Globalization with Labor Market Frictions and Non-Scale Growth

We analyze the interaction between globalization and labor market frictions in a dynamic general equilibrium North-South non-scale growth model with endogenous Northern innovation and endogenous Southern imitation. The employment, growth and relative-wage effects of globalization are shown to depend qualitatively on the degree of Northern labor market frictions. We demonstrate that Northern countries with particular severe labor market frictions benefit from globalization in terms of employment and growth. We also analyze whether stricter intellectual property rights protection in the South, rising R&D subsidies in the North or an increase in Northern labor market flexibility alleviate or aggravate globalization effects.Globalization, Quality-Ladder Model, Non-Scale Growth, Frictional Unemployment, Firing Costs

Globalization, Labor Market Rigidities and Multiple Equilibria

This paper analyses the effects of globalization, stricter intellectual property rights protection and different labor market policies in a dynamic North-South general equilibrium model with non-scale growth. To this aim, we generalize the Schumpeterian product-lifecycle model of Dinopoulos and Segerstrtom (2003) by adding frictional unemployment and firing costs to their framework. We find that the effects on North-South wage inequality, employment and growth depend qualitatively on the level of Northern firing costs. Contrary to the special case of perfect labor market flexibility studied by Dinopoulos and Segerstrom, globalization may not benefit anymore both the South in terms of a relative-wage catch up and the North in terms of a temporary innovation and growth push.Economic Growth, North-South Trade, Globalization, Frictional Unemployment, Firing Costs

The Conundrum of Recovery Policies: Growth or Jobs?

This paper adopts a Neo-Schumpeterian approach to macroeconomics, by proposing a model which includes fully-endogenous growth, involuntary search-based unemployment, and financial frictions. The model analyzes the effects of several recovery policies used by governments to fight unemployment or/and enhance growth. Employment protection legislation reduces growth and unemployment. Policies that reduce the cost of job vacancies decrease unemployment and raise growth. Industrial policies in the form of production subsidies to young small firms, production taxes to adult large firms, and R&D subsidies increase growth and unemployment. Policies that reduce financial frictions accelerate growth but exert an ambiguous effect on unemployment.fully- endogenous growth, Schumpeterian unemployment, financial frictions, recovery policies, vacancy creation

Statin-induced myopathic changes in primary human muscle cells and reversal by a prostaglandin F2 alpha analogue

Statin-related muscle side effects are a constant healthcare problem since patient compliance is dependent on side effects. Statins reduce plasma cholesterol levels and can prevent secondary cardiovascular diseases. Although statin-induced muscle damage has been studied, preventive or curative therapies are yet to be reported. We exposed primary human muscle cell populations (n = 22) to a lipophilic (simvastatin) and a hydrophilic (rosuvastatin) statin and analyzed their expressome. Data and pathway analyses included GOrilla, Reactome and DAVID. We measured mevalonate intracellularly and analyzed eicosanoid profiles secreted by human muscle cells. Functional assays included proliferation and differentiation quantification. More than 1800 transcripts and 900 proteins were differentially expressed after exposure to statins. Simvastatin had a stronger effect on the expressome than rosuvastatin, but both statins influenced cholesterol biosynthesis, fatty acid metabolism, eicosanoid synthesis, proliferation, and differentiation of human muscle cells. Cultured human muscle cells secreted ω-3 and ω-6 derived eicosanoids and prostaglandins. The ω-6 derived metabolites were found at higher levels secreted from simvastatin-treated primary human muscle cells. Eicosanoids rescued muscle cell differentiation. Our data suggest a new aspect on the role of skeletal muscle in cholesterol metabolism. For clinical practice, the addition of omega-n fatty acids might be suitable to prevent or treat statin-myopathy

Júlio Dinis, apologista da Kunstreligion : influência de uma corrente de pensamento europeu no percurso literário dinisiano

