As forests change, tree physiology responds to changes in resource demands. The impact of Pinus taeda (loblolly pine) mortality on physiology of successional hardwoods is unknown. Liquidambar syraciflua (sweetgum) and loblolly pine individuals were measured for resource-use during a simulated southern pine beetle mortality event where several pines underwent a girdling treatment. Sweetgum next to untreated pines had significantly higher sapflow every month, markedly throughout post-mortality months. Sapflow and photosynthetic capacity significantly declined in girdled pines before needle discoloration. Nitrogen concentration of senesced pine and sweetgum leaves significantly increased from pre-mortality to post-mortality. Pine mortality led to increases in sweetgum water use and leaf nitrogen content. A shift in species dominance from loblolly pine to sweetgum would reduce water lost by pine transpiration during sweetgum dormancy by approximately 154 mm. These data indicate significant responses to disturbance and seasonal resource demands in this forest type.

No description available.

An increasing trend in mass mortality events (MMEs) has been observed in recent years, leading to an increased study of these events and their causes. Still to be investigated are the immediate and long-term effects of these environmental disturbances. Microbial communities found on and within the carcass are a major contributor to decomposition. With an increased biomass from several carcasses, transfer of these microbes to secondary death events may be affected. For this project, several simulated MMEs were used in conjunction with a secondary death event to observe the effects of transfer between the microbial communities and changes in the communities over time. It was found that microbial diversity decreases over time as decomposition progresses, and that an initial difference which can be observed between skin and internal microbial communities homogenizes over time. This result will contribute to an understanding of microbial succession and the impact of increasing MMEs.

Cathepsin S is a protease important in major histocompatibility complex (MHC) class II antigen presentation and also in degrading the extracellular matrix. Studies, most of them experimental, have shown that cathepsin S is involved in different pathological conditions such as obesity, inflammation, atherosclerosis, diabetes, and cancer.    The overall hypothesis of this report is that high levels of circulating cathepsin S, is a biomarker that reflects pathology induced by inflammation and obesity. The overall aim of this report was to investigate possible associations between circulating cathepsin S, inflammation, glucometabolic disturbance, and its associated diseases in the community. As cathepsin S appears to be a novel risk marker for several pathological conditions, we also wanted to examine the effect of dietary intervention on circulating cathepsin S concentrations.    This thesis is based on data from three community-based cohorts, the Uppsala longitudinal study of adult men (ULSAM), the prospective investigation of the vasculature in Uppsala seniors (PIVUS), and a post-hoc study from the randomized controlled NORDIET trial.    In the first study, we identified a cross-sectional positive association between serum cathepsin S and two markers of cytokine-mediated inflammation, CRP and IL-6. These associations were similar in non-obese individuals. In longitudinal analyses, higher cathepsin S at baseline was associated with higher CRP and IL-6 levels after six years of follow-up. In the second study, we identified a cross-sectional association between increased serum levels of cathepsin S and reduced insulin sensitivity. These associations were similar in non-obese individuals. No significant association was observed between cathepsin S and insulin secretion. In longitudinal analysis, higher cathepsin S levels were associated with an increased risk of developing diabetes during the six-year follow-up. In the third study, we found that higher serum levels of cathepsin S were associated with increased mortality risk. Moreover, in the ULSAM cohort, serum cathepsin S was independently associated with cause-specific mortality from cardiovascular disease and cancer. In the fourth study, we identified that adherence to an ad libitum healthy Nordic diet for 6 weeks slightly decreased the levels of plasma cathepsin S in normal or marginally overweight individuals, relative to the control group. Changes in circulating cathepsin S concentrations were correlated with changes in body weight, LDL-C, and total cholesterol.    Conclusion: This thesis shows that circulating cathepsin S is a biomarker that independently reflects inflammation, insulin resistance, the risk of developing diabetes, and mortality risk. Furthermore, a Nordic diet moderately reduced cathepsin S levels in normal-weight and overweight men and women. This effect may be partially mediated by diet-induced weight loss and possibly by reduced LDL-C concentrations.

The study of the relationship between socioeconomic characteristics and mortality patterns has been a traditional research focus in demography, representing one of the core areas of the discipline. In Latin America, there is an important set of studies that show a significant inverse relationship between socioeconomic status and mortality rates. However, mainly due to limitations in the available data, we know very little about the specific relation between educational attainment and adult mortality. This inverse relationship between educational attainment and mortality rates provides just the tip of the iceberg for a large set of questions: How wide are educational differences in overall adult mortality in Argentina? Does the association between educational attainment and adult mortality vary by age group, gender and region? Are there unique adult mortality patterns by education among specific causes of death? Has the adult mortality differential by education attainment widened or narrowed as education attainment increased between 1991 and 2010? The main objective of this research was to describe and analyze the relationship between educational attainment and adult mortality patterns during the 1991-2010 period in Argentina. The data used in this study come from the Argentinian Mortality Files for the period 1991-2010 and from the 1991, 2001 and 2010 Argentinian Censuses. Results show a clear gradient in the specific mortality rates according to educational groups, for both sexes and for all age groups. The existence and direction of this relationship was as expected; however, the magnitude of educational differences was much higher than what has been found in other countries. The data also exhibited a clear declining trend in mortality inequalities by education as age increased. Educational differences in overall adult mortality did not display an increasing pattern over time. The year 2001, which was characterized by serious economic and social crisis in the country, displayed the highest educational inequalities in mortality in comparison to either 1991 or 2010. The findings of this dissertation are relevant to policy questions about health care and social inequalities in death. / text

