The river, the railroad tracks, and the towers: How residents' worldview and use value transformed Wilton Manors into a diverse, gay-friendly, urban village

This case study examines the factors that shaped the identity and landscape of a small island-urban-village between the north and south forks of the Middle River and north of an urban area in Broward County, Florida. The purpose of the study is to understand how Wilton Manors was transformed from a “whites only” enclave to the contemporary upscale, diverse, and third gayest city in the U.S. by positing that a dichotomy for urban places exists between their exchange value as seen by Logan and Molotch and the use value produced through everyday activity according to Lefebvre. Qualitative methods were used to gather evidence for reaching conclusions about the relationship among the worldview of residents, the tension between exchange value and use value in the restructuration of the city, and the transformation of Wilton Manors at the end of the 1990s. Semi-structured, in-depth interviews were conducted with 21 contemporary participants. In addition, thirteen taped CDs of selected members of founding families, previously taped in the 1970s, were analyzed using a grounded theory approach. My findings indicate that Wilton Manors’ residents share a common worldview which incorporates social inclusion as a use value, and individual agency in the community. This shared worldview can be traced to selected city pioneers whose civic mindedness helped shape city identity and laid the foundation for future restructuration. Currently, residents’ quality of life reflected in the city’s use value is more significant than exchange value as a primary force in the decisions that are made about the city’s development. With innovative ideas, buildings emulating the new urban mixed-use design, and a reputation as the third gayest city in the United States, Wilton Manors reflects a worldview where residents protect use value as primary over market value in the decisions they make that shape their city but not without contestation.^

Reactive Oxygen Species via Redox Signaling to PI3K/AKT Pathway Contribute to the Malignant Growth of 4-Hydroxy Estradiol-Transformed Mammary Epithelial Cells

The purpose of this study was to investigate the effects of 17-β-estradiol (E2)-induced reactive oxygen species (ROS) on the induction of mammary tumorigenesis. We found that ROS-induced by repeated exposures to 4-hydroxy-estradiol (4-OH-E2), a predominant catechol metabolite of E2, caused transformation of normal human mammary epithelial MCF-10A cells with malignant growth in nude mice. This was evident from inhibition of estrogen-induced breast tumor formation in the xenograft model by both overexpression of catalase as well as by co-treatment with Ebselen. To understand how 4-OH-E2 induces this malignant phenotype through ROS, we investigated the effects of 4-OH-E2 on redox-sensitive signal transduction pathways. During the malignant transformation process we observed that 4-OH-E2 treatment increased AKT phosphorylation through PI3K activation. The PI3K-mediated phosphorylation of AKT in 4-OH-E2-treated cells was inhibited by ROS modifiers as well as by silencing of AKT expression. RNA interference of AKT markedly inhibited 4-OH-E2-induced in vitro tumor formation. The expression of cell cycle genes, cdc2, PRC1 and PCNA and one of transcription factors that control the expression of these genes – nuclear respiratory factor-1 (NRF-1) was significantly up-regulated during the 4-OH-E2-mediated malignant transformation process. The increased expression of these genes was inhibited by ROS modifiers as well as by silencing of AKT expression. These results indicate that 4-OH-E2-induced cell transformation may be mediated, in part, through redox-sensitive AKT signal transduction pathways by up-regulating the expression of cell cycle genes cdc2, PRC1 and PCNA, and the transcription factor – NRF-1. In summary, our study has demonstrated that: (i) 4-OH-E2 is one of the main estrogen metabolites that induce mammary tumorigenesis and (ii) ROS-mediated signaling leading to the activation of PI3K/AKT pathway plays an important role in the generation of 4-OH-E2-induced malignant phenotype of breast epithelial cells. In conclusion, ROS are important signaling molecules in the development of estrogen-induced malignant breast lesions.