2,364 research outputs found

    The role of actors in the policy design process: introducing design coalitions to explain policy output

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    Despite a renaissance of policy design thinking in public policy literature and a renewed interest in agency in the policy process literature, agency in the policy design process has, so far, not received systematic attention. Understanding the agency at play when designing policy, however, is crucial for better comprehension of policy design choices and varia- tion in policy design across cases. Here, we build on the hierarchical structure of design elements that constitute each policy and analyse how actors position themselves during a policy design process in relation to individual design elements. Our aim is to establish dif- ferent actors’ roles in shaping the policy output in an inductive, single-case study using the empirical case of the Swiss renewable energy feed-in tariff. Notably, we find agency in the form of coalitions which emerge around particular design elements. Based on our repre- sentative analysis, we derive the generalisable concept of design coalitions that we define as relational structures of actors who gather around and advocate for specific policy design elements during the policy design process. Policy design coalitions are dynamic through- out the design process and strategic and constitute the determinants in translating policy problems into final policy designs during policy designing. Our approach allows us to shed light on the role of agency in the policy design process in general

    Empirical macromodels under test: a comparative simulation study of the employment effects of a revenue neutral cut in social security contributions

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    In the paper we simulate a revenue-neutral cut in the social security contribution rate using five different types of macro- / microeconomic models, namely two models based on time-series data where the labour market is modelled basically demand oriented, two models of the class of computable equilibrium models which are supply oriented and finally a firm specific model for international tax burden comparisons. Our primary interest is in the employment effects the models predict due to the cut in the contribution rate. It turns out that qualitatively all models considered predict an increase in employment three years after the cut. But the employment effects differ considerably in magnitude, which follows immediately from the different behavioral assumptions underlying the different models. -- In dem Beitrag wird der BeschĂ€ftigungseffekt infolge einer aufkommensneutralen Senkung der SozialversicherungsbeitrĂ€ge simuliert. Zu diesem Zweck werden fĂŒnf unterschiedliche ökonomische Modelle verwendet, namentlich zwei Modelle, die auf Zeitreihendaten aufbauen und in denen der Arbeitsmarkt ĂŒberwiegend von der Nachfrageseite dominiert wird, zwei Modelle aus der Klasse der computable equilibrium models, die typischerweise angebotsorientiert sind, und ein mikroökonomisches, firmenspezifisches Steuerbelastungsvergleichsmodell. Alle Simulationsergebnisse der Modelle weisen auf einen, wenngleich teilweise kleinen, positiven BeschĂ€ftigungseffekt hin, der sich allerdings betrĂ€chtlich in seiner GrĂ¶ĂŸenordnung unterscheidet. Dies ist eine unmittelbare Folge aus den unterschiedlichen Verhaltensannahmen, die den einzelnen Modellen unterliegen.

    Glutathione deficiency down-regulates hepatic lipogenesis in rats

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    <p>Abstract</p> <p>Background</p> <p>Oxidative stress is supposed to increase lipid accumulation by stimulation of hepatic lipogenesis at transcriptional level. This study was performed to investigate the role of glutathione in the regulation of this process. For that purpose, male rats were treated with buthionine sulfoximine (BSO), a specific inhibitor of Îł-glutamylcysteine synthetase, for 7 days and compared with untreated control rats.</p> <p>Results</p> <p>BSO treatment caused a significant reduction of total glutathione in liver (-70%), which was attributable to diminished levels of reduced glutathione (GSH, -71%). Glutathione-deficient rats had lower triglyceride concentrations in their livers than the control rats (-23%), whereas the circulating triglycerides and the cholesterol concentrations in plasma and liver were not different between the two groups of rats. Livers of glutathione-deficient rats had lower mRNA abundance of sterol regulatory element-binding protein (SREBP)-1c (-47%), Spot (S)14 (-29%) and diacylglycerol acyltransferase 2 (DGAT-2, -27%) and a lower enzyme activity of fatty acid synthase (FAS, -26%) than livers of the control rats. Glutathione-deficient rats had also a lower hepatic activity of the redox-sensitive protein-tyrosine phosphatase (PTP)1B, and a higher concentration of irreversible oxidized PTP1B than control rats. No differences were observed in protein expression of total PTP1B and the mature mRNA encoding active XBP1s, a key regulator of unfolded protein and ER stress response.</p> <p>Conclusion</p> <p>This study shows that glutathione deficiency lowers hepatic triglyceride concentrations via influencing lipogenesis. The reduced activity of PTP1B and the higher concentration of irreversible oxidized PTP1B could be, at least in part, responsible for this effect.</p

    Empirical Macromodels Under Test

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    This paper examines the employment effects of a revenue-neutral cut in the social security contribution rate in Germany by running policy simulations in four different types of macroeconomic models. Two models are based on time-series data where the labor market is modeled basically demand oriented, whereas the other two models are supply oriented computable general equilibrium models. While the predicted employment effects of the cut in the contribution rate are qualitatively similar across models three years after the cut, they differ considerably in magnitude. These differences can to a large extent be attributed to differences in the basic structure of the models. Of special importance is how prices and wages react in each model to the cut in the social security tax rate on one side, and the necessary increase of the indirect tax rate on the other side. The results, therefore, provide a guideline for assessing the outcome of policy simulations and for the further development of macroeconomic models suitable for this kind of experiments

