Wildfires in Western North America have become more frequent and intense in recent years. Wildfire smoke can cause adverse health impacts creating an urgent public health concern. This study compares wildfire smoke preparedness and response plans developed by jurisdictions and institutions in western North America, including counties, cities, states, provinces, and universities. We used qualitative content analysis methods to assess the characteristics of 20 wildfire smoke preparedness and response plans. The majority of the plans included strategies related to air quality monitoring, household-level exposure reduction, and risk communication. Wildfire smoke poses a bigger risk to susceptible and/or vulnerable populations, however, 25% of the plans did not include strategies related to targeted outreach for at-risk populations. Since wildfire smoke plans are a relatively new strategy within emergency response, a “gold” standard set of components has yet to be established, therefore,  significant variations of included plan components exist. To improve these plans, it is crucial to enhance targeted outreach programs for vulnerable populations, develop a standardized framework for preparedness, and integrate plans with existing public health frameworks. Additionally, training for first responders on health impacts and investing in air quality monitoring are essential. Future research should focus on evaluating the effectiveness of outreach strategies, conducting longitudinal health studies, and analyzing the economic impacts of wildfire smoke preparedness. By addressing these recommendations and pursuing further research, jurisdictions can enhance their wildfire smoke preparedness and response plans, ultimately protecting public health more effectively.

For biomass derived molecules to serve as precursors for biofuel and other related energy sources, more stable and efficient catalysts are needed. Drawing inspiration from enzymes, our group has recently shown that a bifunctional acid–base metal–organic framework (MOF) with co-localized acid and base sites outperforms a MOF with randomly dispersed acid and base sites as a catalyst for the aldol condensation of biomass-derived carbonyls. These active acid–base sites are composed of a primary amine and carboxylic acid. However, to further improve catalytic activity a templated framework with secondary amine and carboxylic acid active sites can be developed. Relative to primary amines, secondary amines should favor the formation of the key enamine intermediate and increase catalytic rates. Framework synthesis and characterization show success of incorporation of the secondary amine, and preliminary catalysis results indicate how successful this secondary amine has been. Overall, this work expands on the previous introduction of metal-organic framework catalysts as an alternative to common industrial catalysts in the biomass upcycling process by exploring the utility of a new templated secondary amine acid–base MOF. 

Fluoride intake is essential for dental health, yet excessive consumption can lead to fluorosis, a condition negatively affecting teeth and bones. Tea, one of the most widely consumed beverages globally, naturally accumulates fluoride, making it a significant but often overlooked dietary source. Black tea is the most popular type of tea consumed in the U.S. In this study we compared fluoride levels across six brands of black tea and investigated how brewing conditions and water sources affect fluoride concentrations in tea. We brewed black tea from six locally popular brands (Lipton, Tazo, Fortnum & Mason, Twinings, Tetly, and Harney & Sons), using two water sources (distilled water and Seattle tap water), with four samples for each brand using both water sources. We brewed 50 mL of water at 100°C, then we let each sample of the tea sit for 5, 10, and 20 minutes. Ion chromatography was used to measure fluoride concentrations at each time interval. We compared these values to the U.S. Environmental Protection Agency's (EPA) recommended fluoride level of 4.0 mg/L. Our results help characterize the variation between brands and the influence of brewing duration on fluoride release. These findings contribute to a better understanding of fluoride exposure from tea consumption, helping consumers make informed choices about their dietary fluoride intake.

Beaver dams can function as natural filters helping decrease pollution in streams, creeks, and rivers. Beaver dams slow down the water flow in a creek or river, forming ponds that help trap excessive nutrients. An excess of nutrients such as phosphate and nitrate can cause eutrophication, leading to increased algal blooms that can produce toxins and ultimately deplete oxygen in the water. This study investigates the ion levels of chloride, fluoride, phosphate, nitrate, sulfate, and bromide upstream and downstream of the major beaver dam at Pipers Creek in North Seattle's Carkeek Park over the course of a year to better understand the long-term impacts of the dam. We collected three water samples at each of eleven sites along the creek, eight upstream from the dam, and three downstream. Ion chromatography was used to measure the concentrations of anions at each site. The results of this study help elucidate the role of beavers in moderating water quality and provide important baseline data documenting seasonal variations in the nutrient load at Pipers Creek. These findings can also be used to better understand the impact of new beaver dams in other freshwater systems.

Low-income communities are often disproportionately exposed to air pollution. High concentrations of pollutants such as particulate matter under 2.5 µm (PM2.5) and human aerosol emissions, including carbon dioxide (CO2), have been linked to various health and cognitive issues. Performance arts, including singing and playing instruments, produce human aerosol emissions and are considered high risk for airborne disease transmission. Our study evaluated the accumulation of CO2 and PM2.5 in high-risk environments (band classrooms) in low-income public schools in King County (WA), to determine whether there is a correlation between accumulation rates and Title 1 designation. Title 1 designation, which provides government funding for schools with a high percentage of students from low-income households, was used to represent low-income communities. We compared four middle schools that qualified for Title 1 designation to one school that did not qualify. Concentrations of CO2 and PM2.5 were measured using the Aranet4 Home CO2 sensor and a PurpleAir Classic sensor for PM2.5. We took a baseline measurement of both concentrations when the classroom was unoccupied. We then analyzed the change in concentration rates when classes were in session, taking into account classroom size and number of students. Our data showed concentrations above recommended levels at 1,370 ppm (parts per million) for CO2 in one of the Title 1 schools suggesting that Title 1 schools may be at greater risk of poor indoor air quality, though additional studies are needed. This additional exposure to pollutants and human aerosol emissions in already high-risk environments like band classrooms may lead to increased airborne disease transmission, highlighting the disparity in healthy learning environments. These classrooms require additional measures to maintain healthy concentrations of CO2 and PM2.5 to reduce the risk of airborne disease transmission particularly in low-income communities. 

Safe drinking water in schools is crucial for children's safety and academic performance. While Seattle Public Schools has tested for some contaminants, such as lead, the district's responsibility for ion-specific testing for anions such as phosphate, bromide, nitrite, nitrate, chloride, sulfate, and sulfite is less clear. High concentrations of anions pose potential health risks, including reduced oxygen in red blood cells, higher risks of tumors in children, and diarrhea. This research investigated the anion concentration in water fountains across seven high schools in the Seattle Public Schools. Twenty-one water samples were collected from seven public high schools and analyzed for anion concentration using ion chromatography. Results were compared to the Environmental Protection Agency's (EPA) maximum contaminant level (MCL). All test samples were below the EPA's MCL. These results suggest that the drinking water in these schools does not pose potential risks to students from anion contamination. While regular monitoring and management are still necessary to maintain safe drinking water, Seattle Public Schools have met the safety requirements for anion concentration in their drinking water. 

The health risks of particulate matter measuring less than 2.5 micrometers (PM2.5)  include: respiratory disease, cardiovascular issues, and cognitive impairments. Its presence near schools and colleges remains underexplored. This study examines the relationship between PM2.5 exposure levels and academic outcomes in community colleges located in historically redlined neighborhoods across four major West Coast cities: Los Angeles and San Diego in California; Portland, Oregon; and the greater Seattle area in Washington. Using data from the PurpleAir Network, state air quality indices, and community college governing bodies, we analyzed and compared PM2.5 levels near institutions located within historically redlined neighborhoods and institutions located outside those neighborhoods. Leveraging the Python programming language and Google Colab, we examined correlations between an institution’s demographic makeup and transfer rates relative to PM2.5 exposure. Data sets obtained were filtered between the hours of 8 AM and 1 PM during the months of January 2024 through December 2024. Our findings indicate a correlation between higher PM2.5 exposure and lower academic performance for colleges serving predominantly racially marginalized communities located within historically redlined neighborhoods. This research reinforces the role of environmental inequities in shaping educational disparities and highlights the need for targeted policies to address air quality in affected communities.

Medium-chain acyl-CoA dehydrogenase deficiency (MCADD) is a fatty acid β-oxidation disease associated with severe hypoglycemia and sudden death. MCADD is caused by biallelic pathogenic variants in the ACADM gene, which codes for a dehydrogenase specific to carnitines C6 through C12. MCADD is included in newborn screening (NBS) and characterized by elevated medium-chain acylcarnitine fats, annotated as C6, C8, and C10:1. Diagnostic testing is performed in plasma. Acylcarnitine results in dried blood spots have been described to differentiate carriers from affected individuals to reduce false positive NBS. Disease sensitivity and specificity, particularly to differentiate carriers from true positive cases, has not been well described in plasma. We posit that MCADD diagnosis will be more accurate if additional ratios beyond the primary disease markers, C6, C8, and C10:1 acylcarnitines, are considered. This study is a retrospective data review of NBS cases that were positive for possible MCADD and diagnostic testing was performed at Seattle Children’s Hospital. Cases are sorted into four groups: MCADD with homozygous disease variants, compound heterozygous MCADD, carriers of MCADD, or true negative. In collaboration with the biostats core service, linear regression models and receiver operator characteristic curves will compare acylcarnitine species and ratios by group. Preliminary results demonstrate that the primary markers associated with MCADD, C10/C2, C10/C6, C8/C2, C8/C10, and C8/Free carnitine, clearly discriminate affected individuals from control cases in plasma. Analysis is in process to compare the different genotypes of affected MCADD from carriers. Uncovering the diagnostic accuracy of plasma acylcarnitine profiles may influence future testing plans and improve the cost-effectiveness of healthcare services. DNA testing remains costly and slow. Additional biomarkers that provide a conclusive diagnosis of MCADD without requiring genetic testing may lead to more equitable patient care.

