955 resultados para ENDOGENOUS HISTAMINE


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Using a data set for the 162 largest Hungarian firms during the period of 1994-1999, this paper explores the determinants of equity shares held by both foreign investors and Hungarian corporations. Evidence is found for a post-privatisation evolution towards more homogeneous equity structures, where dominant categories of Hungarian and foreign owners aim at achieving controlling stakes. In addition, focusing on firm-level characteristics we find that exporting firms attract foreign owners who acquire controlling equity stakes. Similarly, firm-size measurements are positively associated with the presence of foreign investors. However, they are negatively associated with 100% foreign ownership, possibly because the marginal costs of acquiring additional equity are growing with the size of the assets. The results are interpreted within the framework of the existing theory. In particular, following Demsetz and Lehn (1985) and Demsetz and Villalonga (2001) we argue that equity should not be treated as an exogenous variable. As for specific determinants of equity levels, we focus on informational asymmetries and (unobserved) ownership-specific characteristics of foreign investors and Hungarian investors.

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Researchers often develop and test conceptual models containing formative variables. In many cases, these formative variables are specified as being endogenous. This article provides a clarification of formative variable theory, distinguishing between the formative latent variable and the formative composite variable. When an endogenous latent variable relies on formative indicators for measurement, empirical studies can say nothing about the relationship between exogenous variables and the endogenous formative latent variable: conclusions can only be drawn regarding the exogenous variables' relationships with a composite variable. The authors also show the dangers associated with developing theory about antecedents to endogenous formative variables at the (aggregate) formative latent variable level. Modeling relationships with endogenous formative variables at the (disaggregate) indicator level informs richer theory development, and encourages more precise empirical testing. When antecedents' relationships with endogenous formative variables are modeled at the formative latent variable level rather than the formative indicator level, theory construction can verge on the superficial, and empirical findings can be ambiguous in substantive meaning.

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Presynaptic NMDA receptors facilitate the release of glutamate at excitatory cortical synapses and are involved in regulation of synaptic dynamics and plasticity. At synapses in the entorhinal cortex these receptors are tonically activated and provide a positive feedback modulation of the level of background excitation. NMDA receptor activation requires obligatory occupation of a co-agonist binding site, and in the present investigation we have examined whether this site on the presynaptic receptor is activated by endogenous glycine or d-serine. We used whole-cell patch clamp recordings of spontaneous AMPA receptor-mediated synaptic currents from rat entorhinal cortex neurones in vitro as a monitor of presynaptic glutamate release. Addition of exogenous glycine or d-serine had minimal effects on spontaneous release, suggesting that the co-agonist site was endogenously activated and likely to be saturated in our slices. This was supported by the observation that a co-agonist site antagonist reduced the frequency of spontaneous currents. Depletion of endogenous glycine by enzymatic breakdown with a bacterial glycine oxidase had little effect on glutamate release, whereas d-serine depletion with a yeast d-amino acid oxidase significantly reduced glutamate release, suggesting that d-serine is the endogenous agonist. Finally, the effects of d-serine depletion were mimicked by compromising astroglial cell function, and this was rescued by exogenous d-serine, indicating that astroglial cells are the provider of the d-serine that tonically activates the presynaptic NMDA receptor. We discuss the significance of these observations for the aetiology of epilepsy and possible targeting of the presynaptic NMDA receptor in anticonvulsant therapy. © 2014 Elsevier Ltd. All rights reserved.

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It is estimated that 69-75 million people worldwide will suffer a traumatic brain injury (TBI) or stroke each year. Brain oedema caused by TBI or following a stroke, together with other disorders of the brain cost Europe €770 billion in 2014. Aquaporins (AQP) are transmembrane water channels involved in many physiologies and are responsible for the maintenance of water homeostasis. They react rapidly to changes in osmolarity by transporting water through their highly selective central pore to maintain tonicity and aid in cell volume regulation. We have previously shown that recombinant AQP1-GFP trafficking occurs in a proteinkinase C-microtubule dependant manner in HEK-293 cells in response to hypotonicity. This trafficking mechanism is also reliant on the presence of calcium and its messenger-binding protein calmodulin and results in increased cell surface expression of AQP1 in a time-scale of ~30 seconds. There is currently very little research into the trafficking mechanisms of endogenous AQPs in primary cells. AQP4 is the most abundantly expressed AQP within the brain, it is localised to the astrocytic end-feet, in contact with the blood vessels at the blood-brain-barrier. In situations where the exquisitely-tuned osmotic balance is disturbed, high water permeability can become detrimental. AQP4-mediated water influx causes rapid brain swelling, resulting in death or long term brain damage. Previous research has shown that AQP4 knock-out mice were protected from the formation of cytotoxic brain oedema in a stroke model, highlighting AQP4 as a key drug target for this pathology. As there are currently no treatments available to restrict the flow of water through AQP4 as all known inhibitors are either cytotoxic or non-specific, controlling the mechanisms involved in the regulation of AQP4 in the brain could provide a therapeutic solution to such diseases. Using cell surface biontinylation of endogenous AQP4 in primary rat astrocytes followed by neutraavidin based ELISA we have shown that AQP4 cell surface localisation increases by 2.7 fold after 5 minutes hypotonic treatment at around 85 mOsm/kg H2O. We have also shown that this rapid relocalisation of AQP4 is regulated by PKA, calmodulin, extra-cellular calcium and actin. In summary we have shown that rapid translocation of endogenous AQP4 occurs in primary rat astrocytes in response to hypotonic stimuli; this mechanism is PKA, calcium, actin and calmodulin dependant. AQP4 has the potential to provide a treatment for the development of brain oedema.

