996 resultados para Gottfried Benn


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Although there is evidence that exact calculation recruits left hemisphere perisylvian language systems, recent work has shown that exact calculation can be retained despite severe damage to these networks. In this study, we sought to identify a “core” network for calculation and hence to determine the extent to which left hemisphere language areas are part of this network. We examined performance on addition and subtraction problems in two modalities: one using conventional two-digit problems that can be easily encoded into language; the other using novel shape representations. With regard to numerical problems, our results revealed increased left fronto-temporal activity in addition, and increased parietal activity in subtraction, potentially reflecting retrieval of linguistically encoded information during addition. The shape problems elicited activations of occipital, parietal and dorsal temporal regions, reflecting visual reasoning processes. A core activation common to both calculation types involved the superior parietal lobule bilaterally, right temporal sub-gyral area, and left lateralized activations in inferior parietal (BA 40), frontal (BA 6/8/32) and occipital (BA 18) regions. The large bilateral parietal activation could be attributed to visuo-spatial processing in calculation. The inferior parietal region, and particularly the left angular gyrus, was part of the core calculation network. However, given its activation in both shape and number tasks, its role is unlikely to reflect linguistic processing per se. A possibility is that it serves to integrate right hemisphere visuo-spatial and left hemisphere linguistic and executive processing in calculation.

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The role of language in exact calculation is the subject of debate. Some behavioral and functional neuroimaging investigations of healthy participants suggest that calculation requires language resources. However, there are also reports of individuals with severe aphasic language impairment who retain calculation ability. One possibility in resolving these discordant findings is that the neural basis of calculation has undergone significant reorganization in aphasic calculators. Using fMRI, we examined brain activations associated with exact addition and subtraction in two patients with severe agrammatic aphasia and retained calculation ability. Behavior and brain activations during two-digit addition and subtraction were compared to those of a group of 11 healthy, age-matched controls. Behavioral results confirmed that both patients retained calculation ability. Imaging findings revealed individual differences in processing, but also a similar activation pattern across patients and controls in bilateral parietal cortices. Patients differed from controls in small areas of increased activation in peri-lesional regions, a shift from left fronto-temporal activation to the contralateral region, and increased activations in bilateral superior parietal regions. Our results suggest that bilateral parietal cortex represents the core of the calculation network and, while healthy controls may recruit language resources to support calculation, these mechanisms are not mandatory in adult cognition.

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 Returning to the Journal of Contemporary History debate on The Holy Reich, this article argues that the notion of 'positive Christianity' as  Nazi 'religious system' has been largely invented. It offers a close analysis of significant public statements on National socialism by three leading Nazis: Adolf Hitler, Gottfried Feder and Alfred Rosenberg.

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Um dos requisitos naturais na modelagem de diversas aplicações na área de banco de dados é a utilização de um mecanismo para controle de versões. Esse mecanismo fornece suporte a um processo evolutivo. Tal suporte permite armazenar os diferentes estágios de uma entidade em tempos distintos, ou sob diferentes pontos de vista. Estudos recentes nessa área mostram a importância de incorporar ao modelo conceitual de banco de dados, um mecanismo para auxiliar no controle da evolução de versões. A evolução de versões apresenta problemas principalmente quando ocorre em uma hierarquia de composição. Por exemplo, se existem objetos compostos fazendo referência à objetos componentes que representam versões, então modificações nos componentes podem causar alterações nos objetos que os referenciam. Normalmente as ações relativas a essas modificações são a notificação ou a propagação de mudanças. Algumas propostas adicionam mecanismos de notificação e propagação ao modelo conceitual utilizado por aplicações não convencionais. Isso é importante porque mecanismos deste tipo auxiliam no controle da integridade de dados e na divulgação de informações sobre as mudanças realizadas no banco de dados. O objetivo do trabalho aqui descrito é apresentar um mecanismo de notificação e propagação, que trata da evolução de dados, para um modelo de versões. É definido um modelo de classes com propriedades e operações que permitem manter e manipular subscrições de eventos referentes à evolução de objetos e versões e reagir diante da ocorrência destes eventos. Para atender os requisitos das diferentes aplicações, esta proposta especifica três estratégias. Cada uma delas apresenta diferentes funcionalidades: notificação ativa (enviar mensagens sobre mudanças ocorridas); notificação passiva (armazenar informações sobre mudanças ocorridas) e propagação (alterar o conteúdo do banco de dados automaticamente). Para validar o mecanismo proposto, uma implementação é apresentada para o sistema Oracle 8.

