My doctoral work aims to construct a theoretical and intellectual framework to understand a set of remarkable developments concerning the Italian discourse on architecture from the early 1950s to the mid 1970s. This was when the term Rationalism and its theoretical body of work acquired renewed prestige replacing the ephemeral aesthetic of the modernist movement with a grounded discourse based on a deep understanding of the city as background of all architectural artifacts. The main hypothesis of my research is that this return to a rational methodology characterized by a deep understanding of architecture's internal building logic and identifiable in the work and ideas expressed in the International section of the XV Triennale Exhibition of 1973 had a significant and lasting impact on the thinking and formation of architecture culture in Italy and worldwide. This dissertation will thus attempt to construct a matrix of historical and methodological associations and demonstrations that validate and legitimize that rational methodology through a close examination of the work and key concepts of Tendenza, a group of architects in the Italy of the 1960s, pointing out their importance in preparing the ground for the International section of the XV Triennale Exhibition of 1973, which represented a major point of arrival and a point of departure for architecture culture in Italy and worldwide.

Thesis (M.S.)--Ohio University, June, 2009. / Title from PDF t.p. Includes bibliographical references.

Thèse (M.Sc.)--Université Laval, 2004. / Bibliogr.: f. 91-102. Publié aussi en version électronique.

Universiẗat, Diss., 2004--Bonn.

Thesis (Ph. D.)--University of Oregon, 2000. / Typescript. Includes vita and abstract. Includes bibliographical references (leaves 215-225). Also available for download via the World Wide Web; free to University of Oregon users.

Tesis

270 pages / I theorize and offer some evidence that humans inadvertently risk exacerbating the loss of maintenance-dependent species on private land by using species-based land-use regulation to seek other benefits. Drawing evidence primarily from the US, I argue that such regulation poses a risk to maintenance-dependent species, that humans routinely disregard this risk, and that this disregard widely serves to defend the power of individuals and organizations to use such regulation to seek other benefits. I suggest this implies that with constraints on public funding, humans might improve the survival of some species by clarifying the purpose of such regulation and considering openly refraining from such regulation for some species. I also suggest such change might depend on articulating the issue as whether the survival of a species could ever depend on individuals having a right to conserve or maintain it without selectively incurring harm from regulation intended to save it.

Endometriosis and breast cancer are sex hormone dependent diseases characterised by the local production of high levels of 17β-oestradiol. The relationship between prostaglandins and sex steroid hormones is one of the focal questions in endometriosis, breast cancer and other sex steroid hormone related disorders. Therefore, the main hypothesis was that the aldo-keto reductase (AKR) 1C isoenzymes are responsible for controlling the availability of 17β-oestradiol, progesterone and prostaglandins in the microenvironment of the endometrium, and surrounding adipose tissues of endometriotic lesions and breast tumours. This was investigated using quantitative real-time polymerase chain reaction (PCR) for measuring the gene expression of AKR1C1-3 enzymes, and prostaglandin E (1-4) and F receptors in the endometrium, and surrounding adipose tissues of endometriotic lesions and breast tumours. This was then followed by investigating the role of one of the AKR1C enzymes - AKR1C3 - by inhibiting its catalysis using bimatoprost, followed by using PGE2 as one of the main candidates acting as a transcription factor for upregulating the expression of AKR1C3 which in turn upregulates the production of the local 17β-oestradiol. The gene expression of AKR1C1 was significantly higher in endometriotic lesions compared to eutopic endometrium of endometriosis patients. However, there was no significant difference in the gene expression of AKR1C (1-3) enzymes in the surrounding adipose tissues of endometriotic lesions between patients with or without endometriosis. Also, there was no significant difference in the gene expression of AKR1C (1-3) enzymes in the breast adipose tissues of patients with breast tumours, regardless of the oestrogen or progesterone receptor status. The gene expression of prostaglandin E (EP) receptor subtype 3 was significantly higher in the endometriotic lesions compared to eutopic endometrium of endometriosis patients. In the omental adipose tissue, there was no significant difference in the gene expression of EP1-4 and FP receptors between endometriosis and non-endometriosis patients. In the breast adipose tissue, there was also no significant difference in the gene expression of EP1-4 and FP receptors in patients with breast cancer regardless of the oestrogen or progesterone receptor status. The inhibitory constant (Ki) of bimatoprost was determined using oestrone as a substrate: Ki = 2.9µM and αKi = 0.7µM. Bimatoprost also significantly inhibited the production of 17β-oestradiol and inhibited the production of 9α,11β PGF2 in a dose dependent manner in the human endometrial cells. The effect of PGE2 on the expression of AKR1C1 and AKR1C3 was assessed in the human endometrial cells. The EP4 receptor agonist, L-902688, increased the gene expression of AKR1C1 and AKR1C3. Despite gene expression elevation, L-902688 did not increase the production of 17β-oestradiol. In conclusion, the results were contradictory and highlighted the need for further investigation into the relationship between prostaglandins and sex steroid hormones in the microenvironment of the endometrium, and surrounding adipose tissues of endometriotic lesions and breast tumours.

