Thesis (doctoral)--Universität, Marburg, 2000.

Work which takes from elsewhere forms an important thread in European art music. There is a long tradition of music which variously borrows, thieves, pastiches, plagiarises, ironically ‘retakes’, hoaxes, impersonates and appropriates. The music I have written for Off the edge, while seeking to honour and add to this thread, also attempts to zoom in upon and make explicit the idea of an ultimate and irreversible composerly self-annihilation, a kind of one-way exit-gate from the world of authored musical works itself made of pieces of music, which so much of this tradition, I feel, points towards. (Of my nine pieces, it is perhaps Time to go—only, with its ‘à la suicide note’ texts and its music that seems to slide in from far beyond the frame that is ‘composer Luke Stoneham’, which manages to get closest to this.) I have chosen the title Off the edge, because all of my music tries to capture a sense of nocturnal peripheral vision: be content with catching glimpses of the composer Luke Stoneham, because as soon as you turn to look at him face-on, he disappears.

Indiana University-Purdue University Indianapolis (IUPUI) / Introduction: Endodontic treatment in teeth with pulp canal obliteration (PCO) is challenging. Guided Endodontic Access (GEA) combines information from a cone-beam computed tomography (CBCT) scan with an intra-oral scan to create a stent that can be used as a guide to treat teeth with PCO. GEA stents designed with traditional palatal accesses were shown to be successful in accurately negotiating these 3D printed teeth with simulated PCO, however, the difference in accuracy between the traditional palatal access compared to a conservative incisal access is not yet known. Objective: This in vitro study compares GEA stents designed with an incisal access approach to GEA stents designed with a traditional palatal access approach. The effect on the overall degree of deviation of the designed access path from the prepared path is evaluated by measuring the degree of angle of deviation and amount of deviation in millimeters. Materials and Methods: A 3-D printed maxillary model of an anonymous patient was used. PCO was simulated in a 3D printed natural #8 using the coDiagnostiX software tooth at two levels: coronal and mid-root. A GEA stent that extended from tooth #3 to tooth #14 with a guide sleeve over the simulated tooth #8 was accessed with a dedicated 1.0 mm diameter and 20 mm length drill that is designed to fit the access sleeve. 15 GEA stents had guides utilized for the incisal access approach, and 15 GEA stents had guides utilized for the traditional palatal access approach. Results: Angle, mesio-distal (base), and mesio-distal (tip) deviations were significantly lower for the incisal access compared to the traditional access. Inciso-apical (base) deviation was significantly more negative for incisal access compared to the traditional access. Bucco-lingual (base) deviation was significantly more negative for traditional access compared to the incisal access, while incisal and traditional accesses were not significantly different for bucco-lingual (tip) deviation. Coronal 1/3 calcification groups had significantly more mesio-distal (base) deviation than the middle 1/3 and no PCO groups. The no PCO group had significantly more negative inciso--apical (base) deviation than the coronal 1/3 calcification and middle 1/3 calcification groups, and the coronal 1/3 calcification group was significantly more negative than the middle 1/3 calcification group. The coronal 1/3 calcification group had significantly more mesio-distal (tip) deviation than the no PCO group. PCO level did not have a significant effect on angle, bucco-lingual (base), or bucco-lingual (tip) deviations. Conclusion: The utilization GEA via incisal access resulted in less degree and amount of drill deviation compared to the traditional access at all levels of calcification, however, the level of PCO did not influence the degree and amount of drill deviation between the incisal and traditional access approaches. It can be concluded that the use of a GEA stent that utilizes an incisal access approach in teeth with PCO will result in a more predictable outcome.

No description available.

