911 resultados para added variable plot
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Chapman Family burial plot, Forest Lawn, Glendale, California. "La Carita" statue.
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It has previously been recognized that the major biochemical toxicity induced by sulphide is due to an inhibition of cytochrome ~ oxidase. Inhibition of this enzyme occurs at 30°C and pH 7.4 with a Ki of approximately 0.2 ~M, and a kon of 104 M-1 s-l, under catalytic conditions. However, the equimo1ar mixture of sulphide and the enzyme shows identical catalytic behaviour to that of the native enzyme. This cannot readily be attributed to rapid dissociation of sulphide, as both spectroscopic and plot analysis indicate the koff value is low. The addition of stoichiometric sulphide to the resting oxidized enzyme gives rise to the appearance of a low-spin ferric-type spectrum not identical with that seen on the addition of excess sulphide to the enzyme aerobically. Sulphide added to the enzyme anaerobically gives rise to another low-spin, probably largely ferric, form which upon admission of oxygen is then converted into a 607 nm species closely resembling Compound C. The 607 nm form is probably the precursor of oxyferricytochrome aa3. The addition of successive a1iquots of Na2S solution to the enzyme induces initial uptake of approximately 3 moles of oxygen per mole of the enzyme. Thus, it is concluded that: 1. the initial product of sulphide-cytochrome c oxidase interaction is not an inhibited form of the enzyme, but the low-spin (oxyferri) ~3+~+ species; 2. a subsequent step in which sulphide reduces cytochrome ~ occurs; 3. the final inhibitory step, in which a further molecule of sulphide binds to the cytochrome ~ iron centre in the cytochrome ~2+~+ species, gives the cytochrome a2+~+-H2S form which is a half-reduced fully inhibited species;4. a 607 run form of the enzyme is produced which may be converted into a catalytically active low-spin (oxyferri) state; and therefore 5. liganded sulphide may be able to reduce the cytochrome 33 -Cu centre without securing the prior reduction of the cytochrome a_ haem group or the Cud centre associated with it.
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Tesis (Maestría en Ciencias para la Planificación de Asentamientos Humanos) U.A.N.L.
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Tesis (Maestría en Salud Pública con Esp. en Odontología Social) U.A.N.L.
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Tesis (Maestría en Ciencias) U.A.N.L.
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Tesis (Maestría en Ciencias de la Administración con Especialidad en Relaciones Industriales) U.A.N.L.
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Tesis (Master en Administración y de Negocios con Especialidad en Producción y Calidad) UANL, 2009.
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UANL
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Latent variable models in finance originate both from asset pricing theory and time series analysis. These two strands of literature appeal to two different concepts of latent structures, which are both useful to reduce the dimension of a statistical model specified for a multivariate time series of asset prices. In the CAPM or APT beta pricing models, the dimension reduction is cross-sectional in nature, while in time-series state-space models, dimension is reduced longitudinally by assuming conditional independence between consecutive returns, given a small number of state variables. In this paper, we use the concept of Stochastic Discount Factor (SDF) or pricing kernel as a unifying principle to integrate these two concepts of latent variables. Beta pricing relations amount to characterize the factors as a basis of a vectorial space for the SDF. The coefficients of the SDF with respect to the factors are specified as deterministic functions of some state variables which summarize their dynamics. In beta pricing models, it is often said that only the factorial risk is compensated since the remaining idiosyncratic risk is diversifiable. Implicitly, this argument can be interpreted as a conditional cross-sectional factor structure, that is, a conditional independence between contemporaneous returns of a large number of assets, given a small number of factors, like in standard Factor Analysis. We provide this unifying analysis in the context of conditional equilibrium beta pricing as well as asset pricing with stochastic volatility, stochastic interest rates and other state variables. We address the general issue of econometric specifications of dynamic asset pricing models, which cover the modern literature on conditionally heteroskedastic factor models as well as equilibrium-based asset pricing models with an intertemporal specification of preferences and market fundamentals. We interpret various instantaneous causality relationships between state variables and market fundamentals as leverage effects and discuss their central role relative to the validity of standard CAPM-like stock pricing and preference-free option pricing.
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This Paper Studies Tests of Joint Hypotheses in Time Series Regression with a Unit Root in Which Weakly Dependent and Heterogeneously Distributed Innovations Are Allowed. We Consider Two Types of Regression: One with a Constant and Lagged Dependent Variable, and the Other with a Trend Added. the Statistics Studied Are the Regression \"F-Test\" Originally Analysed by Dickey and Fuller (1981) in a Less General Framework. the Limiting Distributions Are Found Using Functinal Central Limit Theory. New Test Statistics Are Proposed Which Require Only Already Tabulated Critical Values But Which Are Valid in a Quite General Framework (Including Finite Order Arma Models Generated by Gaussian Errors). This Study Extends the Results on Single Coefficients Derived in Phillips (1986A) and Phillips and Perron (1986).
Harsanyi’s Social Aggregation Theorem : A Multi-Profile Approach with Variable-Population Extensions
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This paper provides new versions of Harsanyi’s social aggregation theorem that are formulated in terms of prospects rather than lotteries. Strengthening an earlier result, fixed-population ex-ante utilitarianism is characterized in a multi-profile setting with fixed probabilities. In addition, we extend the social aggregation theorem to social-evaluation problems under uncertainty with a variable population and generalize our approach to uncertain alternatives, which consist of compound vectors of probability distributions and prospects.
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Affiliation: Pascal Michel : Département de pathologie et microbiologie, Faculté de médecine vétérinaire
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Affiliation: Unité de recherche en Arthrose, Centre de recherche du Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame