Plagued Bodies and Spaces: Medicine, Trade, and Death in Ottoman Egypt and Tunisia, 1705-1830 CE

This dissertation examines the history of the bubonic plague, trade, and imperialism in Ottoman Egypt and Tunisia between the eighteenth and nineteenth centuries. Before there was a cure for Yersenia pestis (the bacteria that causes the bubonic plague), the disease posed a demographic crisis in North Africa and disrupted merchant trade, funeral rites, and social life. When the epidemic struck, it generated anxiety and fear among authorities and laypeople alike, thus spawning a call to action by those who were directly impacted by the disease. This research shows how contagion theory, merchant capital, and political leadership influenced the ability for state and non-state actors to manage several plague outbreaks in Ottoman Egypt and Tunisia. What it goes to show is how autochthons and denizens incorporated quarantine in port areas, utilized popular healing techniques, and buried the recently plagued corpses. Eighteenth-century Egyptians and Tunisians experienced plague in a number of ways, however, the customs and habits that authorities, merchants, and ʿulamāʾ (scholars) exercised dovetailed with their access to resources and power. The plague outbreaks during the eighteenth century also coincided with the expansion of merchant capital in Egypt and Tunisia—mostly with the East India Company and the Royal African Company. These constituents and their agents influenced the ability of goods and people to migrate across the Mediterranean Sea and across the African continent. While power dynamics were more horizontal in the early eighteenth century, the French military occupation (1798-1801) was a major site of contestation for how local authorities managed the plague outbreaks in Egypt. Two consequences of the bubonic plague epidemic are that officials labeled marginalized groups as vectors of disease and non-elites plague victims often lacked commemoration. Overall, this project sheds light on the political developments and tensions during several major epidemics in Cairo and Tunis while attending to nascent modernization projects in North Africa

GPR30 Contributes to Estrogen-Induced Thymic Atrophy

The mechanisms by which prolonged estrogen exposures, such as estrogen therapy and pregnancy, reduce thymus weight, cellularity, and CD4 and CD8 phenotype expression, have not been well defined. In this study, the roles played by the membrane estrogen receptor, G protein-coupled receptor 30 (GPR30), and the intracellular estrogen receptors, estrogen receptor α (ERα) and β (ERβ), in 17β-estradiol (E2)-induced thymic atrophy were distinguished by construction and the side-by-side comparison of GPR30-deficient mice with ERα and ERβ gene-deficient mice. Our study shows that whereas ERα mediated exclusively the early developmental blockage of thymocytes, GPR30 was indispensable for thymocyte apoptosis that preferentially occurs in T cell receptor β chain−/low double-positive thymocytes. Additionally, G1, a specific GPR30 agonist, induces thymic atrophy and thymocyte apoptosis, but not developmental blockage. Finally, E2 treatment attenuates the activation of nuclear factor-κ B in CD25−CD4−CD8− double-negative thymocytes through an ERα-dependent yet ERβ- and GPR30-independent pathway. Differential inhibition of nuclear factor-κB by ERα and GPR30 might underlie their disparate physiological effects on thymocytes. Our study distinguishes, for the first time, the respective contributions of nuclear and membrane E2 receptors in negative regulation of thymic development