Das lineare Chromosom von S.lividans zeichnet sich durch eine hohe Variabilität insbesondere der chromosomalen Endbereiche aus. Hier finden sich unter anderen auch verschiedene Gene, die bisher einzigartig sind. Nach Klonierung der Gene in E.coli wurden die entsprechenden Genprodukte als His-Tag Fusionsproteine überproduziert, aufgereinigt und zur Herstellung von Antikörpern verwendet. Der untersuchte Abschnitt, als Ganzes und in Unterabschnitten, wurde auf einem Hoch Kopien Vektor in S.lividans transformiert. In extra hierfür konstruierten Vektorsystemen erfolgte die Produktion von His-Tag Proteinen in S.lividans. Nach Fusion von potentiellen Promoterbereichen mit dem promoterlosen EGFP-Gen, gelang deren Identifizierung in enhanced green fluorescent protein (EGFP) produzierenden S.lividans Transformanten. Mit Hilfe eines Vektors, der ein Temperatur sensitives Replikon besitzt, wurden Gene durch die Integration eines Hygromycin-Resistenzgenes ersetzt, bzw. als Fusionsgen mit dem EGFP-Gen erstellt. Ein Flavoprotein wurde zur Homogenität gereinigt. Es wurde nachgewiesen, dass in S.lividans pro Monomer ein FAD-Molekül interagiert. Physiologische Studien zeigen, dass die Synthese des chromosomal determinierten Proteins in S.lividans nur erfolgt, wenn dieser Stamm ein Plasmid- oder chromosomal- kodiertes Thiostrepton Resistenzprotein (23S rRNA Methylase) enthält. Es muss geschlussfolgert werden, dass die Methylierung der 23S rRNA die Translation verschiedener mRNAs beeinflusst. Die Synthese dieses Proteins ist des Weiteren abhängig von hohen Konzentrationen an NaCl und KCl im Medium, wie auch die zweier Aldo-Keto Reduktasen. Disruptionsmutanten eines dieser zwei Aldo-Keto Reduktase-Gene zeigen jeweils eine erhöhte und verfrühte Produktion eines rot gefärbten Mycel-assoziierten Antibiotikums (Undecylprodigiosin), während die eines weiteren (Actinorhodin) unbeeinflusst blieb.

Prostate cancer is the most commonly diagnosed non-skin cancer in men and the second leading cause of cancer death in the United States. Prostate cancer, like many cancers, is a disease that generally requires a long period of time to develop and grow before it becomes detectable. This long period of latency makes prostate cancer a candidate for dietary chemoprevention. Soy and selenium (Se), are associated with a decreased risk of prostate cancer. We previously showed that high dietary intake of selenium (Se) and soy isoflavones decreased the expression of the androgen receptor (AR) and AR-regulated genes in the prostates of healthy rats. In this study we hypothesized that the downregulation of AR and AR-regulated genes would inhibit tumorigenesis in the transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse. Mice were fed one of two stock diets with or without a supplement of Se in a 2 X 2 factorial design. The stock diets provided high or low dietary isoflavones. Mice were exposed to the diets from conception and sacrificed at 18 or 24 weeks of age. Prostate histopathology, urogenital tract (UGT) weight, serum IGF-1 levels, and the expression of AR and AR-regulated genes in the dorsolateral prostate was examined using quantitative PCR and Western blotting. Urogenital tract (UGT) weight was reduced compared to control in all dietary groups containing high Se, isoflavones, or both at 24 weeks (p<0.005). Dietary isoflavones delayed tumor progression and downregulated protein levels of AR, AR-regulated genes, and upregulated the protective FOXO1 and FOXO3a transcription factors. High dietary isoflavones also decreased the phosphorylation of the IGF-1R. The only main effect of Se was the upregulation of AKR1C14 the enzyme that deactivates 5&aplha;-DHT.This study identifies a previously unknown effect of isoflavones in the upregulation of FOXO expression and confirms previous studies of isoflavones' anticancer effects. Further research is needed to find a protective dose or form of Se and to elucidate the mechanism of isoflavones.