Through the production of a 150-page policy report, our team analyzes international activity in the Arctic related to the loss of summertime sea ice that opens new shipping routes, creates new opportunities for research extraction, and dramatically impacts the way of life for Indigenous Arctic communities, notably the Inuit. In the past decades, the Inuit and other Arctic Indigenous peoples have organized and created for themselves significant political power, leading to self-determination and self-governance initiatives and involvement in the Arctic Council, which is the leading forum for decision-making on Arctic issues. However, the growing economic value of the region also attracts non-Arctic states like China, who want to become a part of decision-making discussions on the region and benefit from the seasonal open ocean in the future. Given the growing power of Indigenous peoples and growing interest in the region, our report addresses two questions: what impact and influence do the policies of Arctic Indigenous Peoples, particularly Inuit, have on the roles of nation-states including non-Arctic nations such as China? And what are the implications of China’s Arctic policy on Arctic Indigenous Peoples, Canada, the United States, and beyond? We use qualitative research methods, mainly the review of primary and secondary source documents that situate our analysis. Our report also draws on meetings with government agencies and indigenous organizations in Ottawa. We will produce a series of recommended policies and areas for further attention that are meant to inform and guide nation states and organizations as they engage in the Arctic. Our analysis of Indigenous and international relations in the Arctic is important because the Arctic represents a unique and unusually successful arena for cooperation between nation states, Indigenous representation, and other non-state actors. This cooperation will only become more vital as global activity in the region increases.

Phagocytosis is a primary function of macrophages that facilitates the elimination of pathogens and the clearance of endogenous and exogenous debris from tissues. This function can become impaired by aging or exposure to environmental toxicants, which may contribute to impaired immune responses and wound healing. To determine the involvement of macrophage phagocytosis in different pathophysiological conditions, we developed an in vitro macrophage phagocytosis assay with lung macrophages and brain microglia from CD-1 mice (three male, three female). The tested groups included an untreated control group, a lipopolysaccharide (LPS)-treated positive control group to increase phagocytosis, a cytochalasin D-treated negative control group to inhibit phagocytosis, and an experimental pioglitazone-treated group to stimulate PPAR-g (nuclear hormone receptor and transcription factor that has been shown to stimulate phagocytosis). We used green fluorescent protein (GFP)-labeled dextran beads opsonized with serum to assess the phagocytotic abilities of the macrophages in each treatment group. We are currently analyzing data that will determine the percentage of macrophages that phagocytosed the beads (GFP+ macrophages) and the average number of beads phagocytosed among GFP+ macrophages per treatment. We predict that there will be fewer GFP+ macrophages in the cytochalasin D-treated group vs. controls, indicating that phagocytosis is properly inhibited. We predict that both LPS and the pioglitazone-treated macrophages will present more GFP uptake and GFP+ cells than the control. A comparison of pioglitazone and LPS uptake will indicate the relative efficacy of pioglitazone in enhancing phagocytosis. Because pioglitazone is thought to stimulate phagocytosis without causing a pro-inflammatory response like LPS does, pioglitazone treatment may be a way to improve the helpful functions of macrophages with impaired phagocytic functions, which can occur with aging or following exposures to environmental toxicants.

Old (> 4 million years ago) ice drilled at the Allan Hills, Antarctica, can help us understand how Earth’s atmosphere has changed in the past. The bubbles trap bits of the atmosphere when they form, which can be analyzed to see what the climate was like. However, the preservation of this old ice depends on ice flow dynamics, possibly including localized shearing (one side of the ice is getting pulled faster than the other), that are difficult to observe. Bubbles in the ice become elongated when the ice around them deforms from strain. Over time, surface tension processes tend to restore bubbles to spherical. Thus, they can indicate the directions of recent or ongoing strain in the ice. We analyze thin/thick section images taken from four samples of Allan Hills ice. The images include information on grain size (size of individual ice crystals) and bubble size, shape, and distribution. We use the Segment Every Grain (SEG) model, a Python package based on the Segment Anything Model developed by Meta, to automatically calculate the sizes and shapes of bubbles in an image. We validate this method by comparing the values it returns with those obtained using another segmenting software, ImageJ, and manually calculated measurements. We can see if automated calculations are reliable enough to use regularly. So far, the SEG model has analyzed one image and it has made mostly correct bubble identification. The data shows that most bubbles are either elongated and small area, or round and large area. It is expected that the SEG and ImageJ models are close to humans in accuracy. The bubble orientations that we measure show the predominant directions of strain in the ice. Future work will use these data along with models of bubble elongation to estimate the strain rates at the Allan Hills.

Infection from Mycobacterium tuberculosis is the leading cause of death due to infectious disease worldwide, with rates of tuberculosis infection greatest in low and middle-income countries (LMICs). Tuberculous meningitis (TBM) is the most severe form of M. tuberculosis disease with nearly half of all cases resulting in death or neurological consequences. Recent studies in our lab have found that single-nucleotide polymorphisms (SNPs) in MUC5AC, a secretory lung mucin, are associated with increased TBM susceptibility, morbidity, and mortality. The purpose of my study is to identify the functional MUC5AC SNP. Four candidate SNPs were selected within the MUC5AC promoter region based on high linkage-disequilibrium scores across multiple global populations with a SNP in the MUC5AC promoter, rs28737416. I utilized molecular cloning techniques to combine a luciferase-expressing plasmid with isolated regions of the human MUC5AC promoter containing the SNPs of interest and subsequently transformed this recombinant plasmid into competent cells. Next, I performed site-directed mutagenesis at the SNPs of interest and am currently transfecting mutants into HEK293T cells to investigate how genotypic variation in each candidate SNP influences promoter function by measuring luciferase expression. I anticipate variants in at least one SNP of interest will reduce gene expression (measured by luciferase expression), indicating functionality. Characterization of this genetic mutation will provide insight into TBM susceptibility across populations and could inform studies of novel therapeutics to treat TBM.