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The successful operation of the regional development – or cohesion – policy of the European Union has a strategic importance from the point of view of the whole integration process. Strengthening economic, social and territorial cohesion and decreasing disparities between member states and regions are not only one of the main priorities of the integration, but at the same time these are justified expectations of the people living in the member states of the union. The cohesion transfers should be spent on those factors which have the biggest contribution to the improvement of development prospects and competitiveness in the given regions. Theories on regional development have controversial conclusions about the long-term formation of development disparities. However, it has become evident that successful development policies are based on endogenous factors, innovation and well-functioning institutions. After examining theoretical considerations and regional disparities the study analyses the impacts of EU regional policy and evaluates the main elements of the proposed regulatory frameworks for the period 2014-2020.

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In this paper we allow the firms to choose their prices and quantities simultaneously. Quantities are produced in advance and their common sales price is determined by the market. Firms offer their “residual capacities” at their announced prices and the corresponding demand will be served to order. If all firms have small capacities, we obtain the Bertrand solution; while if at least one firm has a sufficiently large capacity, the Cournot outcome and a model of price leadership could emerge.

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This paper adds to the growing literature on endogenous timing of decisions in duopolies. We show for a price-setting duopoly game with sufficiently asymmetric and strictly convex cost functions that the less efficient firm moves first while the more efficient moves second with a higher price than the less efficient firm.

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Our paper investigates exclusive dealing and purchasing in successive duopolies. First we show that using a limited set of feasible contracts, exclusive dealing and purchasing is going to be preferred, regardless of the level of product differentiation. In the next step, we make the choice of quality endogenous and derive the equilibrium conditions for qualities under the aforementioned contractual arrangement. Our final proposition shows that in this case the choice of quality depends exclusively on the valuation of the median consumer.

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We determine the endogenous order of moves in which the firms set their prices in the framework of a capacity-constrained Bertrand-Edgeworth triopoly. A three-period timing game that determines the period in which the firms announce their prices precedes the price-setting stage. We show for the non-trivial case (in which the Bertrand-Edgeworth triopoly has only an equilibrium in non-degenerated mixed-strategies) that the firm with the largest capacity sets its price first, while the two other firms set their prices later. Our result extends a finding by Deneckere and Kovenock (1992) from duopolies to triopolies. This extension was made possible by Hirata's (2009) recent advancements on the mixed-strategy equilibria of Bertrand-Edgeworth games.

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The main focus of this thesis was to gain a better understanding about the dynamics of risk perception and its influence on people’s evacuation behavior. Another major focus was to improve our knowledge regarding geo-spatial and temporal variations of risk perception and hurricane evacuation behavior. A longitudinal dataset of more than eight hundred households were collected following two major hurricane events, Ivan and Katrina. The longitudinal survey data was geocoded and a geo-spatial database was integrated to it. The geospatial database was composed of distance, elevation and hazard parameters with respect to the respondent’s household location. A set of Bivariate Probit (BP) model suggests that geospatial variables have had significant influences in explaining hurricane risk perception and evacuation behavior during both hurricanes. The findings also indicated that people made their evacuation decision in coherence with their risk perception. In addition, people updated their hurricane evacuation decision in a subsequent similar event.

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Thesis (Ph.D.)--University of Washington, 2016-08

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In Sudanese women with (n = 60) and without (n = 65) pre-eclampsia, circulating lipids, plasma and red cell saturated and monounsaturated fatty (MUFA) acids and dimethyl acetals (DMAs) were investigated. DMAs are an indirect marker of levels of plasmalogens, endogenous antioxidants, which play a critical role in oxidative protection, and cholesterol homeostasis. The pre-eclamptics had higher C18:1n-9 (p < 0.001) and ΣMUFA (p < 0.01) in plasma free fatty acids, C16:1n-7, C18:1n-9, ΣMUFA; 16:0/16:1n-7 (p < 0.01) in erythrocyte choline phosphoglycerides (ePC) and 16:1n-7, 18:1n-7 and 16:0/16:1n-7 (p < 0.01) in erythrocyte ethanolamine phosphoglycerides (ePE). In contrast, the DMAs 18:0, 18:1 and ΣDMAs in ePE, and 16:0, 18:0 and ΣDMAs in ePC were reduced (p < 0.001) in the pre-eclamptic women. This study of pregnant women with high carbohydrate and low fat background diet suggests pre-eclampsia is associated with oxidative stress and enhanced activity of the microsomal enzyme stearyl-CoA desaturase (delta 9 desaturase), as assessed by palmitic/palmitoleic (C16:0/C16:n-1) and stearic/oleic (C18/C18:1n-9) ratios.