988 resultados para Flow Stability


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Choosing a financially strong insurance company is important when buying health insurance. You want the company to still be in business when you have claims, which can be 20 to 30 years from now. Insurance companies selling insurance in Iowa have met the minimum legal standards to be licensed by the State of Iowa Insurance Division. This licensure doesn’t mean the company has a high financial stability rating. Several independent rating agencies evaluate the financial stability of insurance companies. The rating for an individual insurance company is an opinion as to its financial strength and ability to pay claims in the future. When evaluating a company, a rating agency may consider a company's balance sheet strength, operating performance and business management and strategies.

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It is widely accepted in the literature about the classicalCournot oligopoly model that the loss of quasi competitiveness is linked,in the long run as new firms enter the market, to instability of the equilibrium. In this paper, though, we present a model in which a stableunique symmetric equilibrium is reached for any number of oligopolistsas industry price increases with each new entry. Consequently, the suspicion that non quasi competitiveness implies, in the long run, instabilityis proved false.

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We develop a coordination game to model interactions betweenfundamentals and liquidity during unstable periods in financial markets.We then propose a flexible econometric framework for estimationof the model and analysis of its quantitative implications. The specificempirical application is carry trades in the yen dollar market, includingthe turmoil of 1998. We find a generally very deep market, withlow information disparities amongst agents. We observe occasionallyepisodes of market fragility, or turmoil with up by the escalator, downby the elevator patterns in prices. The key role of strategic behaviorin the econometric model is also confirmed.

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In this paper, we discuss pros and cons ofdifferent models for financial market regulationand supervision and we present a proposal forthe re-organisation of regulatory and supervisoryagencies in the Euro Area. Our arguments areconsistent with both new theories and effectivebehaviour of financial intermediaries inindustrialized countries. Our proposed architecturefor financial market regulation is based on theassignment of different objectives or "finalities"to different authorities, both at the domesticand the European level. According to thisperspective, the three objectives of supervision- microeconomic stability, investor protectionand proper behaviour, efficiency and competition- should be assigned to three distinct Europeanauthorities, each one at the centre of a Europeansystem of financial regulators and supervisorsspecialized in overseeing the entire financialmarket with respect to a single regulatoryobjective and regardless of the subjective natureof the intermediaries. Each system should bestructured and organized similarly to the EuropeanSystem of Central Banks and work in connectionwith the central bank which would remain theinstitution responsible for price and macroeconomicstability. We suggest a plausible path to buildour 4-peak regulatory architecture in the Euro area.

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Deletion or substitution of the serine-rich N-terminal stretch of grass phytochrome A (phyA) has repeatedly been shown to yield a hyperactive photoreceptor when expressed under the control of a constitutive promoter in transgenic tobacco or Arabidopsis seedlings retaining their native phyA. These observations have lead to the proposal that the serine-rich region is involved in negative regulation of phyA signaling. To re-evaluate this conclusion in a more physiological context we produced transgenic Arabidopsis seedlings of the phyA-null background expressing Arabidopsis PHYA deleted in the sequence corresponding to amino acids 6-12, under the control of the native PHYA promoter. Compared to the transgenic seedlings expressing wild-type phyA, the seedlings bearing the mutated phyA showed normal responses to pulses of far-red (FR) light and impaired responses to continuous FR light. In yeast two-hybrid experiments, deleted phyA interacted normally with FHY1 and FHL, which are required for phyA accumulation in the nucleus. Immunoblot analysis showed reduced stability of deleted phyA under continuous red or FR light. The reduced physiological activity can therefore be accounted for by the enhanced destruction of the mutated phyA. These findings do not support the involvement of the serine-rich region in negative regulation but they are consistent with a recent report suggesting that phyA turnover is regulated by phosphorylation.

