio. It is thus also important to study the hedging strategies an insurer should follow to mitigate its exposure to this risk. In Chapter 5, we study the risk-minimizing strategies for a life insurance contract when no mortality-linked financial assets are traded on the financial market. We here extend Dahl and Moller’s results and show that the risk-minimizing strategy of a life insurance contract is given by a weighted average of risk-minimizing strategies of purely financial claims, where the weights are given by the (stochastic) survival probabilities. In Chapter 6, we first study the application of the HJM methodology to the modelling of a longevity bonds market and describe a coherent theoretical setting in which we can properly define the longevity bond prices. Then, we study the risk-minimizing strategies for pure endowments and annuities portfolios when these longevity bonds are traded. Finally, the fourth part deals with the design of ALM strategies for a non-life insurance portfolio. In particular, this chapter aims at studying the risk-minimizing strategies for a non life insurance company when inflation risk and interest rate risk are taken into account. We derive the general form of these strategies when the cumulative payments of the insurer are described by an arbitrary increasing process adapted to the natural filtration of a general marked point process and when the inflation and the term structure of interest rates are simultaneously described by the HJM model of Jarrow and Yildirim. We then systematically apply this result to four specific models of insurance claims. We first study two ``collective' models. We then study two ``individual' models where the claims are notified at a random time and settled through time.

<p>Under det gångna århundradet ökade den förväntade livslängden avsevärt såväl i Sverige som i övriga världen. 1900-talets förbättrade livslängd drevs inledningsvis av en minskad barnadödlighet medan de senare årtiondena kännetecknades av minskad dödlighet i höga åldrar.</p><p>En åldrande befolkning innebär ökade krav på sjukvård, äldreomsorg och inte minst pensionssystem. Pålitliga prognoser för vår framtida livslängd behövs för att beräkna de resurser som nämnda verksamheter kommer att ta i anspråk och utgör förutsättningen för en rättvis prissättning av försäkringsprodukter med levnadsrisk.</p><p>Lee-Carter-modellen är en av vår tids tongivande modeller för mortalitetsprognostisering. Modellen används här för att göra livslängdsprognoser utifrån svenska mortalitetsdata; prognoserna jämförs sedan med observerade utfall.</p><p>Mot bakgrund av resultatet diskuteras levnadsrisk med fokus på pensioner.</p><p>Inte oväntat presterar prognoserna ingen felfri bild av verkligheten och prognosfelet varierar i storlek mellan skattningarna; att använda dem som underlag för pensionsberäkningar hade i förlängningen varit ohållbart. Exemplet illustrerar på samma gång vår osäkerhet inför framtidens livslängdsutveckling och svårigheten i att prognostisera den.</p> / <p>During the past century, Sweden along with many other countries experienced a sharp decline in mortality rates. The increased life expectancy was initially propelled by mortality reductions among infants and subsequently by a survival improvement in advanced ages.</p><p>An ageing population has large implications for those providing services to the elderly, such as medical care and pensions, whilst also addressing the need for accurate and reliable mortality forecasts and projection methods.</p><p>The Lee-Carter model is the current gold standard for mortality forecasting and has been widely adopted in several studies. Here, the model is applied on Swedish mortality data; the projections are then compared to the observed lifespan development. Against this backdrop, a discussion on longevity risk in pensions schemes follows.</p><p>The forecasts performed in this study do not perfectly reflect the observed mortality change in the examined period; furthermore, the variation of the estimation errors limits the actuarial value of the projections. The findings illuminate the uncertainty that surrounds our future life expectancy as well as the difficulties associated with forecasting it.</p>

A series of laboratory accelerated immersion tests are used to examine the effects of different chemicals found in municipal solid waste leachate, geomembrane thickness, and incubation temperatures on the degradation of different high density polyethylene geomembranes. It was found that surfactant was the key leachate constituent affecting antioxidant depletion while salts accelerated degradation of the mechanical properties, especially stress crack resistance. Immersed in synthetic leachate, the time to nominal failure at 35oC was predicted to be 62% longer for the 2.5 mm, and 12% longer for the 2.0 mm, than for the 1.5 mm geomembrane tested. The antioxidant depletion in synthetic leachate and air at temperatures > 85oC was consistent with what would be expected from Arrhenius modeling based on data from lower temperatures (≤ 85oC). However, the early depletion rates in water incubation decreased with the increase of the temperature above 100oC. It was also found that at temperatures above 100oC, there was significant change in the polymer morphology that affected the stress crack resistance at early incubation times prior to polymer degradation. Large-scale geosynthetic liner longevity simulators (GLLSs) which simulated field conditions were used to investigate the susceptibility of pre-aged high density polyethylene geomembranes to stress cracking and to evaluate the performance of geomembranes under a 150 mm sand protection layer. A pre-aged geomembrane with a 560 g/m2 geotextile protection layer experienced brittle rupture at local gravel indentations. The time to failure was correlated to the incubation temperatures. The use of a sand protection layer not only delayed antioxidant depletion compared to that with a traditional geotextile protection but also substantially reduced the long-term tensile strains in the geomembrane below the allowable strain limits. / Thesis (Ph.D, Civil Engineering) -- Queen's University, 2013-11-26 12:36:01.538

This qualitative phenomenological dissertation explored The Departmental Work Lives of Full-Time Non-Tenure Track Faculty (FTNTT) at two public four-year universities located in the Southeastern region of the United States. This study is based on interviews with twelve (FTNTT) faculty members representing departments traditionally associated within the College of Arts and Sciences. This study found FTNTT faculty participants highly credentialed and reasonably satisfied in their positions. This study adds the descriptor heterogeneous to FTNTT faculty members’ job roles, work environments, daily engagements, and work experiences and contradicts existing literature that finds FTNTT faculty positions to be resource deficit and administratively non-supporting. Literature surrounding FTNTT faculty, Agency Theory, and the concepts of Agency of Perspective, Agency of Action, and Action of Avoidance informed this study. This study extended Agency of Action to include intentional, strategic behaviors of inaction (coined within this study as Action of Avoidance) toward the departmental contexts of policies and practices concerning discipline, employability, employment longevity, and personal FTNTT faculty career trajectories. Agency Theory, Agency of Perspective, Agency of Action, and Action of Avoidance, as identified by the researcher, emerged as strong frameworks used by FTNTT faculty to construct behaviors to successfully navigate long-term careers under short-term conditions. Based on FTNTT faculty responses, this study outlines policies and practices that are perceived as supportive or non-supportive. Policymakers may use this data to inform strategies for improving support among FTNTT faculty members.

La première augmentation de la longévité en laboratoire fût observée à la suite d’une intervention nutritionnelle consistant en une réduction de l’apport alimentaire chez le rat. Plus tard, ce phénomène a été reproduit dans de très nombreuses espèces et référé en tant que restriction calorique. Le développement des techniques de biologie moléculaire moderne a permis de montrer dans des organismes modèles simples que cette flexibilité du processus de vieillissement était régulée par des facteurs génétiques. De fait, plusieurs mécanismes cellulaires ont alors pu être identifiés comme responsables de ce contrôle du vieillissement. Ces voies de régulation ont révélées être conservées entre les espèces, depuis les levures jusqu’aux organismes multicellulaires tels que le nématode, la mouche ou la souris, suggérant l’existence d’un programme universel de vieillissement dans le vivant. La levure s’est avéré à plusieurs reprises être un modèle puissant et fiable pour la découverte de gènes impliqués dans ce phénomène. Mon étude a consisté au développement d’un nouveau modèle unicellulaire d’étude du vieillissement à travers l’espèce Schizosaccharomyces pombe appelée aussi levure à fission. La première étape de mon travail a montré que les voies de détection des nutriments gouvernées par la