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Cette thèse présente une méthode performante pour le calcul des capacités parasites dues aux interconnexions des circuits intégrés. Il s'agit de calculer la charge des conducteurs, comme la dérivée normale à la surface de ces conducteurs, du potentiel solution de l'équation de Laplace sur des couches horizontales, la valeur du potentiel étant fixée constante sur chaque conducteur. La difficulté de la résolution numérique provient de la complexité des structures : sur une portion de circuit d'une surface d'un centimètre carré et d'une hauteur de quelques microns, il peut y avoir plus d'un kilomètre d'interconnexions, c'est-à-dire de fils conducteurs enchevêtrés. Une méthode de domaines fictifs avec multiplicateurs de Lagrange surfaciques est utilisée. Elle donne une formulation mixte du problème, couplant le potentiel sur un domaine parallélépipédique contenant le circuit, et la charge à la surface des conducteurs. Nous en proposons une approximation, qui tient compte du saut du gradient du potentiel à travers la surface des conducteurs dans la discrétisation du potentiel, tout en menant à un système que l'on peut résoudre par une méthode rapide. Cette approximation garantit une bonne convergence du calcul de la charge vers la valeur réelle, sans condition de compatibilité contraignante entre les maillages de volume et de surface. Une implémentation efficace en dimension 3, avec laquelle nous avons effectué des tests numériques sur des structures réelles, permet de montrer l'intérêt de la méthode, en temps de calcul et en place mémoire.

Le caoutchouc industriel est présent dans de nombreuses applications, de la plus basique à la plus technique. Son mode de défaillance prépondérant est la rupture due à la propagation de fissures par fatigue : les sollicitations mécaniques ainsi que l'atmosphère extérieure provoquent dans un premier temps l'apparition d'une amorce de fissure. Sous l'effet des sollicitations mécaniques, cette fissure se propage jusqu'à rupture de la pièce. L'objectif de ce travail est de faciliter la simulation numérique de la propagation de fissures dans les élastomères. Pour cela, on utilise la méthode des éléments finis étendus X-FEM. Cette méthode a été développée afin de limiter le recours au remaillage dans le cadre de la fissuration des métaux. En outre, elle permet d'enrichir l'approximation éléments finis par des fonctions provenant de la physique du problème. La première partie de ce travail consiste à adapter cette méthode à la mécanique non-linéaire de la rupture. On s'intéresse en particulier au choix de la formulation de résolution ainsi qu'à la recherche de fonctions d'enrichissement adaptées. Dans un deuxième temps, on s'intéresse à l'enrichissement des formulations mixtes pour la gestion de la contrainte d'incompressibilité. Des stratégies ont été développées afin de préserver la stabilité de ces formulations. Ces enrichissements permettent la vérification de la condition inf-sup dans le cas de trous, des inclusions et des fissures sous l'hypothèse des petites perturbations. Enfin, dans une troisième partie, on détaille l'application du concept de forces configurationnelles comme critère directionnel pour la propagation de fissures 2D et 3D.

Does monetary policy affect the real economy? If so, what is the transmission mechanism or channel through which these effects occur? These two questions are among the most important and controversial in macroeconomics. This dissertation presents some new empirical evidence that addresses each question for the U.S. and Chinese economies. Literature on monetary transmission suggests that the monetary policy can take effect on the real economy through several ways. The most noteworthy one is credit channels, including the bank lending channel and the interest channel. First, I use a new method to test for structural breaks in the U.S. monetary policy history and present some new empirical evidence to support an operative bank lending channel in the transmission mechanism of monetary policy. Results show that an operative bank lending channel existed in 1955 to 1968, and its impact on the economy has become much smaller since 1981, but it still has a significant buffering effect on output by attenuating the effect of the interest channel. Second, I adopt the recently developed time series technique to explore the puzzling negative correlation between output and stock returns in China currently, and posit that it is due to a negative link between monetary policy and stock returns when monetary policy increases output. The monetary policy has not been transmitted well in the public sector which is the principal part of Chinese stock market, and increased investment capital from monetary expansion goes to real estate sector instead of the stock market. Last, I demonstrate how monetary policy has been transmitted into the public and private sectors of China through the credit channel. The fundamental identification problem inherent in using aggregated data that leads to failure in isolating demand shock from supply shock is explicitly solved by introducing control factors. I find that the monetary policy has great impact on private sector rather than public sector through credit channel in China. These findings have important practical implications for U.S. and China’s economic development by improving the efficiency of the monetary policy because a comprehensive understanding of monetary transmission will lead to better policy design.

