This thesis analyzes attitudes about race in Brazil in three research sites conducted in 2008 and 2009. The first research site was Salvador, Bahia where I asked a total of twelve students and professors their opinions about the importance of discussing race relations in Brazil and their views on Affirmative Action. These participants were mostly white middle-class students and professors. The second site was in the periferia of Zona Sul in the neighborhood of Capelinha, São Paulo. I interviewed four residents about the importance of race in Brazil. Here, the residents were mostly non-white, from various states in the north and northeast, and were working class. The last research site was Cooperifa, which is a spoken word movement located near Capelinha in Zona Sul. I found that non-white periferia residents subscribed to the same racial attitudes as the middle-class white participants when discussing the importance of race as a social phenomenon. In turn, I found that Cooperifa participants perceived white privilege as a social phenomenon that needs to be challenged. This thesis examines the links across these three sites and draws from theories of whiteness to understand them. / text

This dissertation proposes a multi-level explanatory framework that strengthens explanations of variation in European Union member states’ compliance with the Anti-Discrimination Directives, and offers novel approaches to testing relationships between key constructs situated at multiple levels of analysis. The framework entails three different yet inter-related levels: system structure, organizational design of public agencies, and the attitudinal and behavioral attributes of civil servants. The theoretical model, proposed in this dissertation, conceptualizes compliance from an integrative approach, and also enables more accurate explanations of the role of information in modifying compliance behavior. This dissertation relies on a multi-method empirical approach, and a combination of secondary and primary sources (i.e. surveys, interviews, observations, and primary documents) to provide answers to the research questions raised in this dissertation.

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The anthracycline quinone, doxorubicin (Adriamycin) is an antineoplastic agent that has substantial therapeutic activity against a broad variety of human cancers. Unfortunately, the use of this agent is limited by its cardiac toxicity, which is associated with free radical formation leading to apoptotic cell death. The goal of this work is to improve our understanding about doxorubicin induced cardiomyopathy and to identify compounds to limit doxorubicin induced cardiomyopathy. The knowledge gained here will have a generalized impact on all cardiac diseases involving oxidative stress and apoptosis. We show that doxorubicin induced apoptosis in primary neonatal rat cardiomyocytes can be attenuated by progesterone (PG). The anti-apoptotic action of PG was blocked by a progesterone receptor antagonist, Mifepristone (MF), indicating a progesterone receptor dependent pathyway. Affymetrix gene analyses found that PG treated cardiomyocytes increased the expression of 180 genes. Among the genes upregulated is NAD(P)H: Quinone Oxidoreductase-1 (NQO1) gene. NQO1 is a flavo-enzyme that can catalyze a two-electron reduction of Dox to a more stable hydroquinone, thereby acting as a defense mechanism against oxidative stress. The induction of NQO1 mRNA and NQO1 activity in cardiomyocytes was observed in a dose and time-dependent manner with PG treatment and was blocked by MF. Induction of NQO1 by b-naphoflavone, an inducer of NQO1, resulted in a decrease in caspase-3 activity. However, inhibition of NQO1 by dicoumarol did not attenuate the cytoprotective effect of PG. This data indicates that although induction of NQO1 can decrease Dox induced apoptosis, this is not the primary mechanism of cytoprotection induced by PG. Microarray analyses revealed that PG induced an increase of Bcl-XL mRNA. Inhibiting the expression of Bcl-XL using siRNA reduced the anti-apoptotic effect of PG, suggesting that Bcl-XL is a key player in PG induced cytoprotection. Western blot analyses indicated that PG induced the expression of Bcl-XL in a dose and time dependent manner consistent with the protective effect of PG. Induction of Bcl-XL by PG was blocked by cyclohexamide, but was not blocked by Actinomycin D indicating that a transcriptionally independent mechanism is responsible for the induction of Bcl-XL by PG. The activity of a bcl-x 3'UTR reporter was induced by PG and blocked by MF. These data suggest that PG may induce stabilization of the Bcl-X mRNA. We further explored the mechanism of PG induced Bcl-XL gene expression by comparing the effect of PG to two other steroids: corticosterone (CT) and retinoic acid (RA). Both CT and RA attenuate Dox induced apoptosis in cardiomyocytes. CT, but not RA or PG induced the activity of a GRE reporter plasmid. Analysis of the 5' region of the Bcl-XL promoter indicated that RA and CT, but not PG induced the activity of the 0.9kb region of the Bcl-XL promoter. The induction of the 0.9kb reporter plasmid by CT was glucocorticoid receptor dependent, since it was inhibited by MF. The Bcl-XL promoter does not contain any glucocorticoid or retinoid response elements, but does have AP-1 and NFkB response elements. CT, but not RA or PG induced the activity of an AP-1 reporter plasmid. RA, but not CT or PG induced the activity of an NFkB reporter plasmid. The induction of the 0.9kb Bcl-XL reporter plasmid by CT was blocked by expression of a dominant negative c-jun, TAM67 as well SB202190 indicating a nongenomic effect of CT in activating the Bcl-XL promoter through a p38 MAPK mediated AP-1 mechanism. Therefore although all three types of nuclear receptor ligands induce bcl-xL expression, the effect of CT is mediated by transcriptional activation by AP-1 signaling while NF-kB transcription factor appears to be involved in RA indced bcl-xL transcription.

