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Träfflista för sökning "WFRF:(Palazzo V) "

Sökning: WFRF:(Palazzo V)

  • Resultat 1-10 av 37
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1.
  • Abel, Ian, 1985, et al. (författare)
  • Multiscale modelling for tokamak pedestals
  • 2018
  • Ingår i: Journal of Plasma Physics. - 0022-3778 .- 1469-7807. ; 84:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Pedestal modelling is crucial to predict the performance of future fusion devices. Current modelling efforts suffer either from a lack of kinetic physics, or an excess of computational complexity. To ameliorate these problems, we take a first-principles multiscale approach to the pedestal. We will present three separate sets of equations, covering the dynamics of edge localised modes (ELMs), the inter-ELM pedestal and pedestal turbulence, respectively. Precisely how these equations should be coupled to each other is covered in detail. This framework is completely self-consistent; it is derived from first principles by means of an asymptotic expansion of the fundamental Vlasov-Landau-Maxwell system in appropriate small parameters. The derivation exploits the narrowness of the pedestal region, the smallness of the thermal gyroradius and the low plasma beta (the ratio of thermal to magnetic pressures) typical of current pedestal operation to achieve its simplifications. The relationship between this framework and gyrokinetics is analysed, and possibilities to directly match our systems of equations onto multiscale gyrokinetics are explored. A detailed comparison between our model and other models in the literature is performed. Finally, the potential for matching this framework onto an open-field-line region is briefly discussed.
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  • Krantz, Tobias, 1971- (författare)
  • Lagskydda lokalt självstyre
  • 2000
  • Ingår i: Upsala nya tidning. - 1104-0173.
  • Tidskriftsartikel (populärvet., debatt m.m.)
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  • Revêchon, Gwladys (författare)
  • Molecular insights into Hutchinson-Gilford progeria syndrome and age-associated disease : from mechanisms to treatment strategy
  • 2019
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Aging is a complex process that occurs as we grow old and is associated with a gradual decline of tissue functions. Scientists have been trying to understand the mechanisms that drive such phenomenon by studying premature aging syndromes and aging-related disorders. The Hutchinson-Gilford progeria syndrome (HGPS) is a lethal segmental genetic disease affecting children at an early age and characterized by accelerated aging-like features including alopecia, loss of subcutaneous adipose tissue and cardiovascular pathologies. This disorder primarily results from the production of a noxious protein called progerin, altering proper tissue homeostasis and functions. Strikingly, HGPS children present an accelerated vascular aging phenotype similar to that of chronic kidney disease (CKD) patients. Indeed, in addition to displaying kidney defects, CKD patients exhibit an accelerated vascular decline. Interestingly, progerin has previously been found expressed in cells and tissues from aged individuals, but its contribution to aging and aging-associated disorders remains poorly understood. Here, we investigated whether and how various levels of progerin are relevant to the development and progression of tissue pathology in HGPS, normal aging and aging-associated diseases, in order to generate a potential new treatment strategy for HGPS in particular. In paper I, to better understand the mechanisms by which progerin accumulation disrupts tissue homeostasis, a humanized HGPS mouse model with overexpression of progerin in the skin was used. We demonstrated that progerin accumulation resulted in impaired tissue homeostasis as a consequence of an aberrant increase in symmetric cell division. Further analysis suggested a potential causal role of the Wnt/β-catenin signaling, associated with mislocalization of the nuclear envelope proteins emerin and nesprin-2. In paper II, to investigate whether a small fraction of progerin-expressing cells in a tissue can lead to tissue pathology during aging, another humanized HGPS mouse model was employed. We showed that continuous expression of progerin in only a few preadipocytes and adipocytes is associated with fibrosis and lipoatrophy over time. This phenotype was combined with increased senescence, persistent DNA damage and cell death, which were found accompanied by macrophage infiltration and systemic inflammation. These results suggested that progerin, despite being expressed in only a low fraction of the cells of a tissue, has the potential to contribute to a common aging-associated phenotype. In paper III, to unravel the possible involvement of progerin expression in age-associated diseases, we used arterial biopsies and blood from CKD patients. We found that progerin