Dans sa provenance platonicienne, l’idéal de l’incarnation de l’Idée doit à la fois affronter des individualités (pré)déterminées et qualitativement différentes (le pluralisme) – qui sont répétitions et répétées elles-mêmes. Il doit devenir le vouloir-dire de la personne qui s’efforce de mettre en œuvre ce dernier et qui cherche à franchir les limites ontologiques de la représentation. Cependant, l’irréalisabilité de la pure répétition du vouloir-dire – ou de n’importe quel « sujet » – atteste de la présence absente du même dans le processus de sa mise en œuvre ; la répétition est toujours déjà répétition différenciatrice, son acte même toujours susceptible d’être perçu comme mimétique en pratique. Lorsque nous « créons », nous cherchons une différence absolue (singularisation) tout en visant l’universalité du vouloir-dire, l’Univocité. Autrement dit, c’est l’inévitabilité de la répétition différenciatrice (« nouveauté ») qui se répète et tend vers un dernier résultat censé être absolument univoque et intersubjectivement compris et jugé. Cette inévitabilité signifie-t-elle une (ou la dernière) impasse théorique – une « fin » – insurmontable ? Comment les artistes, les historiens d’art et les philosophes s’y prennent-ils ? Entre l’origine et le futur de l’art, quelle puissance de la répétition devrait-on y chercher pour ne plus répéter « une répétition pour toute » ? / From its Platonic source, the ideal of embodiment of Idea must face individualities which are (pre)determined and qualitatively different – and are themselves repetitions repeated. It must become “what-is-wanted-to-be-said” or “meaning” (“vouloir-dire”) of the person who endeavors to realize it and to attempt to exceed the ontological limits of representation. Meanwhile, the unrealizability of pure repetition of the “vouloir-dire” – like any other “subject matter” – testifies to the absent presence of the same in the process of its realization; each and every repetition is always already a differential repetition, and its act itself always susceptible to be taken as mimetic in practice. When we “create”, we search for the absolute difference (singularization) while aiming at a universality of the “vouloir-dire”, Univocity. Put another way, it is the inevitability of the differential repetition (“newness”) that repeats itself and moves towards the last outcome that is meant to be unique in itself and intersubjectively understood and judged. Does this inevitability point towards a (or the last) insurmountable theoretical stalemate – “an end”? How do artists, art-historians, and philosophers deal with this problem? Between the origin and the future of art, what sort of force of repetition do we have to look for in order to finally no longer repeat “one repetition for all”?

