Nonlinear monetary policy rules: some new evidence for the US

This paper dreives optimal monetary policy rules in setups where certainty equivalence does not hold because either central bank preferences are not quadratic, and/or the aggregate supply relation is nonlinear. Analytical results show that these features lead to sign and size aymmetries, and nonlinearities in the policy rule. Reduced-form estimates indicate that US monetary policy can be characterized by a nonlinear policy rule after 1983, but not before 1979. This finding is consistent with the view that the Fed`s inflation preferences during the Volcker-Greenspan regime differ considerably from the ones during the Burns-Miller regime

NONLINEAR MONETARY POLICY RULES: SOME NEW EVIDENCE FOR THE US

This paper dreives optimal monetary policy rules in setups where certainty equivalence does not hold because either central bank preferences are not quadratic, and/or the aggregate supply relation is nonlinear. Analytical results show that these features lead to sign and size aymmetries, and nonlinearities in the policy rule. Reduced-form estimates indicate that US monetary policy can be characterized by a nonlinear policy rule after 1983, but not before 1979. This finding is consistent with the view that the Fed`s inflation preferences during the Volcker-Greenspan regime differ considerably from the ones during the Burns-Miller regime.

Correlated percolation and the correlated resistor network

We present some exact results on percolation properties of the Ising model, when the range of the percolating bonds is larger than nearest-neighbors. We show that for a percolation range to next-nearest neighbors the percolation threshold Tp is still equal to the Ising critical temperature Tc, and present the phase diagram for this type of percolation. In addition, we present Monte Carlo calculations of the finite size behavior of the correlated resistor network defined on the Ising model. The thermal exponent t of the conductivity that follows from it is found to be t = 0.2000 +- 0.0007. We observe no corrections to scaling in its finite size behavior.Comment: 16 pages, REVTeX, 6 figures include

Development and validation of a gene expression test to identify hard-to-heal chronic venous leg ulcers

Background: Chronic venous leg ulcers pose a significant burden to healthcare systems, and predicting wound healing is challenging. The aim of this study was to develop a genetic test to evaluate the propensity of a chronic ulcer to heal. Methods: Sequential refinement and testing of a gene expression signature was conducted using three distinct cohorts of human wound tissue. The expression of candidate genes was screened using a cohort of acute and chronic wound tissue and normal skin with quantitative transcript analysis. Genes showing significant expression differences were combined and examined, using receiver operating characteristic (ROC) curve analysis, in a controlled prospective study of patients with venous leg ulcers. A refined gene signature was evaluated using a prospective, blinded study of consecutive patients with venous ulcers. Results: The initial gene signature, comprising 25 genes, could identify the outcome (healing versus non‐healing) of chronic venous leg ulcers (area under the curve (AUC) 0·84, 95 per cent c.i. 0·73 to 0·94). Subsequent refinement resulted in a final 14‐gene signature (WD14), which performed equally well (AUC 0·88, 0·80 to 0·97). When examined in a prospective blinded study, the WD14 signature could also identify wounds likely to demonstrate signs of healing (AUC 0·73, 0·62 to 0·84). Conclusion: A gene signature can identify people with chronic venous leg ulcers that are unlikely to heal

Detection of six serotypes of botulinum neurotoxin using fluorogenic reporters

Methods that do not require animal sacrifice to detect botulinum neurotoxins (BoNTs) are critical for BoNT antagonist discovery and the advancement of quantitative assays for biodefense and pharmaceutical applications. Here we describe the development and optimization of fluorogenic reporters that detect the proteolytic activity of BoNT/A, B, D, E, F, and G serotypes in real time with femtomolar to picomolar sensitivity. Notably, the reporters can detect femtomolar concentrations of BoNT/A in 4 h and BoNT/E in 20 h, sensitivity that equals that of animal-based methods. The reporters can be used to determine the specific activity of BoNT preparations with intra- and inter-assay coefficients of variation of approximately 10%. Finally, we find that the greater sensitivity of our reporters compared with those used in other commercially available assays makes the former attractive candidates for high-throughput screening of BoNT antagonists

Multilevel first-order system least squares for elliptic grid generation

A new fully variational approach is studied for elliptic grid generation (EGG). It is based on a general algorithm developed in a companion paper [A. L. Codd, T. A. Manteuffel, and S. F. McCormick, SIAM J. Numer. Anal., 41 (2003), pp. 2197--2209] that involves using Newton's method to linearize an appropriate equivalent first-order system, first-order system least squares (FOSLS) to formulate and discretize the Newton step, and algebraic multigrid (AMG) to solve the resulting matrix equation. The approach is coupled with nested iteration to provide an accurate initial guess for finer levels using coarse-level computation. The present paper verifies the assumptions of the companion work and confirms the overall efficiency of the scheme with numerical experiments

Mechanistic insights of epithelial protein lost in neoplasm in prostate cancer metastasis

EPLIN is frequently downregulated or lost in various cancers. The purpose of this study was to evaluate the importance of EPLIN in prostate cancer progression, with particular focus on the mechanistic implications to elucidate EPLIN's tumour suppressive function in cancer. EPLIN expression was evaluated in prostate cancer cell lines and tissues. PC‐3 and LNCaP EPLINα overexpression models were generated through transfection with EPLINα sequence and EPLIN knockdown was achieved using shRNA in CA‐HPV‐10 cells. Functional assays were performed to evaluate cellular characteristics and potential mechanisms were evaluated using a protein microarray, and validated using western blot analysis. EPLIN expression was reduced in clinical prostate cancer sections, including hyperplasia (p≤0.001) and adenocarcinoma (p=0.005), when compared to normal prostate tissue. EPLINα overexpression reduced cell growth, migration and invasion, and influenced transcript, protein and phosphoprotein expression of paxillin, FAK and Src. EPLIN knockdown increased the invasive and migratory nature of CA‐HPV‐10 cells and also induced changes to FAK and Src total and/or phospho expression. Functional characterisation of cellular migration and invasion in addition to FAK and Src inhibition demonstrated differential effects between control and EPLINα overexpression and EPLIN knockdown cell lines. This study highlights that EPLIN expression in prostate cancer is able to influence several aspects of cancer cell characteristics, including cell growth, migration and invasion. The mechanism of the tumour suppressive action of EPLIN remains to be fully elucidated; and this study proposes a role for EPLIN's ability to regulate the aggressive characteristics of prostate cancer cells partially through regulating FAK/Src signalling