was expressed at low frequencies in 70% of the CKD patients arteries (in up to 7.4% of the cells), which was associated with an increase in DNA damage. When searching for the cause of progerin expression, we identified the LMNA c.1824C>T mutation in both the blood and arteries. Our data further suggested that progerinexpressing cells might arise during vascular regeneration, by proliferation of progenitor cells. In paper IV, to examine the mechanisms associated with telomere dysfunction in HGPS, we employed various in vitro systems and a severe progeroid mouse model of skin. We demonstrated that telomere dysfunction leads to the production of non-coding RNAs, which activates the DNA damage response signaling. Treatment with telomeric sequence-specific antisense oligonucleotides not only repressed this signaling, but also significantly improved both the healthspan and lifespan of HGPS mice. This thesis provides novel findings about the complex molecular mechanisms underlying progerin expression in HGPS, and its possible contribution to aging and CKD-related early vascular aging, all of which led to the discovery of a potential new treatment approach for HGPS.
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  • Moradi, Fatemeh, 1985- (författare)
  • Working out work : from personal informatics to redesigning work
  • 2016
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • "Personal Informatics" (PI) and "Quantified Self" (QS) are two contemporary notions in the field of Human–Computer Interaction. Such hardware and software systems gather personalized quantified data and visualize them for the purpose of supporting self-reflection. Many of these systems focus on breaking the habit of prolonged sitting and increasing physical activity in our daily lives. The problems associated with the sedentary lifestyle and prolonged hours of sitting have been noted in many studies. In fact, stationary behavior is a risk factor for cardiovascular disease, diabetes and certain types of type of cancer. Nowadays we, as adults, spend more than 8 hours a day on work and work-related activities. As a consequence, the time spent sitting in office workspaces contributes to the majority of stationary behavior in our daily lives. Throughout history, designers and technocrats have constantly redesigned workspaces in attempts to increase work productivity and efficiency. Thus "modern" office work configuration includes desks and stationary computers and so office workers have become accustomed to prolonged sitting in their workplaces.    In relation to this research problem, I have worked on my PhD thesis within the context of a four-year cross disciplinary research project in which we have been exploring ways of increasing physical activity and breaking the habit of prolonged sitting among office workers. This is a thesis in informatics and closely allied to medicine and it focuses on studying how contemporary office work affects the body and how to redesign this context. For this thesis, I conducted three empirical studies and designed and developed two prototypes - the "NEAT Lamp" and the "Talking Tree". The "Sport Co." study was the first quantitative study, and was followed by two qualitative observational ethnographic studies – the "Housing Co." study and the "Health Co." study. The research process adopted during the work can be described as an intertwined process consisting of three methodological approaches: observational ethnographic studies, concept development and prototyping. These three came together to form a coherent contextual design process for tackling the research question, "How can we approach the design of work in today's offices in order to make office workers more physically active in their workspaces?"  This process resulted in five papers presenting various aspects and results of the research conducted. The results cover the role of bodies at work by considering the history of work design, knowledge about the local movement and mobility patterns of office workers in modern office spaces and eventually the design and evaluation of the two prototypes introduced in this thesis. Finally, I conclude this thesis by highlighting my overall contributions. The first contribution targets designers willing to design for increasing physical activity and breaking the habit of prolonged sitting in workspaces. In relation to this I introduce a design space as a tool for understanding the design of work in relation to worker’s bodies. The second contribution highlights how observational ethnographic studies, concept development, and prototyping can be combined when exploring the context of physical activity in office environments and it shows how contextual design might be a suitable approach for such studies. In addition, it emphasizes ways for how we can redesign work and expand our contextual knowledge. This, by examining and evaluating interactive prototypes in real office settings.
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