Rising atmospheric carbon dioxide levels have driven research into efficient gas separation materials. Polymers of intrinsic microporosity (PIMs) is one promising solution due to their rigid, porous structures and processability, allowing them to be turned into thin films for membrane-based gas separations. My research focuses on enhancing the carbon dioxide selectivity of helicene-based PIMs through post-synthetic modification of these polymers. I have synthesized a small molecule model of the PIM to screen for amine substitution conditions and ensure the viability of post-synthetic modification on the larger helicene-based PIM. Characterization techniques, multinuclear NMR and mass spectrometry, have verified the synthesis and amination of my model system. By incorporating nucleophilic amines into PIMs, these polymers can feature enhanced binding to electrophilic carbon dioxide, thereby increasing the interactions with carbon dioxide over other mixed gases, leading to separation. In my future studies, I will extend these modifications to the helicene-base PIM, fabricate films and evaluate their properties. Surface area measurements using N₂ gas sorption methods and CO₂ absorption isotherms will quantify gas-binding affinity and separation performance.

Glaciers have long been used as the bellwethers of climate change, given their ability to store gases, dust, microbes, and other environmental materials in their layers; tracking their recession has also been an important visual indicator of climate change. In this research, I examine how anions in newly exposed vary with depth. To do this, I took samples from exposed vertical ice faces on the Coleman glacier, on the north face of Mount Baker. Samples were thawed and analyzed using ion chromatography.  Trace amounts of chloride, nitrate, sulfate, and phosphate were found in each sample. The ion concentrations showed no trend with depth, and the ice itself appeared uniform. This is in contrast from vertical cores taken from solid ice in numerous other surveys, which show distinct annual layers and variation. This suggests that the ice at vertical faces has different properties from that at the top layers, including in its ability to trap environmental markers. Further research is needed to confirm this difference and examine which of these markers is most affected. Increased understanding of these markers could give more insight into how glaciers change over time and interact with their environment.

Stiffness measures derived from MR Elastography have shown value in guiding treatment decisions and monitoring effectiveness of therapies for liver disease but it requires extra hardware, longer scan duration and is susceptible to motion and breathing artifacts. Recent studies have revealed a strong linear correlation between water diffusion and tissue stiffness, demonstrating that Diffusion Weighted MRI (DWI) can be used to estimate stiffness values in liver tissue. DWI-derived stiffness values may help evaluate treatment-induced changes in breast cancer but to our knowledge, this has not yet been tested. The purpose of my ongoing study is to calibrate DWI estimates of tissue stiffness for the breast by optimizing DWI parameters (diffusion weightings, or ‘b-values’) and  calibration coefficients (a, b), evaluating the potential of stiffness measures for monitoring response to neoadjuvant chemotherapy (NAC) in breast cancer. We collected baseline and early treatment MRI exams from 25 patients undergoing NAC in this IRB approved study along with their treatment outcomes based on pathologic response post completion of NAC. I evaluated  the stiffness values obtained from different b-value pairs (low b-values: 100/200; high b-values: 800,1500,2000 s/mm²) and calibration coefficients(a,b=-9.7,13.9:-10.8,17.5:-8.8,21.2) and compared it to the invasive breast cancer stiffness values reported in literature. I also evaluated the performance of the optimized parameters to predict treatment response. The optimal b-value pairing (b=200,1500s/mm²) and coefficients a=-9.7,b=13.9 produced stiffness values consistent with literature. Using this approach, the performance for predicting treatment outcomes between responder and non-responder groups was AUC=0.84. These preliminary findings suggest that DWI based virtual elastography could serve as a non-invasive tool to assess tumor stiffness and track treatment efficacy, potentially improving breast cancer management.

The widespread use of makeup raises concerns about bacterial contamination, which can lead to acne, rashes, pink eye, and staph infections. Despite these risks, hygiene practices in cosmetic use, especially in public settings, are often overlooked. This study investigates bacterial contamination in both personal makeup products and in-store testers to assess potential health risks. Swab samples were collected from used personal cosmetics and store testers at popular beauty retailers, focusing on mascaras, foundation bottles, lipsticks, and sponges. Samples were transferred to nutrient-rich media plates, incubated at 37°C for 24–48 hours, and analyzed through colony-forming unit (CFU) counts and Gram staining for bacterial classification. Preliminary results suggest that store testers contain higher bacterial loads than personal products, emphasizing the need for improved hygiene practices in retail environments. These findings could encourage cosmetic brands and retailers to implement better sanitation protocols, such as stricter single-use applicator policies or improved packaging designs, to limit bacterial contamination and promote safer cosmetic use.

The angiopoietin-Tie2 signaling pathway is central to regulating vascular stability, remodeling, and permeability. Angiopoietin-1 (Ang1) promotes pAKT activation and vascular stability and regeneration, whereas Ang2 antagonizes these effects, leading to leaky vasculature. Although Tie2’s association with α5β1 integrin has been implicated in mediating these divergent outcomes, the requirement of direct F-domain ligand binding for integrin recruitment remains unclear. Here, we report the development and mechanistic evaluation of a de novo designed Tie2 mini binder (Tmb) that selectively targets the Tie2 receptor without engaging α5β1 integrin. Using an AI-based protein design pipeline, we designed Tmb with high affinity (KD ≈ 0.65 nM) for Tie2, as confirmed by CryoEM analysis, which demonstrated that Tmb accurately recapitulates its designed structure. When conjugated to multivalent scaffolds, Tmb effectively clusters Tie2 receptors, recapitulating the signaling profile of native Ang1. Notably, high valency Tmb constructs (e.g., H8T) robustly activated pAKT and induced nuclear FOXO1 exclusion, mirroring the pro-survival and vascular stabilizing effects of Ang1, despite lacking the capacity to bind α5β1 integrin directly. Detailed cellular assays revealed that Tie2 clustering leads to the formation of two distinct complexes: a Tie2–α5β1 integrin complex that facilitates focal adhesion assembly and cell migration via pCAS recruitment, and a Tie2–tight junction complex (comprising ZO1, claudin-5, and occludin) that underpins vascular barrier integrity. Importantly, competitive binding studies demonstrated that integrin recruitment to the Tie2 complex does not require direct F-domain engagement. In human iPSC-derived diabetic blood vessel organoids, treatment with Tmb-based Tie2 agonists ameliorated diabetic vasculopathy phenotypes by reducing pathogenic collagen IV deposition, restoring tight junction organization, and lowering nuclear FOXO1 levels. These findings provide novel insights into the mechanistic interplay between Tie2, integrin, and junctional proteins, and underscore the therapeutic potential of synthetic Tie2 agonists in vascular repair and diabetic vasculopathy.

Over a hundred years after the Spanish Flu, the influenza A virus (IAV) remains a leading cause of respiratory infections and mortality worldwide. The proliferation of IAV causes many of the symptoms associated with IAV clinical disease. However, the severity of acute lung injury (ALI) from IAV is primarily driven by the host's immune response to infection. The mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated protein kinase (ERK) signaling cascade is a highly conserved pathway that is activated during lung injury and inflammation in both rodents and humans. Two MEK isoforms, MEK1 (Map2k1) and MEK2 (Map2k2), activate downstream effectors, ERK1 and ERK2, and control critical cellular processes, including the intensity and duration of inflammatory signaling. Our prior research revealed that MEK2-deficient mice exhibited improved weight recovery and overall fitness during IAV infection, suggesting that MEK2 is a host response exacerbating ALI during IAV infection. During IAV infection, excessive pro-inflammatory cytokine production drives immune cell recruitment into the lungs, leading to collateral tissue damage that impairs organ function and exacerbates disease. We hypothesize that MEK2 enhances immune cell recruitment to the lungs, enhancing inflammation, which may occur through exuberant chemokine signaling. To investigate this, we infected MEK2-deficient and wild-type mice with mouse-adapted IAV (H1N1, PR8) and collected cells from bronchoalveolar lavage (BAL) and lung homogenates. Using flow cytometry, we found reduced immune cell recruitment, including decreased numbers of monocytes, dendritic cells, monocyte-macrophages, CD4+ T-cells, CD8+ T-cells, and B-cells. Next, we assessed levels of key chemokines known to attract monocytes and lymphocytes by measuring their gene expression in the lungs and protein levels in the BAL. Investigating MEK2’s impact on chemokine signaling will elucidate the mechanism by which MEK2 perpetuates lung inflammation and injury during IAV infection and will guide the development of future host-directed therapies for IAV-induced lung damage.