The northeastern quadrant of Washington State is an area of vast public lands. It includes 2-3 National Forests, three State Forests, three Indian Reservations, five Wildlife Areas, and 28 Sno-Parks that contain a wide variety of recreational amenities, including kayaking, rafting, horseback riding, snowshoeing, skiing, camping, and backpacking, among others. This area is also part of the Okanogan Dry Forest and Canadian Rockies Mountains ecoregions, which are characterized by dense coniferous forests that are easily ignitable. As a result, the region is regularly impacted by devastating wildfires, which are accompanied by heavy smoke and pose significant threats to local air quality, small town economies, and natural resources. The purpose of this project is to understand how smoke and fire impact two important resources serving tourists in the area: outdoor recreational amenities, and the production of apples and wine. To investigate these impacts, I reviewed data on recent fires that caused damage to orchard and vineyard land, tribal land, recreational land, and private real estate, looking at the cost of this damage in terms of lives and property lost and the particular impacts of smoke hazards. This data was augmented with interviews of local real estate agents, business owners, and members of the Washington State Department of Natural Resources. The final results I'm expecting from this research is on how recreational amenties are impacted by mega-fires that causes devestating damage towards the forest, recreation amenties, local tribes, people lives,property, public health and the community. By doing this reserch it help me get better understanding how we should managed fire on recreational areas in the Okanogan Highlands area by following proper fire suppression tactics and resources. The results of this project help us better understand the growing effects of fire and smoke on this region in general, and on recreational and tourist activity in particular.

Photoreceptor cells in the retina use several opsin proteins to detect light and confer visual information. Mutations to genes encoding opsins are associated with varying degrees of color blindness and retinal degeneration. In a previous mouse model for color blindness the retina degenerated, with a significant reduction of healthy cones by 3 months (Ma, et al., 2022, Human Gene Therapy). I am characterizing a new mouse line that was gene edited to lack both blue and green sensitive cone opsins, making it a double knock out. We fix and embed the eyes before freezing them, and then I stain frozen eye sections with fluorescent antibodies.  Using a high-resolution microscope, I am able to examine retina health and cone populations. I am comparing knockout animals with a wild type strain of normal mice and a retinal degeneration strain processed in the same way. I confirmed the absence of both blue and green cone opsin in the knockout mice, and despite being a model for color blindness, the mice maintain a healthy population of ospin-less cones for at least one year. However, at one year the knockout mice have approximately 30% fewer cones in their retinas than normal mice. The populations of dying cells and immune response cells in the knockout retinas match those seen in the wild type retinas, and are significantly lower than the populations seen in the degeneration model. This suggests that the retina is not in an active state of degeneration for at least one year. This model will be useful for future development of cone opsin gene therapies, and can serve as a model for color blindness. It also has implications for the health of cones without the cone opsin protein.

For people living with epilepsy (PWE), anti-seizure medicines (ASMs) are the primary treatment option. However, 30% of PWE are unable to control their seizures with ASMs because they have drug-resistant epilepsy (DRE). Pathological mechanisms that contribute to DRE are not currently understood. Nevertheless, both clinical and preclinical data indicate potential involvement of changes in the architecture of neuronal networks. I used a clinically relevant rat model of temporal lobe epilepsy, and novel medication in food delivery system to confirm DRE, or failure to reduce their baseline seizure frequency by 50% with two or more clinically used ASMs. I hypothesized that the DRE animals would have lowered neuronal cell density compared to the those with drug-sensitive epilepsy (DSE). All rats were euthanized at the end of a 6-week treatment period to process the brains for immunohistochemical labeling of mature neurons with the antibody, NeuN. Total percent staining area was quantified in the hippocampus, piriform cortex, and somatosensory cortex of brains. No differences in NeuN immunoreactivity were observed between DSE and DRE animals in any brain region. However, NeuN levels in animals with epilepsy, regardless of treatment outcome, trended lower than naïve animals without epilepsy in the CA1 and dentate gyrus regions of the hippocampus. Together, these data suggest that neuron density may not be driving pharmacoresistance. However, it is possible that the ratio between excitatory and inhibitory neurons may be disrupted in DRE. This underscores the need for future studies to quantify neuronal subtypes, providing a more nuanced understanding of the underlying mechanisms of pharmacoresistance. These studies play a crucial role in guiding future research into novel treatments designed for DRE.

The technology industry has developed rapidly since the last decade of the 20th century. It has provided a large amount of job positions for cities. However, when society was getting back to the pre-pandemic condition in 2022, the tech industry announced layoffs. More than 188,568 workers were unemployed in the United States. My research focuses on the indirect effect of mass tech layoffs. The indirect effect is the employment changes of other companies in the same community as the firm that announced the layoffs. In other words, the indirect effect measures the impact on the locals. The research topic is to analyze the short-term effect of technology industry layoffs in 2022, focusing on the indirect effect on the labor market. I measured the relationship between every sector’s employment, except the technology sector, and tech layoffs in this city using fixed effects models. After layoffs, numerous unemployed people are looking for jobs. Many people have to find other jobs to support their family or themselves. They are more likely to look for jobs in the same city because it is the easiest way to overcome adversity. Therefore, employment in other companies will increase. The anticipated result is that the correlation is positive, meaning when layoffs happen, employment in other non-tech industries will increase.