Changing the rules of the game : banks and community-oriented economic development

Thesis (M.C.P.)--Massachusetts Institute of Technology, Dept. of Urban Studies and Planning, 1983.MICROFICHE COPY AVAILABLE IN ARCHIVES AND ROTCH.Bibliography: leaves 121-124.by David Stone Flad.M.C.P

MRI substrates of specific neuropsychological dysfunctions within and across FTD genotypes at the presymptomatic and symptomatic disease stage

Neuropsychologische Defizite, wie Apraxie, spielen für neurodegenerative Erkrankungen, speziell auch für Frontotemporale Demenzen (FTD), eine wichtige Rolle. In dieser Arbeit zeige ich abgegrenzte atrophische Areale der Hirnrinde, die für Apraxie und die Leistung im Trail Making Test (TMT) innerhalb einer Kohorte von familiärer FTD relevant sind. Mit einer Stichprobe von 472 Probanden aus der GENFI Studie, demonstriere ich einen Hypothesen getriebenen Ansatz um kortikale atrophische Areale zu identifizieren, die mit spezifischen neuropsychologischen Defiziten zusammenhängen: dadurch konnte ich atrophische Areale im prämotorischen Cortex, Inferioren Frontalcortex und der Pars opercularis des Inferioren Frontalcortex identifizieren, die speziell mit Apraxie zusammenhängen; sowie Areale im Frontalcortex, die mit der Leistung im TMT zusammenhängen. Zusätzlich präsentiere ich einen alternativen Weg, um das Problem multipler Vergleiche von kortikalen Strukturen zu lösen, indem eine permutationsbasierte Maximum Statistik berechnet wird, welche die Identifikation kleiner Areale ermöglicht. Zuletzt zeige ich eine Analyse über präsymptomatische Effekte und diskutiere deren Schwierigkeiten und Limitationen: in den zuvor identifizierten Arealen konnte ich keine präsymptomatische Degeneration feststellen. Schließlich trägt diese Arbeit zur wissenschaftlichen Forschung im Bereich der Apraxie, familiärer FTD sowie genereller Zusammenhänge von neuropsychologischen Defiziten und Hirnrindenbereichen bei.Neuropsychological deficits, as apraxia, play an important role for neurodegenerative dementias, including frontotemporal dementia (FTD). In this work I delineate cortical atrophy areas relevant for apraxia and Trail Making Test (TMT) performance within a genetic frontotemporal lobar degeneration (FTLD) cohort. Using 472 subjects from the GENFI study, I demonstrate a hypothesis-driven approach for the identification of cortical atrophy areas related to specific neuropsychological dysfunctions: through this I identified atrophy in the premotor cortex, inferior frontal and frontal opercular areas to be specifically related to apraxia; and areas in the frontal cortex to be related to TMT performance. In addition, I present an alternative way of correcting my results within a surface-based approach for multiple comparisons using a permutation based maximum statistic, facilitating the identification of small areas. Lastly, I present an analysis about presymptomatic effects and discuss its limitations and difficulties: I could not delineate presymptomatic cortical degeneration in the previously identified areas. As a result, this work contributes to research about apraxia, genetic FTLD and general relations of neuropsychological functions with cortical areas