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In this study, we report the effect of fatty acids on the Thy-1 antigen mRNA decay. Low serum and synthetic medium culture conditions were used to demonstrate that fatty acids, which are important metabolites involved as second messengers in signal transduction, also influence the steady-state mRNA level. Detailed analysis demonstrated that polyunsaturated lipids attached to bovine serum albumin, such as linoleic, linolenic, and arachidonic acids, modulate gene expression specifically in the S1A T lymphoma cell line by inducing a 3-5-fold increase in the steady-state Thy-1 mRNA level, concomitant with a twofold increase in cell surface expression. A similar modulation was observed in the immature CD4-CD8- T cell precursors but not in mature thymocytes. Nuclear run-on and transfection experiments indicated that the observed Thy-1 mRNA level is post-transcriptionally regulated and that the presence of the coding region is sufficient for this adaptive response. A mechanism without a requirement for protein kinase C activation, but involving Ca2+ entry, could account for this difference in Thy-1 mRNA stability.

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Monitoring and management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is a standard of care after traumatic brain injury (TBI). However, the pathophysiology of so-called secondary brain injury, i.e., the cascade of potentially deleterious events that occur in the early phase following initial cerebral insult-after TBI, is complex, involving a subtle interplay between cerebral blood flow (CBF), oxygen delivery and utilization, and supply of main cerebral energy substrates (glucose) to the injured brain. Regulation of this interplay depends on the type of injury and may vary individually and over time. In this setting, patient management can be a challenging task, where standard ICP/CPP monitoring may become insufficient to prevent secondary brain injury. Growing clinical evidence demonstrates that so-called multimodal brain monitoring, including brain tissue oxygen (PbtO2), cerebral microdialysis and transcranial Doppler among others, might help to optimize CBF and the delivery of oxygen/energy substrate at the bedside, thereby improving the management of secondary brain injury. Looking beyond ICP and CPP, and applying a multimodal therapeutic approach for the optimization of CBF, oxygen delivery, and brain energy supply may eventually improve overall care of patients with head injury. This review summarizes some of the important pathophysiological determinants of secondary cerebral damage after TBI and discusses novel approaches to optimize CBF and provide adequate oxygen and energy supply to the injured brain using multimodal brain monitoring.

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Fibrin has been long used clinically for hemostasis and sealing, yet extension of use in other applications has been limited due to its relatively rapid resorption in vivo, even with addition of aprotinin or other protease inhibitors. We report an engineered aprotinin variant that can be immobilized within fibrin and thus provide extended longevity. When recombinantly fused to a transglutaminase substrate domain from α(2)-plasmin inhibitor (α(2)PI(1-8)), the resulting variant, aprotinin-α(2)PI(1-8), was covalently crosslinked into fibrin matrices during normal thrombin/factor XIIIa-mediated polymerization. Challenge with physiological plasmin concentrations revealed that aprotinin-α(2)PI(1-8)-containing matrices retained 78% of their mass after 3 wk, whereas matrices containing wild type (WT) aprotinin degraded completely within 1 wk. Plasmin challenge of commercial sealants Omrixil and Tisseel, supplemented with aprotinin-α(2)PI(1-8) or WT aprotinin, showed extended longevity as well. When seeded with human dermal fibroblasts, aprotinin-α(2)PI(1-8)-supplemented matrices supported cell growth for at least 33% longer than those containing WT aprotinin. Subcutaneously implanted matrices containing aprotinin-α(2)PI(1-8) were detectable in mice for more than twice as long as those containing WT aprotinin. We conclude that our engineered recombinant aprotinin variant can confer extended longevity to fibrin matrices more effectively than WT aprotinin in vitro and in vivo.

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Although the histogram is the most widely used density estimator, itis well--known that the appearance of a constructed histogram for a given binwidth can change markedly for different choices of anchor position. In thispaper we construct a stability index $G$ that assesses the potential changesin the appearance of histograms for a given data set and bin width as theanchor position changes. If a particular bin width choice leads to an unstableappearance, the arbitrary choice of any one anchor position is dangerous, anda different bin width should be considered. The index is based on the statisticalroughness of the histogram estimate. We show via Monte Carlo simulation thatdensities with more structure are more likely to lead to histograms withunstable appearance. In addition, ignoring the precision to which the datavalues are provided when choosing the bin width leads to instability. We provideseveral real data examples to illustrate the properties of $G$. Applicationsto other binned density estimators are also discussed.