In conclusion, SED is a predictor of stroke mortality. Both childhood and adulthood SED were related to the risk of stroke. Stroke mortality increased with improving SED at a lower stage of development, while it decreased with SED improvement at a higher stage of development. The analysis was conducted among middle- or high-income countries/regions as data only available there. Investigation for low-income countries is warranted as data become available. / Keywords. Socioeconomic development; stroke; mortality / Socioeconomic development (SED) relates to the prevalence of risk factors of stroke and influence health policy. We aim to explore the association of (SED) in childhood and adulthood with stroke mortality among countries/regions, and to examine its impact on time trend of stroke mortality. / The ecological study used data on stroke mortality in five-year age group among countries/regions with death registry covering > 70% population provided by the World Health Organization. SED was measured by Human Development Index (HDI), a composite indicator with longevity, education and standard of living, obtained from the United Nations. Mortality rates (1950-2003) were averaged over three years and in logarithmical scale. HDI from 1960 to 2003 were available for this analysis. The effect of HDI on stroke mortality was analyzed and the major confounders, such as prevalence of hypertension, smoking, diabetes, obesity, and the level of dietary fat and alcohol consumption were adjusted for using regression model. / The results revealed that stroke mortality was inversely associated with HDI in childhood and adulthood respectively. Childhood HDI explained 36% of variance of stroke mortality among countries/regions in men and 35% in women; while adulthood HDI interpreted 34% in men and 52% in women (P < 0.01); annual change of stroke mortality was inversely associated with that of HDI. The peak of stroke mortality was exhibited at HDI = 0.79-0.83 for men and 0.80-0.83 for women. Stroke mortality increased with HDI where HDI < 0.79 for men and 0.80 for women, while it decreased with HDI improvement where HDI > 0.83 for men and women. Controlling for confounders did not materially change the results. / Wu, Shenghui. / Adviser: Xin-Hua Zhang. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3468. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 189-218). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