Does monetary policy affect the real economy? If so, what is the transmission mechanism or channel through which these effects occur? These two questions are among the most important and controversial in macroeconomics. This dissertation presents some new empirical evidence that addresses each question for the U.S. and Chinese economies. Literature on monetary transmission suggests that the monetary policy can take effect on the real economy through several ways. The most noteworthy one is credit channels, including the bank lending channel and the interest channel. First, I use a new method to test for structural breaks in the U.S. monetary policy history and present some new empirical evidence to support an operative bank lending channel in the transmission mechanism of monetary policy. Results show that an operative bank lending channel existed in 1955 to 1968, and its impact on the economy has become much smaller since 1981, but it still has a significant buffering effect on output by attenuating the effect of the interest channel. Second, I adopt the recently developed time series technique to explore the puzzling negative correlation between output and stock returns in China currently, and posit that it is due to a negative link between monetary policy and stock returns when monetary policy increases output. The monetary policy has not been transmitted well in the public sector which is the principal part of Chinese stock market, and increased investment capital from monetary expansion goes to real estate sector instead of the stock market. Last, I demonstrate how monetary policy has been transmitted into the public and private sectors of China through the credit channel. The fundamental identification problem inherent in using aggregated data that leads to failure in isolating demand shock from supply shock is explicitly solved by introducing control factors. I find that the monetary policy has great impact on private sector rather than public sector through credit channel in China. These findings have important practical implications for U.S. and China’s economic development by improving the efficiency of the monetary policy because a comprehensive understanding of monetary transmission will lead to better policy design.

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No description available.

Abstract Melatonin is an important modulator of several physiological and behavioural processes, and it influences the function of many different tissues. Melatonin has effective antioxidative properties, but some of its actions in mammals are also mediated through the MT1 and MT2 melatonin receptors. Antioxidative properties are seen especially when the melatonin concentration is high (≥ nM), and melatonin's affinity for its receptors appears at lower concentrations (pM). Recently, the involvement of melatonin in protecting the heart against cardiac diseases, including myocardial infarction (MI), has been brought out. MI alters the structure and function of myocardium, attenuating for example cardiac contractility by affecting the amount and function of the essential Ca2+ handling proteins, dihydropyridine receptor (DHPR), ryanodine receptor (RyR2) and sarco-endoplasmic reticulum (SR) Ca2+-ATPase2 (SERCA2). MI also evokes many adaptive responses in organisms, such as elevated production of atrial and brain natriuretic peptides (ANP and BNP). In this thesis, the expression of MT1 and MT2 receptor mRNAs was investigated in several rat tissues. Furthermore, the effect of MI and exogenous melatonin on the rat endogenous melatonin and on the expression of cardiac MT1, MT2, DHPR, RyR2 and SERCA2 proteins was evaluated. The concentrations of ANP and BNP were also measured after post-MI melatonin administration. The results show the expression of MT1 and/or MT2 receptor mRNAs in the hypothalamus, retina, small intestine, liver and heart, which indicates that at least some effects of melatonin could be mediated through the receptors in these tissues. Melatonin synthesis in the pineal gland increased rapidly in response to MI, supporting an important role of endogenous melatonin in protecting the heart after MI. Furthermore, exogenous melatonin altered the mRNA expression of DHPR, RyR2 and SERCA2 after MI, suggesting that melatonin might contribute to the post-infarction cardiac contractile function. The results also revealed a novel, positive relationship between melatonin and ANP, and thereby bring out one more possible way of melatonin to protect the heart against MI-induced injuries. Taken together, the present thesis (i) supports the notion that melatonin is an important endogenous protective agent of the organism, and (ii) extends our knowledge of melatonin's post-infarction cardioprotective actions. / Tiivistelmä Melatoniini osallistuu monien fysiologisten toimintojen ja käyttäytymisen säätelyyn sekä vaikuttaa useiden eri kudosten toimintaan. Melatoniini on tehokas antioksidantti, mutta jotkut sen vaikutuksista välittyvät myös MT1 ja MT2 melatoniini reseptorien kautta. Antioksidatiiviset vaikutukset tulevat esiin erityisesti silloin, kun melatoniinin pitoisuus on korkea (≥ nM). Alhaisemmilla pitoisuuksilla (pM) on puolestaan havaittavissa melatoniinin sitoutuminen reseptoreihinsa. Viime aikoina on tullut esille melatoniinin mahdollinen suojavaikutus sydänsairauksia, kuten sydäninfarkteja, vastaan. Sydäninfarkti muuttaa sydänlihaksen rakennetta ja toimintaa esimerkiksi vaikuttamalla supistuksen kannalta välttämättömien proteiinien, dihydropyridiini reseptorin (DHPR), ryanodiini reseptorin (RyR2) ja sarko-endoplasmakalvoston Ca2+-ATPaasi2:n (SERCA2) lukumääriin ja toimintaan, ja sitä kautta muun muassa heikentää sydämen supistuvuutta. Sydäninfarkti laukaisee elimistössä myös monia adaptiivisia vasteita, kuten eteispeptidin (ANP) ja aivojen natriureettisen peptidin (BNP) lisääntyneen erityksen. Tässä väitöstyössä tutkittiin MT1 ja MT2 reseptorien mRNAn ilmentymistä useissa rotan eri kudoksissa. Lisäksi tutkittiin sydäninfarktin ja eksogeenisen melatoniinin vaikutuksia rotan endogeeniseen melatoniiniin sekä sydämen MT1, MT2, DHPR, RyR2 ja SERCA2 proteiinien ekspressioon. Myös ANP ja BNP pitoisuudet mitattiin. Tulokset osoittivat MT1 ja/tai MT2 reseptori mRNAn ilmentymisen hypotalamuksessa, silmän verkkokalvolla, ohutsuolessa, maksassa ja sydämessä, minkä perusteella ainakin osa melatoniinin vaikutuksista saattaisi olla reseptorivälitteisiä näissä kudoksissa. Tulosten mukaan käpyrauhasen melatoniinisynteesi lisääntyi nopeasti sydäninfarktin jälkeen, mikä tukee käsitystä endogeenisen melatoniinin tärkeästä roolista infarktin jälkeisessä sydämen suojauksessa. Lisäksi eksogeeninen melatoniini muutti DHPR:n, RyR2:n ja SERCA2:n mRNA ekspressiota infarktin jälkeen, mikä voisi merkitä, että melatoniini saattaa vaikuttaa infarktin jälkeiseen sydämen supistuvuuteen. Tulosten osoittama positiivinen riippuvuus melatoniinin ja ANP:n välillä tuo puolestaan esille yhden uuden mahdollisen keinon, jonka kautta melatoniini voisi suojata sydäntä infarktin aiheuttamia vaurioita vastaan. Yhteenvetona voidaan todeta, että tämä väitöstyö (i) tukee käsitystä, että endogeenisella melatoniinilla on tärkeä merkitys elimistön suojaamisessa, ja (ii) laajentaa tietämystämme infarktin jälkeisistä melatoniinin sydäntä suojaavista vaikutuksista.

