Browsing by Author "Wu, Xi"
Now showing 1 - 3 of 3
Results Per Page
Sort Options
Item Adverse Selection and Advantageous Selection in Insurance Markets(2014-08-08) Wu, XiThis dissertation consists of three essays about adverse selection and advantageous selection in life insurance and health insurance markets. Firstly, I confirm the advantageous selection in voluntary private health insurance markets in Europe and detect the sources of such advantageous selection by using data from Survey of Health, Ageing and Retirement in Europe (SHARE). Specifically, I find, on the extensive margin, individuals with symptom are less likely to own VPHI than those without any symptom; on the intensive margin, the more the number of symptoms the individual has, the less likely she has VPHI. Same conclusion can be obtained when using a subjective measure of health. The sources of this advantageous selection include asset, education, longevity expectations, as well as cognitive ability. Conditional on these factors, individuals whose health is worse are more likely to purchase VPHI. Secondly, I identify the adverse selection problem in life insurance markets in the presence of both adverse and advantageous private information. Conventional theory for private information of adverse selection predicts a positive correlation between insurance coverage and ex post risk. However, Cawley and Philipson (1999) reported a neutral or even negative correlation between mortality risk and insurance coverage in the life insurance market. A recent growing literature has shown that such puzzle could be attributed to the multiple dimensions of private information coexisting in the market. Specifically, I provide evidence of the existence of private information both on mortality risk and on life insurance preferences. I show that these two dimensions of private information have an offsetting effect on the relationship between subsequent mortality and life insurance purchases, which makes the identification of the private information on mortality risk difficult under the traditional setting. Instead, I apply the mixture density model and successfully detect a positive correlation between individual mortality and insurance coverage. Moreover, I examine the mortality risk related to each of the two main types of life insurance contracts ? term and whole life insurance. Our two-period model shows that, given an individual, the relative income, rather than the risk, dominates the choice between whole and term life insurance policies, indicating that a systematic risk difference between these two pools should not be observed. Moreover, when the income of these two periods are the same, whole life insurance policies, the one with more capability of avoiding reclassification risk, would be always favored if the individual is risk averse. Empirical results support the conclusions made in the theoretical model. This paper also, empirically confirms the partial lock-in of consumers embodied in the more front-loading contract as proposed by Hendel and Lizzeri (2003). Specifically, I find as a more front-loaded contract, whole life insurance policy is associated with a lower lapsation rate and thus retains a healthier pool after 65 years old.Item Integrated 3D Acid Fracturing Model for Carbonate Reservoir Stimulation(2014-06-23) Wu, XiAcid fracturing is one of the stimulation methods used in carbonate formations and has been proved effective and economical. Because of the stochastic nature of acidizing in carbonate formation, designing and optimizing acid fracture treatment today still remain challenging. In the past, a simple acid fracture conductivity correlation was usually considered sufficient to estimate the overall average fracture conductivity in the formation, leading to the computation of the productivity index for fractured well performance. However, the nature of heterogeneity could not be included in the modeling. Understanding the important role of heterogeneity to stimulation performance becomes a crucial step in design and optimization of acid fracture jobs. In order to study the effect of this stochastic nature on acid fracturing, a fully 3D acid reaction model was developed based on the geostatistical parameters of the formation. It is possible to describe local conductivity distribution related to acid transport and reaction process. In this study, we have developed a new interactive workflow allowing the model of the fracture propagation process, the acid etching process and the well production interactively. This thesis presents the novel approach in integrating fracture propagation, acid transport and dissolution, and well performance models in a seamless fashion for acid fracturing design. In this new approach, the fracture geometry data of a hydraulic fracture is first obtained from commercial models of hydraulic fracture propagation, and then the 3D acid fracture model simulates acid etching and transport from the fracture propagation model using the width distribution as the initial condition. We then calculate the fracture conductivity distribution along the created fracture considering the geostatistical parameters such as permeability correlation length and standard deviation in permeability of the formation. The final step of the approach is to predict well performance after stimulation with a reservoir flow simulator. The significant improvements of the new approach are two folds: (1) capturing the geostatistical effect of the formation; and (2) modeling the acid etching and transport more accurately. The thesis explains the methodology and illustrates the application of the approach with examples. The results from this study show that the new model can successfully design and optimize acid fracturing treatments.Item Novel Insights into the Regulation of Autophagy in Saccharomyces Cerevisiae(2011-12-15) Wu, Xi; Tu, BenjaminAutophagy is an evolutionarily conserved pathway for the degradation of intracellular contents. How autophagy is regulated, especially upon changes in metabolic and nutritional state, remains poorly understood. In Saccharomyces cerevisiae, autophagy is normally triggered by nutrient starvation. However, by using a prototrophic strain, I discovered that autophagy can be strongly induced upon switch from a rich medium (YPL) to a minimal medium (SL) without nutrient starvation. This new autophagy-inducing condition was termed SL-induced autophagy. Growth measurement confirmed that SL-induced autophagy was important for cellular homeostasis and growth following medium switch. A genetic screen uncovered IML1, NPR2, NPR3 and PBP1, which are all required for SL-induced autophagy, but not for nitrogen-starvation-induced autophagy. Iml1p, Npr2p and Npr3p function in the same complex and regulate autophagosome formation. During SL-induced autophagy, Iml1p can localize to the pre-autophagosomal structures, consistent with the role of the Iml1p complex in autophagosome formation. Moreover, a conserved domain in Iml1p was identified to be required for SL-induced autophagy as well as complex formation. I discovered that sulfur containing amino acids, but not non-sulfur containing amino acids, can specifically inhibit SL-induced autophagy. I further demonstrated that cysteine is a key metabolite that inhibits SL-induced autophagy by regulating cellular processes related to cysteine metabolism. Cysteine does not suppress SL-induced autophagy by regulating oxidative stress, protein urmylation and thiolation of cytosolic tRNAs. Future studies will be required to reveal the exact mechanism through which cysteine inhibits SL-induced autophagy. I also discovered that autophagy can be significantly induced upon depletion of a Fe-S cluster containing protein, Rli1p, and other factors that are also involved in rRNA processing and translation initiation. Interestingly, IML1, NPR2, NPR3 and PBP1 are also important for Rli1p-depletion-induced mitophagy. These results strongly suggest the mechanistic link between SL-induced autophagy and ribosome biogenesis or translation regulation. Collectively, my studies have demonstrated the existence of additional mechanisms that regulate autophagy in response to relatively more subtle changes in metabolic and nutritional state.