In this work we explore the collider prospects for the asymptotic safety scenario being realized as a quantum theory of gravity. Testing gravity at colliders becomes a real possibility in the case of extra dimensional models, or with additional physics leading to a fundamental scale of gravity significantly lower than the Planck mass. We present several approximations for the full non-perturbative renormalization group running, and show how these can be implemented at the level of the graviton wave-function renormalization. The issue of scale identi fication of the physical process with the renormalization group scale k is clarified and several different choices are compared. The various approximations are resolved and shown in most cases to generate scheme independent results. On the phenomenological side, we investigate two separate observables. First, at tree-level we present results on LHC di-muon production due to asymptotically safe gravitons. By including fixed point scaling Kaluza- Klein modes, the predicted signal is enhanced and simultaneously problems associated with the breakdown of perturbative unitarity are reduced. At the one-loop level, we outline our calculation for the contribution to electro-weak precision observables originating from asymptotically safe gravity. New bounds are derived which show different behaviour as a function of the number of extra dimensions compared with previous effective field theory results. Finally, we comment on possible further directions for exploring the frontier of collider physics and quantum gravity.

Zugl.: Dortmund, Univ., Diss., 2007

Reproduction de : Thèse de doctorat : Psychologie et psychologie clinique : Lyon 2 : 2002. / Titre provenant de l'écran-titre. Bibliogr.

Zugl.: Dortmund, Univ., Diss., 2009

Zugl.: Augsburg, Univ., Diss., 2008

Thesis (Ph. D.)--University of Texas at Austin, 2000. / Vita. Includes bibliographical references (leaves 126-131). Available also in a digital version from Dissertation Abstracts.

Thesis (doctoral)--Wissenschaftliche Hochschule für Unternehmensführung, Koblenz, 1999.

Zugl.: Bratislava, Comenius-Univ., Diss., 2009

Waardenburg-Shah syndrome (WS4, MIM_277580) is a congenital developmental disorder characterized by pigmentary abnormalities of the skin, eyes and hair, sensorineural deafness and intestinal aganglionosis (HSCR; Hirschsprung disease). Mutations in the coding regions of EDN3, EDNRB, or SOX10 account for 65-85% of the WS4 patients. These mutations are not fully penetrant, contributing to the phenotypic variability of WS4. We screened these genes in a three-generation family (14 individuals; three members affected with HSCR only and one affected with “partial’ WS4 –iris heterochromia and HSCR-). A novel heterozygous missense mutation was identified in EDNRB. EDNRB encodes the EDNRB receptor, which is essential for the differentiation of the neural crest cells into melanocytes, enteric ganglia and Schwann cells. The mutation was present in four affected and three unaffected family members. In the EDNRB isoforms 1 and 2, the mutation results in the replacement of the translation initiation codon methionine (Met) with a valine (Val) and such replacement (M1V) would theoretically abolish the use of the translation initiation codon. However, in EDNRB isoform 3, the replacement is at Met91 (M91V) and is predicted benign. Since different EDNRB transcripts are expressed concomitantly in the still developing newborn's gut, we theorized that the intra-familial variability of the phenotype could be related to the expression ratio between benign and damaging isoforms. We examined the consequences of M1V or M91V in their respective isoforms. Constructs containing either wild-type cDNA of isoform 1 and 3 or their mutated counterpart were transiently transfected into Human Embryonic Kidney 293 cell (HEK293). Confocal and immunoblot experiments showed that EDNRB M1V generated a shortened protein (starting from Met46); the wild-type-EDNRB isoform 3 or its mutant (p.M91V) were only found in the cytosol. Although EDNRB M1V was able to generate a shorter protein, the later failed to translocate onto the cell membrane, theoretically, affecting signal-transduction. Isoform 3 did not seem to play a role as cellular receptor. We also identified a c.-248G/A rare change at the 5’-untranslated region (5’UTR) of EDN3 (EDNRB ligand) which was predicted to affect translation efficiency. The presence of this variant in affected individuals but not in healthy carriers of the EDNRB mutation, suggests that both variants are necessary for the disease manifestation. Variations within the disease phenotype may be due to each individual’s genetic background. To identify other susceptibility loci, we carried out whole-genome linkage scan in this family using a high density SNP assay. Merlin software was used for parametric and non-parametric linkage. A susceptibility locus on chromosome 4q13.3-q24 was identified by both nonparametric and parametric linkage analyses, with LOD scores of 1.204 and 1.7109 respectively. Haplotype analysis refined the region to a 27.76 cM interval, in which genes involved in neuron development reside. To conclude, the novel EDNRB M1V mutation in this family may lead to HSCR and/or WS4 when in conjunction with other genetic lesions, such as the EDN3 5’UTR rare variation and/or a not yet identified susceptibility locus on chromosome 4q13.3-q24. / published_or_final_version / Surgery / Master / Master of Philosophy

This report is the Austrian contribution to the European TSER research project "SMEPOL" ("SME policy and the regional dimension of innovation"). The objective of this project is to analyze innovation policies aiming at SMEs, to evaluate their effectiveness and to propose potential improvements. For this purpose, important innovation support instruments for SMEs in several European regions - Upper Austria, the Triangle region in southern Jutland (Denmark), Lombardy and Apulia in Italy, Limburg in the Netherlands, Wallonia, northern and south-eastern Norway, Valencia in Spain, parts of London and its outer metropolitan area - have been investigated. This report focusses on the region of Upper Austria. It has four major parts: First, an introductory text describing the conceptual model of the research, its design and methodology, and presenting the investigated Austrian region. Second, a description of the national and regional innovation support system in general and an analysis of those support instruments which are most important for innovation activities of SMEs in particular. Third, an investigation of the innovativeness of SMEs in Upper Austria, the innovation barriers, and the effects of the selected support instruments on the firms' innovation activities. Fourth, conclusions regarding the strengths and weaknesses of the innovation support instruments and proposals for improvements. (author's abstract, ed. M.Putz) / Series: SRE - Discussion Papers