Policy bias and agriculture: partial and general equilibrium measures

The paper examines the impact of industrial protection, agricultural export taxes, and overvaluation of the exchange rate on the balance between the agricultural and non-agricultural sectors. A variety of agricultural terms-of-trade indices are constructed to measure the policy bias against agriculture in a general equilibrium framework that incorporates traded and non-traded goods. These general equilibrium measures are compared to earlier work in a partial equilibrium framework assuming perfect substitutability between domestic and traded goods. Starting from a stylized computable general equilibrium (CGE) model of Tanzania, we simulate a 25 percent tariff on non-agriculture and a 25 percent export tax on agriculture. We also consider the impact of changes in the equilibrium exchange rate. The results indicate that the partial equilibrium measures miss much of the action operating through indirect product and factor market linkages, while overstating the strength of the linkages between changes in the exchange rate and prices of traded goods on the agricultural terms of trade.Terms of trade., Equilibrium (Economics) Mathematical models., Tanzania., Computable general equilibrium (CGE)., Agricultural trade.,

Evaluating Component Migration: Comparing Two Generations of the INBONE(®) Total Ankle Replacement.

Although total ankle replacement (TAR) designs have radically evolved, the compressive forces at the ankle can cause aseptic loosening, talar subsidence, and implant failure. The purpose of the present report was to compare the implant migration associated with the INBONE(®) I, a TAR system with a stemmed talar component, and the newer generation INBONE(®) II, a TAR system without a stemmed talar component (Wright Medical Technology, Inc., Arlington, TN). Because core decompression could weaken the integrity of the talus, we hypothesized that the stemmed component would result in greater implant migration. A total of 35 consecutive patients (age 58.2 ± 12.1 years; 23 men) were included. Of these 35 patients, 20 (57.1%) had been treated with the INBONE(®) I and 15 (42.9%) with the INBONE(®) II. To assess implant migration, using anteroposterior radiographs, the distance from the apex of the tibial component to the most distal aspect of the talar stem or to the mid-saddle of the nonstemmed component was measured. The measurements were recorded from the immediate postoperative radiographs and the 12-month postoperative radiographs. Implant migration was quantified as the difference between the 12-month and the immediate postoperative measurements. Despite our hypothesis, no significant difference was found in implant migration between the INBONE(®) I (0.7 ± 1.2 mm) and INBONE(®) II (0.6 ± 1.3 mm, p = .981). However, previously published data have suggested that implant migration can continue for ≥2 years after surgery. Therefore, additional investigations with larger sample sizes and longer follow-up periods are needed to draw definitive conclusions

Identification of a Core Amino Acid Motif within the α Subunit of GABAARs that Promotes Inhibitory Synaptogenesis and Resilience to Seizures

The fidelity of inhibitory neurotransmission is dependent on the accumulation of γ-aminobutyric acid type A receptors (GABAARs) at the appropriate synaptic sites. Synaptic GABAARs are constructed from α(1-3), β(1-3), and γ2 subunits, and neurons can target these subtypes to specific synapses. Here, we identify a 15-amino acid inhibitory synapse targeting motif (ISTM) within the α2 subunit that promotes the association between GABAARs and the inhibitory scaffold proteins collybistin and gephyrin. Using mice in which the ISTM has been introduced into the α1 subunit (Gabra1-2 mice), we show that the ISTM is critical for axo-axonic synapse formation, the efficacy of GABAergic neurotransmission, and seizure sensitivity. The Gabra1-2 mutation rescues seizure-induced lethality in Gabra2-1 mice, which lack axo-axonic synapses due to the deletion of the ISTM from the α2 subunit. Taken together, our data demonstrate that the ISTM plays a critical role in promoting inhibitory synapse formation, both in the axonic and somatodendritic compartments