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A Dieta Cetogênica é caracterizada pelo alto teor de gordura e baixo teor de carboidratos e proteínas, e tem sido proposta como benéfica em crianças com desordens epiléticas que não respondem ao tratamento convencional de drogas anti-epiléticas. O retardo de crescimento é um importante inconveniente desta dieta e as causas metabólicas ainda não estão bem caracterizadas. O objetivo desse estudo é examinar a variação de peso corporal e de tecido adiposo de ratos Wistar tratados com a dieta cetogênica durante 6 semanas, e a atividade da fração citosólica da enzima fosfoenolpiruvato carboxicinase (PEPCK) no tecido adiposo. Os ratos alimentados com a dieta cetogênica apresentaram uma diminuição do peso corporal, mas um significante aumento de tecido adiposo. A razão tecido adiposo/peso corporal apresentou diferenças entre os ratos cetogênicos e os controles já na primeira semana de tratamento, cerca de 2 vezes maior nos ratos cetogênicos. A lipogênese visceral foi mantida por um aumento na atividade da PEPCK, objetivando o fornecimento de glicerol-3- fosfato para a síntese de triacilglicerol e este acúmulo de gordura foi acompanhado por intolerância à glicose. Não foram observadas mudanças na glicemia e lipidemia basais. Estes dados contribuem para o entendimento dos efeitos metabólicos da dieta cetogênica e sugere alguns riscos potenciais desta dieta.

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A partir de uma grande base de dados fornecida por uma instituição de microcrédito do nordeste brasileiro, a relação entre parentesco e inadimplência é analisada. O presente trabalho mostra evidências de que o parentesco entre membros de um grupo solidário afeta positivamente a adimplência. Grupos em que todos os membros possuíam algum laço de parentesco entre si apresentaram uma probabilidade 24% menor de inadimplência do que grupo sem esses laços. Além disso, quando considerado apenas o primeiro empréstimo, grupos com 100% de parentesco entre os membros apresentaram uma probabilidade 45% menor de inadimplência em comparação com membros sem relações de parentesco. Os resultados deste trabalho também mostram que há uma relação negativa entre parentesco e probabilidade de mudança na formação de um grupo solidário. Essas análises permitem fazer inferências acerca dos mecanismos pelos quais o parentesco afeta o desempenho do microcrédito. Os resultados sugerem que o parentesco possui um benefício maior no processo de autosseleção do grupo. Além disso, os resultados também sugerem que o impacto positivo do parentesco nas atividades de automonitoramento compensa o enfraquecimento das atividades de enforcement.

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This paper examines the efects of the transfer of credit risk associated with bank loans. We are interested in (a) whether the transfer of credit risk has any impact on the intensity with which banks monitor their borrowers and (b) whether credit risk transfer infuences the amount of financing that is provided to firms in an economy. Our model first develops conditions under which bank finance is available to firrms, mainly in the spirit of Holmstrom/Tirole (1997). We then introduce projects with uncorrelated pay-offs and argue that one possible economic rationale for credit risk transfer is diversi¯cation. We analyze whether and how within this scenario the transfer of the credit risk of loans changes a bank's incentives to monitor its debtors. Finally we investigate whether and what kind of impact this may have on the amount of ¯nancing available to firms in an economy. Our results indicate that the monitoring incentives are being eroded indeed and that credit risk transfer can increase the overall amount of obtainable funds in an economy.

