The Impact of Stochastic Interest and Mortality Rates on Ruin Probability and Annuitization Decisions Faced by Retirees

This dissertation focuses on two issues in retirement planning. The first issue, annuitization problem, provides insight on how interest rates may affect annuitization decisions for retirees under an all-or-nothing framework. The second issue, ruin probability, studies the probability for a retired individual who might run out of money, under a fixed consumption strategy before the end of his/her life under stochastic hazard rates. These two financial problems have been very important in personal finance for both retirees and financial advisors throughout the world, especially in the developed countries as the baby boom generation nears retirement. They are the direct results of both longevity risk and demise of Defined Benefit (DB) pension plans. The existing literature of the annuitization problem, such as Richard (1975), concludes that it is always optimal to annuitize with no bequest motives under a constant interest rate. To see the effect of stochastic interest rates on the annuitization decisions under a constrained consumption strategy without bequest motives, we present two life cycle models. They investigate the optimal annuitization strategy for a retired individual whose objective is to maximize his/her lifetime utility under a variety of institutional restrictions, in an all-or-nothing framework. The individual is required to annuitize all his/her wealth in a lump sum at some time at retirement. The first life cycle model we have presented assumes full consumption after annuity purchasing. A free boundary exists in this case upon the assumption of constant spread between the expected return of the risky asset and the riskless interest rate. The second life cycle model applies the optimal consumption strategy after annuitization, and numerical analysis shows that it is always optimal to annuitize no matter what the current interest rate is. This conclusion is based on the assumption of constant risk premium, no loads and no bequest motives. Historical data show that mortality rates for human beings behave stochastically. Motivated by this, we study the ruin probability for a retired individual who withdraws $1 per annum with various initial wealth for log-normal mortality with constant drift and volatility, which is a special form of the most widely accepted Lee-Carter model. This problem is converted to a Partial Differential Equation (PDE) and solved numerically by the Alternative Direction Implicit (ADI) method. For any given initial wealth, ruin probability can be obtained for various initial hazard rates. The correlation between the wealth process and the mortality process slightly affects the ruin probability at time zero

dbOGAP - An Integrated Bioinformatics Resource for Protein O-GlcNAcylation

<p>Abstract</p> <p>Background</p> <p>Protein O-GlcNAcylation (or O-GlcNAc-ylation) is an O-linked glycosylation involving the transfer of β-<it>N</it>-acetylglucosamine to the hydroxyl group of serine or threonine residues of proteins. Growing evidences suggest that protein O-GlcNAcylation is common and is analogous to phosphorylation in modulating broad ranges of biological processes. However, compared to phosphorylation, the amount of protein O-GlcNAcylation data is relatively limited and its annotation in databases is scarce. Furthermore, a bioinformatics resource for O-GlcNAcylation is lacking, and an O-GlcNAcylation site prediction tool is much needed.</p> <p>Description</p> <p>We developed a database of O-GlcNAcylated proteins and sites, dbOGAP, primarily based on literature published since O-GlcNAcylation was first described in 1984. The database currently contains ~800 proteins with experimental O-GlcNAcylation information, of which ~61% are of humans, and 172 proteins have a total of ~400 O-GlcNAcylation sites identified. The O-GlcNAcylated proteins are primarily nucleocytoplasmic, including membrane- and non-membrane bounded organelle-associated proteins. The known O-GlcNAcylated proteins exert a broad range of functions including transcriptional regulation, macromolecular complex assembly, intracellular transport, translation, and regulation of cell growth or death. The database also contains ~365 potential O-GlcNAcylated proteins inferred from known O-GlcNAcylated orthologs. Additional annotations, including other protein posttranslational modifications, biological pathways and disease information are integrated into the database. We developed an O-GlcNAcylation site prediction system, OGlcNAcScan, based on Support Vector Machine and trained using protein sequences with known O-GlcNAcylation sites from dbOGAP. The site prediction system achieved an area under ROC curve of 74.3% in five-fold cross-validation. The dbOGAP website was developed to allow for performing search and query on O-GlcNAcylated proteins and associated literature, as well as for browsing by gene names, organisms or pathways, and downloading of the database. Also available from the website, the OGlcNAcScan tool presents a list of predicted O-GlcNAcylation sites for given protein sequences.</p> <p>Conclusions</p> <p>dbOGAP is the first public bioinformatics resource to allow systematic access to the O-GlcNAcylated proteins, and related functional information and bibliography, as well as to an O-GlcNAcylation site prediction tool. The resource will facilitate research on O-GlcNAcylation and its proteomic identification.</p