Injustice has permeated the criminal legal system and its punitive regime for as long as this society has existed. The rapidly expanding American carceral state arose from a myriad of retributive policies and legislation that became prevalent throughout the last quarter of the twentieth century. There is currently an abundance of research focused on the effects of incarceration on people of diverse racial, ethnic, and socioeconomic backgrounds. A crucial gap in prison reform research remains the effects of this system of punishment on LGBTQ+ people. My research endeavor aims to address that fact and reveal how individuals with queer sexual or gender identities have been impacted by this system within Washington State. The institutions that exact punishment in this state operate both on a heteronormative apparatus and a gender binary. My thesis involves placing formerly incarcerated LGBTQ+ people at the forefront of prison reform research to highlight their distinctive adversities and establish policy proposals to ameliorate them. I conducted interviews with people who fit this demographic to bring to light their lived experiences and discover what practices, policies, and changes they want to see implemented. The findings illustrate a need for reform in areas including programming opportunities, support systems, healthcare accessibility, gender-affirming care, therapeutic services, housing assignments, reentry assistance, and equitable treatment overall. Incarcerated LGBTQ+ individuals are subjected to exacerbated punishment from correctional staff and other incarcerated individuals, which leads to difficulties with interpersonal dynamics and an overall suppression of identity. Faced with heightened vulnerabilities while incarcerated, LGBTQ+ people maintain resilient attitudes as they reenter society and positively transform their lives. The voices of this community in this research illuminates the necessity of addressing LGBTQ+ rights within prison reform efforts.

Autism is a neurodevelopmental condition characterized by social-communication differences and restricted, repetitive behaviors (American Psychological Association, 2013). While racial disparities in autism prevalence have been documented, not much research has examined how these differences appear in autism screening measures. This study investigates racial differences in Autism Spectrum Quotient (AQ) scores among non-autistic Asian and White adults to assess potential biases in autism screening. Using data from three NIH-funded studies (COBRA, BEAM, and The Korean Study), AQ scores from 166 participants (n=102 White, n=64 Asian) will be analyzed through t-tests and Repeated Measures Analysis of Variance (ANOVA) to compare total and subscale scores. Preliminary observation suggests that non-autistic Asian participants may be more likely to score higher on the AQ, raising concerns about false positives in autism screenings. Understanding these differences will help improve diagnostic accuracy, reduce disparities, and promote equitable access to neurodevelopmental resources.

First-generation college students (FGCS), those first in their families to pursue or complete a college degree, are a widely studied demographic across psychological research. However, much of the literature on FGCS examines their mental health and life experiences through a deficit framework, focused on systemic obstacles to success and categorizing students as “at risk”. Additionally, some research fails to recognize the importance of intersectionality, viewing FGCS’s mental health as separate from its systemic, social, and institutional contexts. To better highlight the assets and intersecting identities of FGCS, this strengths-based presentation explores existing literature about their mental health experiences, describes their risk and protective factors in developing mental health symptoms and conditions, and proposes mental health initiatives for FGCS and, specifically for, Latine FGCS. I use insights from interviews with Latine FGCS as illustrative examples to further demonstrate the importance of considering context and intersectionality in this area of psychological research.

Proteins in the NFкB family are transcription factors that modulate the expression of genes relating to immunity and inflammation. One protein within this family is the p50/RelA heterodimer which includes a structured DNA-binding domain and a Transcription Activation Domain (TAD) which is intrinsically disordered, or naturally lacking secondary and tertiary structure. Previous studies have shown that interactions between the DNA-binding domain and TAD affect DNA binding affinity and specificity. With the goal of further assessing and comparing the interactions between intrinsically disordered and structured domains in proteins of this family, we have worked to troubleshoot and optimize protocols relating to expressing and purifying human p50/RelA protein. I analyzed the efficiency of multiple chromatography steps and introduced changes to improve yield. Optimization of the expression and purification protocols will enable future investigations into the DNA binding activity of this protein.

As digital platforms increasingly influence financial markets, the role of social media engagement in shaping stock performance has gained growing attention. This study investigates the link between social media activity and stock prices, focusing on Reddit, a prominent platform for individual investors to share opinions. Analyzing daily data on the most frequently discussed stocks on Reddit, we examine how discussion volume and sentiment of investors drive stock price movements. Our findings reveal that both discussion volume and positive sentiment are significantly associated with rising stock prices. Additionally, we observed a nonlinear relationship between sentiment, mentions, and stock performance. Specifically, discussion volume exhibited a negative nonlinear relationship with stock prices, while positive sentiment showed a positive nonlinear effect. These results provide insights for investors and financial analysts, highlighting the value of monitoring social media trends to inform investment strategies. f

Corn, a crucial agricultural commodity, serves as a fundamental input. Its economic importance has made government subsidies a vital policy instrument to stabilize corn supply and prices To investigate the relationship between corn subsidies and prices, we compiled yearly data on U.S. corn prices, subsidies, exports, production, and inflation from 1980 to 2023. Employing linear and nonlinear regression models, we analyzed the role of corn subsidies in shaping corn prices while controlling for other factors. Our results suggest a statistically significant negative relationship between subsidies and corn prices. Interestingly, this negative relationship weakens at higher subsidy levels, revealing a curvilinear relationship. This implies that while subsidies can lower prices to benefit consumers and stimulate the economy, excessive subsidies may reduce the magnitude of price decreases and dampen producers’ incentives by further suppressing prices and revenue. Our findings offer valuable insights for policymakers, showing the need for careful calibration of subsidies to balance consumer benefits with producer sustainability. We also suggest potential avenues for further exploration to extend this work

TBC domain containing kinase (TBCK) is an understudied protein with three domains: a pseudokinase; Tre-2, Bub2, and Cdc16; and rhodanese, and is highly expressed in the brain. Homozygous mutations in TBCK cause a rare neurodegenerative disorder in children, which clinically presents as syndrome infantile encephalopathy, brain atrophy, cerebellar hypoplasia, and muscle hypotonia. Two mutations in particular, Arg126Stop and Arg511His in the pseudokinase and TBC domains respectively, are commonly found among TBCK patients. The progression of the disease is characterized by a global regression in brain development, severe intellectual disability, and premature death in acute cases. The pathogenic mechanism underlying TBCK syndrome is unclear, but past studies show that TBCK patient neurons demonstrate aberrant metabolite buildup in the lysosome likely resulting from abnormal lysosomal activity. Immunoprecipitation mass spectrometry was performed for wild type TBCK in both N terminal and C terminal tags, revealing a preliminary list of both known and unknown interactors for TBCK. To further investigate the early developmental implications of mutant TBCK, CRISPR/Cas9 directed mutagenesis is being used to generate two induced pluripotent stem cell (iPSC) lines harboring the Arg126Stop and Arg511His mutants for subsequent differentiation into neural progenitor cells (NPC) and neurons. Immunofluorescent imaging of the mutant NPCs will confirm the recapitulation of growth and lysosomal defects present in patient cells. To analyze the effect of TBCK mutation on lysosomal function/content, we will immuno-isolate lysosomes through lysosome immunoprecipitation (Lyso-IP) and identify proteomic changes through mass spectrometry. While providing a crucial in vitro cell model of two common patient mutations, these experiments will offer critical insight into cellular dysfunctions that contribute to TBCK disease states.

Dynamics of activity across the cerebral cortex at the mesoscopic scale – coordinated fluctuations of local populations of neurons — are essential to perception and cognition and relevant to computations like sensorimotor integration and goal-directed task engagement. However, understanding direct causal links between population dynamics and behavior requires the ability to manipulate mesoscale activity and observe the effect of manipulation across multiple brain regions simultaneously. Here, we develop a novel system enabling simultaneous recording and manipulation of activity across the dorsal cortex of awake mice, compatible with large-scale electrophysiology from any region across the brain. Transgenic mice expressing the GCaMP calcium sensor are injected systemically with an adeno-associated virus driving expression of the ChrimsonR excitatory opsin. This strategy drives expression of the blue-excited calcium indicator, GCaMP, in excitatory neurons and red-excited Chrimson opsin in inhibitory neurons. The light channels of the imaging and the opsin do not interfere. We demonstrate widefield single-photon calcium imaging and simultaneous galvo-targeted laser stimulation over the entire dorsal cortical surface and find that the spatial and temporal resolution of the stimulus is suitable for targeting many specific cortical regions in short periods of time. The calcium indicator responded to the laser within 30 ms, and the activity returned to baseline within 100 ms after laser offset. The area of effect was as small as 3 mm² for the lowest laser power or as large as 10 mm² for the largest laser power. Moreover, the preparation is stable over many months and is thus well-suited for long-term behavioral experiments. The ability to stimulate and measure anywhere on the dorsal cortical surface of the brain will allow us to design computational models describing how causal manipulation impacts neural dynamics, especially in the context of designing closed-loop systems to control neural activity and behavior. 

Autism is a neurodevelopmental disorder characterized by differences in social-communication and the presence of restricted and repetitive behaviors and interests. Many autistic individuals engage in “camouflaging” to hide or change their behaviors associated with autism to avoid social stigma. This study aims to explore neurophysiological characteristics underlying camouflaging. Electroencephalography (EEG) is a popular psychophysiological tool that measures brain activity through oscillatory patterns, reflecting various cognitive and emotional processes. Specifically, during “resting state” (when the brain is exposed to minimal external stimuli), theta waves have been shown to have increased activity during periods of increased cognitive load, attentional demands, and task difficulty – mental states that all relate to camouflaging based on qualitative research.  Participants included autistic (n=108) as well as non-autistic adults (n=85), between the ages of 15 and 31 years. Participants completed the Camouflaging Autistic Traits Questionnaire (CAT-Q) which measured three domains of camouflaging in autism: compensation, masking, and assimilation. EEG recordings were taken during resting state and oscillatory activity in the theta frequency band (4-8 Hz) will be analyzed. Our hypothesis is that camouflaging traits will be positively correlated with theta wave activity.  Camouflaging can lead to various challenges for autistic individuals, including depression and anxiety. Thus, identifying the proposed analyses could provide valuable insight into the cognitive and emotional processes of camouflaging, ultimately contributing to a better understanding and potential treatment for mental health challenges faced by the autistic community.