sérine/thréonine protéine kinase A (Pka1) et la sérine/thréonine kinase Sck2 contrôlent le vieillissement chronologique de ces cellules comme il était connu dans la levure Saccharomyces cerevisiae. Ceci permit de valider l’utilisation de la levure à fission pour l’étude du vieillissement. Ensuite, nous avons analysé plus en détail l’effet pro-vieillissement du glucose en étudiant le rôle de sa détection par le récepteur membranaire Git3 couplé à la protéine G (Gpa2) en amont de la kinase Pka1. La perte du signal du glucose par la délétion de Git3 imite partiellement l’effet d’augmentation de longévité obtenu par baisse de la concentration en glucose dans le milieu. De plus, l’effet néfaste du signal du glucose est maintenu en absence de tout métabolisme du glucose suite à la mutation des hexokinases, premières enzymes de la glycolyse. L’ensemble de ces résultats suggèrent que la signalisation du glucose est prédominante sur son métabolisme pour son effet pro-vieillissement. D’autre part, à la fois la suppression de cette signalisation et la baisse de niveau de glucose disponible allongent la durée de vie en corrélation avec une augmentation de la résistance au stress, une hausse d’activité mitochondriale et une baisse de production de radicaux libres. Finalement, le criblage d’une banque de surexpression d’ADNc a permis d’identifier plusieurs gènes candidats responsables de ces effets en aval de la voie de signalisation Git3/PKA. La recherche sur les mécanismes moléculaires du vieillissement propose une nouvelle approche, un nouvel angle de vue, pour la compréhension des fonctions cellulaires et promet d’apporter de précieuses clefs pour mieux comprendre certaines maladies. En effet, le vieillissement est la première cause d’apparition de nombreuses affections comme les cancers, les maladies cardiovasculaires et métaboliques ou les maladies neurodégénératives tels que les syndromes d’Alzheimer et de Parkinson. / The first increase in life span due to man’s intervention was obtained with rats subjected to a diet reduced in calorie intake. Later, this phenomenon was repeated with many other species and referred as diet restriction or calorie restriction. The development of modern Molecular Biology approaches and the use of simple model organisms demonstrated that the rate of aging was regulated by genetic traits. Indeed, several cellular mechanisms were identified as responsible for the control of aging. These regulatory pathways appear to be conserved throughout species, from yeast to multicellular organisms like nematode, fly and mice, thus suggesting the existence of a universal program of aging. Yeast proved several times to be a powerful and reliable model for discovering genes involved in the regulation of aging. My study consisted in developing Schizosaccharomyces pombe (also called fission yeast) as a new unicellular model to study aging. The first step of my work was to show that pathways of nutrient detection through kinases involving Pka1 and Sck2 control chronological aging in S. pombe, as it was previously demonstrated in Saccharomyces cerevisiae. This first work validated the use of fission yeast for the study of aging. Subsequently, we analysed in more detail the pro-aging effect of glucose focusing on the role of its signalling through the G-protein Gpa2-coupled membrane receptor Git3, which acts upstream of Pka1. The loss of the glucose signal due to deletion of Git3 mimics partially the effect of increasing longevity by reducing glucose in the medium. Moreover, detrimental effects of glucose signal are maintained in absence of sugar metabolism following loss of hexokinases, the first enzymes of glycolysis. Together, these results suggest that the pro-aging effects of glucose signalling are predominant over those due to metabolism of this sugar. Moreover, both obliteration of this signalling pathway and decrease of glucose availability extend life span, and correlate with an increase in stress resistance, in mitochondrial activity and a lower production of free radicals. Finally, screening a cDNA-overexpression library allowed us to identify several genes candidates responsible for the effects on longevity downstream of Git3/Pka1. Research in the molecular mechanisms of aging propose holds the promise to bring precious clues as to this mysterious processes affecting all living creatures, and paves the way to unravel the underlying causes of many human diseases. Indeed, aging is the first cause of numerous late-onset pathologies including cancers, cardiovascular diseases or neurodegenerative diseases like Alzheimer and Parkinson syndromes.

