Thesis (Ph. D.)--Pennsylvania State College, 1933. / Cover title. "Bibliography on amplifiers": p. 8.

Thesis (Ph. D.)--University of Hawaii at Manoa, 2004. / Includes bibliographical references (leaves 198-219).

No description available.

Thesis--Utrecht. / Vita. Includes bibliographical references.

Thesis--Utrecht. / Vita. Includes bibliographical references.

Thesis--Utrecht. / Vita. Includes bibliographical references.

The parcel shelf in a car is one of the things that are most exposed to ultraviolet light and heat. The sunlight causes ultraviolet radiation and excessive heat to this area. This can cause the material to degrade, fade or drift in colour. The parcel shelf production is today divided between three producers. This requires a good contact and cooperation between the different actors. As the automobile industry is a very complex industry, high demand is required of everyone involved. The goal of this study was to find improvements that could lead to a better ultraviolet and heat protection. Volvo Cars provided material and the experiments were held on their test facility. The tests were conducted based on the Volvo Cars requirements and methods. A Weather-Ometer is used to simulate the ultraviolet light and heat, the same way a parcel shelf is exposed to outdoors. Chemical analyses are used to determine whether there is any difference in the material when it is aged in a Weather-Ometer or not. The parcel shelf is made of needle punched, dispersed dyed polyester. The results showed that the present parcel shelf material does indeed show a colour shift after ageing. The authors present a number of suggestions to improve the material's characteristics. For example, Volvo could consider using an acrylic non-woven instead of polyester. Dyes that withstand ultraviolet radiation better can also be chosen and a variety of ultraviolet absorbers can be added. 2-(2-hydroxy-5-carboxy-phenyl)-2H-benzotriazole, Tinuvin P, 327 [2-(2-hydroxy-5-methyl-phenyl) 2H-benzotriazole, 2-(3,5-butyl-6-hydroxy)-2H-2-chloro-benzotriazole respectively] and 2,4-dihydroxy-benzophenone are example of absorbers that can be added to make the ultraviolet resistance better. / Program: Textilingenjörsutbildningen

Ph.D. / Molecular and Medical Genetics / The objective of this study is to examine, in light of the expression of multiple p53 family member isoforms, the specific role of p73 in malignant conversion, cellular response to DNA damage, and direct or indirect cooperation with other p53 family members in a clonal model of epidermal carcinogenesis. We first focused on the role of p73 in malignant conversion. Whether sporadic or siRNA induced, loss of p73 in initiated p53+/+ keratinocytes lead to conversion to squamous cell carcinoma (SCC) in vivo which was reversible upon reconstitution of TAp73α but not ΔNp73α. Second, we investigated the cellular response to ionizing radiation (IR) in the presence and absence of p73, showing that loss of p73 at malignant conversion was associated with resistance to IR in vitro. The loss of radiation sensitivity and malignant conversion was characterized by reduced steady state DNA binding levels of transcriptionally active p63 isoforms to the p21 promoter, failure to induce specific p53 family transcriptional targets, and failure to arrest in G1. Reconstitution of TAp73α, but not ΔNp73α, increased steady state DNA binding capabilities of TAp63β, TAp63γ, and ΔNp63γ, and steady state levels of p53 family target mRNA, but did not restore cellular sensitivity to IR. We thus uncovered a functional cooperation between TA isoforms of p73 and p63 and showed that p73-mediated DNA damage response was uncoupled from its tumor suppressive role. We observed preferential DNA binding of the inhibitory ΔNp63α isoform both in vitro and invivo in SCC suggesting that in the absence of TAp73α a balance is tipped toward DNA binding of the inhibitory isoforms. Third, we studied the role of the p53 family inkeratinocyte response to UVB. Tumorigenic cells lacking p73 that were resistant to IR remained sensitive to UVB, accompanied by DNA binding of the TAp63γ isoform, suggesting that keratinocyte response to UVB is not dependent upon p73 and suggesting a hierarchy of p53 family member responses to DNA damage. Finally, we examined TAp73α interaction with the p53 family inhibitor Mdm2. Mdm2 was in complex with DNA-bound p53 family members in malignant cells, but reconstitution of cells withTAp73α correlated with removal of Mdm2 from the complex, making them more like primary keratinocytes or initiated cells. Like the initiated cells, cells expressing TAp73α were refractory to treatment with the Mdm2-p53 inhibitor Nutlin-3 while cells lacking p73 expression or expressing ΔNp73α were sensitive. Thus, we suggest that p73 may be acting as a molecular shield to keep p53 family member inhibitors, such as ΔNp63α andMdm2, at bay. Further understanding of p53 family interplay in tumor development and DNA damage response could lead to new therapies or optimization of current therapeutic strategies in solid tumors of epithelium, particularly where deregulation or loss of p63 and p73 expression is associated with increased tumor invasiveness, treatment resistance, and poor patient prognosis.