Discrete charging of metallic grains: Statistics of addition spectra

We analyze the statistics of electrostatic energies (and their differences) for a quantum dot system composed of a finite number $K$ of electron islands (metallic grains) with random capacitance-inductance matrix $C$, for which the total charge is discrete, $Q=Ne$ (where $e$ is the charge of an electron and $N$ is an integer). The analysis is based on a generalized charging model, where the electrons are distributed among the grains such that the electrostatic energy E(N) is minimal. Its second difference (inverse compressibility) $\chi_{N}=E(N+1)-2 E(N)+E(N-1)$ represents the spacing between adjacent Coulomb blockade peaks appearing when the conductance of the quantum dot is plotted against gate voltage. The statistics of this quantity has been the focus of experimental and theoretical investigations during the last two decades. We provide an algorithm for calculating the distribution function corresponding to $\chi_{N}$ and show that this function is piecewise polynomial.Comment: 21 pages, no figures, mathematical nomenclature (except for Abstract and Introduction

On Renyi entropies characterizing the shape and the extension of the phase space representation of quantum wave functions in disordered systems

We discuss some properties of the generalized entropies, called Renyi entropies and their application to the case of continuous distributions. In particular it is shown that these measures of complexity can be divergent, however, their differences are free from these divergences thus enabling them to be good candidates for the description of the extension and the shape of continuous distributions. We apply this formalism to the projection of wave functions onto the coherent state basis, i.e. to the Husimi representation. We also show how the localization properties of the Husimi distribution on average can be reconstructed from its marginal distributions that are calculated in position and momentum space in the case when the phase space has no structure, i.e. no classical limit can be defined. Numerical simulations on a one dimensional disordered system corroborate our expectations.Comment: 8 pages with 2 embedded eps figures, RevTex4, AmsMath included, submitted to PR

Wild-Type, but Not Mutant N296H, Human Tau Restores Aβ-Mediated Inhibition of LTP in Tau−/− mice

Microtubule associated protein tau (MAPT) is involved in the pathogenesis of Alzheimer’s disease and many forms of frontotemporal dementia (FTD). We recently reported that Aβ-mediated inhibition of hippocampal long-term potentiation (LTP) in mice requires tau. Here, we asked whether expression of human $MAPT$ can restore Aβ-mediated inhibition on a mouse $Tau−/−$ background and whether human tau with an FTD-causing mutation (N296H) can interfere with Aβ-mediated inhibition of LTP. We used transgenic mouse lines each expressing the full human $MAPT$ locus using bacterial artificial chromosome technology. These lines expressed all six human tau protein isoforms on a $Tau−/−$ background. We found that the human wild-type $MAPT$ H1 locus was able to restore Aβ$_{42}$-mediated impairment of LTP. In contrast, Aβ$_{42}$ did not reduce LTP in slices in two independently generated transgenic lines expressing tau protein with the mutation N296H associated with frontotemporal dementia (FTD). Basal phosphorylation of tau measured as the ratio of AT8/Tau5 immunoreactivity was significantly reduced in N296H mutant hippocampal slices. Our data show that human $MAPT$ is able to restore Aβ$_{42}$-mediated inhibition of LTP in $Tau−/−$ mice. These results provide further evidence that tau protein is central to Aβ-induced LTP impairment and provide a valuable tool for further analysis of the links between Aβ, human tau and impairment of synaptic function.MVC was supported by a Wellcome Trust OXION Training Fellowship and an equipment grant from Alzheimer’s Research UK. MVC is funded by the Institute for Life Sciences University of Southampton. RW-M was supported by a Wellcome Trust Research Career Development Fellowship (073141/Z/03/Z), CurePSP and the Alzheimer’s Society; FD held a Wellcome Trust DPhil in Neuroscience (075406/Z/04/A), and CMP is funded by the Gerald Kerkut Trust and IfLS. We thank Hana N. Dawson and Michael P. Vitek for Tau−/− mice. We thank Jenny Dworzak for her participation at an early phase of this project