O principal objetivo desta tese consiste na análise da possível influência de uma corrente de pensamento europeu no percurso literário dinisiano. Considera-se que esse percurso inicia em 1861, quando Joaquim Guilherme Gomes Coelho – usando pela primeira vez o pseudónimo de Júlio Dinis – publica três poemas num «periódico de poesias inéditas», A Grinalda, e termina nos primeiros dias de setembro de 1871, com a revisão do manuscrito da sua última Crónica da Aldeia, Os Fidalgos da Casa Mourisca. A corrente de pensamento acima referida constituiu-se como um paradigma filosófico da modernidade, de influência hegeliana, e é comummente designada por Kunstreligion (religião da arte), por ter conhecido o seu centro teórico na Alemanha, embora, a partir de 1850, se tenha expandido por outros países europeus, onde a sua receção se efetuou, pri-meiramente, de forma pontual, por parte de alguns artistas – entre eles o nosso Júlio Dinis, mas também Antero de Quental – que começaram então a exaltar a arte como religião, da qual o artista, assumindo funções ministeriais, se apresenta como sacerdote. A missão a cumprir seria a de educar e civilizar o povo europeu, num tempo em que as sociedades da Europa ocidental experienciam um acelerado processo de secularização. Desta forma, na segunda metade do século XIX, o conceito de Kunstreligion radicaliza-se, começando a exprimir uma relação de concorrência, no espaço público, entre a arte e a religião oficial – no caso português, entre a arte e o catolicismo. Essa concorrência expressa-se, sobretudo, através da atitude dos artistas, que, com a sua prática artística, intervêm criticamente na sociedade, com o intento de ajudar a (re)construí-la, veiculando os valores inerentes à ideo-logia que defendem – e a Kunstreligion difunde enquanto corrente estético-filosófica.The main objective of this thesis is to investigate the possible influence of a European cur-rent of thought in Dinisian’s literary career. It is considered that this career begins in 1861, when Joaquim Guilherme Gomes Coelho – using, for the first time, the pseudonym of Júlio Dinis – publishes three poems in a «periodical paper of unpublished poems», A Grinalda, and concludes in the first days of September 1871 with the revision of the manuscript of his last Crónica da Aldeia, Os Fidalgos da Casa Mourisca. The European current of thought mentioned above formed itself as a philosophical para-digm of the modernity, of Hegelian influence, and is usually called Kunstreligion (Art Re-ligion), because of having known its theoretical core in Germany, although after 1850 it has expanded to other European countries, where its reception occurred at first individually by some artists – among them our Júlio Dinis, but also Antero de Quental – who began to exalt art as religion, from which the artist presents himself as a priest, in the way that he assumes ministerial functions. Therefore, the artist has a mission to perform in order to educate and civilize the European people, at a time when Western European societies are undergoing an accelerated process of secularization. In this way, in the second part of the nineteenth century the concept of Kunstreligion radicalise itself and begins to express a relationship of concurrence, in the public place, between art and official religion – in the particular case of Portugal, between art and Catholicism. This concurrence expresses itself, above all, in artists’ attitudes who critically intervene in society with their artistic practice intending to help to (re)build it. In doing so, artistes convey the values which are inherent in the ideology they defend – and Kunstreligion spreads as an aesthetic-philosophical cur-rent

A molecular signature of myalgia in myotonic dystrophy 2

Background: Chronic muscle pain affects close to 20% of the population and is a major health burden. The underlying mechanisms of muscle pain are difficult to investigate as pain presents in patients with very diverse histories. Treatment options are therefore limited and not tailored to underlying mechanisms. To gain insight into the pathophysiology of myalgia we investigated a homogeneous group of patients suffering from myotonic dystrophy type 2 (DM2), a monogenic disorder presenting with myalgia in at least 50% of affected patients. Methods: After IRB approval we performed an observational cross-sectional cohort study and recruited 42 patients with genetically confirmed DM2 plus 20 healthy age and gender matched control subjects. All participants were subjected to an extensive sensory-testing protocol. In addition, RNA sequencing was performed from 12 muscle biopsy specimens obtained from DM2 patients. Findings: Clinical sensory testing as well as RNA sequencing clearly separated DM2 myalgic from non-myalgia patients and also from healthy controls. In particular pressure pain thresholds were significantly lowered for all muscles tested in myalgic DM2 patients but were not significantly different between non-myalgic patients and healthy controls. The expression of fourteen muscle expressed genes in myalgic patients was significantly up or down-regulated in myalgic compared to non-myalgic DM2 patients. Interpretation: Our data support the idea that molecular changes in the muscles of DM2 patients are associated with muscle pain. Further studies should address whether muscle-specific molecular pathways play a significant role in myalgia in order to facilitate the development of mechanism-based therapeutic strategies to treat musculoskeletal pain

