Pregnancy presents an immunological conflict. The fetus, despite expressing foreign paternal antigens, does not face rejection by the maternal immune system. Instead, the maternal immune system accepts the semi-allogeneic fetus. This process is called maternal-fetal immune tolerance, a regulated process at the maternal-fetal interface. This tolerance is not one dimensional, and is carried out by numerous immune cell populations, which provide protection to the fetus without causing detriment to the mothers ability to fight infection. Among contributors to immune tolerance, myeloid-derived suppressor cells (MDSC’s), and regulatory T-cells (Tregs), share suppressive functions. MDSC’s, immature myeloid cells, inhibit T-cell activation and processes related to inflammation. On the other hand, Tregs enforce peripheral tolerance and inhibit effector T-cells such as CD4’s. It is unclear if both act through complementary mechanisms during pregnancy. Although both MDSC’s and Tregs are recognized individually as key players in immune tolerance during pregnancy, how they interact, co-regulate, or potentially act synergistically during the period of gestation is not yet fully understood. This project presents a review of recent literature focusing on the development, function, and dynamics of MDSCs and Tregs in pregnancy. Peer-reviewed sources published within the past five years will be analyzed to clarify how immunosuppression is carried out during pregnancy. Emphasis is placed on their roles at the maternal-fetal interface and how their dysregulation may contribute to adverse pregnancy outcomes.

Breast cancer research has advanced significantly in recent years, leading to the identification of three key receptors as actionable targets for treatment: estrogen, progesterone, and HER2. Drugs that target these receptors demonstrated dramatic improvements in women who express these markers. However, one subtype of breast cancer, triple-negative breast cancer (TNBC), lacks expression of all three receptors, resulting in limited treatment options and rapid tumor progression. Identifying a molecular target that promotes TNBC malignancy is critical for developing a therapy that improves patient survival. Recent studies identified pyruvate dehydrogenase kinase 4 (PDK4), a metabolic enzyme involved in regulating glucose oxidation, as a potential driver of tumor growth and therapy resistance in TNBC. In this study, we investigated the impact of PDK4 inhibition on cell growth and migration in TNBC. Using Western blotting, we found that PDK4 is overexpressed in a TNBC cell model. This elevated expression is a common feature of the TNBC subtype and may contribute to its aggressive behavior and poor clinical outcomes. To further explore the therapeutic potential of targeting PDK4, we tested an orally bioavailable inhibitor, PDK4-In-1, using cell proliferation assays and a modified scratch assay. Treatment with PDK4-In-1 reduced TNBC cell proliferation and migration. These findings suggest that PDK4 overexpression plays a key role in TNBC progression and highlights it as a potential therapeutic target. Ongoing research will focus on validating these findings in patient-derived models and across multiple TNBC cell lines.

The Aleutian Islands support a diverse community of cormorants, including Urile urile (Red-faced Cormorant), Urile pelagicus (Pelagic Cormorant), and Nannopterum auritum (Double-crested Cormorant), along with a potentially distinct and understudied form referred to as "Kenyon’s Shag" (Urile kenyoni, KESH). First identified from skeletal remains by Doug Causey, KESH displays a suite of unique traits including smaller adult body size, distinct skeletal features, and facial coloration patterns not fully aligning with either PECO or RFCO. Despite these differences, it remains unclear whether KESH represents a valid species, a morphological variant, or a hybrid form. This project combines field sampling across multiple Aleutian and Bering Sea localities with genetic analysis to address three primary questions: (1) Can KESH individuals be distinguished using molecular markers? (2) How genetically divergent are KESH individuals from other cormorants in the region? (3) What is the phylogenetic relationship among Aleutian Urile species? In addition, the project seeks to develop rapid diagnostic tools for species identification. Broader evolutionary hypotheses suggest KESH may represent a relic lineage persisting after Pleistocene range shifts, a stable hybrid between RFCO and PECO, or an emergent taxon under selection for distinct ecological traits. Regardless of its taxonomic outcome, the study of KESH highlights important evolutionary dynamics within seabird populations and contributes to our understanding of avian diversity and speciation in remote high-latitude ecosystems.

In older individuals, there is a decrease in immunity and an increase in the incidence of leukemia associated with dysfunctional lymphopoiesis. The homeobox transcription factor Hoxa9 is heavily involved in the regulation of hematopoiesis. In early hematopoietic stem cells (HSCs), it is highly expressed, but downregulated upon commitment to a specific lineage. Animals deficient in Hoxa9 display an "aged" hematopoietic phenotype, with HSCs biased towards commitment to a myeloid lineage. Prior research has shown that Hoxa9 is a negative regulator of the cyclin-dependent kinase inhibitor p16ink4a. p16ink4a is upregulated both as an individual ages and in the absence of Hoxa9. Ablation of p16ink4a in Hoxa9-deficient animals results in a restoration of lymphopoiesis. These animals display a balanced blood cell compartment, closer to that as observed in wildtype mice, however their HSC compartment still displays a myeloid bias. To understand the role of Hoxa9 and p16ink4a in lymphopoiesis and the myeloid bias that presents with age, the bone marrow of Hoxa9 -/- and p16ink4a -/- mice in addition to Hoxa9 -/- p16ink4a -/- double knockout animals was studied using cytokine stimulation and CFU assays.