Thesis (M.S.)--University of Michigan, 1989.

Thesis (M.S.)--University of Michigan, 1996. / Includes bibliographical references.

Thesis (M.S.)--University of Michigan, 1995.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1968. / Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M.S.)--University of Michigan, 1995.

Thesis (M.S.)--University of Wisconsin--Madison, 1980. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 63-65).

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<p> <b>Objectives:</b> Mothers of low socioeconomic status (SES) and of non-Hispanic black race deliver prematurely more often. The goal of my dissertation was to improve understanding of the mechanism of disproportionate premature birth in low SES women. I tested a psychological and physiological stress explanation of prematurity risk, estimated the effect of the Affordable Care Act (ACA) Medicaid expansion on gestational age (GA), and estimated how the ACA Medicaid expansion effect was influenced by race. <i><b>Data and Methods:</b></i> I developed a conceptual framework of how psychological and physiological stress increase premature birth risk utilizing Appraisal and pathophysiology theory. I generated hypotheses about how financial risk removal would impact GA and tested them utilizing variation in expansions in Medicaid eligibility for pregnant women in three matched state pairs and distribution of the Earned Income Tax Credit (EITC). I utilized data from the Pregnancy Risk Assessment Monitoring System and performed multivariate ordinal regressions. I also used national birth record data and exploited state variation in ACA Medicaid expansion status to estimate the impact on GA in non-Hispanic black and all other mothers using multivariate linear regressions and linear probability models. </p><p> <b>Results:</b> Hypothesis testing based on two of the three Medicaid expansion for pregnant women state pairs and the EITC analyses resulted in significant evidence (one-sided p-values &lt; 0.05) for a direct pathway between psychological stress concerning financial risk, physiological stress, and GA. The ACA Medicaid expansion was associated with an increase in GA for non-Hispanic black mothers (+34 hours), a decrease for all other mothers (&ndash;6 hours), and a 3% decrease (95% CI = &ndash;5% to &ndash;2%) in the incidence of early term or shorter gestation births for non-Hispanic black mothers. </p><p> <b>Conclusions:</b> Decreasing financial risk for low SES women with Medicaid or the EITC is associated with increased GA. The higher premature birth risk in this population is likely the result of a direct pathway involving psychological and physiological stress. Other financial risk removal strategies should be investigated. The ACA Medicaid expansion did not meaningfully influence GA on a weekly scale but did moderately decrease overall preterm birth risk in non-Hispanic black mothers.</p><p>

Gestational diabetes mellitus can have devastating effects in the health of the mother and child. While pregnancy rates are decreasing, prevalence of GDM is increasing, and it is estimated that up to 9% of pregnancies are complicated by diabetes in the United States. Traditional treatment and monitoring of gestational diabetes mellitus relies on patient’s compliance to document glycemic levels. This proposed study will evaluate the effectiveness of telemedicine using a wireless glucose meter that transmits information to the providers in real time. The prospective open cohort randomized clinical trial will take place in medical centers around Boston. Two hundred participants diagnosed with gestational diabetes will be recruited over a period of 24 months from these centers and randomly placed into two groups. One group will follow traditional treatment, and the intervention group will be asked to use iGlucose meter system. Glycemic levels and frequency of prenatal visits will be evaluated and analyzed. If telemedicine proves to be efficacious in treating GDM, this would give providers a new treatment plan to consider to effectively manage blood glucose levels and reduce poor perinatal outcomes related to gestational diabetes mellitus.

Preeclampsia is an increasingly prevalent disorder of placentation that has very limited options for treatment. The disease is characterized by aberrant invasion of placental trophoblasts into the decidualized maternal endometrium. In order to identify pathways of therapeutic interest during placentation, we are focusing on the pathway of the neuropeptide kisspeptin and its receptor KISS1R, both highly expressed in the human placenta. Early functional studies of the ligand-receptor system identified a role for kisspeptin in the inhibition of cancer metastasis. Parallels exist between cancer and placentation, suggesting the possibility of an inhibitory role for kisspeptin during pregnancy as well. Existing functional data supports kisspeptin's inhibitory influence on cellular invasion, but the mechanism remains unknown. Evidence for the localization of the KISS1R receptor in the current literature was established via a nonspecific antibody and requires further investigation. Current literature suggests involvement of the ERK (extracellular signal-regulated kinase) pathway as well. Our work aims to solidify the localization of kisspeptin and KISS1R, avoiding the use of KISS1R antibodies. Using immunohistochemistry for protein localization of kisspeptin and placental fractionation followed by quantitative PCR analysis for gene expression, we provide evidence of kisspeptin's restriction to the syncytiotrophoblast layer of the placenta, and KISS1R gene expression limited to the villous cytotrophoblast layer. This distribution of ligand and receptor suggests a paracrine mechanism for kisspeptin action, with syncytiotrophoblasts secreting kisspeptin to act on its receptor on the villous cytotrophoblast layer, and thus restricting cytotrophoblast invasion. We further attempt to support these data with the use of laser capture microdissection of placental tissue to isolate the different layers, followed by quantitative PCR. This technique introduced a particularly challenging aspect of working with the placenta: maintaining tissue morphology while also preserving RNA integrity. This thesis outlines our troubleshooting process for that technique and introduces alternatives for future work. We also employed Western blot analysis of ERK activation to establish the mechanism of kisspeptin's inhibitory effect on fractionated trophoblasts.