941 resultados para Differential calculus in Banach spaces
Resumo:
A coercive estimate for a solution of a degenerate second order di fferential equation is installed, and its applications to spectral problems for the corresponding dif ferential operator is demonstrated. The suffi cient conditions for existence of the solutions of one class of the nonlinear second order diff erential equations on the real axis are obtained.
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Previous studies in mice with hypervitaminosis A have demonstrated that fat-storing cells (hepatic stellate cells-HSCs) participate in schistosomal granuloma fibrogenesis. The origin of such cells in portal areas, away from the Disse spaces, was herein investigated. HSCs were identified in frozen sections of the liver by means of Sudan III staining. They appeared as red-stained cells disposed along the sinusoids of normal mice, but were never found within portal spaces. However, in the chronically inflamed portal spaces of Capillaria hepatica-infected mice, Sudan III-positive cells were frequently present among leukocytes and fibroblast-like cells. Thus, there are no resident HSCs in portal spaces, but their presence there in chronic inflammatory processes indicates that they are able to migrate from peri-sinusoidal areas in order to reach the portal areas.
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To study the functional role of individual alpha1-adrenergic (AR) subtypes in blood pressure (BP) regulation, we used mice lacking the alpha1B-AR and/or alpha1D-AR with the same genetic background and further studied their hemodynamic and vasoconstrictive responses. Both the alpha1D-AR knockout and alpha1B-/alpha1D-AR double knockout mice, but not the alpha1B-AR knockout mice, had significantly (p < 0.05) lower levels of basal systolic and mean arterial BP than wild-type mice in nonanesthetized condition, and they showed no significant change in heart rate or in cardiac function, as assessed by echocardiogram. All mutants showed a significantly (p < 0.05) reduced catecholamine-induced pressor and vasoconstriction responses. It is noteworthy that the infusion of norepinephrine did not elicit any pressor response at all in alpha1B-/alpha1D-AR double knockout mice. In an attempt to further examine alpha1-AR subtype, which is involved in the genesis or maintenance of hypertension, BP after salt loading was monitored by tail-cuff readings and confirmed at the endpoint by direct intra-arterial recording. After salt loading, alpha1B-AR knockout mice developed a comparable level of hypertension to wild-type mice, whereas mice lacking alpha1D-AR had significantly (p < 0.05) attenuated BP and lower levels of circulating catecholamines. Our data indicated that alpha1B- and alpha1D-AR subtypes participate cooperatively in BP regulation; however, the deletion of the functional alpha1D-AR, not alpha1B-AR, leads to an antihypertensive effect. The study shows differential contributions of alpha1B- and alpha1D-ARs in BP regulation.
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L’informe que es presenta en aquest llibre és el resultat d’un nou acord de col·laboració entre el Programa de les Nacions Unides per als Assentaments Humans (ONU-Habitat) i l’Institut de Seguretat Pública de Catalunya, impulsat amb l’objectiu de millorar la seguretat en esdeveniments públics en els espais urbans a l’Àfrica. La fase pilot es va dur a terme el 2010, durant els dos seminaris de formació realitzats a Mollet del Vallès (Barcelona) com a part de la Plataforma Policia per al Desenvolupament Urbà (PPUD). En aquest informe es descriuen els orígens i l’estat de la iniciativa i resumeix els resultats. També s’inclouen algunes recomanacions per a millorar la seguretat d’esdeveniments públics. Font d'informació: http://www.onuhabitat.org.
Resumo:
In order to understand relationships between executive and structural deficits in the frontal cortex of patients within normal aging or Alzheimer's disease, we studied frontal pathological changes in young and old controls compared to cases with sporadic (AD) or familial Alzheimer's disease (FAD). We performed a semi-automatic computer assisted analysis of the distribution of beta-amyloid (Abeta) deposits revealed by Abeta immunostaining as well as of neurofibrillary tangles (NFT) revealed by Gallyas silver staining in Brodman areas 10 (frontal polar), 12 (ventro-infero-median) and 24 (anterior cingular), using tissue samples from 5 FAD, 6 sporadic AD and 10 control brains. We also performed densitometric measurements of glial fibrillary acidic protein, principal compound of intermediate filaments of astrocytes, and of phosphorylated neurofilament H and M epitopes in areas 10 and 24. All regions studied seem almost completely spared in normal old controls, with only the oldest ones exhibiting a weak percentage of beta-amyloid deposit and hardly any NFT. On the contrary, all AD and FAD cases were severely damaged as shown by statistically significant increased percentages of beta-amyloid deposit, as well as by a high number of NFT. FAD cases (all from the same family) had statistically more beta-amyloid and GFAP than sporadic AD cases in both areas 10 and 24 and statistically more NFT only in area 24. The correlation between the percentage of beta-amyloid and the number of NFT was significant only for area 24. Altogether, these data suggest that the frontal cortex can be spared by AD type lesions in normal aging, but is severely damaged in sporadic and still more in familial Alzheimer's disease. The frontal regions appear to be differentially vulnerable, with area 12 having the less amyloid burden, area 24 the less NFT and area 10 having both more amyloid and more NFT. This pattern of damage in frontal regions may represent a strong neuroanatomical support for the deterioration of attention and cognitive capacities as well as for the presence of emotional and behavioral troubles in AD patients.