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We analyze which normal form solution concepts capture the notion offorward induction, as defined by van Damme (JET, 1989) in the classof generic two player normal form games preceded by an outsideoption. We find that none of the known strategic stability concepts(including Mertens stable sets and hyperstable sets) captures this form of forward induction. On the other hand, we show that the evolutionary concept of EES set (Swinkels, JET, 1992) is always consistent with forward induction.

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We argue the importance both of developing simple sufficientconditions for the stability of general multiclass queueing networks and also of assessing such conditions under a range of assumptions on the weight of the traffic flowing between service stations. To achieve the former, we review a peak-rate stability condition and extend its range of application and for the latter, we introduce a generalisation of the Lu-Kumar network on which the stability condition may be tested for a range of traffic configurations. The peak-rate condition is close to exact when the between-station traffic is light, but degrades as this traffic increases.

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Effet d'un bolus intraveineux de phénylephrine ou d'éphedríne sur le flux sanguin cutané lors d'une anesthésie rachidienne Introduction : La phénylephrine et l'éphedrine sont des substances vaso-actives utilisées de routine pour corriger des épisodes d'hypotension artérielle induits par l'anesthésie intrarachidienne. L'influence de ces deux vasopresseurs sur le flux sanguin cutané (FSC) dans ce contexte n'a jusqu'à maintenant pas été décrite. Cette étude évalue l'effet d'une injection intraveineuse de 75 µg de phénylephrine ou de 7.5 mg d'éphedrine sur le FSC mesuré par Laser Doppler, dans les zones concernées parle bloc sympathiqué induit par l'anesthésie intrarachidienne (membres inférieurs) et dans les zones non concernées (membres supérieurs). Méthode :Après acceptation par le Comité d'Éthique, et obtention de leur accord écrit, 20 patients devant subir une intervention chirurgicale élective en décubitus dorsal sous anesthésie. intrarachidienne ont été inclus dans cette étude randomisée en double insu. Le FSC a été mesuré en continu par deux sondes fixées l'une à la cuisse (zone avec bloc sympathique) et l'autre sur l'avantbras (zone sans bloc sympathique). Les valeurs de FSC ont été enregistrées après l'anesthésie rachidienne (valeur contrôle), puis après l'injection i.v. dè phénylephrine (10 patients) ou d'éphedrine (10 patients) pour corriger une hypotension définie comme une chute de 20 mmHg de la pression artérielle systolique. Les variations de FSC exprimées en pourcentage de la valeur contrôle moyenne (+/- écart type) ont été analysées par le test t de Student. Résultats :Les données démographiques des patients et le niveau sensitif induit par l'anesthésie rachidienne sont similaires dans les deux groupes. Aux doses utilisées, seule l'éphedrine restaure la pression artérielle aux valeurs précédant l'anesthésie rachidienne. La phénylephrine augmente le FSC de l'avant-bras de 44% (+/- 79%) et de la cuisse de 34% (+/-24%), alors que l'éphedrine diminue le débit sanguin cutané de l'avant-bras de 16% (+/- 15%) et de la cuisse de 22% (+/-11%). Conclusion : L'injection intraveineuse de phénylephrine et d'éphedrine ont des effets opposés sur le flux sanguin cutané, et cette réponse n'est pas modifiée par le bloc sympathique.. Cette différence peut s'expliquer par la distribution des sous-types de récepteurs adrénergiques alpha et leur prédominance relative dans les veines et les artères de différents diamètres perfusant le tissu sous-cutané et la peau. L'éphedrine, èn raison de sa meilleure efficacité pour traiter les épisodes d'hypotension artérielle après anesthésie intrarachidienne devrait être préféré à la phénylephrine, leurs effets opposés sur le flux sanguin cutané n'étant pas pertinents en pratique clinique. SUMMARY Background: Phenylephrine or ephedrine is routinely used to correct hypotensive episodes fallowing spinal anaesthesia (SA). The influence of these two vasopressors on skin blood flow (SBF) has not yet been described. We have therefore evaluated the effects of an i.v. bolus of 75 µg phenylephrine or 7.5 mg of ephedrine on SBF measured by laser Doppler flowmetry during sympathetic blockade induced by SA. Methods: With Ethical Committee approval and written consent, 20 patients scheduled for elective procedures in supine position under SA were enrolled in this double-blind randomized study. SBF was measured continuously by two probes fixed at the thigh (area with sympathic blockade) and forearm level (area without sympathic blockade) respectively. SBF values were recorded after SA (control values) and then after a bolus administration of phenylephriné (n=10) or ephedrine (n=10) when systolic blood pressure decreased by 20 mmHg. Changes were expressed as percentage of control SBF values and analysed by Student's paired t-test. Results: Patient characteristics and dermatomal sensory levels were similar in both groups. Phenylephrine increases mean SBF at the forearm level by 44% (79%) [mean (SD)j and at the thigh by 34% (24%). Ephedrine decreases SBF at the forearm level by 16% (15%) and at the thigh by 22% (il%). Ephedrine bolus restores arterial blood pressure to pre-anaesthesia values, whereas phenylephrine does not. Conclusion: Administratión of phenylephrine and ephedrine has opposite effects on skin blood flow and sympathetic blockade does not modify this response. These findings could be explained by the distribution of the alpha-adrenoréceptor subtypes and their relative predominance among veins and arteries of different size perfusing the subcutaneous tissue and the skin. Ephedrine, due to its better efficacy to correct hypotensive episodes following SA, should be preferred, to phenylephrine, their opposite effects on SBF being not relevant for clinical practice.

