Metallic thin fi lms on stepped surfaces: lateral scattering of quantum well states

Quantum well states of Ag films grown on stepped Au(111) surfaces are shown to undergo lateral scattering, in analogy with surface states of vicinal Ag(111). Applying angle resolved photoemission spectroscopy we observe quantum well bands with zone-folding and gap openings driven by surface/interface step lattice scattering. Experiments performed on a curved Au(111) substrate allow us to determine a subtle terrace-size effect, i.e., a fine step-density-dependent upward shift of quantum well bands. This energy shift is explained as mainly due to the periodically stepped crystal potential offset at the interface side of the film. Finally, the surface state of the stepped Ag film is analyzed with both photoemission and scanning tunneling microscopy. We observe that the stepped film interface also affects the surface state energy, which exhibits a larger terrace-size effect compared to surface states of bulk vicinal Ag(111) crystals

DEVELOPMENT AND APPLICATIONS OF TIME-DEPENDENT DENSITY MATRIX FUNCTIONAL THEORY

En esta tesis estudiamos las teorías sobre la Matriz Densidad Reducida (MDR) como un marco prometedor. Nos enfocamos sobre esta teorías desde dos aspectos: Primero, usamos algunos modelos sencillos hechos con dos partículas las cuales estan armónicamente confinadas como una base para ilustrar la utilidad de la matriz densidad. Para tales sistemas, usamos la MDR de un cuerpo para calcular algunas cantidades de interés tales como densidad de momentum. Posteriormente obtenemos los orbitales naturales y su número de ocupación para algunos de los modelos, y en uno de los casos expresamos la MDR de dos cuerpos de manera exacta en términos de la MDR de un cuerpo. También usamos el teorema diferencial del virial para establecer una descripción unificada de la familia entera de estos sistemas modelo en términos de la densidad. En la seguna parte cambiamos a casos fuera del equilibrio y analizamos la así llamada jerarquía BBGKY de ecuaciones para describir la evolución temporal de un sistema de muchos cuerpos en términos de sus MDRs (a todos los órdenes). Proveemos un exhaustivo estudio de los desafíos y problemas abiertos ligados a la truncación de tales jerarquías de ecuaciones para hacerlas aplicables. Restringimos nuestro análisis a la evolución acoplada de la MDR de uno y dos cuerpos, donde los efectos de correlación de alto orden estan embebidos dentro de la aproximación usada para cerrar las ecuaciones. Probamos que dentro de esta aproximación, el número de electrones y la energía total se conservan, sin importar la aproximación usada. Luego, demostramos que aplicando los esquemas de truncación de estado base para llevar los electrones a comportamientos indeseables y no físicos, tales como la violación e incluso la divergencia en la densidad electrónica local, tanto en regímenes correlacionados débiles y fuertes.

Density-potential mapping in the standard and quantum electrodynamical time-dependent density functional theory

131 p.

Analysis and control of transient spectra using time-dependent density functional theory.

215 p.

Age-dependent decrease in glutamine synthetase expression in the hippocampal astroglia of the triple transgenic Alzheimer's disease mouse model : mechanism for deficient glutamatergic transmission?

Astrocytes are fundamental for brain homeostasis and the progression and outcome of many neuropathologies including Alzheimer's disease (AD). In the triple transgenic mouse model of AD (3xTg-AD) generalised hippocampal astroglia atrophy precedes a restricted and specific beta-amyloid (A beta) plaque-related astrogliosis. Astrocytes are critical for CNS glutamatergic transmission being the principal elements of glutamate homeostasis through maintaining its synthesis, uptake and turnover via glutamate-glutamine shuttle. Glutamine synthetase (GS), which is specifically expressed in astrocytes, forms glutamine by an ATP-dependent amination of glutamate. Here, we report changes in GS astrocytic expression in two major cognitive areas of the hippocampus (the dentate gyrus, DG and the CA1) in 3xTg-AD animals aged between 9 and 18 months. We found a significant reduction in Nv (number of cell/mm(3)) of GS immunoreactive (GS-IR) astrocytes starting from 12 months (28.59%) of age in the DG, and sustained at 18 months (31.65%). CA1 decrease of GS-positive astrocytes Nv (33.26%) occurs at 18 months. This Nv reduction of GSIR astrocytes is paralleled by a decrease in overall GS expression (determined by its optical density) that becomes significant at 18 months (21.61% and 19.68% in DG and CA1, respectively). GS-IR Nv changes are directly associated with the presence of A beta deposits showing a decrease of 47.92% as opposed to 23.47% in areas free of A beta. These changes in GS containing astrocytes and GS-immunoreactivity indicate AD-related impairments of glutamate homeostatic system, at the advanced and late stages of the disease, which may affect the efficacy of glutamatergic transmission in the diseased brain that may contribute to the cognitive deficiency.

Mechanisms Responsible for the Trophic Effect of Beta-Adrenoceptors on the I-to Current Density in Type 1 Diabetic Rat Cardiomyocytes

Background/Aims: In diabetic ventricular myocytes, transient outward potassium current (I-to) amplitude is severely reduced because of the impaired catecholamine release that characterizes diabetic autonomic neuropathy. Sympathetic nervous system exhibits a trophic effect on I-to since incubation of myocytes with noradrenaline restores current amplitude via beta-adrenoceptor (beta AR) stimulation. Here, we investigate the intracellular signalling pathway though which incubation of diabetic cardiomyocytes with the beta AR agonist isoproterenol recovers I-to amplitude to normal values. Methods: Experiments were performed in ventricular myocytes isolated from streptozotocin-diabetic rats. I-to current was recorded by using the patch-clamp technique. Kv4 channel expression was determined by immunofluorescence. Protein-protein interaction was determined by coimmunoprecipitation. Results: Stimulation of beta AR activates first a G alpha s protein, adenylyl cyclase and Protein Kinase A. PKA-phosphorylated receptor then switches to the G alpha i protein. This leads to the activation of the beta AR-Kinase-1 and further receptor phosphorylation and arrestin dependent internalization. The internalized receptor-arrestin complex recruits and activates cSrc and the MAPK cascade, where Ras, c-Raf1 and finally ERK1/2 mediate the increase in Kv4.2 and Kv4.3 protein abundance in the plasma membrane. Conclusion: beta(2)AR stimulation activates a G alpha s and G alpha i protein dependent pathway where the ERK1/2 modulates the Ito current amplitude and the density of the Kv4.2 and Kv4.2 channels in the plasma membrane upon sympathetic stimulation in diabetic heart.