Ce mémoire présente, dans une première partie, une étude détaillée de la mortalité adulte des Canadiens-français nés entre 1620 et 1749. Des résultats inédits sont présentés sous forme de tables de mortalité abrégées avec entrées échelonnées. La comparaison de celles-ci permet de décrire les différences de comportement observées entre les hommes et les femmes, les populations de régions urbaines et rurales ainsi que trois groupes de générations s’étant succédé au cours de la période étudiée. Dans une deuxième partie, une étude de cas visant à confirmer l’influence du caractère familial sur la longévité est présentée. Une famille se distinguant par les durées de vie exceptionnellement longues de plusieurs de ses membres est comparée à une famille fictive de référence, représentative de la population moyenne de l’époque. Les résultats opposant ces deux familles consistent en des âges moyens au décès et des proportions de survivants à différents âges. Cette deuxième étude s’inscrit dans le prolongement des recherches effectuées avec les ascendances de Jeanne Calment et Marie-Louise Meilleur. Les informations tirées des registres paroissiaux du Québec ancien et consolidées informatiquement par le Programme de recherche en démographie historique (PRDH) dans une base de données appelée Registre de la population du Québec ancien (RPQA) constituent la source exploitée pour la réalisation des deux parties du mémoire. / This thesis presents, in the first part, a detailed study of adult mortality of French-Canadians born between 1620 and 1749. New time published results are presented in the form of abridged life tables with staggered entries. The life tables are compared to ascertain behavioural differences between men and women, between residents of urban and rural regions and across three generations during the period studied. In the second part, the thesis presents a case study conducted to test the influence of inheritance on human longevity. A family distinguished by the exceptional longevity of several of its members is compared to a reference fictional family representative of the average population of the time. Evidence provided on these two families consists of mean ages at death and proportions of survivors at different ages. This case study builds on research conducted with the ancestry of Jeanne Calment and Marie Louise Meilleur. Information drawn from the parish registers of old Quebec computerized by the Programme de recherche en démographie historique (PRDH) in a database called Registre de la population du Québec ancien (RPQA) is the primary source used for the life tables and case study.

L’ubiquitin-fold modifier (UFM1) fait partie de la classe 1 de la famille de protéine ubiquitin-like (Ubl). UFM1 et Ub ont très peu d’homologie de séquence, mais partagent des similarités remarquables au niveau de leur structure tertiaire. Tout comme l’Ub et la majorité des autres Ubls, UFM1 se lie de façon covalente à ses substrats par l’intermédiaire d’une cascade enzymatique. Il est de plus en plus fréquemment rapporté que les protéines Ubls sont impliquées dans des maladies humaines. Le gène Ufm1 est surexprimé chez des souris de type MCP développant une ischémie myocardique et dans les îlots de Langerhans de patients atteints du diabète de type 2. UFM1 et ses enzymes spécifiques, UBA5, UFL1 et UFC1, sont conservés chez les métazoaires et les plantes suggérant un rôle important pour les organismes multicellulaires. Le Caenorhabditis elegans est le modèle animal le plus simple utilisé en biologie. Sa morphologie, ses phénotypes visibles et ses lignées cellulaires ont été décrits de façon détaillée. De plus, son cycle de vie court permet de rapidement observer les effets de certains gènes sur la longévité. Ce modèle nous permet de facilement manipuler l’expression du gène Ufm1 et de mieux connaître ses fonctions. En diminuant l’expression du gène ufm-1 chez le C.elegans, par la technique de l’ARN interférence par alimentation, nous n’avons observé aucun problème morphologique grave. Les vers ressemblaient aux vers sauvages et possédaient un nombre de progéniture normal. Cependant, les vers sauvage exposés à l’ARNi d’ufm-1 vivent significativement moins longtemps que les contrôles et ce, de façon indépendante de la voie de signalisation de l’insuline/IGF. Chez le C. elegans la longévité et la résistance au stress cellulaire sont intimement liées. Nous n’avons remarqué aucun effet d’ufm-1 sur le stress thermal, osmotique ou oxydatif, mais il est requis pour la protection contre le stress protéotoxique. Il est également nécessaire au maintien de l’intégrité neuronale au cours du vieillissement des animaux. L’ensemble de nos données nous renseigne sur les fonctions putatives du gène Ufm1. / The ubiquitin-fold modifier (UFM1) is part of the type 1 class of the family of ubiquitin-like protein (Ubl). UFM1 and Ub have very little sequence homology but share remarkable similarities in their tertiary structure. Like Ub and most other UBLS, UFM1 binds covalently to its substrates through an enzymatic cascade. It is frequently reported that UBLs are involved in human diseases. UFM-1 is overexpressed in mice developing a myocardial ischemia and in the islets of patients suffering from type 2 diabetes. UFM1 and its specific enzymes, UBA5, UFL1, and UFC1 are conserved in metazoans and plants suggesting an important role in multicellular organisms. Caenorhabditis elegans is one of the the simplest animal models used in biology. Some features such as morphology, visible phenotypes and cell lineage have completely been described. The short lifecycle of C. elegans makes it easy to observe gene effects on longevity. This model allows us to easily manipulate the expression of the Ufm1 gene and learn more about its putative functions. To study putative functions of Ufm1, we decreased the expression of ufm-1 using RNA interference introduces through feeding. No gross morphological disturbances were observed; worms resembled wild type and had a normal brood size. However, worms exposed to ufm-1 RNAi had a significantly shorter lifespan than the controls. This effect is independent of the insulin/IGF pathway, which is a major axis of longevity genetics. In C. elegans longevity and cellular stress resistance are intimately linked. We have observed no effect of ufm-1 on thermal, osmotic or oxidative stress, but it is required for protection against proteotoxic stress. It is also necessary to maintain neuronal integrity during aging. Together, our results shed light on putative functions of Ufm1 gene.