Cancer immunotherapy, specifically Adoptive Cell Therapy (ACT), has revolutionized treatment approaches using genetically modified T cells to recognize and eliminate cancer cells. However, tumors combat this by creating an immunosuppressive tumor microenvironment (TME) blocking effective antitumor immune responses.  Dendritic cells (DCs) are innate immune cells that act as messengers between the innate and adaptive systems.   In the Oda lab we have designed Dual Costimulatory Receptor (DCRs) that combine a FLT3L or CD40L ectodomain with different costimulatory endodomains (e.g. CD40, 4-1BB, OX40), to provide both T cell-extrinsic and -intrinsic costimulatory signals.  These DCRs are expressed on the surface of antigen specific T cells, and the combination of these signals allows for enhanced tumor antigen presentation and dendritic cell activation, leading to an increase of the immune response to target and destroy cancer tumors. I will investigate how incorporating DCRs on T cells will enhance ACT effectiveness. I hypothesize these DCR signals on T cells will enhance dendritic cell function in the TME, allowing for increased T cell activation and antitumor immune responses. To test this, I will conduct in vitro coculture experiments to determine how DCR-T cells, dendritic cells, and pancreatic cancer cells interact together. I will study the interactions of these immune cells using live cell imaging technology such as the Incucyte. Additionally, I will analyze the phenotypes of our distinct cell populations via flow cytometry.  This research aims to enhance the development of immunotherapy for Pancreatic and all solid cancers by improving the recognition of cancer cells from the immune system. These results could help pave the way for improving solid tumor cancer treatment.

While taking multiple general science courses and dance courses as a double-degree student, I have devised creative ways to balance my studying and dance training. One involved creating dance choreography to memorize organic chemistry reactions, which inspired me to choreograph a dance piece named after the motor cortex “Homunculus” for Aura Dance Company’s (RSO) annual spring show in 2023. This sparked my interest in organizing a project to teach this learning structure that may be useful to others. With help from Professor Hannah Wiley and MFA candidate Beth Twigs, I designed dance workshops for my peers to learn more about neuroscience and dance. NeuroDance is a multidimensional project to educate students about neuroscience through dance-making tools. The project involved organizing workshops where participants learned movements inspired by molecular neuroscience, neuroanatomy, and skeletal anatomy. Participants modeled ions, neurons, and planes of movement through facilitated movement phrases and seeds. To assess learning outcomes, quizzes were given before and after the workshops. Volunteers were recruited from on-campus social, dance, and neuroscience groups, and outreach will occur via social media and posters. The data from the learning aspect of these workshops house the scientific results, but the movement observed served as the foundation for a larger choreographic work presented in the Department of Dance’s Dance Majors Concert (2025). The physicality and repetition inherent in dance offer a unique and enriching platform for learning. I aim further to explore the potential of dance education in STEM with this pilot study.

The Kinnar are a South Asian genderqueer community, who possess the power of shraap or ashirwaad - the power to curse or bless. The use their powers to perform blessing (badhai), sex, and begging work. While they are regarded as deities and a "third gender," they have historically been othered in South Asia's dominant colonial, cultural, and religious archives. These archives paradoxically narrate the Kinnar as less-than-human and more-than-human, trapping them in the ontological category of the "non-human." In my multi-genre, multi-modal book, Of Ghosts & Gods, I seek to understand the development of Kinnar identity and de-humanization. I ask three main, interwoven questions: (1) How do Kinnar peoples narrativize themselves? (2) How have their identities and lives been (de)constructed under various empires (Mughal, British, contemporary Hindu fundamentalist)? (3) How have they managed to survive - despite and with - a paradoxical identity under empire? I amalgamate several Kinnar testimonies, Hindu epics, Burke Museum archives, and personal experiences to get at this inquiry. I bring these sources together through ethnographic and critically fabulative methodologies, in an effort to amplify and ally with Kinnar voices. Through this book, I want to help visibilize the Kinnar peoples in ways they may wish to be made visible. It is important to do so, as imperial projects invested in eliminating the Kinnar relied on gross misrepresentation of the community to justify their dehumanization. The urgency of this work increases when we recognize that the Hindu-fundamentalist administration of 2025 India continues this work, limiting Kinnar livelihoods through its unquestioned religious assumptions. I am not a member of the Hijra, Kinnar, Khwajasarai or other South Asian genderqueer communities. To re-write archival violence therefore, Of Ghosts & Gods strives to place Kinnar voices before my own. 

Recent advances in ultra-high-resolution frequency comb spectroscopy have enabled the observation of previously unresolved spectroscopic details in small molecular systems. However, current theoretical frameworks are insufficient to fully describe the complex interactions between internal and overall rotational angular momenta, and higher frequency vibrational modes, particularly in molecules with multiple internal rotors. This work focuses on elucidating the coupled torsional, rotational, and vibrational kinematics of dimethyl sulfide (DMS), an asymmetric top with two internal methyl rotors which generate a rich and highly structured spectrum. We develop a general theoretical approach that incorporates torsional angular momenta into the overall molecular framework by systematically coupling the individual degrees of freedom, which are initially described in their well-known primitive bases, into a fully symmetrized torsion-rotation-vibration Hamiltonian. Through this systematic approach, interactions between the overall rotational and internal angular momenta of the methyl groups are explicitly addressed, capturing the effects of intrinsic Coriolis couplings and the tunneling splittings of the rotors. The resulting eigenstates and energy spectrum are analyzed to predict spectroscopic transitions, which are then compared with experimental findings, allowing the assignment of observed peaks to specific ground and excited quantum states. This rigorous treatment provides insights into nontrivial state mixing and previously unresolved splittings observed in high-resolution spectra. The methods developed in this work offer a pathway toward more accurate analysis of complex molecular systems and clusters, with broader applicability to high-resolution spectroscopy in atmospheric, astrochemical, and low-temperature environments.

Gray whales in the North Pacific annually migrate north to the Gulf of Alaska and the Bering Sea, and their migration route bypasses the Salish Sea. Roughly a dozen of these whales, commonly called “the Sounders,” have detoured their migration into North Puget Sound since the 1990s. These whales have been observed feeding on ghost shrimp in the intertidal area of sediment beaches in North Puget Sound, using a high risk strategy of feeding on shrimp at high tides. This feeding strategy leaves large indents, or “feeding pits”, in the sediment that are revealed at low tide and can provide insight into the Sounders’ feeding habits and contribute to a deeper understanding of the North Pacific gray whale population. My research focused on locational trends of gray whale feeding pits on Jetty Island West beach, and I observed longitudinal locations of specific pits in the intertidal zone to investigate feeding patterns. I observed feeding pits with drone imagery collected at low tide and compiled into aerial maps, or “orthomosaics,” and I compared feeding pits in different longitudes to observe where on the beach whales are feeding. Two seasons of feeding pit imagery were collected from late winter and spring of 2024 and 2025, and I have analyzed the imagery using ArcGIS pro. Survey site area ranged from approximately 0.09km² to 0.4 km² for different maps. The non-invasive nature of drone photogrammetry has recently increased its use in marine and biological research, and this method of data collection is ideal for surveying gray whale pits on Jetty Island. Because of the increased risk of feeding in higher tidal zones, I expect to find higher concentrations of feeding pits at lower tidal zones.

Seabirds are considered a strong indicator species for ecosystem health due to their visibility, lack of behavioral and phenotypic plasticity, and high trophic level.  Current declines in seabird populations are often attributed to bottom-up ecosystem control regulating upper trophic level populations. These bottom-up effects might be caused by reductions in marine productivity due to climate change. I performed statistical and graphical analyses on the National Audubon Society’s Christmas Bird Count data from Puget Sound and water chemistry data from the Ocean Research College Academy’s moored and deployable sensors. This allowed me to identify possible relationships between bird populations and water chemistry from 2009 to 2024 in the Possession Sound estuary. My initial analyses demonstrated the expected decline in collective seabirds counted, however certain pelagic species experienced unexpected increases. Further investigation is required to determine whether the increase was caused by ecosystem dynamics or improved count methods. My initial analyses did not indicate any relationship between water chemistry and bird populations. The lack of apparent relationship may be due to the water chemistry changes having impacts on primary productivity and indirect bottom-up trophic cascades, which could have a significant lag time in effects on bird populations. My analysis also does not account for environmental factors in disparate migration sites or breeding colonies that might affect bird populations. 

Photovoice is an innovative, visual research method that aims to capture more nuanced aspects of caregiving and family relations through photographs and storytelling. This study seeks to better understand the cultural, emotional, and practical aspects of caregiving in families affected by HIV. The project involves six semi-structured focus group discussions – three with mothers and three with fathers. Participants are trained in ethical photography and asked to take photos inspired by specific caregiving questions such as “What does being a parent mean to you?” The images captured serve as discussion prompts during group discussions, helping illuminate family structures, caregiving roles, and the challenges faced in raising HIV-exposed but uninfected children. Discussions are transcribed, and the qualitative data are analyzed using inductive thematic analysis to explore common caregiving patterns and the impact of parental HIV on caregiving dynamics. Preliminary findings are expected to highlight the critical roles of fathers in caregiving and identify strategies to better support families in nurturing child development. These findings inform future interventions and policies designed to support HIV-exposed children and their caregivers, with a focus on the unique caregiving challenges in high-HIV-prevalence contexts. As a research team member, I contribute by developing Standard Operating Procedures (SOPs) for study methodologies, managing qualitative data, coordinating team communication, and assisting with data analysis and dissemination.