Britain enjoys a rich historical tradition of popular protest and collective action. Due to their public and publicized nature, sporting events have been recognized increasingly as venues in which broader cultural and political meanings are enacted and debated in the postwar period. This project examines how social anxieties about immigration, unemployment, and government repression were represented and contested through violence and eventually racist aggression at football matches. From 1968 to the mid-1970s, violence among fans and with police became expected on a weekly basis within and outside British football stadiums as new forms of spectator allegiance and sports consumption emerged. British football became a contested cultural and institutional site of racisms, violence, masculinities, and national mythologies. Rather than examining football per se, the principal aim of this project is to investigate how this distinct cultural milieu became a site for the British government to enact violence against working-class citizens by manipulating moral anxieties, physical environments, police tactics, and legal prosecution. Whereas many British sociologists have focused on the motivation of crowd behavior and the group dynamics among supporter gangs, this paper looks at the response of the state, local police authorities, and the Home Office and Department of Environment. Politicians concerned with British sport helped to create oppositional, aggressive and disciplinary environments that promoted mutually reciprocating violent environments. Beginning in the late 1970s, spectators not only participated in violence, but also racial abuse, in stadium environments. Several fans protested the emergence of successful black footballers, who came to represent conflicts about immigration, job and housing competition, and race riots in postwar Britain. The environment became a cultural location that several groups recognized as a platform for the contestation and manipulation of racial and class conflict: it garnered activism from the neo-fascist National Front, spawned several anti-racist organizations, captured the attention of the Home Office responsible for public order, and garnered extensive national press coverage. Consequently, the football environment not only mirrored social and political hostilities, but produced them as well.

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The interaction of different formulations of the antifungal drug amphotericin B (AmB) with model cell membranes was studied and new techniques of measuring this interaction using electrochemical and/or spectroscopic methods were developed. Two model cell membrane systems were used: sterol-free lipid monolayers adsorbed to a Hg electrode and sterol-free or sterol-containing floating lipid monolayers on a Langmuir trough. Electrochemical control over the adsorbed monolayer allowed the defectiveness of the layer to be varied and the interaction of AmB with both well-ordered and defective monolayers characterized. Measurements of monolayer capacitance and permeability were used to indicate the nature of the interaction. Capacitance provides a measure of the lipid organization, while permeability was measured via electro reduction of thallium (I)cation. The three AmB formulations and two control samples were examined and showed different interaction behaviour. The disruption of lipid order and permeabilization induced by the two commercial formulations correlated generally with in vivo studies of their toxicity. An experimental and possibly less toxic AmB formulation made monolayer significantly more permeable. In situ fluorescence microscopy of the monolayer on Hg was carried out after introducing a low concentration of fluorophore into the layer. Fluorescence intensity as a function of electrode potential was measured and was used to characterize the lipid on Hg model membrane system before we attempted to measure AmB's influence on the fluorescence. The fluorescence excitation and emission spectra of AmB itself were measured ex situ for two of the formulations. Using added surfactant to control AmB aggregation state, the relationship between AmB aggregation and its fluorescence properties was examined. We discovered AmB to have unusual dual fluorescence properties, the extent of which differed between formulations. We measured AmB's fluorescence in situ as the drug interacted with floating lipid monolayers on the Langmuir trough. Both the variation in fluorescence during compression of a mixed AmB/lipid monolayer and penetration of AmB into a phospholipid monolayer were measured. This experimental setup was configured to collect fluorescence only from AmB at the monolayer, and not from AmB in bulk solution. Fluorescence excitation was made using a laser diode extracted from a consumer electronics device.

The first objective of this thesis was to assess the feasibility of designing a “smart” degradable polymer that can release anti-inflammatory drugs in response to inflammatory-related enzymes. The drug polymer was synthesized using diisocyanates, poly(caprolactone)diols, and oxaceprol (OC) biomonomers. Biodegradation studies demonstrated that the trimethylhexamethylene diisocyanate-based drug polymer responded to an inflammatory enzyme to release more OC, while a 1, 12-diisocyanatododecane analog demonstrated minimal drug release. The drug delivery response was believed to be a direct function of the molecular structure and distribution of the hard segment. The second objective of this thesis was to elucidate the anti-inflammatory mechanisms of OC by investigating its effects on cytokine-induced monocytic-cells adhesion in human umbilical vein endothelial cells (HUVECs) in vitro. Results showed that OC had no direct effect on the monocyte-endothelium adhesion, suggesting that OC may mediate inflammation by mechanisms other than those suggested by the literature.