Elderly Vietnamese immigrants experience unique stressors and healthcareincompatibilities that demand an examination of the quality of their physician-patientinteractions. Previous studies on Vietnamese American health disparities demonstrate concernsover stroke rates, heart disease, and reluctance to communicate with health providers. Particularstructural, political, cultural, and behavioral effects resulting from forcible immigration from theVietnam War and communism have exacerbated healthcare complications. To study the depth ofthese effects, I surveyed and interviewed Vietnamese individuals sixty years of age or older whoimmigrated to America. These surveys and interviews allowed participants to rate their primarycare physicians on different metrics to demonstrate their level of satisfaction with theirpatient-physician interactions holistically and to connect these ratings to their personal levels ofintegration within American society and ability to navigate American healthcare systems. Theresults surprisingly demonstrate an overwhelmingly positive response towards Americanhealthcare,highlighting not the challenges that Vietnamese elderly face in regards to achievingsatisfactory levels of healthcare, but rather the means through which they have overcome thedifficulties of acculturation and gained access to quality healthcare. My findings indicate successstories in traversing the difficult realm of healthcare for these Vietnamese elderly individuals,whether through their education and information seeking or through caretakers who are capableof providing for them and provide insight into how we can extend this success to others stillstruggling to find quality healthcare. To expand upon these findings, I suggest conductingsimilar surveys and interviews, but with a larger sample of Vietnamese Americans, includingdiversity in education, income, class, employment, and family/home life, as this study was mostlimited by its small and non-diverse sample.

Changes in the levels of circulating proteins are associated with Alzheimer's disease (AD), whereas their pathogenic roles in AD are unclear. Here, we identified soluble ST2 (sST2), a decoy receptor of interleukin-33-ST2 signaling, as a new disease-causing factor in AD. Increased circulating sST2 level is associated with more severe pathological changes in female individuals with AD. Genome-wide association analysis and CRISPR-Cas9 genome editing identified rs1921622 , a genetic variant in an enhancer element of IL1RL1, which downregulates gene and protein levels of sST2. Mendelian randomization analysis using genetic variants, including rs1921622 , demonstrated that decreased sST2 levels lower AD risk and related endophenotypes in females carrying the Apolipoprotein E (APOE)-ε4 genotype; the association is stronger in Chinese than in European-descent populations. Human and mouse transcriptome and immunohistochemical studies showed that rs1921622 /sST2 regulates amyloid-beta (Aβ) pathology through the modulation of microglial activation and Aβ clearance. These findings demonstrate how sST2 level is modulated by a genetic variation and plays a disease-causing role in females with AD.