Discharge planning is an important component of safe and efficient hospital care. We are interested in how patients who live in a baseline unsafe situation conceptualize a “safe” discharge plan. Thus, our study aimed to understand the needs, perspectives, and priorities of patients experiencing homelessness as they prepare to leave the hospital. We conducted qualitative semi-structured interviews in 2023-2024 at a large urban, public, safety-net hospital in the Pacific Northwest. Any adult patient admitted to an acute care general medicine service who was living homeless was eligible. Patients with severe cognitive or mental health disorders that precluded consent process were excluded. This study was approved by our institutional IRB. Patients experiencing homelessness shared their perspectives on discharge planning in three major themes: 1) basic needs, 2) barriers to stability, and 3) role of healthcare systems. Within the theme of basic needs, respondents identified the importance of physical survival: shelter/warmth, protection from violence, and treatment for major injuries or illness. They identified key barriers to stability: loss of property, legal concerns, and financial challenges. While many respondents were hopeful that the role of the healthcare system might be to assist in these issues, they also acknowledged the existence of significant resource constraints. Many reflected on the way that U.S. society views poverty and the impact of policy and funding to what is feasible by healthcare providers. Several participants were aware of interventions that the healthcare system puts into place to achieve better outcomes but noted these may still be out of reach when basic needs are not met. We found that patients experiencing homelessness were overwhelmingly focused on achieving their basic needs, including physical survival and environmental stability. Current discharge processes should be tailored to individual lived experiences, especially with regards to housing status.

The early 20th-century publishing landscape in England remains largely undocumented in a structured dataset, despite the availability of bibliographic records in The English Catalogue of Books. Issued annually by Publishers’ Circular, these catalogs document books, laws, and government reports published in the United Kingdom from the mid-19th to early 20th century. Digitized versions, made available through the HathiTrust digital library, contain Optical Character Recognition (OCR)-generated text that often includes errors and inconsistencies, making automated data extraction challenging. Our project focused on refining and formatting bibliographic data from these files by developing tailored regular expressions and Python-based parsing techniques for each catalog year. This work was a necessary step toward the eventual creation of an open-access dataset covering books published between 1900 and 1928. In Summer 2024, we refined parsing methods to identify and correct inconsistencies in the raw OCR text for catalog years 1902–1922, building on prior work. These improvements increased the number of extracted publication entries by 15.4% across the catalog collection, adding approximately 16,500 additional book records. The structured data enabled content analysis of bibliographic trends, including authorship patterns, publisher prominence, and thematic categorization. Using SQL-based keyword searches, we examined colonial publication networks, identifying the prevalence of colonial discourse and associated geographical trends. Additionally, we parsed Hebrew-language publications to analyze Jewish authorship and the locations of Hebrew book publishing in early 20th-century England. By structuring historical bibliographic data, this project provides a valuable resource for researchers studying literary trends, publishing industry shifts, and broader cultural patterns. Our work contributes to ongoing efforts to digitize The English Catalogue of Books and deepen insights into the evolution of the British literary landscape.

Transgender and nonbinary individuals (TNB) face significant discrimination in healthcare settings, which is strongly associated with disparities in alcohol use and treatment access. These barriers often result in delayed or avoided care, exacerbating both physical and mental health issues. The literature reflects a lack of comprehensive understanding and research regarding the specific systemic barriers contributing to avoidance of alcohol healthcare among TNB individuals. This study aims to assess how healthcare experiences influence decisions to engage with alcohol healthcare within the TNB community and discusses future considerations for improvement. TNB adults (N = 26) completed an individual qualitative interview either in-person or online. As part of a larger semi-structured interview about alcohol use, participants were asked about their experiences discussing alcohol use and/or receiving alcohol interventions from medical providers. Participants identified as 30.8% transfeminine, 26.9% transmasculine, and 57.7% nonbinary and were between the ages of 18 and 57. The interview was audio recorded and transcribed by HIPAA-compliant Zoom and transcripts were then cross-checked and edited to ensure their accuracy. Ongoing qualitative analysis is conducted in Dedoose to identify emerging themes. Interactive coding procedures included two coders completing deductive codes identified with prior literature and two coders independently using inductive coding to identify new themes. Discrepancies are identified and discussions support reaching consensus. Understanding the intersection of healthcare mistreatment and substance use disorders in this demographic will inform future policies and interventions designed to create more inclusive and supportive healthcare environments for TNB individuals.

Extracellular vesicles (EVs) are lipid-bilayer membrane-enclosed structures that cells produce and use for intercellular communication. Within the context of cancer, EVs have been shown to enhance cancer development by delivering cargo from malignant cells to recipient cells to promote survival, proliferation, and invasion. In a previous project, I conducted a chemical screen alongside my graudate mentor and other undergraduates to determine kinases that were important to EV biogenesis. One hit was the JNK pathway, which decreased EV production when inhibited. I studied the pathway in further detail utilizing a variety of experimental techniques to establish its importance for EV generation, and I was able to conclude that JNK regulates EV biogenesis. Another facet of cancer development is oxidative stress, caused by reactive oxygen species (ROS). When unregulated, these highly reactive free radicals and molecules derived from oxygen can damage DNA, facilitate metastasis, and aid in cancer progression. Given that surrounding literature revealed that JNK is activated by ROS, I hypothesized a connection between ROS and EV production. This project aims to more directly uncover the impact of ROS on EV generation by manipulating ROS-related genes in vivo. To do this, I knocked down ROS generator genes such as Dual Oxidase (Duox) in Drosophila melanogaster. I quantified ROS levels by staining the dissected tumor tissues with an ROS probe to ensure that the genes were functioning as expected. Then, I stained the tissues for phospho-JNK as a proxy for ROS quantification and to measure JNK activity. Finally, I conducted live imaging of the tumor tissues to quantify EV generation. I anticipate that impairing ROS generation will inhibit JNK activation, subsequently leading to a decrease in EV production. Understanding how factors involved in cancer development function in relation to each other is crucial for discovering novel cancer therapeutics.

Extracellular vesicles (EVs) are essential mediators in intercellular communication secreted by cells to transfer bioactive cargo that lead to biological effects. The crucial roles EVs have in maintaining biological homeostasis are similarly found within cancer cells in the tumor microenvironment, where they promote cell growth/survival, invasion, and metastasis. Investigating methods to reduce tumor-cell derived EVs could provide substantial remedies for cancer patients. One pathway of interest in cancer is the cellular response to reactive oxygen species (ROS)—highly reactive molecules which tumor cells use for oncogenic signaling, to damage macromolecules, and drive tumor progression. Modulation of ROS levels may yield anticancer effects, but research about the role of ROS in EV biogenesis has not been conducted. To assess their connection, I used MDA-MB-231 human breast cancer cells as an in vitro model for EV biogenesis. My interest in ROS and EVs began when I assisted my graduate mentor in an extensive chemical screen and found kinase inhibitors that altered EV production via an EV isolation protocol. From these hits, I identified ROS-activated pathways that promote cancer progression as important players in EV production. I then tested if chemicals known to directly affect ROS alter EV production by isolating and quantifying EVs and by imaging their production from MDA-MB-231 cells. To provide a comprehensive understanding of the pathway, I validated upstream interactions of EV biogenesis by measuring the production of ROS using a chemical marker that emits green fluorescence when oxidized. From this data, I can determine if there is a direct interaction between ROS and EV production. An understanding of EV biogenesis and its connection to ROS and cancer progression may unveil new opportunities for novel cancer therapeutics.

Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are neurodevelopmental conditions that are known to co-occur with decreased sleep quality and quantity. ASD is characterized by social communication differences and restricted, repetitive behaviors and interests.  ADHD is characterized by inattention and/or hyperactivity/impulsivity. Previous research found higher instances of sleep disruptions within adults with ADHD as well as autistic populations compared to neurotypical adults. However, quantitative data around the associations between ASD and sleep disruptions is sparse.  This leads to our research question which is, how does sleep disruption affect autistic, autistic + ADHD adult’s sleep quality and quantity compared to neurotypical adults? We hypothesize that ASD+ADHD and ASD adults have experience higher sleep disruptions (fewer hours of sleep and lower quality) compared to non-autistic adults. Participants included autistic adults (n=66), autistic adults with ADHD (n=39), and non-autistic adults (n=221) enrolled in the NIH-funded COBRA and BEAM studies, which investigated how the brain processes sensory and visual information.  Autism diagnoses were confirmed using standard assessments (such as Autism Diagnostic Observation Schedule, 2nd Edition, Autism Quotient) by clinicians.  Participants self-reported ADHD diagnoses, sleep quantity (hours per night on weekdays, hours per night on weekends), and sleep quality (over the past week on a 4-point Likert scale). An ANOVA will be used to compare sleep quality and quantity between diagnostic groups. Understanding neurodivergent populations’ sleep quality and quantity helps improve public health communication around sleep health, which is particularly important population health issue given the link between sleep, mental and physical health. Finally, identifying populations most in need of sleep interventions helps us address the increased number of adults with sleep disturbance and disorders.

The Pacific Northwest (PNW) saw an unprecedented heatwave between June 25 to July 3 of 2021, with temperatures reaching up to 15℃ above the climatological mean. Previous studies have focused on this event’s impacts on plants in Western Washington and Oregon through direct observations, or have focused on the economic implications from poor crop turnout. We used remote sensing data to take a holistic approach and examined how all plants throughout the PNW fared during and after this historical heatwave. We found that solar induced fluorescence (SIF) and near-Infrared reflectance of vegetation (NIRv), two remotely sensed vegetation health markers, had regionally dependent plant responses to the extreme heat. In particular, anomalously high SIF regions coincided with anomalously high photosynthetically active radiation (PAR) regions due to low cloud cover. As SIF has been used as a proxy for gross primary productivity (GPP), our findings begs the question: was the elevated SIF during the heatwave indicative of higher GPP, or was the SIF response an artifact of the higher radiation? Our study aims to further our understanding of how extreme events impact plant health, which is increasingly important as heatwaves become more intense and frequent in the future.

In the developing brain of a fruit fly (Drosophila melanogaster), neural stem cells, called neuroblasts, divide to produce new cells that will become neurons. These divisions follow strict biological rules, but because many factors influence how and when neuroblasts divide, predicting their behavior is challenging. While lab experiments provide crucial insights, they are often limited in how many conditions can be tested at once (genetic, physical, or otherwise). To address these limitations, we developed an agent-based computer model that simulates neuroblast divisions and their interactions with neighboring cells. Our model allows exploration of different conditions to predict how neuroblasts behave in complex environments. This work focuses on three key hypotheses about neuroblast behavior: (1) post stem cell division, the larger cells are more likely to remain as stem cells, (2) the cell positioned on top during division will keep its stem cell identity, and (3) clustering of differentiated neural cells on the membrane of a neuroblast suppresses their division. To investigate these hypotheses, we examine emergent behaviors in our model through size-based, location-based, and clustering-based differentiation rules. By adjusting parameters such as cell placement, division timing, and proximity to other neuroblasts, we analyze how these factors influence neuroblast fate. We validate model predictions against experimental data by comparing division patterns observed in simulations to those seen in Drosophila brains through live imaging. By combining computational modeling with experimental data, this work provides a framework for understanding the factors responsible for neural development. Our findings will refine existing models of neural stem cell behavior and help guide future experiments, making it easier to uncover the fundamental rules of brain development.

This project analyzes the Blade Runner films in order to rethink the cyborg, a theory articulated by Donna Haraway as a metaphor that transgresses binaries which uphold systems of oppression, such as the distinctions between male/female, organic/inorganic, and human/nonhuman. For Haraway, the cyborg is a paragon of agency and liberation; however, Blade Runner imagines a world in which cyborgs – in this case human-like androids called replicants – entrench capitalist ideals in addition to racist and anthropocentric hierarchies. In the films, the replicants are coded as ambiguous racial Others who flexibly inhabit the symbolic position of Black, Asian, and white persons. Yet they are still placed above non-white humans within the racial hierarchy of the films because of their contributions to the capitalist and colonial projects of the future. In other words, they take on the role of a “model minority” desired for their production of capital, yet despised for being quintessentially non-human. The replicant-cyborg in Blade Runner reflects the societal desire for a class of laborers that will submit to capitalist interests, demonstrating (contra Haraway) its failure to disrupt established systems of power. However, while this paper interrogates our faith in the potential of the cyborg, it would be remiss to disavow this figure completely. In light of the cyborg’s associations with capitalist ideals, how might we reconsider it and our relationship with new technologies as they emerge? How can we conceptualize a future in which entanglements with technology are liberating rather than oppressive? These are ongoing questions for this project, which I explore in returning to Blade Runner.

6PPD-Quinone (6PPD-Q) is a toxic transformation product of the tire rubber additive, 6PPD, that has been identified as the primary cause of Coho Salmon (Oncorhynchus kisutch) mortality in watersheds impacted by roadway runoff. Recent studies have focused on quantifying the lethal concentration of 6PPD-Q, identifying the major sources, and predicting the environmental release from rubber products. Organic chemical release from solids is typically evaluated with solvent extraction where organic solvent and solid are contacted, releasing the leachable chemicals for measurement. However, different solvents and methods introduce inconsistencies in leaching data from different laboratories. This study evaluates the impact of solvent choice on 6PPD-Q extraction from crumb rubber. I will quantify 6PPD-Q concentrations in methanol, ethyl acetate, or acetone during storage after rubber extractions. Determining the best solvent for 6PPD-Q that promotes the most recovery and stability is essential for data quality. After this study, desorption and resorption rates of 6PPD-Q onto various crumb rubbers will be measured.  These studies aim to improve study design for leaching assessments and enhance our understanding of the persistence and mobility of 6PPD-Q in the environment.

Downregulation of the mTOR complex has been shown to increase lifespan and delay development of multiple organisms, including Drosophila melanogaster. Rapamycin, an inhibitor of this complex, is undergoing FDA-approved clinical trials as a promising anti-aging drug. However the impact of genetic variation on rapamycin's response is unknown. Our study of 140+ genetically diverse Drosophila strains revealed significant variation in pupation time after rapamycin exposure, however, the underlying mechanisms of this variation remain poorly understood. Surprisingly, this sensitivity does not correlate with genetic variation in or around the mTOR gene. We therefore hypothesize that differences in phosphorylation of downstream mTOR targets may explain this variation. Currently, we are using multiple approaches to investigate how activation of downstream targets differs between highly resistant and sensitive strains. We aim to characterize the phosphoproteome of first instar Drosophila larvae from highly sensitive and resistant strains. First instar larvae were treated with rapamycin for 12 hours, followed by mass spectrometry analysis to identify phosphorylation changes in mTOR pathway targets. To validate that 12 hours of treatment induces a rapamycin response, we monitored the growth of a parallel group of larvae until 72 hours and measured their size. Sensitive DGRP strains, 348 and 517, showed a twofold reduction in length when treated with 20uM rapamycin compared to control (p-value <0.0001), while the resistant strain, 441, showed no significant decrease. Comparing the phosphoproteome of multiple resistant and sensitive lines will uncover molecular factors associated with resistance or sensitivity. Additionally, whole-larvae RNA-seq will assess the expression profile of these factors, revealing whether gene expression of tor pathway-related genes contributes to sensitivity. Understanding the mechanisms behind rapamycin resistance or sensitivity is critical for its clinical application. This project highlights the value of accounting for genetic variation in drug development, guiding future approaches for developing new drugs.

The Svoboda Diaries Project (SDP) is an interdisciplinary digital humanities effort dedicated to preserving and analyzing a collection of historical diaries. Written by Joseph Svoboda, a British steamship purser, these diaries span 40 years and offer firsthand insights into the daily life, healthcare practices, social networks, economic conditions, and cultural landscape of 19th century Iraq. Due to the unstructured and handwritten nature of these texts, analysis of them could benefit from computational techniques. Our research specifically addresses this challenge by extracting and analyzing references to food, medicine, symptoms, and healthcare providers, making these diaries a valuable resource for studying historical medical practices. To extract key terms from the diaries, we apply Natural Language Processing (NLP) methods,  which allow computers to interpret human language. Specifically, we use Named Entity Recognition (NER), a technique that identifies and categorizes entities or terms such as foods, medicines, illnesses, and doctors within the diaries. This type of extraction allows us to transform narrative into a format that is more amenable to analysis using automated methods. Once extracted, we visualize these relationships through network visualizations—graphical representations that illustrate connections between different entities in the text. These visualizations help us trace the circulation of medical knowledge, showing who prescribed what, which remedies were most common in the diaries, and how treatment preferences may have varied depending on provider perspectives. We aim to directly link healthcare providers with the remedies they recommended, allowing us to understand patterns of medical practice at the time. Structuring historical information into data-driven models allows us to examine cultural and economic influences on healthcare. Beyond this specific case, our research demonstrates how data science can be applied to historical texts, enabling researchers to discover patterns in historical healthcare practices across different time periods and regions.

Directly converting fibroblasts (that make up scar tissue) into skeletal or heart muscle without a pluripotent intermediate (direct skeletal muscle or cardiac reprogramming) is one of the most promising methods for regenerating lost muscle tissue, but its low efficiency in human cells remains a significant obstacle toward clinical application. In collaboration with the Institute of Protein Design, UW, we have designed several synthetic minibinders against receptor kinases which are highly specific to their cognate receptor. Utilizing these minibinders we have created a new class of designed protein, called heterofusions, that fuse two unrelated minibinders together to force the two cognate receptor kinases together in an unnatural pairing, which could elicit novel signaling responses not achievable using natural ligands. However, which heterofusions elicit novel signaling is unknown. We aim to use direct skeletal muscle and cardiac reprogramming systems, which would benefit from this novel signaling, to screen which heterofusions elicit novel signaling to increase efficiency. To do this I developed an inducible direct cardiac reprogramming system and we also used a previously established inducible direct skeletal muscle reprogramming system to be backgrounds for screening heterofusions, with efficiency determined by imaging cardiac and skeletal muscle development makers. We found a few heterofusions, including that which brings together TrkA and BMPRII (TAB2), increased the efficiency of skeletal muscle reprogramming. I found in signaling experiments using Chinese hamster ovary cells modified to express human TrkA and BMPRII that TAB2 upregulates pERK and pCREB. Interestingly, pCREB is not part of native TrkA or BMPRII signaling, meaning novel signaling is occuring. Additionally, I have shown pCREB inhibition with a small molecule impairs direct skeletal reprogramming and TAB2’s ability to increase efficiency, showing pCREB is TAB2’s mechanism of increasing efficiency. These results show heterofusions novel signaling abilities and its applications in revolutionizing regenerative therapies.