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This article is an introduction to Malliavin Calculus for practitioners.We treat one specific application to the calculation of greeks in Finance.We consider also the kernel density method to compute greeks and anextension of the Vega index called the local vega index.
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Our understanding of how genotype determines phenotype in primary dystonia is limited. Familial young-onset primary dystonia is commonly due to the DYT1 gene mutation. A critical question, given the 30% penetrance of clinical symptoms in DYT1 mutation carriers, is why the same genotype leads to differential clinical expression and whether non-DYT1 adult-onset primary dystonia, with and without family history share pathophysiological mechanisms with DYT1 dystonia. This study examines the relationship between dystonic phenotype and the DYT1 gene mutation by monitoring whole-brain structure using voxel-based morphometry. We acquired magnetic resonance imaging data of symptomatic and asymptomatic DYT1 mutation carriers, of non-DYT1 primary dystonia patients, with and without family history and control subjects with normal DYT1 alleles. By crossing the factors genotype and phenotype we demonstrate a significant interaction in terms of brain anatomy confined to the basal ganglia bilaterally. The explanation for this effect differs according to both gene and dystonia status: non-DYT1 adult-onset dystonia patients and asymptomatic DYT1 carriers have significantly larger basal ganglia compared to healthy subjects and symptomatic DYT1 mutation carriers. There is a significant negative correlation between severity of dystonia and basal ganglia size in DYT1 mutation carriers. We propose that differential pathophysiological and compensatory mechanisms lead to brain structure changes in non-DYT1 primary adult-onset dystonias and DYT1 gene carriers. Given the range of age of onset, there may be differential genetic modulation of brain development that in turn determines clinical expression. Alternatively, a DYT1 gene dependent primary defect of motor circuit development may lead to stress-induced remodelling of the basal ganglia and hence dystonia.
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Following a scheme of Levin we describe the values that functions in Fock spaces take on lattices of critical density in terms of both the size of the values and a cancelation condition that involves discrete versions of the Cauchy and Beurling-Ahlfors transforms.
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We investigated how synaptic plasticity is related to the neurodegeneration process in the human dorsolateral prefrontal cortex. Pre- and postsynaptic proteins of Brodmann's area 9 from patients with Alzheimer's disease (AD) and age-matched controls were quantified by immunohistochemical methods and Western blots. The main finding was a significant increase in the expression of postsynaptic density protein PSD-95 in AD brains, revealed on both sections and immunoblots, while the expression of spinophilin, associated to spines, remained quantitatively unchanged despite qualitative changes with age and disease. Presynaptic protein alpha-synuclein indicated an increased immunohistochemical level, while synaptophysin remained unchanged. MAP2, a somatodendritic microtubule protein, as well as AD markers such as amyloid-beta protein and phosphorylated protein tau showed an increased expression on immunosections in AD. Altogether these changes suggest neuritic and synaptic reorganization in the process of AD. In particular, the significant increase in PSD-95 expression suggests a change in NMDA receptors trafficking and may represent a novel marker of functional significance for the disease.
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Males of plants with separate sexes are often more prone to attack by herbivores than females. A common explanation for this pattern is that individuals with a greater male function suffer more from herbivory because they grow more quickly, drawing more heavily on resources for growth that might otherwise be allocated to defence. Here, we test this 'faster-sex' hypothesis in a species in which males in fact grow more slowly than hermaphrodites, the wind-pollinated annual herb Mercurialis annua. We expected greater herbivory in the faster-growing hermaphrodites. In contrast, we found that males, the slower sex, were significantly more heavily eaten by snails than hermaphrodites. Our results thus reject the faster-sex hypothesis and point to the importance of a trade-off between defence and reproduction rather than growth.
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The thesis discusses games and the gaming experience. It is divided into two main sections; the first examines games in general, while the second concentrates exclusively on electronic games. The text approaches games from two distinct directions by looking at both their spatiality and their narrativity at the same time. These two points of view are combined right from the beginning of the text as they are used in conceptualising the nature of the gaming experience. The purpose of the thesis is to investigate two closely related issues concerning both the field of game studies and the nature of games. In regard to studying games, the focus is placed on the juxtaposition of ludology and narratology, which acts as a framework for looking at gaming. In addition to aiming to find out whether or not it is possible to undermine the said state of affairs through the spatiality of games, the text looks at the interrelationships of games and their spaces as well as the role of narratives in those spaces. The thesis is characterised by discussing alternative points of view and its hypothetical nature. During the text, it becomes apparent that the relationship between games and narratives is strongly twofold: on one hand, the player continuously narrativizes the states the game is in while playing, while the narratives residing within the game space form their own partially separate narrative spaces, on the other. These spaces affect the conception the player has of the game states and the events taking place in the game space itself.