Diss. (sammanfattning) Umeå : Umeå universitet, 2009. / Härtill 4 uppsatser.

Thesis (Ph.D. in Microbiology) -- University of Colorado Denver, 2007. / Typescript. Abstract available online via ProQuest Digital Dissertations. Includes bibliographical references (leaves 207-223).

Oxygen Transport Membranes (OTMs) can drastically reduce the energy and cost demands of processes that require pure oxygen, as they offer the possibility to combine a separation unit with a chemical reactor. One of the most commercially viable applications of OTMs is the partial oxidation of hydrocarbons for syngas production. A typical OTM configuration is a sequential arrangement of layers, i.e. an inactive support, a fuel oxidation layer, a dense layer and an oxygen reduction layer. However, one of the limitations of the OTM system is the low catalytic activity and stability of the materials currently used for the fuel oxidation layer. Moreover, the traditional deposition techniques that are used for the catalysts preparation are difficult to perform, as the fuel oxidation layer is buried deeply in the structure of the OTM. To simplify the OTM fabrication and improve the catalysts activity and stability, this thesis explores the exsolution of Ni nanoparticles from two different host lattice compositions, as potential materials for the fuel oxidation layer of OTMs. The (La₀.₇₅Sr₀.₂₅)(Cr₀.₅Mn₀.₄₅Ni₀.₅)O₃ (LSCMNi5) perovskite was selected, as the first candidate material for the OTMs. During reduction, the exsolution of Ni nanoparticles from the perovskite lattice took place and enhanced significantly the catalytic activity of the material regarding methane conversion. However, these nanoparticles were oxidised during the first hours of the testing and slowly reincorporated into the perovskite structure, leading to drop in the performance. Thereafter, the (La₀.₇₅Sr₀.₂₅)(Cr₀.₅Mn₀.₄₅Ni₀.₅)O₃ (LSCMNi5) perovskite was selected as an alternative composition. When the oxide lattice was sufficiently reduced, the exsolution of Fe-Ni alloy nanoparticles occurred. The catalytic testing suggested that the Fe-Ni alloy nanoparticles on LSCFNi5 presented lower activity for methane conversion comparing to the Ni nanoparticles on LSCMNi5, but higher stability in oxidising conditions. By increasing the Ni doping on the B-site of LSCF to 15 mol%, the catalytic activity of the material regarding methane conversion was increased and exceeded that of LSCMNi5. A CH₄ conversion of 70% was achieved, which was 20 times higher than that of the initial LSCF perovskite. Therefore, by tailoring the perovskite composition and the exsolution of the Fe-Ni alloy nanoparticles, it was possible to synthesize a material for the fuel oxidation layer of OTMs, which combined the high catalytic activity of Ni and the good redox stability of Fe.

<p>Pancreatic endocrine tumors (PETs) may cause typical syndromes of hormone excess, or appear clinically non-functioning without hormonal symptoms. PETs occur sporadically, in association with the multiple endocrine neoplasia type 1 (MEN1) syndrome, or rarely the von Hippel-Lindau syndrome. Molecular genetic investigations may reveal pathways important for tumor development, and be of clinical use.</p><p>The aim of this thesis was to investigate regulation of different genes involved in cell proliferation, and relate findings to signs of malignancy in PETs.</p><p>The MEN1 gene on chromosome 11q13 was mutated in three out of eleven sporadic malignant PETs. Two nonsense mutations, causing truncation of the protein, and one missense mutation were found.</p><p>Relation of allelic loss at 11q13 and 3p25 to malignant behavior was observed in sporadic PETs. Allelic loss at 18q21 was found in a subset of sporadic and MEN1-associated PETs, and mutation analysis of Smad4 excluded a tumor suppressor gene function.</p><p>In PETs with allelic loss on chromosome 3p25, mutation analysis of WNT7A and HDAC11 excluded function as tumor suppressor genes.</p><p>Menin, encoded by the MEN1 gene, was reported to regulate expression of the cyclin-dependent kinase inhibitors CDKN2C/p18, CDKN1B/p27, and CDKN2B/p15 in mouse pancreatic islet tumor models. Here, the mRNA expression of these genes was not related to MEN1 gene mutations in human PETs.</p><p>Cyclin-dependent kinase 4 (CDK4) and the protooncogene c-Myc were found to be overexpressed regardless of MEN1 gene mutational status of the PETs. The CDK4 gene was neither amplified nor mutated. Targeting of CDK4 may present an alternative to traditional chemotherapy of PETs in the future.</p>

