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Abstract Using bootstrap simulations, asset allocations that mimic real-world lifecycle fund behavior are shown to have lower accumulation efficiency than several available alternatives. The alternatives include fixed stock/bond allocation with [...]

Abstract Target-date mutual funds are likely to increase in popularity because they are now one of the three approved default options for many retirement plans. In the retirement years, target-date [...]

Abstract Much research has addressed the question of how much money can safely be withdrawn from a retirement portfolio without prematurely running out of money (shortfall risk). Instead of constant [...]

Abstract This paper reconciles previous research outcomes and explains why prior studies offer conflicting recommendations regarding the decision to delay Social Security payments. Using a bootstrap, this paper determines the [...]

The effects of endotoxin on ethanol-dependent free radical generation in the liver and subsequent trapping of these free radicals in the bile are investigated using spin-trapping techniques. The free radical adducts in the bile were identified using their electron paramagnetic resonance spectra. Results reveal that treatment with endotoxin enhances the generation of free radicals through Kupffer cells and catalytic metals modulation.

The hypothesis that increases in glucose utilization (Rg) after intrapulmonary lipopolysaccharide (LPS) challenge is confined to the respiratory system was tested by measuring Rg of the whole lung and bronchoalveolar lavage (BAL) fluid cells after a challenge. Increases in Rg in the whole lung but not in BAL cells were observed after intravenous LPS challenge. In contrast, intratracheal LPS challenge increased Rg in BAL cells but not in the whole lung. These results indicated that increases in Rg are confined to the respiratory system.

Experimental study of the effect of acute alcohol treatment on tissue uptake of glucose under basal conditions or after a hyperinsulinemic euglycemic clamp in fasted rats shows that acute alcohol weakens basal and hormone-induced glucose uptake in a tissue-specific manner. Decreased glucose recycling in humans after acute alcohol uptake can also be attributed to this inhibitory effect of alcohol on glucose use in skeletal muscles. Alcohol inhibits insulin-stimulated glucose use selectively in muscles, having no effects on other tissues.

Administration of epinephrine in animals generated hyperglycemia, which results due to acceleration of glucose production in the liver. Infusion of acute ethanol reduces the glucose production, but does not inhibit it completely. The glucose production impairment is achieved through lowered responsiveness of the liver to adrenergic stimulation.

Inhibition of nitric oxide release in endotoxemic rats enhance the formation of super oxide anion. Nitric oxide acts as a remover of toxic radicals such as super oxide by inhibiting free radical formation from peroxidase. Thus, nitric oxide maintains tissue integrity during inflammatory process. The inhibition of nitric oxide synthase by N-omega-nitro-L-arginine methyl ester (L-NAME) disrupts the normal balance between oxide and superoxide, resulting in tissue injury.

The role of complement factors in the activation of Kupffer cells and polymorphonuclear neutrophils (PMN) during hepatic ischemia and reperfusion were studied in rats. Preischemic depletion of serum complement reduced plasma glutathione oxidation and accumulation of PMNs. Cobra venum factor, injected to simulate complement activation, produced an opposite reaction. Results suggest that complement activation can induce parenchymal necrosis but requires other mediators to cause severe parenchymal damage.