Alcohol Promotes Mammary Tumor Growth through Activation of VEGF-Dependent Tumor Angiogenesis

Alcohol consumption has been recognized as a risk factor for breast cancer. Experimental studies demonstrate that alcohol exposure promotes the progression of existing mammary tumors. However, the mechanisms underlying this effect remain unclear. In the present study, the role of vascular endothelial growth factor (VEGF) in alcohol promotion of breast cancer development was investigated using a mouse xenograft model of mammary tumors and a three-dimensional (3D) tumor/endothelial cell co-culture system. For the mouse xenograft model, mouse E0771 breast cancer cells were implanted into the mammary fat pad of C57BL6 mice. These mice were exposed to alcohol in their drinking water. For the 3D co-culture system, E0771 cells and MDA-MB231 breast cancer cells were co-cultured with SVEC4-10EE2 and human umbilical vein endothelial cells, respectively. The results demonstrated that alcohol increased tumor angiogenesis and accelerated tumor growth. Furthermore, it appeared that alcohol induced VEGF expression in breast cancer cells in vitro and in vivo. Blocking VEGF signaling by SU5416 inhibited tumor angiogenesis in the 3D tumor/endothelial cell co-culture system. Furthermore, injection of SU5416 into mice inhibited alcohol-promoted mammary tumor growth in vivo. These results indicate that alcohol may promote mammary tumor growth by stimulating VEGF-dependent angiogenesis

Identification and Characterization of Key Chemical Constituents in Processed Gastrodia elata Using UHPLC-MS/MS and Chemometric Methods

© The Author(s) 2019. Background. Obesity is a major medical issue nationally, with rates continually increasing. In obese patients, minimal data exist for appropriate dosing of acyclovir to decrease the rates of nephrotoxicity. The purpose of this study was to determine the prevalence of and risk factors associated with acyclovir-induced nephrotoxicity. Methods. A retrospective case-control of patients who received intravenous acyclovir for \u3e48 hours at University of Mississippi Medical Center over a 4-year period were evaluated to elucidate the prevalence of acyclovir-induced nephrotoxicity. Additionally, risk factors for the development of nephrotoxicity, including the effect of obesity and dosing strategy, were assessed. Results. One hundred fifteen patients were included in the study. A total of 24 (21%) patients developed nephrotoxicity after acyclovir exposure and were in the Risk (9.6%), Injury (4.3%), and Failure (7%) categories, defined by the RIFLE criteria. Neither acyclovir dosage, fluid status, nor baseline characteristics, other than obesity, varied between those who developed nephrotoxicity vs those who did not. Independent predictors of nephrotoxicity were obesity (odds ratio [OR], 3.2; 95% confidence interval [CI], 1.19-8.67) and receipt of vancomycin (OR, 4.73; 95% CI, 1.57-14.25). No differences in vancomycin dosing or concentrations were observed between the patients who developed nephrotoxicity and those who did not. Conclusions. In this study, nephrotoxicity occurred in 21% of patients receiving acyclovir. Concomitant vancomycin receipt and obesity led to higher rates of toxicity. Efforts should be made to target obese patients on acyclovir plus vancomycin and discontinue therapy in patients not warranting antiviral coverage to minimize chances of toxicity

Multiple Gravity Assist Spacecraft Trajectories Design Based on BFS and EP_DE Algorithm

