A quality-index of poverty measures

The multitude of available poverty measures can confuse a policy maker who wants to evaluate a poverty-reduction policy. We proposes a rule for ranking poverty measures by use of the food-gap, calculated as the cost-difference between a household’s normative food basket, derived from a healthy diet, and the actually chosen food basket. The rationale for this indicator is based on the fact, that (1) basic food needs reflect an ultimate necessity, (2) food expenditure is highly divisibility, thus allowing for efficient marginal substitution between competing necessities when the household’s economic hardship increases. For these reasons we believe this to be an objective indicator for the sacrifice in the standard of living of a family under economic stress. A household is identified as ‘truly’ poor or non-poor by a given poverty measure if the diagnoses coincide and vice versa. The ranking is obtained by a gain-function, which adds up congruent and deducts contradicting outcomes for each poverty measure. We calculate four types of gain-functions –of headcounts, food-gaps, FGT-like powered food-gaps and an augmented version of the latter. The poverty measures include expenditure-based, income-based, relative, absolute, mixed measures and a multidimensional measure of social deprivation. The most qualitative measure is found to be Ravallion’s Food Energy Intake and Share measure, though it suffers from a possible bias, since it includes the food-norm in its design. The 60%-median income measure from all sources ranks highest among the unbiased measures. The absolute poverty measure yields the worst performance.poverty measures, food poverty, evaluation of poverty reduction policies

Domain Wall Fermions and MC Simulations of Vector Theories

It is known that domain wall fermions may be used in MC simulations of vector theories. The practicality and usefulness of such an implementation is investigated in the context of the vector Schwinger model, on a 2+1 dimensional lattice. Preliminary results of a Hybrid Monte Carlo simulation are presented.Comment: Talk presented at LATTICE96(chirality in qcd), 3 pages in LaTex, 4 Postscript figure

Symmetric stability of compressible zonal flows on a generalized equatorial β plane

Sufficient conditions are derived for the linear stability with respect to zonally symmetric perturbations of a steady zonal solution to the nonhydrostatic compressible Euler equations on an equatorial � plane, including a leading order representation of the Coriolis force terms due to the poleward component of the planetary rotation vector. A version of the energy–Casimir method of stability proof is applied: an invariant functional of the Euler equations linearized about the equilibrium zonal flow is found, and positive definiteness of the functional is shown to imply linear stability of the equilibrium. It is shown that an equilibrium is stable if the potential vorticity has the same sign as latitude and the Rayleigh centrifugal stability condition that absolute angular momentum increase toward the equator on surfaces of constant pressure is satisfied. The result generalizes earlier results for hydrostatic and incompressible systems and for systems that do not account for the nontraditional Coriolis force terms. The stability of particular equilibrium zonal velocity, entropy, and density fields is assessed. A notable case in which the effect of the nontraditional Coriolis force is decisive is the instability of an angular momentum profile that decreases away from the equator but is flatter than quadratic in latitude, despite its satisfying both the centrifugal and convective stability conditions

Targeting the Mevalonate Pathway Suppresses VHL-Deficient CC-RCC through an HIF-Dependent Mechanism.

Clear cell renal cell carcinoma (CC-RCC) is a devastating disease with limited therapeutic options available for advanced stages. The objective of this study was to investigate HMG-CoA reductase inhibitors, also known as statins, as potential therapeutics for CC-RCC. Importantly, treatment with statins was found to be synthetically lethal with the loss of the von Hippel-Lindau (VHL) tumor suppressor gene, which occurs in 90% of CC-RCC driving the disease. This effect has been confirmed in three different CC-RCC cell lines with three different lipophilic statins. Inhibition of mevalonate synthesis by statins causes a profound cytostatic effect at nanomolar concentrations and becomes cytotoxic at low micromolar concentrations in VHL-deficient CC-RCC. The synthetic lethal effect can be fully rescued by both mevalonate and geranylgeranylpyrophosphate, but not by squalene, indicating that the effect is due to disruption of small GTPase isoprenylation and not the inhibition of cholesterol synthesis. Inhibition of Rho and Rho kinase (ROCK) signaling contributes to the synthetic lethality effect, and overactivation of hypoxia-inducible factor signaling resulting from VHL loss is required. Finally, statin treatment is able to inhibit both tumor initiation and progression of subcutaneous 786-OT1-based CC-RCC tumors in mice. Thus, statins represent potential therapeutics for the treatment of VHL-deficient CC-RCC. Mol Cancer Ther; 17(8); 1781-92. ©2018 AACR

Editing in America

A survey and discussion of modern copy editors that attempts to provide perspective on their role in the communications and publishing industry. This capstone compares past research perspectives on copy editors with new survey responses to create a modern context for professional copy editors, discussing their skills, work environment, outlook, and professional role. This research also discusses the influence of evolving technologies on the role of copy editors and their perspectives

Differentiation of murine B cells induced by chondroitin sulfate B

A two-step culture system was used to investigate the role of chondroitin sulfate (CS) B, which is mitogenic to B cells, in differentiation of B cells. Mouse spleen B cells were incubated for 3 days with CSB in the presence of interleukin (IL)-4 and IL-5. After washing, the cells were replated at 10(5) viable cells/well and recultured without CSB in the presence of IL-4 and IL-5. CSB dose-dependently increased IgM production, the greatest enhancement being 450%. Dextran sulfate had a similar effect, whereas other glycosaminoglycans, CSA, CSC, heparin and hyaluronic acid, were marginally effective. Treatment of B cells with CSB resulted in increases in the number of IgM-secreting cells and numbers of CD138-positive cells and CD45R/B220-negative cells. CSB-induced IgM production was inhibited by the protein kinase C (PKC) inhibitor GF109203X but not by the phosphatidylinositol 3-kinase (P13K) inhibitor wortmannin. These results demonstrated that CSB promoted differentiation of B cells in the presence of IL-4 and IL-5 and suggested that PKC but not P13K is crucial for CSB-induced IgM production.</p

On the width of the equatorial deep jets

The equatorial deep jets (EDJ) are a striking feature of the equatorial ocean circulation. In the Atlantic Ocean, the EDJ are associated with a vertical scale of between 300 and 700 m, a time scale of roughly 4.5 years and upward energy propagation to the surface. It has been found that the meridional width of the EDJ is roughly 1.5 times larger than expected based on their vertical scale. Here we use a shallow water model for a high order baroclinic vertical normal mode to argue that mixing of momentum along isopycnals can explain the enhanced width. A lateral eddy viscosity of 300 m2 s−1 10 is found to be sufficient to account for the width implied by observations

Kinome rewiring reveals AURKA limits PI3K-pathway inhibitor efficacy in breast cancer.

Dysregulation of the PI3K-AKT-mTOR signaling network is a prominent feature of breast cancers. However, clinical responses to drugs targeting this pathway have been modest, possibly because of dynamic changes in cellular signaling that drive resistance and limit drug efficacy. Using a quantitative chemoproteomics approach, we mapped kinome dynamics in response to inhibitors of this pathway and identified signaling changes that correlate with drug sensitivity. Maintenance of AURKA after drug treatment was associated with resistance in breast cancer models. Incomplete inhibition of AURKA was a common source of therapy failure, and combinations of PI3K, AKT or mTOR inhibitors with the AURKA inhibitor MLN8237 were highly synergistic and durably suppressed mTOR signaling, resulting in apoptosis and tumor regression in vivo. This signaling map identifies survival factors whose presence limits the efficacy of targeted therapies and reveals new drug combinations that may unlock the full potential of PI3K-AKT-mTOR pathway inhibitors in breast cancer