Pancreatic endocrine tumors (PETs) may cause typical syndromes of hormone excess, or appear clinically non-functioning without hormonal symptoms. PETs occur sporadically, in association with the multiple endocrine neoplasia type 1 (MEN1) syndrome, or rarely the von Hippel-Lindau syndrome. Molecular genetic investigations may reveal pathways important for tumor development, and be of clinical use. The aim of this thesis was to investigate regulation of different genes involved in cell proliferation, and relate findings to signs of malignancy in PETs. The MEN1 gene on chromosome 11q13 was mutated in three out of eleven sporadic malignant PETs. Two nonsense mutations, causing truncation of the protein, and one missense mutation were found. Relation of allelic loss at 11q13 and 3p25 to malignant behavior was observed in sporadic PETs. Allelic loss at 18q21 was found in a subset of sporadic and MEN1-associated PETs, and mutation analysis of Smad4 excluded a tumor suppressor gene function. In PETs with allelic loss on chromosome 3p25, mutation analysis of WNT7A and HDAC11 excluded function as tumor suppressor genes. Menin, encoded by the MEN1 gene, was reported to regulate expression of the cyclin-dependent kinase inhibitors CDKN2C/p18, CDKN1B/p27, and CDKN2B/p15 in mouse pancreatic islet tumor models. Here, the mRNA expression of these genes was not related to MEN1 gene mutations in human PETs. Cyclin-dependent kinase 4 (CDK4) and the protooncogene c-Myc were found to be overexpressed regardless of MEN1 gene mutational status of the PETs. The CDK4 gene was neither amplified nor mutated. Targeting of CDK4 may present an alternative to traditional chemotherapy of PETs in the future.

No description available.

We employ income projection models based on human capital dynamics in order to assess quantitatively the role that educational improvements are expected to play as a driver of future income convergence in Europe. We concentrate on income convergence dynamics between emerging economies in Central and Eastern Europe and Western European countries during the next 50 years. Our results indicate that improvements in human capital contribute significantly to the income convergence potential of European emerging economies. Using realistic scenarios, we quantify the effect that future human capital investments paths are expected to have in terms of speeding up the income convergence process in the region. The income projection exercise shows that the returns to investing in education in terms of income convergence in Europe could be sizeable, although it may take relatively long for the poorer economies of the region to rip the growth benefits. (authors' abstract) / Series: Department of Economics Working Paper Series

Thesis (Ph.D. in Toxicology) -- University of Colorado Denver, 2008. / Typescript. Includes bibliographical references (leaves 144-170). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

Humanitarian interventions tend to be justified by claims to the existence of an obligation upon ‘us' (the benevolent saviours) to intervene militarily when a state is responsible for large-scale atrocity crimes against its own population. However, this justification is paradoxical, given that there is rarely held to exist a commensurate obligation to address structural violence (even when ‘we' may be partly responsible for, or complicit within, structures that are violent). The paradox arises because structural violence can be harmful – even evil – in its own right, and can also lead to – or exacerbate – direct violence. Hence, intervening militarily, and inevitably causing further harm in the act of intervening, results in a moral shortfall. This shortfall is indicative of a prevailing understanding of harm that is blind to the potential for structures to be violent. In responding to the paradox, I adopt a critical cosmopolitan perspective to argue that because structural violence can be harmful on a great scale, and because it is co-constitutive of direct violence, we ought not to countenance intervening with the use of military force (with what this brings in the form of inevitable intended and unintended harm) to stop direct violence without also considering and addressing violent structures, especially if they are violent structures that we are, ourselves, embedded within. Therefore, it is morally imperative to engage in an ongoing process of illumination and addressing of evil structures to rectify the harms they cause, alongside any efforts to stem direct violence, if any sort of intervention is to be legitimate and just. This requires us to a) expand our understanding of harm and evil at the global level, and b) engage in consistent and sustained deliberative processes that bring to the forefront structural violence and structural underpinnings of direct violence.

Taste buds are chemosensory endorgans embedded in the oral epithelium composed of cells that undergo continuous replacement. Mature taste cells live on average 10-14 days and are replaced by new cells when they die. However, the mechanism by which taste cells are produced and integrated into the taste bud as mature taste cells remains unknown. Previous studies approached this issue from either cell cycle gene expression properties or lineage tracing of precursor cells. In our study, we apply a new fate mapping technique that combines these two ideas. This technique, Mosaic Analysis with Double Markers, allows for simultaneous gene knockout and subsequent tracking of single cells. This allows us to study the potency of precursor cells supplying the taste bud while analyzing how gene function regulates the maturation pathway these taste cells take. The following experiments illustrate the initial phase of this investigation.