The paper deals with the multiple gravity assist trajectories design. In order to improve the performance of the heuristic algorithms, such as differential evolution algorithm, in multiple gravity assist trajectories design optimization, a method combining BFS (breadth-first search) and EP DE (differential evolution algorithm based on search space exploring and principal component analysis) is proposed. In this method, firstly find the possible multiple gravity assist planet sequences with pruning based BFS and use standard differential evolution algorithm to judge the possibility of all the possible trajectories. Then select the better ones from all the possible solutions. Finally, use EP DE which will be introduced in this paper to find an optimal decision vector of spacecraft transfer time schedule (launch window and transfer duration) for each selected planet sequence. In this paper, several cases are presented to prove the efficiency of the method proposed

Enhanced Anaerobic Biodegradation of Benzoate Under Sulfate-Reducing Conditions With Conductive Iron-Oxides in Sediment of Pearl River Estuary

Anaerobic biodegradation of aromatic compounds under sulfate-reducing conditions is important to marine sediments. Sulfate respiration by a single bacterial strain and syntrophic metabolism by a syntrophic bacterial consortium are primary strategies for sulfate-dependent biodegradation of aromatic compounds. The objective of this study was to investigate the potential of conductive iron oxides to facilitate the degradation of aromatic compounds under sulfate-reducing conditions in marine sediments, using benzoate as a model aromatic compound. Here, in anaerobic incubations of sediments from the Pearl River Estuary, the addition of hematite or magnetite (20 mM as Fe atom) enhanced the rates of sulfate-dependent benzoate degradation by 81.8 and 91.5%, respectively, compared with control incubations without iron oxides. Further experiments demonstrated that the rate of sulfate-dependent benzoate degradation accelerated with increased magnetite concentration (5, 10, and 20 mM). The detection of acetate as an intermediate product implied syntrophic benzoate degradation pathway, which was also supported by the abundance of putative acetate- or/and H2-utilizing sulfate reducers from microbial community analysis. Microbial reduction of iron oxides under sulfate-reducing conditions only accounted for 2–11% of electrons produced by benzoate oxidation, thus the stimulatory effect of conductive iron oxides on sulfate-dependent benzoate degradation was not mainly due to an increased pool of terminal electron acceptors. The enhanced rates of syntrophic benzoate degradation by the presence of conductive iron oxides probably resulted from the establishment of a direct interspecies electron transfer (DIET) between syntrophic partners. In the presence of magnetite, Bacteroidetes and Desulfobulbaceae with potential function of extracellular electron transfer might be involved in syntrophic benzoate degradation. Results from this study will contribute to the development of new strategies for in situ bioremediation of anaerobic sediments contaminated with aromatic compounds, and provide a new perspective for the natural attenuation of aromatic compounds in iron-rich marine sediments

MetaboSearch: Tool for Mass-Based Metabolite Identification Using Multiple Databases

Searching metabolites against databases according to their masses is often the first step in metabolite identification for a mass spectrometry-based untargeted metabolomics study. Major metabolite databases include Human Metabolome DataBase (HMDB), Madison Metabolomics Consortium Database (MMCD), Metlin, and LIPID MAPS. Since each one of these databases covers only a fraction of the metabolome, integration of the search results from these databases is expected to yield a more comprehensive coverage. However, the manual combination of multiple search results is generally difficult when identification of hundreds of metabolites is desired. We have implemented a web-based software tool that enables simultaneous mass-based search against the four major databases, and the integration of the results. In addition, more complete chemical identifier information for the metabolites is retrieved by cross-referencing multiple databases. The search results are merged based on IUPAC International Chemical Identifier (InChI) keys. Besides a simple list of m/z values, the software can accept the ion annotation information as input for enhanced metabolite identification. The performance of the software is demonstrated on mass spectrometry data acquired in both positive and negative ionization modes. Compared with search results from individual databases, MetaboSearch provides better coverage of the metabolome and more complete chemical identifier information. Availability: The software tool is available at http://omics.georgetown.edu/MetaboSearch.html