Introduction: Evidence-based treatments (EBT), such as cognitive behavioral therapy (CBT) remain underused in community mental health (CMH) settings in part due to financial, time, and geographical barriers associated with training clinicians in-person. Virtual EBT training offers a potentially cost-effective and feasible alternative; however, limited research has examined its effectiveness in improving clinicians' perceived knowledge and skills for treating youth with various mental health conditions. The current study uses benchmarking analyses to compare change in perceived knowledge and skill levels for treating youth with depression, anxiety, trauma and behavior problems among clinicians trained in-person versus those trained online. Method: Participants included 1,250 Washington State CMH clinicians (Mage=35.58 years, SD=12.12, 92% Master’s level) involved in the CBT+ initiative, a Washington statewide EBT training program. Of these clinicians, 658 attended training in-person (years 2016–2019), while 592 participated virtually (years 2020–2023). Clinicians self-reported their perceived knowledge and skill levels for treating youth with depression, anxiety, trauma, and behavior problems before training and after completing a six-month consultation period. Results: Preliminary analyses using paired samples t-tests revealed that across all disorders, perceived knowledge and skill scores significantly increased from pre-training to post consultation for in-person training clinicians (all p’s < .001, Cohen's d ranged from .93 to 1.61), as well as virtual training clinicians (all p’s < .001, Cohen's d ranged from 0.75 to 1.73). Benchmarking analyses will be conducted to compare effect sizes for changes in perceived knowledge and skill levels between clinicians trained in-person and those trained virtually. Discussion: As the need for youth mental health services continues to grow, it is vital to evaluate alternative training methods to expand access to high-quality mental healthcare.

Upon nerve injury and neurodegeneration, neuron regeneration is crucial to maintain proper function. However, this natural process happens infrequently and slowly. Neuron regeneration is known to be mediated by the activity of nerve growth factor (NGF) in neurons, which binds to two receptors: tropomyosin receptor kinase A (TrkA) and p75 neurotrophin receptor (p75NTR). Previous studies have shown that engaging the receptor p75NTR activates a signaling pathway that also triggers a pain response, thus it would be ideal to have a ligand that only activates TrkA for neuron regeneration without initiating the pain response. In collaboration with the Institute for Protein Design (IPD), this study investigated an AI-designed TrkA agonist that specifically binds to and activates only the TrkA receptor. We used fibroblasts transdifferentiated into neurons as a model to study the efficiency of this TrkA agonist. Western blotting was used to study the phosphorylation of the proteins downstream of TrkA in the signaling pathway, such as pPLCγ, pAkt, and pErk, and the activity of transient receptor potential vanilloid 1 (TRPV1), a calcium channel that indicates the sensitivity of a neuron. Immunofluorescence staining was used to examine the expression of calcitonin gene-related peptide (CGRP), a neuropeptide involved in pain perception. We found that the designed TrkA agonist generates a similar level of activation of downstream proteins as NGF while successfully preventing the expression of pain response markers. Directly injecting NGF as a treatment for neurodegenerative diseases is generally not considered viable as it often induces significant pain, therefore this TrkA agonist has the potential for therapeutic use.

Natural growth factors like fibroblast growth factor (FGF) are essential for maintaining pluripotency in induced pluripotent stem cells (iPSCs). However, current limitations of native growth factors include signal instability, off-target pathway activation, and dependence of xenogenic components for production. To address these issues, we developed a synthetic protein, C6-79C, which consists of six scaffolded subunits of a de novo designed FGFR1/2c binder, mb7. While mb7 functions as an FGF pathway inhibitor, the hexameric C6-79C acts as a receptor tyrosine kinase (RTK) agonist, providing more isoform-specific and prolonged signaling compared to native FGF. We formulated SynGrow, replacing FGF with C6-79C in minimal E8 media, and compared its performance against commercial media. Our study focused on three objectives: (1) comparing the expression of pluripotency markers (Oct4, NANOG, SOX2, and TRA1-60) in cells grown in SynGrow versus commercial media, and (2) evaluating morphology and viability under different media change regimens (daily, every other day, or no change). iPSCs grown in SynGrow exhibited superior morphology compared to those in mTeSR (commercial media). Pluripotency markers (Oct4, NANOG, and SOX2) were expressed at similar levels in both media, with SynGrow also showing higher expression of TRA1-60 across passages, confirmed by flow cytometry. Future evaluations will assess germ layer marker expression following directed differentiation. Our findings demonstrate that synthetic protein-based media formulations, like SynGrow, can effectively replace native growth factor-based media. This approach offers stable, prolonged, and xeno-free alternatives for stem cell culture, with broad implications for improving reproducibility and safety in regenerative medicine and cell-based therapies. 

Salivary glands are organs in the mouth which produce and secrete saliva, a multifunctional fluid crucial for processes including oral cavity lubrication, digestion, and antimicrobial functions. Diabetes mellitus has been associated with salivary gland dysfunction and harmful oral consequences including severe tooth decay and disrupted wound healing, yet it is not currently known what cell populations are affected in salivary glands and how this disease affects cell organization, function, and metabolic response. One model for diseases in human tissues are organoids, three-dimensional multicellular systems derived from stem cells which self-organize to mimic the structure and function of tissues in vivo when given the right cues. Dr. Devon Ehnes in the Ruohola-Baker Lab recently created a protocol to develop salivary gland organoids from induced pluripotent stem cells (iPSCs), and through additional culture in a high-glucose media along with inflammatory cytokines, this organoid has been used to study how diabetes affects salivary glands. Preliminary analysis has suggested acinar and ductal cell dysfunction and mitochondrial stress as causes of salivary gland dysfunction, but further work is necessary to understand how this diabetic environment leads to changes in cell function and mitochondrial activity. Here, I use a human iPSC-derived organoid model to assess how diabetic conditions affect the expression and localization of the acinar marker AMY1A, the ductal marker KRT19, the cell stress marker FOXO1, and the mitochondrial marker ATPB to determine the mechanisms for salivary gland dysfunction in diabetes.

Alzheimer's disease (AD) affected approximately 6.9 million Americans aged 65 and older in 2024, and it is projected to rise to 13 million by 2050 (Alzheimer’s Association, 2024). AD is characterized by progressive cognitive decline, but sleep disruption is an often overlooked symptom that emerges early in the disease's progression. Evidence suggests that AD-related sleep disturbance may originate from dysfunction in the circadian system, particularly in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN regulates sleep-wake cycles, and recent findings from de la Iglesia lab have shown that specific SCN neurons exhibit a daily rhythm of fiber expansion and retraction. This study aims to investigate how aging and AD affect SCN structural plasticity; this could help explain circadian disturbances in AD patients. I aim to identify the age at which abnormal circadian phenotypes emerge in a mouse model of AD which shows circadian disruptions. We are currently comparing activity patterns of AD mice ages 6 to 16-months old with their wild-type littermate controls using behavioral running wheel data. We hypothesize that the AD mice will exhibit a decreased mean total sleep and shorter circadian period in constant darkness. While these symptoms are common with aging in healthy mice, we expect that they will appear earlier in AD mice than in their wild-type littermates, as disrupted sleep is an early-onset symptom of AD. Future studies will assess whether these symptoms are associated with deficits in daily structural plasticity of the SCN. By elucidating the relationship between AD, SCN neuronal structure, and circadian rhythm disruptions, this research aims to provide insights into the mechanisms underlying sleep disturbances in AD patients. Understanding these processes could potentially lead to the development of targeted interventions to mitigate sleep disruptions and slow disease progression in AD patients.

Human tooth development is a complex and tightly regulated process that involves multiple signaling pathways and specialized proteins coordinating enamel formation. Enamel, the hardest tissue in the human body, is secreted by ameloblasts, which follow a distinct developmental process. Disruptions in these processes can lead to enamel-related disorders, such as amelogenesis imperfecta, a genetic condition characterized by defective enamel formation. A key factor in this disorder is WDR72, a gene that encodes the tryptophan-aspartate repeat domain 72 (WDR72) protein, which is critical for intracellular trafficking during enamel maturation. Although WDR72 has been studied in animal models, its precise localization and function in human fetal tooth buds remain incompletely understood. To address this question, I cryosectioned human fetal tooth samples at 19 and 22 gestational weeks and performed immunochemistry staining to visualize WDR72 alongside key enamel proteins. I performed cryosectioning to prepare thin tissue sections of each tooth bud sample, followed by immunohistochemical staining with antibodies specific to WDR72. I then imaged selected sections under a fluorescence microscope. Preliminary results suggest distinct WDR72 distribution in regions corresponding to secretory ameloblasts. These findings offer insights into the localization of WDR72 during tooth formation and lay the groundwork for future studies on the mechanisms of tooth regeneration. 