Le présent mémoire s’inscrit dans un projet, financé par le CRSH, visant l’étude des conditions de vie dans l’enfance et la survie aux grands âges L’augmentation de la longévité et de la mortalité observée dans les pays industrialisés depuis plus d’un siècle ont mené à l’émergence d’un courant de recherche visant à identifier les causes de ces progrès. Il a été soulevé que les conditions de vie dans l’enfance pourraient y jouer un rôle. L’objectif de ce mémoire est donc de mettre en lumière les déterminants qui sont en cause en étudiant la mortalité au-delà de 40 ans d’une population urbaine canadienne-française en phase d’industrialisation, soit, celle de la ville de Québec au début du 20ème siècle. Plus spécifiquement, une analyse descriptive de la population étudiée sera effectuée et suivra une analyse statistique à l’aide de modèles de risques proportionnels de Cox qui prendront en compte différentes facettes des conditions de vie. Au coeur de ce mémoire a été l’élaboration d’une base de données se basant sur le Canadian Families Project et créée à partir du recensement canadien de 1901. Cette dernière nous a permis de dresser un portrait des conditions de vie dans l’enfance, telles qu’elles étaient au tournant du 20ème siècle, de la population étudiée. Nous avons complété cette base de données en recueillant des informations sur les mariages à l’aide des fichiers de du projet BALSAC ainsi que les âges au décès des individus de l’échantillon en consultant les fiches de l’État civil. Nous avons pu mettre en lumière que les individus ayant passé leur enfance dans un ménage de type complexe affichent une mortalité moins élevée (de près de 35%) que pour les structures familiales simples. De plus, les individus qui ont grandi dans un ménage dont le chef était bilingue ou occupait un emploi qualifié ont des risques de mortalité inférieurs de près du tiers par rapport aux autres. Nous avons aussi trouvé que les résidents de la Basse-Ville courraient un risque de mortalité jusqu’à 50% plus élevé que celui de ceux provenant d’autres districts de la ville. / This thesis is part of a project, financed by the CRSH, aiming at the study of early-life conditions and survival later in life. The increase in longevity in industrialized countries over the last century has lead to emergence of a research trend seeking to identify the causes of this progress. It has been remarked that the life conditions during childhood may have played a role in this progress. The goal of this thesis is to put forward the determining factors that are in cause by studying the mortality beyond the age of 40 of the population of a French Canadian city going through an industrialization phase, i.e. Quebec City at the beginning of the twentieth century. More specifically, a descriptive analysis of the population studied will be done and will follow a statistical analysis with the help of Cox proportional hazard models that will take the different aspects of life conditions into account. At the heart of this thesis is the elaboration of a database based on the Canadian Families Project, created from the 1901 Canadian census. The latter has allowed us to draw a portrait of the living conditions during childhood of the studied population, as they were at the turn of the 20th century. We collected information from the BALSAC project files for weddings and from files of the civil status for the age at death of sampled individuals to complement the database. We were able to see that individuals who spent their childhood within a complex type of household had lower risk of mortality (nearly 35% lower) than those who grew up in simple family structures. Moreover, children who lived in a household whose head was bilingual or skilled have mortality risk reduced by almost a third. We also found that residents of the Basse-Ville have higher risk, up to 50%, than residents from other districts of the city.

No description available.