Adopted children often have trauma–related emotional and behavioral problems, such as depression, anger, and anxiety, and these problems can continue to exist after adoption. Post-adoption, the adoptive family’s impact on these problems is not well understood. The current study examines the relationship between adopted children’s trauma symptoms and family communication – a construct that is associated with child social-emotional adjustment in traditional, biological families. Data was collected from adoptive families who were recruited to participate in a therapeutic family intervention. The results revealed a significant negative correlation between family communication and trauma-related emotional and behavioral problems in adopted children; specifically, the healthier the family communicated, the less problems the adopted child exhibited. Further, we wanted to determine if a similar relationship was found between biological children’s emotional problems in adoptive families and family communication. The results revealed a similar relationship: the healthier the family communicated, the less emotional problems the biological children experienced. The results of this study indicate that family communication may be a significant factor when considering the severity of adopted children’s trauma-related emotional and behavioral problems post-adoption.

As the threat of antimicrobial-resistant infections continues to rise, the need for novel antibiotics grows. Targeting virulence factors in bacterial pathogens is one potential strategy for antibiotic development because inhibiting virulence would decrease the ability of the pathogen to evade the host immune response. This strategy may decrease the development of resistance since the treatment is not directly bactericidal and there is less selective pressure put on the bacteria population. Our goal is to discover new virulence genes in Bacillus anthracis that could potentially be a therapeutic target. Specifically, we are interested in finding genes that allow B. anthracis to acquire iron from the host. For bacterial pathogens, iron is critical for growth and often a limiting nutrient in the host. It has been linked with proper functioning of electron transfer proteins and superoxide dismutase enzymes. In B. anthracis infection, iron is acquired from host hemoglobin through a hemolytic pathway, but the complete mechanism of this is unknown. Approximately 1000 transposon mutants of B. anthracis were screened for the inability to acquire iron from hemoglobin, and five were deficient in acquiring iron from hemoglobin in in vitro assays. Of those five mutant strains, only one (9F12) also exhibited an in vivo phenotype using the wax worm model of infection. The gene disrupted in the 9F12 transposon mutant is the dUTPase/aminopeptidase gene. Our aim in this study is to confirm that the disruption of the dUTPase gene leads to the inability to acquire iron from hemoglobin in B. anthracis. Using targeted mutagenesis, we created an insertional mutant strain to disrupt the dUTPase gene and we are currently testing it, along with WT and 9F12, for the ability to grow in iron-limited conditions with or without hemoglobin. Confirmation of this phenotype will demonstrate that the dUTPASE/aminopeptidase gene is important for iron acquisition from hemoglobin and will support further studies to understand the role of this gene in the virulence of B. anthracis.

Aquatic parameters such as increased temperatures and dissolved oxygen levels is critical in determining the survival and ability to thrive of trout species, including the Bonneville cutthroat trout. Bonneville cutthroat trout (Oncorhynchus clarkia Utah), a subspecies of Yellowstone cutthroat trout, originated in the Bonneville Basin and is native to many river basins in Utah, Wyoming, Idaho, and Nevada(Duff 1996). East Canyon Creek is a headwater tributary in the Weber River Basin of northern Utah, and a stream where Bonneville cutthroat trout are native. However, due to the introduction of nonnative trout and multiple causes of habitat quality decline, they no longer occur in the stream. Over the summer of 2018, I participated in data collection which assessed the habitat qualities of East Canyon Creek. This data includes temperature, aquatic, and riparian qualities. Data on the corresponding summer for dissolved oxygen is available as well. When compared to Colorado’s Coldwater Criteria, it appears that the temperatures of East Canyon Creek exceeded the acute (22.1°C) and chronic (17.0°C) upper thermal thresholds for cutthroat trout(Todd et al 2008). When compared to the acute (5.0 mg/L) and chronic (6.0 mg/L) dissolved oxygen minimum concentrations(Null et al 2017), East Canyon Creek’s concentrations appear to have dropped below the identified concentrations. The objective of this paper is to statistically analyze the temperature and dissolved oxygen data on East Canyon Creek from 2018, and determine if a restoration project of Bonneville cutthroat trout in East Canyon Creek would be successful. Through the data analysis, we have found that water temperatures during the summer months have significantly exceeded both acute and chronic upper survival limits, and that dissolved oxygen concentrations are significantly lower than the minimum chronic survival level, indicating that East Canyon Creek is not yet suitable for a successful reintroduction of Bonneville cutthroat trout.

The BRCA1 gene encodes an 1863 amino acid protein that is relevant in many essential biological pathways, most notably DNA damage response and tumor suppression. In many instances, BRCA1's functions depend on interaction with other cellular components. One such binding partner is P53, another important tumor-suppressing protein that cooperates with BRCA1 to inhibit cancer cell growth. However, the nature of this interaction is not yet fully understood. Here we developed a biochemical assay to investigate the exact binding site for P53 in the central domain of BRCA1. The discovery of such binding sites allows future studies to identify the precise amino acid residues involved in binding and better predict the effect of mutations in the binding site on BRCA1's ability to inhibit carcinogenesis.

Breast cancer (BC) is the second most commonly diagnosed cancer among American women after skin cancer. Traditional treatments of BC include surgery, radiation, and chemotherapy therapy; however, these treatments are non-specific and potentially kill peripheral, healthy cells. There emerges a need for more specific treatments, most notably to develop chemotherapy agents that target a unique feature of the cancer cells. Interestingly, 70% of BC cells upregulate estradiol-dependent pathway, a characteristic essential for rapid cell growth. Current BC drugs, such as Herceptin and Tamoxifen, have targeted this pathway to preferentially kill BC cells. However, most women relapse within 15 years due to drug-resistance. Thus, there is a need for new chemotherapeutic drugs. Our research group studies a novel estrogen-receptor targeting drug: Est-3-Melex. This compound has the estradiol molecule linked to a DNA alkylating agent, Melex. We hypothesize that Est-3-Melex enters the cancer cells via an interaction between the estradiol moiety and the estrogen receptor alpha (ER-alpha). ER-alpha then enters the nucleus and binds to Estrogen Response Elements on the DNA. This movement positions the Melex moiety on the DNA and allows the transfer of a methyl group to the N3 adenine on the DNA. In this project, we test the hypothesized mechanism of action of our compound. Since Est-3-Melex has a DNA methylation component (Melex) conjugated to estrogen, our hypothesis is that after the drug binds to the estrogen receptor in the cytosol, it translocates to the nucleus, specifically methylates the N3-region of adenine bases, eventually triggering cell death.