On the use of kinetic energy preserving DG-schemes for large eddy simulation

Recently, element based high order methods such as Discontinuous Galerkin (DG) methods and the closely related flux reconstruction (FR) schemes have become popular for compressible large eddy simulation (LES). Element based high order methods with Riemann solver based interface numerical flux functions offer an interesting dispersion dissipation behavior for multi-scale problems: dispersion errors are very low for a broad range of scales, while dissipation errors are very low for well resolved scales and are very high for scales close to the Nyquist cutoff. In some sense, the inherent numerical dissipation caused by the interface Riemann solver acts as a filter of high frequency solution components. This observation motivates the trend that element based high order methods with Riemann solvers are used without an explicit LES model added. Only the high frequency type inherent dissipation caused by the Riemann solver at the element interfaces is used to account for the missing sub-grid scale dissipation. Due to under resolution of vortical dominated structures typical for LES type setups, element based high order methods suffer from stability issues caused by aliasing errors of the non-linear flux terms. A very common strategy to fight these aliasing issues (and instabilities) is socalled polynomial de-aliasing, where interpolation is exchanged with projection based on an increased number of quadrature points. In this paper, we start with this common no model or implicit LES (iLES) DG approach with polynomial de-aliasing and Riemann solver dissipation and review its capabilities and limitations. We find that the strategy gives excellent results, but only when the resolution is such, that about 40% of the dissipation is resolved. For more realistic, coarser resolutions used in classical LES e.g. of industrial applications, the iLES DG strategy becomes quite inaccurate. We show that there is no obvious fix to this strategy, as adding for instance a sub-grid-scale models on top doesn't change much or in worst case decreases the fidelity even more. Finally, the core of this work is a novel LES strategy based on split form DG methods that are kinetic energy preserving. The scheme offers excellent stability with full control over the amount and shape of the added artificial dissipation. This premise is the main idea of the work and we will assess the LES capabilities of the novel split form DG approach when applied to shock-free, moderate Mach number turbulence. We will demonstrate that the novel DG LES strategy offers similar accuracy as the iLES methodology for well resolved cases, but strongly increases fidelity in case of more realistic coarse resolutions. (C) 2017 Elsevier Inc. All rights reserved

MRI substrates of specific neuropsychological dysfunctions within and across FTD genotypes at the presymptomatic and symptomatic disease stage

Neuropsychologische Defizite, wie Apraxie, spielen für neurodegenerative Erkrankungen, speziell auch für Frontotemporale Demenzen (FTD), eine wichtige Rolle. In dieser Arbeit zeige ich abgegrenzte atrophische Areale der Hirnrinde, die für Apraxie und die Leistung im Trail Making Test (TMT) innerhalb einer Kohorte von familiärer FTD relevant sind. Mit einer Stichprobe von 472 Probanden aus der GENFI Studie, demonstriere ich einen Hypothesen getriebenen Ansatz um kortikale atrophische Areale zu identifizieren, die mit spezifischen neuropsychologischen Defiziten zusammenhängen: dadurch konnte ich atrophische Areale im prämotorischen Cortex, Inferioren Frontalcortex und der Pars opercularis des Inferioren Frontalcortex identifizieren, die speziell mit Apraxie zusammenhängen; sowie Areale im Frontalcortex, die mit der Leistung im TMT zusammenhängen. Zusätzlich präsentiere ich einen alternativen Weg, um das Problem multipler Vergleiche von kortikalen Strukturen zu lösen, indem eine permutationsbasierte Maximum Statistik berechnet wird, welche die Identifikation kleiner Areale ermöglicht. Zuletzt zeige ich eine Analyse über präsymptomatische Effekte und diskutiere deren Schwierigkeiten und Limitationen: in den zuvor identifizierten Arealen konnte ich keine präsymptomatische Degeneration feststellen. Schließlich trägt diese Arbeit zur wissenschaftlichen Forschung im Bereich der Apraxie, familiärer FTD sowie genereller Zusammenhänge von neuropsychologischen Defiziten und Hirnrindenbereichen bei.Neuropsychological deficits, as apraxia, play an important role for neurodegenerative dementias, including frontotemporal dementia (FTD). In this work I delineate cortical atrophy areas relevant for apraxia and Trail Making Test (TMT) performance within a genetic frontotemporal lobar degeneration (FTLD) cohort. Using 472 subjects from the GENFI study, I demonstrate a hypothesis-driven approach for the identification of cortical atrophy areas related to specific neuropsychological dysfunctions: through this I identified atrophy in the premotor cortex, inferior frontal and frontal opercular areas to be specifically related to apraxia; and areas in the frontal cortex to be related to TMT performance. In addition, I present an alternative way of correcting my results within a surface-based approach for multiple comparisons using a permutation based maximum statistic, facilitating the identification of small areas. Lastly, I present an analysis about presymptomatic effects and discuss its limitations and difficulties: I could not delineate presymptomatic cortical degeneration in the previously identified areas. As a result, this work contributes to research about apraxia, genetic FTLD and general relations of neuropsychological functions with cortical areas