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Recent regulatory efforts aim at lowering the cyclicality of bank lending because of its potential detrimental effects on financial stability and the real economy. We investigate the cyclicality of SME lending by local banks with vs. without a public mandate, controlling for location, size, loan maturity, funding structure, liquidity, profitability, and credit demand-side factors. The public mandate is set by local governments and stipulates a deviation from strict profit maximization and a sustainable provision of financial services to local customers. We find that banks with a public mandate are 25 percent less cyclical than other local banks. The result is credit supply-side driven and especially strong for savings banks with high liquidity and stable deposit funding. Our findings have implications for the banking structure, financial stability and the finance-growth nexus in a local context.

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The general idea of this research is to analyze overall firm performance before and after the global financial crisis of 2008. The main question is: What kind of strategies did companies adopt that led to positive business performance after the crisis? Are there any particular competitive advantages that bring better performance in the case of an economic downturn? This research focuses on competitive advantage gained by resource-based view attributes of a product (quality, durability and prestige) and dynamic capabilities (strategic flexibility in product development and technological innovation ability). The economic crisis setting provides a proper background to analyze the competitive advantage strategies in a dynamic, low-probability environment to determine which are most worth adopting in the business world. I employ an OLS regression analysis in order to measure the business performance of 136 Brazilian firms across four years – 2002, 2005, 2008 and 2012. The findings indicate that even though all of the strategic resources and capabilities positively influence firm performance in expansionary periods, only the superior product characteristics are pertinent in surviving an economic downturn.

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Recent regulatory efforts aim at lowering the cyclicality of bank lending because of its potential detrimental effects on financial stability and the real economy. We investigate the cyclicality of SME lending by local banks with vs. without a public mandate, controlling for location, size, loan maturity, funding structure, liquidity, profitability, and credit demand-side factors. The public mandate is set by local governments and stipulates a deviation from strict profit maximization and a sustainable provision of financial services to local customers. We find that banks with a public mandate are 25 percent less cyclical than other local banks. The result is credit supply-side driven and especially strong for savings banks with high liquidity and stable deposit funding. Our findings have implications for the banking structure, financial stability and the finance-growth nexus in a local context.

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Autism comprises a heterogeneous group of neurodevelopmental disorders that affects the brain maturation and produces sensorial, motor, language and social interaction deficits in early childhood. Several studies have shown a major involvement of genetic factors leading to a predisposition to autism, which are possibly affected by environmental modulators during embryonic and post-natal life. Recent studies in animal models indicate that alterations in epigenetic control during development can generate neuronal maturation disturbances and produce a hyper-excitable circuit, resulting in typical symptoms of autism. In the animal model of autism induced by valproic acid (VPA) during rat pregnancy, behavioral, electrophysiological and cellular alterations have been reported which can also be observed in patients with autism. However, only a few studies have correlated behavioral alterations with the supposed neuronal hyper-excitability in this model. The aim of this project was to generate an animal model of autism by pre-natal exposure to VPA and evaluate the early post-natal development and pre-puberal (PND30) behavior in the offspring. Furthermore, we quantified the parvalbumin-positive neuronal distribution in the medial prefrontal cortex and Purkinje cells in the cerebellum of VPA animals. Our results show that VPA treatment induced developmental alterations, which were observed in behavioral changes as compared to vehicle-treated controls. VPA animals showed clear behavioral abnormalities such as hyperlocomotion, prolonged stereotipies and reduced social interaction with an unfamiliar mate. Cellular quantification revealed a decrease in the number of parvalbumin-positive interneurons in the anterior cingulate cortex and in the prelimbic cortex of the mPFC, suggesting an excitatory/inhibitory unbalance in this animal model of autism. Moreover, we also observed that the neuronal reduction occurred mainly in the cortical layers II/III and V/VI. We did not detect any change in the density of Purkinje neurons in the Crus I region of the cerebellar cortex. Together, our results strengthens the face validity of the VPA model in rats and shed light on specific changes in the inhibitory circuitry of the prefrontal cortex in this autism model. Further studies should address the challenges to clarify particular electrophysiological correlates of the cellular alterations in order to better understand the behavioral dysfunctions