On a large class of two-dimensional anisotropic meshes, the inf-sup condition (stability) is proved for the triangular and quadrilateral finite element pairs suggested by Bernardi/Raugel and Fortin. As a consequence the pairs ${\cal P}_2-{\cal P}_0$, ${\cal Q}_2-{\cal P}_0$, and ${\cal Q}_2^\prime-{\cal P}_0$ turn out to be stable independent of the aspect ratio of the elements.

In this thesis we analyse the high-order in time discontinuous Galerkin nite element method (DGFEM) for second-order in time linear abstract wave equations. Our abstract approximation analysis is a generalisation of the approach introduced by Claes Johnson (in Comput. Methods Appl. Mech. Engrg., 107:117-129, 1993), writing the second order problem as a system of fi rst order problems. We consider abstract spatial (time independent) operators, highorder in time basis functions when discretising in time; we also prove approximation results in case of linear constraints, e.g. non-homogeneous boundary data. We take the two steps approximation approach i.e. using high-order in time DGFEM; the discretisation approach in time introduced by D Schötzau (PhD thesis, Swiss Federal institute of technology, Zürich, 1999) to fi rst obtain the semidiscrete scheme and then conformal spatial discretisation to obtain the fully-discrete formulation. We have shown solvability, unconditional stability and conditional a priori error estimates within our abstract framework for the fully discretized problem. The skew-symmetric spatial forms arising in our abstract framework for the semi- and fully-discrete schemes do not full ll the underlying assumptions in D. Schötzau's work. But the semi-discrete and fully discrete forms satisfy an Inf-sup condition, essential for our proofs; in this sense our approach is also a generalisation of D. Schötzau's work. All estimates are given in a norm in space and time which is weaker than the Hilbert norm belonging to our abstract function spaces, a typical complication in evolution problems. To the best of the author's knowledge, with the approximation approach we used, these stability and a priori error estimates with their abstract structure have not been shown before for the abstract variational formulation used in this thesis. Finally we apply our abstract framework to the acoustic and an elasto-dynamic linear equations with non-homogeneous Dirichlet boundary data.