My doctoral thesis “Essays on Lifetime Uncertainty: Models, Applications, and Economic Implications” addresses economic and mathematical aspects pertaining to uncertainties in human lifetimes. More precisely, I commence my research related to life insurance markets in a methodological direction by considering the question of how to forecast aggregate human mortality when risks in the resulting projections is important. I then rely on the developed method to study relevant applied actuarial problems. In a second strand of research, I consider the uncertainty in individual lifetimes and its influence on secondary life insurance market transactions. Longevity risk is becoming increasingly crucial to recognize, model, and monitor for life insurers, pension plans, annuity providers, as well as governments and individuals. One key aspect to managing this risk is correctly forecasting future mortality improvements, and this topic has attracted much attention from academics as well as from practitioners. However, in the existing literature, little attention has been paid to accurately modeling the uncertainties associated with the obtained forecasts, albeit having appropriate estimates for the risk in mortality projections, i.e. identifying the transiency of different random sources affecting the projections, is important for many applications. My first essay “Coherent Modeling of the Risk in Mortality Projections: A Semi-Parametric Approach” deals with stochastically forecasting mortality. In contrast to previous approaches, I present the first data-driven method that focuses attention on uncertainties in mortality projections rather than uncertainties in realized mortality rates. Specifically, I analyze time series of mortality forecasts generated from arbitrary but fixed forecasting methodologies and historic mortality data sets. Building on the financial literature on term structure modeling, I adopt a semi-parametric representation that encompasses all models with transitions parameterized by a Normal distributed random vector to identify and estimate suitable specifications. I find that one to two random factors appear sufficient to capture most of the variation within all of our data sets. Moreover, I observe similar systematic shapes for their volatility components, despite stemming from different forecasting methods and/or different mortality data sets. I further propose and estimate a model variant that guarantees a non-negative process of the spot force of mortality. Hence, the resulting forward mortality factor models present parsimonious and tractable alternatives to the popular methods in situations where the appraisal of risks within medium or long-term mortality projections plays a dominant role. Relying on a simple version of the derived forward mortality factor models, I take a closer look at their applications in the actuarial context in the second essay “Applications of Forward Mortality Factor Models in Life Insurance Practice. In the first application, I derive the Economic Capital for a stylized UK life insurance company offering traditional product lines. My numerical results illustrate that (systematic) mortality risk plays an important role for a life insurer's solvency. In the second application, I discuss the valuation of different common mortality-contingent embedded options within life insurance contracts. Specifically, I present a closed-form valuation formula for Guaranteed Annuity Options within traditional endowment policies, and I demonstrate how to derive the fair option fee for a Guaranteed Minimum Income Benefit within a Variable Annuity Contract based on Monte Carlo simulations. Overall my results exhibit the advantages of forward mortality factor models in terms of their simplicity and compatibility with classical life contingencies theory. The second major part of my doctoral thesis concerns the so-called life settlement market, i.e. the secondary market for life insurance policies. Evolving from so-called “viatical settlements” popular in the late 1980s that targeted severely ill life insurance policyholders, life settlements generally involve senior insureds with below average life expectancies. Within such a transaction, both the liability of future contingent premiums and the benefits of a life insurance contract are transferred from the policyholder to a life settlement company, which may further securitize a bundle of these contracts in the capital market. One interesting and puzzling observation is that although life settlements are advertised as a high-return investment with a low “Beta”, the actual market systematically underperformed relative to expectations. While the common explanation in the literature for this gap between anticipated and realized returns falls on the allegedly meager quality of the underlying life expectancy estimates, my third essay “Coherent Pricing of Life Settlements under Asymmetric Information” proposes a different viewpoint: The discrepancy may be explained by adverse selection. Specifically, by assuming information with respect to policyholders’ health states is asymmetric, my model shows that a discrepancy naturally arises in a competitive market when the decision to settle is taken into account for pricing the life settlement transaction, since the life settlement company needs to shift its pricing schedule in order to balance expected profits. I derive practically applicable pricing formulas that account for the policyholder’s decision to settle, and my numerical results reconfirm that---depending on the parameter choices---the impact of asymmetric information on pricing may be considerable. Hence, my results reveal a new angle on the financial analysis of life settlements due to asymmetric information. Hence, all in all, my thesis includes two distinct research strands that both analyze certain economic risks associated with the uncertainty of individuals’ lifetimes---the first at the aggregate level and the second at the individual level. My work contributes to the literature by providing both new insights about how to incorporate lifetime uncertainty into economic models, and new insights about what repercussions---that are in part rather unexpected---this risk factor may have.

Not available / text

No abstract available. / Thesis (M.P.H.)-University of KwaZulu-Natal, Durban, 2006.

Cathepsin S is a protease important in major histocompatibility complex (MHC) class II antigen presentation and also in degrading the extracellular matrix. Studies, most of them experimental, have shown that cathepsin S is involved in different pathological conditions such as obesity, inflammation, atherosclerosis, diabetes, and cancer. The overall hypothesis of this report is that high levels of circulating cathepsin S, is a biomarker that reflects pathology induced by inflammation and obesity. The overall aim of this report was to investigate possible associations between circulating cathepsin S, inflammation, glucometabolic disturbance, and its associated diseases in the community. As cathepsin S appears to be a novel risk marker for several pathological conditions, we also wanted to examine the effect of dietary intervention on circulating cathepsin S concentrations. This thesis is based on data from three community-based cohorts, the Uppsala longitudinal study of adult men (ULSAM), the prospective investigation of the vasculature in Uppsala seniors (PIVUS), and a post-hoc study from the randomized controlled NORDIET trial. In the first study, we identified a cross-sectional positive association between serum cathepsin S and two markers of cytokine-mediated inflammation, CRP and IL-6. These associations were similar in non-obese individuals. In longitudinal analyses, higher cathepsin S at baseline was associated with higher CRP and IL-6 levels after six years of follow-up. In the second study, we identified a cross-sectional association between increased serum levels of cathepsin S and reduced insulin sensitivity. These associations were similar in non-obese individuals. No significant association was observed between cathepsin S and insulin secretion. In longitudinal analysis, higher cathepsin S levels were associated with an increased risk of developing diabetes during the six-year follow-up. In the third study, we found that higher serum levels of cathepsin S were associated with increased mortality risk. Moreover, in the ULSAM cohort, serum cathepsin S was independently associated with cause-specific mortality from cardiovascular disease and cancer. In the fourth study, we identified that adherence to an ad libitum healthy Nordic diet for 6 weeks slightly decreased the levels of plasma cathepsin S in normal or marginally overweight individuals, relative to the control group. Changes in circulating cathepsin S concentrations were correlated with changes in body weight, LDL-C, and total cholesterol. Conclusion: This thesis shows that circulating cathepsin S is a biomarker that independently reflects inflammation, insulin resistance, the risk of developing diabetes, and mortality risk. Furthermore, a Nordic diet moderately reduced cathepsin S levels in normal-weight and overweight men and women. This effect may be partially mediated by diet-induced weight loss and possibly by reduced LDL-C concentrations.