Scene memory and spatial inhibition in visual search

Abstract: Any object-oriented action requires that the object be first brought into the attentional foreground, often through visual search. Outside the laboratory, this would always take place in the presence of a scene representation acquired from ongoing visual exploration. The interaction of scene memory with visual search is still not completely understood. Feature integration theory (FIT) has shaped both research on visual search, emphasizing the scaling of search times with set size when searches entail feature conjunctions, and research on visual working memory through the change detection paradigm. Despite its neural motivation, there is no consistently neural process account of FIT in both its dimensions. We propose such an account that integrates (1) visual exploration and the building of scene memory, (2) the attentional detection of visual transients and the extraction of search cues, and (3) visual search itself. The model uses dynamic field theory in which networks of neural dynamic populations supporting stable activation states are coupled to generate sequences of processing steps. The neural architecture accounts for basic findings in visual search and proposes a concrete mechanism for the integration of working memory into the search process. In a behavioral experiment, we address the long-standing question of whether both the overall speed and the efficiency of visual search can be improved by scene memory. We find both effects and provide model fits of the behavioral results. In a second experiment, we show that the increase in efficiency is fragile, and trace that fragility to the resetting of spatial working memory

Subclinical myocardial injury in patients with Facioscapulohumeral muscular dystrophy 1 and preserved ejection fraction - assessment by cardiovascular magnetic resonance

Background: Facioscapulohumeral muscular dystrophy type 1 (FSHD1) is an autosomal dominant and the third most common inherited muscle disease. Cardiac involvement is currently described in several muscular dystrophies (MD), but there are conflicting reports in FSHD1. Mostly, FSHD1 is recognized as MD with infrequent cardiac involvement, but sudden cardiac deaths are reported in single cases. The aim of this study is to investigate whether subclinical cardiac involvement in FSHD1 patients is detectable in preserved left ventricular systolic function applying cardiovascular magnetic resonance (CMR). Methods: We prospectively included patients with genetically confirmed FSHD1 (n = 52, 48 ± 15 years) and compared them with 29 healthy age-matched controls using a 1.5 T CMR scanner. Myocardial tissue differentiation was performed qualitatively using focal fibrosis imaging (late gadolinium enhancement (LGE)), fat imaging (multi-echo sequence for fat/water-separation) and parametric T2- and T1-mapping for quantifying inflammation and diffuse fibrosis. Extracellular volume fraction was calculated. A 12-lead electrocardiogram and 24-h Holter were performed for the assessment of MD-specific Groh-criteria and arrhythmia. Results: Focal fibrosis by LGE was present in 13 patients (25%,10 men), fat infiltration in 7 patients (13%,5 men). T2 values did not differ between FSHD1 and healthy controls. Native T1 mapping revealed significantly higher values in patients (global native myocardial T1 values basal: FSHD1: 1012 ± 26 ms vs. controls: 985 ± 28 ms, p < 0.01, medial FSHD1: 994 ± 37 ms vs. controls: 982 ± 28 ms, p = 0.028). This was also evident in regions adjacent to focal fibrosis, indicating diffuse fibrosis. Groh-criteria were positive in 1 patient. In Holter, arrhythmic events were recorded in 10/43 subjects (23%). Conclusions: Patients with FSHD1 and preserved left ventricular ejection fraction present focal and diffuse myocardial injury. Longitudinal multi-center trials are needed to define the impact of myocardial changes as well as a relation between myocardial injury and arrhythmias on long-term prognosis and therapeutic decision-making. Trial Registration: ISRCTN registry with study ID ISRCTN13744381

Statins aggravate the risk of insulin resistance in human muscle

Beside their beneficial effects on cardiovascular events, statins are thought to contribute to insulin resistance and type-2 diabetes. It is not known whether these effects are long-term events from statin-treatment or already triggered with the first statin-intake. Skeletal muscle is considered the main site for insulin-stimulated glucose uptake and therefore, a primary target for insulin resistance in the human body. We analyzed localization and expression of proteins related to GLUT4 mediated glucose uptake via AMPKα or AKT in human skeletal muscle tissue from patients with statin-intake >6 months and in primary human myotubes after 96 h statin treatment. The ratio for AMPKα activity significantly increased in human skeletal muscle cells treated with statins for long- and short-term. Furthermore, the insulin-stimulated counterpart, AKT, significantly decreased in activity and protein level, while GSK3ß and mTOR protein expression reduced in statin-treated primary human myotubes, only. However, GLUT4 was normally distributed whereas CAV3 was internalized from plasma membrane around the nucleus in statin-treated primary human myotubes. Statin-treatment activates AMPKα-dependent glucose uptake and remains active after long-term statin treatment. Permanent blocking of its insulin-dependent counterpart AKT activation may lead to metabolic inflexibility and insulin resistance in the long run and may be a direct consequence of statin-treatment