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This study investigates the intra-individual stability of the speed of several motor tasks and the intensity of associated movements in 256 children (131 girls, 125 boys) from the Zurich generational study using the Zurich neuromotor assessment battery (ZNA) over a 12-year period from the age of 6 to 18 years. The stability was assessed by correlograms of standard deviation scores calculated from age- and gender-adjusted normative values and compared with standing height and full scale intelligence quotient (IQ). While motor tasks of hand, finger and foot (HFT) and contralateral associated movements (CAM) exhibited a moderate stability (summary measure as correlation coefficients between two measurements made 4 years apart: .61 and .60), other tasks (dynamic balance, static balance and pegboard) were only weakly stable (.46, .47 and .49). IQ and height were more stable than neuromotor components (.72 and .86). We conclude that the moderately stable HFT and CAM may reflect "motor traits", while the stability of the pegboard and balance tasks is weaker because these skills are more experience related and state-dependent.

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This paper presents a classical Cournot oligopoly model with some peculiar features: it is non--quasi--competitive as price under N-poly is greater than monopoly price; Cournot equilibrium exists and is unique with each new entry; the successive equilibria after new entries are stable under the adjustment mechanism that assumes that actual output of each seller is adjusted proportionally to the difference between actual output and profit maximizing output. Moreover, the model tends to perfect competition as N goes to infinity, reaching the monopoly price again.

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Euglycemic hyperinsulinemia stimulates both sympathetic nerve activity and blood flow to skeletal muscle, but the mechanism is unknown. Possible mechanisms that may stimulate muscle blood flow include neural, humoral, or metabolic effects of insulin. To determine whether such insulin-induced vasodilation is modulated by stimulation of adrenergic or cholinergic mechanisms, we obtained, in eight healthy lean subjects, plethysmographic measurements of calf blood flow during 3 h of hyperinsulinemic (1 mU.kg-1.min-1) euglycemic clamp performed alone or during concomitant beta-adrenergic (propranolol infusion), cholinergic (atropine infusion), or alpha-adrenergic (prazosin administration) blockade. Euglycemic hyperinsulinemia alone increased calf blood flow by 38 +/- 10% (means +/- SE) and decreased vascular resistance by 27 +/- 4% (P < 0.01). The principal new observation is that these insulin-induced vasodilatory responses were not attenuated by concomitant propranolol or atropine infusion, nor were they potentiated by prazosin administration. In conclusion, these findings provide evidence that during euglycemic hyperinsulinemia in lean healthy humans stimulation of muscle blood flow is not mediated primarily by beta-adrenergic or cholinergic mechanisms. Furthermore, alpha-adrenergic mechanisms do not markedly limit insulin-induced stimulation of muscle blood flow.