An Outline of a Progressive Resolution to the Euro-area Sovereign Debt Overhang: How a Five year Suspension of the Debt Burden Could Overthrow Austerity

The present study puts forward a plan for solving the sovereign debt crisis in the euro area (EA) in line with the interests of the working classes and the social majority. Our main strategy is for the European Central Bank (ECB) to acquire a significant part of the outstanding sovereign debt (at market prices) of the countries in the EA and convert it to zero-coupon bonds. No transfers will take place between individual states; taxpayers in any EA country will not be involved in the debt restructuring of any foreign eurozone country. Debt will not be forgiven: individual states will agree to buy it back from the ECB in the future when the ratio of sovereign debt to GDP has fallen to 20 percent. The sterilization costs for the ECB are manageable. This model of an unconventional monetary intervention would give progressive governments in the EA the necessary basis for developing social and welfare policies to the benefit of the working classes. It would reverse present-day policy priorities and replace the neoliberal agenda with a program of social and economic reconstruction, with the elites paying for the crisis. The perspective taken here favors social justice and coherence, having as its priority the social needs and the interests of the working majority

Bayesian Image Quality Transfer with CNNs: Exploring Uncertainty in dMRI Super-Resolution

In this work, we investigate the value of uncertainty modeling in 3D super-resolution with convolutional neural networks (CNNs). Deep learning has shown success in a plethora of medical image transformation problems, such as super-resolution (SR) and image synthesis. However, the highly ill-posed nature of such problems results in inevitable ambiguity in the learning of networks. We propose to account for intrinsic uncertainty through a per-patch heteroscedastic noise model and for parameter uncertainty through approximate Bayesian inference in the form of variational dropout. We show that the combined benefits of both lead to the state-of-the-art performance SR of diffusion MR brain images in terms of errors compared to ground truth. We further show that the reduced error scores produce tangible benefits in downstream tractography. In addition, the probabilistic nature of the methods naturally confers a mechanism to quantify uncertainty over the super-resolved output. We demonstrate through experiments on both healthy and pathological brains the potential utility of such an uncertainty measure in the risk assessment of the super-resolved images for subsequent clinical use.Comment: Accepted paper at MICCAI 201

Automatic, fast and robust characterization of noise distributions for diffusion MRI

Knowledge of the noise distribution in magnitude diffusion MRI images is the centerpiece to quantify uncertainties arising from the acquisition process. The use of parallel imaging methods, the number of receiver coils and imaging filters applied by the scanner, amongst other factors, dictate the resulting signal distribution. Accurate estimation beyond textbook Rician or noncentral chi distributions often requires information about the acquisition process (e.g. coils sensitivity maps or reconstruction coefficients), which is not usually available. We introduce a new method where a change of variable naturally gives rise to a particular form of the gamma distribution for background signals. The first moments and maximum likelihood estimators of this gamma distribution explicitly depend on the number of coils, making it possible to estimate all unknown parameters using only the magnitude data. A rejection step is used to make the method automatic and robust to artifacts. Experiments on synthetic datasets show that the proposed method can reliably estimate both the degrees of freedom and the standard deviation. The worst case errors range from below 2% (spatially uniform noise) to approximately 10% (spatially variable noise). Repeated acquisitions of in vivo datasets show that the estimated parameters are stable and have lower variances than compared methods.Comment: v2: added publisher DOI statement, fixed text typo in appendix A

An operator expansion for the elastic limit

A leading twist expansion in terms of bi-local operators is proposed for the structure functions of deeply inelastic scattering near the elastic limit $x \to 1$, which is also applicable to a range of other processes. Operators of increasing dimensions contribute to logarithmically enhanced terms which are supressed by corresponding powers of $1-x$. For the longitudinal structure function, in moment ($N$) space, all the logarithmic contributions of order $\ln^k N/N$ are shown to be resummable in terms of the anomalous dimension of the leading operator in the expansion.Comment: 9 pages, 1 figure, uses REVTEX 3.1 and axodra

Wide-angle elastic scattering and color randomization

Baryon-baryon elastic scattering is considered in the independent scattering (Landshoff) mechanism. It is suggested that for scattering at moderate energies, direct and interchange quark channels contribute with equal color coefficients because the quark color is randomized by soft gluon exchange during the hadronization stage. With this assumption, it is shown that the ratio of cross sections $R_{\overline{p} p/ p p}$ at CM angle $\theta = 90^0$ decreases from a high energy value of R_{\pbar p / pp} \approx 1/2.7, down to R_{\pbar p / pp} \approx 1/28, compatible with experimental data at moderate energies. This sizable fall in the ratio seems to be characteristic of the Landshoff mechanism, in which changes at the quark level have a strong effect precisely because the hadronic process occurs via multiple quark scatterings. The effect of color randomization on the angular distribution of proton-proton elastic scattering and the cross section ratio $R_{np/pp}$ is also discussed.Comment: 18 pages, latex2e, 4 uuencoded figures, include

