Constructing the Vulvar Pain Assessment Questionnaire Inventory

The goals of this program of research were to examine the link between self-reported vulvar pain and clinical diagnoses, and to create a user-friendly assessment tool to aid in that process. These goals were undertaken through a series of four empirical studies (Chapters 2-6): one archival study, two online studies, and one study conducted in a Women’s Health clinic. In Chapter 2, the link between self-report and clinical diagnosis was confirmed by extracting data from multiple studies conducted in the Sexual Health Research Laboratory over the course of several years. We demonstrated the accuracy of diagnosis based on multiple factors, and explored the varied gynecological presentation of different diagnostic groups. Chapter 3 was based on an online study designed to create the Vulvar Pain Assessment Questionnaire (VPAQ) inventory. Following the construct validation approach, a large pool of potential items was created to capture a broad selection of vulvar pain symptoms. Nearly 300 participants completed the entire item pool, and a series of factor analyses were utilized to narrow down the items and create scales/subscales. Relationships were computed among subscales and validated scales to establish convergent and discriminant validity. Chapters 4 and 5 were conducted in the Department of Obstetrics & Gynecology at Oregon Health & Science University. The brief screening version of the VPAQ was employed with patients of the Program in Vulvar Health at the Center for Women’s Health. The accuracy and usefulness of the VPAQscreen was determined from the perspective of patients as well as their health care providers, and the treatment-seeking experiences of patients was explored. Finally, a second online study was conducted to confirm the factor structure, internal consistency, and test-retest reliability of the VPAQ inventory. The results presented in these chapters confirm the link between targeted questions and accurate diagnoses, and provide a guideline that is useful and accessible for providers and patients.

Retro-Neoliberalism: Elite Counter-Protest in Latin America, 1940-1975

This research challenges the origin story of neoliberalism in Latin America. Drawing on archival data from the Mont Pèlerin Society and the personal archives of leading but neglected figures in the post-war push to rebuild economic liberalism, I present a historical geography of elite counter-protest that both predates and broadens the generally accepted “birth” of neoliberalism in 1970s Chile. Beginning in the 1940s, Latin American elites found common cause with key figures from economic liberalism’s most radical wing: the Austrian School. While existing literature links the onset of neoliberalism in Chile to the Austrian School, particularly with respect to the School’s influence on the early Mont Pèlerin Society, this dissertation is the first comprehensive inquiry to place the Austrian tradition in the ideational and organizational landscape of Latin America. Embracing a new mission that promised to save the soul of Western civilization, Latin America’s retro-neoliberal leaders collaborated with transnational actors to build a network of Austrian-inspired think-tanks and institutes of higher learning in the region. These organizations, in turn, served as recruiting mechanisms to found the Hispanic quarter of the Mont Pèlerin Society, which was dominated not (as might be assumed) by Chileans, but rather by retro-neoliberal elites from Mexico, Argentina, Guatemala, and Venezuela. By 1975, when scholars began analyzing how a run-of-the-mill economics department had been transformed into a bastion of free-market thinking in Chile, an entire neoliberal university was up and running in Guatemala, exposing all students, regardless of discipline, to the Austrian tradition – the crowning achievement of Latin America’s retro-neoliberal network. Investigating, and accounting for, the development and impact of this initiative sheds new light on the neoliberal landscape in Latin America, and raises important questions for the study of neoliberalism more broadly.

Salmonella Enterica serovar Typhimurium Infection in Mouse Pregnancy

Salmonella are Gram-negative, intracellular food-borne pathogens that cause pregnancy complications. In pregnant mice, Salmonella enterica serovar Typhimurium (S.Tm) infection results in placental bacterial replication, inflammation, necrosis, and fetal loss by unknown mechanisms. Necroptosis, or programmed necrosis mediated by RIPK3 (receptor-interacting protein kinase 3), an inflammatory cell death pathway, is implicated in the pathogenesis of S.Tm in non-pregnant mice. This goal of this thesis was to investigate the role of necroptosis in the pathogenesis of S.Tm infection during mouse pregnancy. I hypothesized that elimination of the key necroptotic cell death protein RIPK3 would decrease placental inflammation and trophoblast cell death, and increase conceptus survival compared to controls. Mice expressing a functional Slc11a1 (encodes the natural resistance-associated macrophage protein 1, NRAMP1) gene with or without RIPK3 function (Ripk3-/-Slc11a1+/+ compared to Slc11a1+/+) were infected with 103 S.Tm by tail vein injection on gestational day (GD) 12. Mice were euthanized on GD 14 (48h post-infection) or GD 15 (72h post-infection) and implantation sites (IS) and maternal serum were harvested for analyses. In nearly all challenged mice (except one outlier), S.Tm were detected in most IS within a litter but there was limited immune cell infiltration, placental damage or cell death in Slc11a1 competent mice regardless of Ripk3 gene deletion. Maternal serum cytokine analyses confirmed lack of maternal immune responses to S.Tm infection. IS amongst the litter of a single dam (Ripk3-/-Slc11a1+/+ at 72h postinfection) displayed heavy but not universal placental S.Tm infection of decidual tissues and spongiotrophoblast, associated with elevated maternal serum pro-inflammatory cytokines. S.Tm infection of the fetal yolk sac (YS) was observed in 54.5% of IS from this dam. YS infection was confirmed in archival samples in mice expressing Ripk3 with intact Slc11a1 and in mice lacking functional Slc11a1. In Slc11a1 incompetent mice, S.Tm were detected in placental labyrinthine trophoblast. Based on the available data, this thesis suggests that Ripk3 and necroptosis have no significant roles in either promotion or prevention of progressive Salmonella infection during mouse pregnancy. It also provides pilot data that NRAMP1 controls placental localization and lethality due to YS infection.