989 resultados para Wolff, Christian, Freiherr von, 1679-1754


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Mode of access: Internet.

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Mode of access: Internet.

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Mode of access: Internet.

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von Lic.Dr. Freiherr von Gall, Lehrer am Realgymnasium und an der Realschule zu Mainz

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von August Freiherr von Gall, Lic.theol., Dr.phil., Professor am Gymn. und Privatdozent a.d. Univ. in Gießen

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This paper examines the relationship between financial performance and ethical screening intensity of a special class of ethical funds that is rooted in Islamic values – Islamic equity funds (IEFs). These faith-based ethical funds screen investments on compliance with Islamic values where conventional interest expense (riba), gambling (maysir), excessive uncertainty (gharar), and non-ethical (non-halal) products are prohibited. We test whether these extra screens affect the financial performance of IEFs relative to non-Islamic funds. Based on a large survivorship-free international sample of 387 Islamic funds, our results show that IEFs on average underperform conventional funds by 40 basis points per month, or 4.8% per year (supporting the underperformance hypothesis). While Islamic funds do not generally perform better during crisis periods, they outperformed conventional funds during the recent sub-prime crisis (supporting the outperformance hypothesis). Using holdings-based measures for ethical screening intensity, results show IEFs that apply more intensive screening perform worse, suggesting that there is a cost to being ethical.

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Von den wirtschaftlich genutzten Fischarten in der Ostsee haben die Plattfische nach Hering, Dorsch und Sprott den vierthöchsten Fanganteil. Mit dem Rückgang des Dorschbestandes wuchs ihr Stellenwert weiter, zumal sie ohnehin eine wertvolle Sortimentsbereicherung für die im Vergleich zur Nordsee deutlich geringere Artenvielfalt an Konsumfischen darstellen. Absolut dominierend ist die Flunder. Hauptfanggebiete der deutschen Plattfischfischerei in der Ostsee sind die Mecklenburger Bucht und die Arkonasee.

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De acordo com Leibniz, nossos raciocínios estão fundados em dois grandes princípios, o Princípio de Razão Suficiente e o Princípio de Contradição. Apesar da reconhecida relevância de tais princípios para sua filosofia, muitas são as interpretações sobre o real papel que eles desempenham dentro dela e sobre a relação deles entre si. Nosso estudo pauta-se não só pela interpretação de Leibniz como pela visão de alguns de seus comentadores, especialmente três deles: Russell, Couturat e Deleuze. Iremos pesquisar, entre outras coisas, se tais princípios são independentes um do outro; se são aplicáveis a todo tipo de verdade; se o Princípio de Perfeição é uma particularização do Princípio de Razão Suficiente ou se é irredutível a ele; e se as verdades da razão são regidas pelo Princípio de Contradição e as verdades de fato são regidas pelo Princípio de Razão Suficiente. A articulação entre tais princípios remete a um terceiro ponto: a concepção da verdade como inclusão do conceito do predicado no sujeito, tema este que iremos analisar com base nos diferentes pontos de vista acerca das proposições essenciais e existenciais. Em relação a esta última, investigaremos se representam ou não uma exceção ao caráter analítico de todas as proposições verdadeiras.

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Levetiracetam (LEV) is a prominent antiepileptic drug (AED) which binds to neuronal synaptic vesicle glycoprotein 2A (SV2A) protein and has reported effects on ion channels, but retains a poorly-defined mechanism of action. Here, we investigate inhibition of voltage-dependent Ca2+ (CaV) channels as a potential mechanism by which LEV imparts effects on neuronal activity. We used electrophysiological methods to investigate the effects of LEV on cholinergic synaptic transmission and CaV channel activity in superior cervical ganglion neurons (SCGNs). In parallel, we investigated effects of the LEV ‘inactive’ R-enantiomer, UCB L060. Thus, LEV, but not UCB L060 (each 100 μM), inhibited synaptic transmission between SCGNs in long-term culture in a time-dependent manner, significantly reducing excitatory postsynaptic potentials (EPSP) following ≥30 min application. In isolated SCGNs, LEV pretreatment (≥1 h), but not acute (5 min) application, significantly inhibited whole-cell IBa amplitude. In current clamp recordings, LEV reduced the amplitude of the afterhyperpolarizing potential (AHP) in a Ca2+-dependent manner, but also increased action potential (AP) latency in a Ca2+-independent manner, suggesting further mechanisms associated with reduced excitability. Intracellular LEV application (4-5 min) caused a rapid inhibition of IBa amplitude to an extent comparable to that seen following extracellular LEV pretreatment ( ≥ 1 h). Neither pretreatment nor intracellular application of UCB L060 produced any inhibitory effects on IBa amplitude. These results identify a stereospecific intracellular pathway by which LEV inhibits presynaptic CaV channels; resultant reductions in neuronal excitability are proposed to contribute to the anticonvulsant effects of LEV.

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Synaptic vesicle glycoprotein (SV)2A is a transmembrane protein found in secretory vesicles and is critical for Ca2+-dependent exocytosis in central neurons, although its mechanism of action remains uncertain. Previous studies have proposed, variously, a role of SV2 in the maintenance and formation of the readily releasable pool (RRP) or in the regulation of Ca2+ responsiveness of primed vesicles. Such previous studies have typically used genetic approaches to ablate SV2 levels; here, we used a strategy involving small interference RNA (siRNA) injection to knockdown solely presynaptic SV2A levels in rat superior cervical ganglion (SCG) neuron synapses. Moreover, we investigated the effects of SV2A knockdown on voltage-dependent Ca2+ channel (VDCC) function in SCG neurons. Thus, we extended the studies of SV2A mechanisms by investigating the effects on vesicular transmitter release and VDCC function in peripheral sympathetic neurons. We first demonstrated an siRNA-mediated SV2A knockdown. We showed that this SV2A knockdown markedly affected presynaptic function, causing an attenuated RRP size, increased paired-pulse depression and delayed RRP recovery after stimulus-dependent depletion. We further demonstrated that the SV2A–siRNA-mediated effects on vesicular release were accompanied by a reduction in VDCC current density in isolated SCG neurons. Together, our data showed that SV2A is required for correct transmitter release at sympathetic neurons. Mechanistically, we demonstrated that presynaptic SV2A: (i) acted to direct normal synaptic transmission by maintaining RRP size, (ii) had a facilitatory role in recovery from synaptic depression, and that (iii) SV2A deficits were associated with aberrant Ca2+ current density, which may contribute to the secretory phenotype in sympathetic peripheral neurons.