INCORPORATING GOVERNMENT PROGRAM PROVISIONS INTO A MEAN-VARIANCE FRAMEWORK

E-V studies traditionally have relied on historical data to calculate returns and variance. Historical data may not fully reflect current conditions, particularly when decisions involve government-supported crops. This paper presents a method for calculating mean and variance using subjectively-estimated data. The method is developed for both government-supported and non-program crops. Comparisons to alternative methods suggest the approach provides reasonable accuracy.Agricultural and Food Policy,

Rate-dependent morphology of Li2O2 growth in Li-O2 batteries

Compact solid discharge products enable energy storage devices with high gravimetric and volumetric energy densities, but solid deposits on active surfaces can disturb charge transport and induce mechanical stress. In this Letter we develop a nanoscale continuum model for the growth of Li2O2 crystals in lithium-oxygen batteries with organic electrolytes, based on a theory of electrochemical non-equilibrium thermodynamics originally applied to Li-ion batteries. As in the case of lithium insertion in phase-separating LiFePO4 nanoparticles, the theory predicts a transition from complex to uniform morphologies of Li2O2 with increasing current. Discrete particle growth at low discharge rates becomes suppressed at high rates, resulting in a film of electronically insulating Li2O2 that limits cell performance. We predict that the transition between these surface growth modes occurs at current densities close to the exchange current density of the cathode reaction, consistent with experimental observations.Comment: 8 pages, 6 fig

Asset liability modelling and pension schemes: the application of robust optimization to USS

This paper uses a novel numerical optimization technique - robust optimization - that is well suited to solving the asset-liability management (ALM) problem for pension schemes. It requires the estimation of fewer stochastic parameters, reduces estimation risk and adopts a prudent approach to asset allocation. This study is the first to apply it to a real-world pension scheme, and the first ALM model of a pension scheme to maximise the Sharpe ratio. We disaggregate pension liabilities into three components - active members, deferred members and pensioners, and transform the optimal asset allocation into the scheme’s projected contribution rate. The robust optimization model is extended to include liabilities and used to derive optimal investment policies for the Universities Superannuation Scheme (USS), benchmarked against the Sharpe and Tint, Bayes-Stein, and Black-Litterman models as well as the actual USS investment decisions. Over a 144 month out-of-sample period robust optimization is superior to the four benchmarks across 20 performance criteria, and has a remarkably stable asset allocation – essentially fix-mix. These conclusions are supported by six robustness checks

Interplay of Mre11 Nuclease with Dna2 plus Sgs1 in Rad51-Dependent Recombinational Repair

The Mre11/Rad50/Xrs2 complex initiates IR repair by binding to the end of a double-strand break, resulting in 5′ to 3′ exonuclease degradation creating a single-stranded 3′ overhang competent for strand invasion into the unbroken chromosome. The nuclease(s) involved are not well understood. Mre11 encodes a nuclease, but it has 3′ to 5′, rather than 5′ to 3′ activity. Furthermore, mutations that inactivate only the nuclease activity of Mre11 but not its other repair functions, mre11-D56N and mre11-H125N, are resistant to IR. This suggests that another nuclease can catalyze 5′ to 3′ degradation. One candidate nuclease that has not been tested to date because it is encoded by an essential gene is the Dna2 helicase/nuclease. We recently reported the ability to suppress the lethality of a dna2Δ with a pif1Δ. The dna2Δ pif1Δ mutant is IR-resistant. We have determined that dna2Δ pif1Δ mre11-D56N and dna2Δ pif1Δ mre11-H125N strains are equally as sensitive to IR as mre11Δ strains, suggesting that in the absence of Dna2, Mre11 nuclease carries out repair. The dna2Δ pif1Δ mre11-D56N triple mutant is complemented by plasmids expressing Mre11, Dna2 or dna2K1080E, a mutant with defective helicase and functional nuclease, demonstrating that the nuclease of Dna2 compensates for the absence of Mre11 nuclease in IR repair, presumably in 5′ to 3′ degradation at DSB ends. We further show that sgs1Δ mre11-H125N, but not sgs1Δ, is very sensitive to IR, implicating the Sgs1 helicase in the Dna2-mediated pathway

Diagnosis and treatment of pediatric acquired aplastic anemia (AAA): An initial survey of the North American Pediatric Aplastic Anemia Consortium (NAPAAC)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106711/1/pbc24875.pd

Neurofibromin Deficient Myeloid Cells are Critical Mediators of Aneurysm Formation In Vivo

Background Neurofibromatosis Type 1 (NF1) is a genetic disorder resulting from mutations in the NF1 tumor suppressor gene. Neurofibromin, the protein product of NF1, functions as a negative regulator of Ras activity in circulating hematopoietic and vascular wall cells, which are critical for maintaining vessel wall homeostasis. NF1 patients have evidence of chronic inflammation resulting in development of premature cardiovascular disease, including arterial aneurysms, which may manifest as sudden death. However, the molecular pathogenesis of NF1 aneurysm formation is unknown. Method and Results Utilizing an angiotensin II-induced aneurysm model, we demonstrate that heterozygous inactivation of Nf1 (Nf1+/−) enhanced aneurysm formation with myeloid cell infiltration and increased oxidative stress in the vessel wall. Using lineage-restricted transgenic mice, we show loss of a single Nf1 allele in myeloid cells is sufficient to recapitulate the Nf1+/− aneurysm phenotype in vivo. Finally, oral administration of simvastatin or the antioxidant apocynin, reduced aneurysm formation in Nf1+/− mice. Conclusion These data provide genetic and pharmacologic evidence that Nf1+/− myeloid cells are the cellular triggers for aneurysm formation in a novel model of NF1 vasculopathy and provide a potential therapeutic target

Imposed currents in galvanic cells

We analyze the steady-state behavior of a general mathematical model for reversible galvanic cells, such as redox flow cells, reversible solid oxide fuel cells, and rechargeable batteries. We consider not only operation in the galvanic discharging mode, spontaneously generating a positive current against an external load, but also operation in two modes which require a net input of electrical energy: (i) the electrolytic charging mode, where a negative current is imposed to generate a voltage exceeding the open-circuit voltage, and (ii) the “super-galvanic” discharging mode, where a positive current exceeding the short-circuit current is imposed to generate a negative voltage. Analysis of the various (dis-)charging modes of galvanic cells is important to predict the efficiency of electrical to chemical energy conversion and to provide sensitive tests for experimental validation of fuel cell models. In the model, we consider effects of diffuse charge on electrochemical charge-transfer rates by combining a generalized Frumkin-Butler-Volmer equation for reaction kinetics across the compact Stern layer with the full Poisson-Nernst-Planck transport theory, without assuming local electroneutrality. Since this approach is rare in the literature, we provide a brief historical review. To illustrate the general theory, we present results for a monovalent binary electrolyte, consisting of cations, which react at the electrodes, and non-reactive anions, which are either fixed in space (as in a solid electrolyte) or are mobile (as in a liquid electrolyte). The full model is solved numerically and compared to analytical results in the limit of thin diffuse layers, relative to the membrane thickness. The spatial profiles of the ion concentrations and electrostatic potential reveal a complex dependence on the kinetic parameters and the imposed current, in which the diffuse charge at each electrode and the total membrane charge can have either sign, contrary perhaps to intuition. For thin diffuse layers, simple analytical expressions are presented for galvanic cells valid in all three (dis-)charging modes in the two subsequent limits of the ratio δ of the effective thicknesses of the compact and diffuse layers: (i) the “Helmholtz limit” (δ → ∞) where the compact layer carries the double layer voltage as in standard Butler-Volmer models, and (ii) the opposite “Gouy-Chapman limit” (δ → 0) where the diffuse layer fully determines the charge-transfer kinetics. In these limits, the model predicts both reaction-limited and diffusion-limited currents, which can be surpassed for finite positive values of the compact layer, diffuse layer and membrane thickness

DNA damage signalling prevents deleterious telomere addition at DNA breaks

The response to DNA damage involves regulation of multiple essential processes to maximize the accuracy of DNA damage repair and cell survival 1. Telomerase has the potential to interfere with repair by inappropriately adding telomeres to DNA breaks. It was unknown whether cells modulate telomerase in response to DNA damage, to increase the accuracy of repair. Here we report that telomerase action is regulated as a part of the cellular response to a DNA double-strand break (DSB). Using yeast, we show that the major ATR/Mec1 DNA damage signalling pathway regulates telomerase action at DSBs. Upon DNA damage, MEC1-RAD53-DUN1-dependent phosphorylation of the telomerase inhibitor Pif1 occurs. Utilizing a separation of function PIF1 mutation, we show that this phosphorylation is required for the Pif1-mediated telomerase inhibition that takes place specifically at DNA breaks, but not telomeres. Hence DNA damage signalling down-modulates telomerase action at a DNA break via Pif1 phosphorylation, thus preventing aberrant healing of broken DNA ends by telomerase. These findings uncover a novel regulatory mechanism that coordinates competing DNA end-processing activities and thereby promotes DNA repair accuracy and genome integrity

Eculizumab treatment: stochastic occurrence of C3 binding to individual PNH erythrocytes

C5 blockade by eculizumab prevents complement-mediated intravascular hemolysis in paroxysmal nocturnal hemoglobinuria (PNH). However, C3-bound PNH red blood cells (RBCs), arising in almost all treated patients, may undergo extravascular hemolysis reducing clinical benefits. Despite the uniform deficiency of CD55 and of CD59, there are always two distinct populations of PNH RBCs, with (C3+) and without (C3-) C3 binding