Les rétinopathies ischémiques (RI) sont la cause majeure de cécité chez les personnes âgées de moins de 65 ans. Il existe deux types de RIs soit la rétinopathie du prématuré (ROP) ainsi que la rétinopathie diabétique (RD). Les RIs sont décrites en deux phases soit la phase de vasooblitération, marquée par une perte importante de vaisseaux sanguins, et une phase de néovascularisation secondaire à lʼischémie menant à une croissance pathologique de vaisseaux. Cette seconde phase peut générer des complications cliniques telles quʼun oedème dans lʼhumeur vitré ainsi que le détachement de la rétine chez les patients déjà atteints dʼune RI. Les traitements approuvés pour les RIs visent à réduire la formation des vaisseaux pathologiques ou lʼoedème; mais ceux-ci malheureusement ne règlent pas les problèmes sous-jacents tels que la perte vasculaire et lʼischémie. La rétine est un tissu hautement vascularisé qui contribue à lʼirrigation et à lʼhoméostasie des neurones. Lʼinteraction neurovasculaire, comprenant de neurones, vaisseaux et cellules gliales, contribue au maintien de cette homéostasie. Durant le développement, les neurones et les cellules gliales jouent un rôle important dans la vascularisation de la rétine en sécrétant des facteurs qui stimulent l'angiogenèse. Cependant, nos connaissances sur lʼinteraction neurovasculaire dans les RIs sont limitées. En identifiant les interactions importantes entre les cellules composant cette unité neurovasculaire dans la rétine, nous pourrons viser des cibles qui engendreront une revascularisation seine afin de diminuer les signes pathologiques chez les patients atteints dʼune RI. Les travaux présentés dans cette thèse visent à mieux expliquer cette interaction neurovasculaire en soulignant des concepts importants propres aux RIs. En utilisant un modèle de rétinopathie induite par lʼoxygène chez la souris, qui reproduit les caractéristiques importantes de la ROP (et en certaines instances, la RD), nous identifions quelques molécules clés jouant un rôle significatif dans les RIs soit la sémaphorine 3A (sema3A), lʼIL-1β, ainsi que le récepteur PAR2. Nos résultats démontrent que Sema3A, sécrétée par les cellules ganglionnaires rétiniennes (CGRs) durant une ischémie, empêche la revascularisation normale et que cette expression est induite par lʼIL-1β provenant des microglies activées. En bloquant Sema3A directement ou via lʼinhibition de lʼIL- 1β, nous remarquons une revascularisation seine ainsi quʼune diminution importante des vaisseaux pathologiques. Cela nous indique que Sema3A est impliquée dans la guidance vasculaire et quʼelle contribue à la pathogenèse des RIs. Lʼactivation de façon exogène de PAR2, identifié aussi comme régulateur du récepteur de lʼIL-1β (IL- 1RI) sur les CGRs, se traduit par une diminution séquentielle de lʼIL-1RI et de Sema3A ce qui mène également à une revascularisation seine. En conclusion, ces travaux soulignent lʼimportance de lʼinteraction neurovasculaire ainsi que la guidance vasculaire dans les RIs. Ils renforcent lʼimportance de la communication entre neurone, vaisseau et microglie dans la pathogenèse des RIs. Finalement, nous identifions quelques molécules clés qui pourront servir comme cibles afin de lutter contre lʼischémie qui cause des problèmes vasculaires chez les patients atteints dʼune RI. / Ischemic retinopathies (IRs), namely, retinopathy of prematurity (ROP) and diabetic retinopathy (DR), are the major cause of blindness in persons under the age of 65. IRs are biphasic disorders described by an initial vasoobliterative phase marked by a persistent microvascular degeneration, which leads to ischemia. Retinal ischemia, secondary to vessel loss, incites a second neovascularization phase represented by an aberrant, misdirected neovessel formation into the vitreous, which can cause adverse clinical complications including vitreous hemorrhaging and tractional retinal detachment. While current treatments aim at reducing vitreous/retinal hemorrhaging and/or pathological pre-retinal neovascularization, these regimens fail to address the underlying problem; that is, microvascular decay and retinal ischemia. The retina is a highly metabolic tissue that requires a significant amount of nutrients and oxygen. This is supplied by an intricate and highly regulated vascular network required to maintain homeostasis and proper function. The intricate cellular interactions in the neurovascular unit – the consortium of vessel, neurons and support glia – are required for regulating and maintaining homeostasis under normal conditions. However, the understanding of how this unit functions under ischemic stress, that which is seen in patients suffering from IRs, is not well defined. The present work underlines several important concepts of neurovascular coupling in IRs in efforts to identify potential therapeutic agents that may help curb retinal ischemia by stimulating normal revascularization. Using a mouse model of oxygen-induced retinopathy (OIR), which reproduces the salient features of ROP (and in some instances DR), we identified key players involved in generating the pathophysiological signatures associated with IRs; namely, semaphorin3A (Sema3A), interleukin-1β (IL-1β) and protease-activated receptor 2 (PAR2). Our results show that neuronal-derived Sema3A, secreted by ischemic retinal ganglion cells (RGCs), acts as a potent vaso-repulsive molecules that impedes normal revascularization. Activated microglia contribute to this process by secreting IL-1β, which induces paracrine release of Sema3A expression contributing to microvascular decay as well as pathological pre-retinal neovascularization. Inhibition of Sema3A or IL-1β translates to rapid revascularization and, as a result, a significant reduction in pathological neovessel formation. These results demonstrate that Sema3A is directly involved in vascular guidance and precipitates the pathophysiological features associated with IRs. PAR2, found on RGCs, was also identified as a key regulatory mechanism involved in dampening IL-1β induced Sema3A mediated vascular decay by reducing IL-1 receptor (IL-1RI). Exogenous activation of neuronal PAR2 translates to a sequential reduction of both IL-1RI and Sema3A resulting in accelerated revascularization and consequentially pre-retinal neovascularization. In conclusion, these studies highlight the importance of neurovascular coupling associated with IRs. Herein, we demonstrate the consorted interaction between neuron, vessel and glia and its impact on shaping the retinal vasculature during disease. Moreover, we underscore the significant impact of neuronal guidance cues in manifesting the salient vascular features of IRs. Finally, we identify key players that may serve as potential therapeutic avenues in curbing retinal ischemia in efforts to reduce vascular complications associated with IRs.