    Pathogenicity of Pythium species to maize

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    AbstractPythium isolates from diseased and dead bait plants of maize and cress grown in compost or various soils (maize fields, parkland under deciduous trees, grassland) were characterised and tested for pathogenicity to maize (Zea mays L.). In pot tests performed under controlled conditions, pathogenicity of the isolates to maize was apparent by reduction of root and shoot growth, whereas damping-off of maize seedlings was less frequent. Contrarily, pea seedlings were killed by pathogenic Pythium isolates. Pythium isolates from diseased maize seedlings and pathogenic strains from other gramineous plants (P. phragmitis, P. aff.phragmitis, P. catenulatum) were not necessarily more virulent to maize compared to isolates originating from dicotyledonous plants (cress). The most virulent isolates originated from compost and caused a reduction of maize shoot growth of up to 60%. Phylogenetic analysis revealed that they were very closely related to P. ultimum var. ultimum and P. arrhenomanes, respectively. Isolates originating from maize fields, grassland and parkland under deciduous trees, a reference culture of P. arrhenomanes and strains of P. phragmitis, P. aff. phragmitis and P. catenulatum with known pathogenicity on reed were non-pathogenic on maize. Isolates from compost, and from maize fields generally had a higher temperature optimum for mycelial growth (30 °C) and a faster growth rate (1.5–2.0 mm h−1) compared to the isolates from parkland under deciduous trees and grassland soil (20–25 °C, ~1.0 mm h−1), respectively. This study indicates a potential impact of pathogenic Pythium on maize plants even in the absence of visible symptoms

    Empirical Macromodels Under Test : A Comparative Simulation Study of the Employment Effects of a Revenue Neutral Cut in Social Security Contributions

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    In the paper we simulate a revenue-neutral cut in the social security contribution rate using five different types of macro- / microeconomic models, namely two models based on time-series data where the labour market is modelled basically demand oriented, two models of the class of computable equilibrium models which are supply oriented and finally a firm specific model for international tax burden comparisons. Our primary interest is in the employment effects the models predict due to the cut in the contribution rate. It turns out that qualitatively all models considered predict an increase in employment three years after the cut. But the employment effects differ considerably in magnitude, which follows immediately from the different behavioral assumptions underlying the different models

    Tetramer enrichment reveals the presence of phenotypically diverse hepatitis C virus-specific CD8+T cells in chronic infection

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    Virus-specific CD8+ T cells are rarely detectable ex vivo by conventional methods during chronic hepatitis C virus (HCV) infection. In this study, however, we were able to detect and characterize HCV-specific CD8+ T cells in all chronically HCV genotype 1a-infected, HLA-A*02:01-positive patients analyzed by performing major histocompatibility complex (MHC) class I tetramer enrichment. Two-thirds of these enriched HCV-specific CD8+ T-cell populations displayed an effector memory phenotype, whereas, surprisingly, one-third displayed a naive-like phenotype despite ongoing viral replication. CD8+ T cells with an effector memory phenotype could not expand in vitro, suggesting exhaustion of these cells. Interestingly, some of the naive-like CD8+ T cells proliferated vigorously upon in vitro priming, whereas others did not. These differences were linked to the corresponding viral sequences in the respective patients. Indeed, naive-like CD8+ T cells from patients with the consensus sequence in the corresponding T-cell epitope did not expand in vitro. In contrast, in patients displaying sequence variations, we were able to induce HCV-specific CD8+ T-cell proliferation, which may indicate infection with a variant virus. Collectively, these data reveal the presence of phenotypically and functionally diverse HCV-specific CD8+ T cells at very low frequencies that are detectable in all chronically infected patients despite viral persistence. IMPORTANCE In this study, we analyzed CD8+ T-cell responses specific for HLA-A*02:01-restricted epitopes in chronically HCV-infected patients, using MHC class I tetramer enrichment. Importantly, we could detect HCV-specific CD8+ T-cell populations in all patients. To further characterize these HCV-specific CD8+ T-cell populations that are not detectable using conventional techniques, we performed phenotypic, functional, and viral sequence analyses. These data revealed different mechanisms for CD8+ T-cell failure in HCV infection, including T-cell exhaustion, viral escape, and functional impairment of naive-like HCV-specific CD8+ T cells

    Modulating the polarization of broadband terahertz pulses from a spintronic emitter at rates up to 10 kHz

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    eliable modulation of terahertz electromagnetic waveforms is important for many applications. Here, we rapidly modulate the direction of the electric field of linearly polarized terahertz electromagnetic pulses with 1–30 THz bandwidth by applying time-dependent magnetic fields to a spintronic terahertz emitter. Polarity modulation of the terahertz field with more than 99% contrast at a rate of 10 kHz is achieved using a harmonic magnetic field. By adding a static magnetic field, we modulate the direction of the terahertz field between angles of, for instance, −53° and 53° at kilohertz rates. We believe our approach makes spintronic terahertz emitters a promising source for low-noise modulation spectroscopy and polarization-sensitive techniques such as ellipsometry at 1–30 THz

    Molecular Sequence of Events and Signaling Pathways in Cerebral Metastases

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    Brain metastases are the leading cause of morbidity and mortality among cancer patients, and are reported to occur in about 40% of cancer patients with metastatic disease in the United States of America. Primary tumor cells appear to detach from the parent tumor site, migrate, survive and pass through the blood brain barrier in order to establish cerebral metastases. This complex process involves distinct molecular and genetic mechanisms that mediate metastasis from these primary organs to the brain. Furthermore, an interaction between the invading cells and cerebral milieu is shown to promote this process as well. Here, we review the mechanisms by which primary cancer cells metastasize to the brain via a mechanism called epithelial-to-mesenchymal transition, as well as the involvement of certain microRNA and genetic aberrations implicated in cerebral metastases from the lung, breast, skin, kidney and colon. While the mechanisms governing the development of brain metastases remain a major hindrance in treatment, understanding and identification of the aforementioned molecular pathways may allow for improved management and discovery of novel therapeutic targets
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