Developmental surface dysgraphia without surface dyslexia

The case is reported of an individual (NK) with a developmental spelling impairment (dysgraphia) who has no apparent problems in reading. His performance is therefore similar to a case of dysgraphia without dyslexia (PJT) reported by Hepner, McCloskey & Rapp (2017), and provides further evidence of a classical dissociation between impaired spelling and preserved reading in individuals with developmental literacy problems. The dissociation is observed when NK is asked to read and spell in either his first (Greek) or his second language (English). An investigation of his spelling performance revealed that his impairment was more selective than that of PJT. Although his spelling of regular words and nonwords was normal, NK had a problem in spelling words with atypical sound-letter associations despite having no problems in reading aloud or understanding the meaning of words of this kind. It is argued that NK’s pattern of performance can be best explained in terms of normal development of an orthographic system that allows access to the meaning and pronunciation of written words during reading. In terms of a dual route model of spelling, his poor spelling appears to be the result of a developmental impairment that impedes access to the orthographic system from phonology and semantics. In terms of the triangle model, his poor spelling appears to be the result of a developmental impairment that affects activation of orthography from semantics

Adrenoceptor-stimulated inflammatory response in stress-induced serum amyloid A synthesis

Rationale Stressful life events are suggested to contribute to the development of various pathologies, such as cardiovascular disorders, whose etiopathogenesis is highly associated with elevated levels of serum amyloid A (SAA) proteins. SAA synthesis inthe liver isregulated bya complex network ofcytokines actingindependently orinconcert withvarious hormones/stimulants including the stress-activated sympathetic nervous system. Objective This study aims to investigate the underlying mechanisms that regulate the stress-induced hepatic synthesis of SAA, with particular focus on adrenoceptors (AR), major components of the sympathoadrenal response to stress. Methods and results We demonstrated that repeated stress elevates IL-1β, IL-6, and TNFα serum levels in mice, accompanied by increased synthesis and secretion of hepatic SAA1/2 and SAA3, an effect that was blocked by AR antagonists. Moreover, stimulation ofα1- andβ1/2-ARsmimics thestress effectonSAA1/2 regulation, whereas α2-AR stimulation exhibitsa relatively weakimpactonSAA.InsupportoftheessentialcytokinecontributionintheAR-agonistinducedSAAproductionisthefactthat theanti-inflammatorydrug,sodiumsalicylate,preventedtheAR-stimulatedhepaticSAA1/2synthesisbyreducingIL-1βlevels, whereasIL-1βinhibitionwithAnakinramimicsthissodiumsalicylatepreventiveeffect,thusindicatingacrucial rolefor IL-1β. Interestingly, the AR-driven SAA3 synthesis was elevated by sodium salicylate in a TNFα-dependent way, supporting diverse and complex regulatory roles of cytokines in SAA production. In contrast to α1/α2-AR, the β1/2-AR-mediated SAA1/2 and SAA3 upregulation cannot be reversed by fenofibrate, a hypolipidemic drug with anti-inflammatory properties. Conclusion Taken together, these findings strongly support a critical role of the AR-stimulated inflammatory response in the hepatic SAA production under stressful conditions, highlighting distinct AR type-specific mechanisms that regulate the hepatic synthesis of SAA1/2 and SAA3.This research was supported by the European Union (European Regional Development Fund-ERDF) and the Greek national funds through the Operational Program "THESSALY-MAINLAND GREECE AND EPIRUS-2007-2013" of the National Strategic Reference Framework (NSRF 2007-2013, Grant 346985/80753) and the National Cancer Institute Intramural Research Program.info:eu-repo/semantics/publishedVersio

Tau mislocation in glucocorticoid-triggered hippocampal pathology

The exposure to high glucocorticoids (GC) triggers neuronal atrophy and cognitive deficits, but the exact cellular mechanisms underlying the GC-associated dendritic remodeling and spine loss are still poorly understood. Previous studies have implicated sustained GC elevations in neurodegenerative mechanisms through GC-evoked hyperphosphorylation of the cytoskeletal protein Tau while Tau mislocation has recently been proposed as relevant in Alzheimer's disease (AD) pathology. In light of the dual cytoplasmic and synaptic role of Tau, this study monitored the impact of prolonged GC treatment on Tau intracellular localization and its phosphorylation status in different cellular compartments. We demonstrate, both by biochemical and ultrastructural analysis, that GC administration led to cytosolic and dendritic Tau accumulation in rat hippocampus, and triggered Tau hyperphosphorylation in epitopes related to its malfunction (Ser396/404) and cytoskeletal pathology (e.g., Thr231 and Ser262). In addition, we show, for the first time, that chronic GC administration also increased Tau levels in synaptic compartment; however, at the synapse, there was an increase in phosphorylation of Ser396/404, but a decrease of Thr231. These GC-triggered Tau changes were paralleled by reduced levels of synaptic scaffolding proteins such as PSD-95 and Shank proteins as well as reduced dendritic branching and spine loss. These in vivo findings add to our limited knowledge about the underlying mechanisms of GC-evoked synaptic atrophy and neuronal disconnection implicating Tau missorting in mechanism(s) of synaptic damage, beyond AD pathology.We would like to thank Rui Fernandes for TEM technical support. IS was supported by the Portuguese Foundation for Science and Technology (FCT).This work was funded by the Portuguese Foundation for Science and Technology (FCT) (grant NMC-113934 to IS and grant SFRH/BPD/80118/2011 to JC), Canon Foundation and project DoIT - Desenvolvimento e Operacionalização da Investigação de Translação (N° do projeto 13853), funded by Fundo Europeu de Desenvolvimento Regional (FEDER) through the Programa Operacional Fatores de Competitividade (POFC).info:eu-repo/semantics/publishedVersio