This project critically examines online narratives about human and more-than-human cloning, with a focus on the spread of misinformation, radicalization, conspiracies, and their dangerous impact. At first glance, discussions about human vs. more-than-human cloning differ significantly. Human cloning is commonly considered morally objectionable, with supporters often forming part of controversial communities. In contrast, more-than-human cloning frequently sparks curiosity and, in some contexts, is encouraged. It is viewed not as an "act against God" but as a testament to human intelligence and dominance. This difference in responses raises many questions: Why are responses so dissimilar? How does online discourse drive these reactions? And can these distinctions--these different understandings of personhood and "life"--reinforce or perpetuate ideologies that cause harm? To answer these questions, I examine academic explorations of cloning and compare them with ones found all across the digital sphere-from social sites such as Reddit, X (formerly known as Twitter), and 4chan, to YouTube comment sections. Using a digital, “websplorer” approach, I analyze different perspectives on cloning, ranging from the "manosphere"-- interconnected misogynist online communities, scientism, and how they relate to the more-than-human. After a critical interrogation of these perspectives, I invite the user to consider an alternative, perhaps more ethical, approach to discussing cloning, one that does not reinforce heteronormativity, human exceptionalism, or pro-eugenic views. This alternative approach includes an exploration and critique of the Western concept of “personhood” and its limitations regarding cloned life, human and more-than-human.

Mitochondrial fusion is essential for cellular function, metabolism, apoptosis, and stress responses. Mitochondrial outer membrane fusion is mediated by two mitofusin paralogs, Mfn1 andMfn2, which are large GTPases that remodel cellular membranes. Membrane fusion likely proceeds through two distinct steps, first tethering two organelles and second lipid mixing; however, much of the mechanism is poorly defined. Previous studies have solved crystal structures of a partial construct of the mitofusins, revealing a GTP dependent conformational change ; however, this is not a complete analysis as at least two states in the catalytic cycle are missing. Our project aims to quantify the conformational changes of Mfn2 throughout the entire mechanism of GTP hydrolysis. To achieve this, we are utilizing a novel transition metal Förster Resonance Energy Transfer (tmFRET) developed by Dr. Gordon and Dr. Zagotta. This system utilizes a noncanonical amino acid as the donor and a transition metal as the acceptor to measure changes as small as 3Å. Currently, we’re mutating the cystines to develop a single donor-acceptor pair, while keeping the stability and GTPase function of Mfn2. Our main approach is to introduce targeted mutations in key cysteine residues and analyze their effects on the protein’s enzymatic activity. Using molecular biology, we design DNA plasmids encoding the mutations,and express and purify the mutant proteins.  Finally we measure the GTPase activity using malachite green assays. Our current findings suggest some mutations have trivial impact on MFN2’s GTP hydrolysis, suggesting that it’s viable. The further goal of our project is to keep only one solvent accessible cysteine while maintaining protein function. This research will further elucidate the mechanism of mitochondrial fusion and its role in disease pathogenesis. Explanding the biophysical understanding of membrane remodeling.

Glioblastomas (GBMs) are highly aggressive brain tumors with poor patient prognosis, necessitating improved preclinical models to evaluate therapeutic strategies. My lab develops cerebral organoids from human pluripotent stem cells, seeded with primary patient tumors to model GBM progression and therapeutic screening. Developing biologically relevant neural organoids provides a platform for integrating patient-derived GBM samples, enabling disease modeling and treatment testing. This study aims to optimize the embedding, cryosectioning and immunofluorescence (IF) staining protocols used to screen key molecular markers and cell populations within the organoids to validate their suitability for GBM tumor engraftment. Fixed organoids, along with embryonic and adult mouse brain tissues, are embedded in OCT to preserve structure and cryosectioned (12–20 μm). IF staining is optimized by adjusting fixation time, permeabilization, blocking reagents, and antibody concentrations to improve specificity and reduce background fluorescence. Markers analyzed so far include SOX2 (neural precursors), PAX6 (radial glia), FOXG1 (forebrain), and TUJ1 (neuronal differentiation). Mouse brain cryosections from newborn (P0) and adult (P56) stages serve as positive controls to validate antibody specificity and distinguish true signals from autofluorescence or non-specific staining. Images are acquired via Olympus scanner and analyzed using OlyViA and NIH Fiji (Enhanced ImageJ). Current efforts focus on optimizing section thickness for clearer images and refining blocking conditions to minimize non-specific binding. We expect the detected fluorescent markers will mirror known cellular and tissue expression patterns, confirming that the organoids exhibit normal human fetal neurodevelopmental characteristics and are biologically relevant for GBM modeling. Future work will expand marker validation to include GFAP (astrocytes), DCX (neurogenesis marker), TBR2 (intermediate progenitors), OLIG2 (oligodendrocyte progenitors), PTPRZ1 (radial glia), IBA1 (microglia) and other cell lineage-specific markers. Establishing reliable staining and imaging conditions is a crucial step toward developing our organoid model to be suitable for exploring GBM tumor biology and potential therapeutic responses.

Stigma related to substance use disorders (SUDs) has profound and far-reaching consequences on individuals’ physical and mental health, as well as their socioeconomic well-being. This can lead to social isolation and can hinder access to treatment. While most stigma reduction interventions target structural stigma (such as educating medical students or professionals who work with individuals with SUDs), our study targets social and self-stigma experienced by individuals ages 21-35 with risky alcohol and/or cannabis use. Our objective is to develop a digital intervention to support individuals who experience substance use related stigma, enabling them to cope with stigma more effectively. Its digital nature allows for increased accessibility, convenience, and consistent support to individuals who might otherwise face barriers in accessing traditional healthcare services. We employ a user-centered design approach, utilizing peer mentoring to reduce self-stigma. Over 3 Zoom sessions, we collaborate with participants to first brainstorm topics that should be included in the intervention, receive feedback on different activities participants might engage in, and finally gather feedback on a prototype of the intervention which includes completing the System Usability Scale. My role involves collaboratively drafting the focus group scripts and facilitating sessions, including engaging participants in activities. From the focus groups, we anticipate that we will better understand important factors that influence the effectiveness of the intervention such as what features are most engaging, what format of content is most effective, and what topics are most relevant to the population. Findings from this project will allow us to design an effective digital intervention that can reach more people and provide an alternative for those who may not be willing or able to access the healthcare system. 

Alterations to sleep structure have been observed in healthy aging humans as well as those diagnosed with Alzheimer’s disease (AD). To gain further insight into how sleep is affected by age and neurodegenerative diseases we will analyze sleep in healthy aged rats and in a transgenic rat model of AD. We collected neural data from the hippocampus of aged  (30-32 months old) and adult rats (4-9 months old) during 30-60 minute sleep sessions before and after the performance of a spatial navigation task. We have collected similar sleep data from transgenic F344AD rats (12 months old; a model of AD) and their wildtype littermates. First, we will combine movement tracking and measures of hippocampal local field potential (LFP) activity in the hippocampus to distinguish periods of awake activity, quiet wakefulness, slow-wave sleep, and REM sleep. Specifically, we will use an established measure, the theta-delta ratio, to distinguish slow-wave sleep from REM sleep. Using this approach, we will characterize the sleep structure of the young and old rats and the AD/control rats to determine if there are any differences in, for example, the amount of time spent in a particular sleep stage or the average length of each stage. In addition, we will investigate whether there are any differences in sleep patterns between shorter (30-60 minute) sleep sessions and longer (4 hour) sleep sessions. These analyses will determine whether our rat models of aging and AD recapitulate the sleep changes seen in aged humans with and without AD.

Protein Kinase Inhibitors (PKIs) are a family of heat stable, high-affinity inhibitors of the catalytic subunit of Protein Kinase A (PKAc). In the presence of Mg-ATP, the three isoforms—PKIα, PKIβ, and PKIγ—bind to PKAc with very low dissociation constants: 0.758nm, 1.875nm, and 0.4142nm respectively. In vitro studies have shown that PKIs can translocate PKAc from the nucleus to the cytoplasm, suggesting a role for PKIs in terminating nuclear cAMP-driven PKA activity. Previous research, including studies from our lab, has found that dysregulated PKAc mutants play a significant role in Cushing’s syndrome, a rare and potentially fatal metabolic disorder caused by excessive cortisol production. Building on these findings, we hypothesized that increasing PKI expression could counteract the hyperactivity of PKAc mutants and reduce cortisol production. To test this, we expressed each PKI isoform in adrenal cell lines and assessed their steroidogenic capacity using biochemical assays such as western blots, RNA-seq, qPCR, and ELISA-based cortisol assays. We observed that PKIα and PKIγ led to a general suppression of steroidogenic associated proteins such as StAR, Cyp11a1 and SF1. This altered proteome was accompanied by significantly suppressed cortisol synthesis only in the PKIα and PKIγ expressing cells. The difference between PKIα/γ and PKIβ was surprising given that all PKI isoforms are postulated to potently inhibit PKAc. Thus, we questioned whether PKIα/γ effects are mediated through PKAc. To answer this, we have cloned mutant PKI isoforms that do not bind PKAc, and confirmed the mutant PKIs do not inhibit PKAc through kinase assays. Our next step is to express the mutant PKI isoforms in adrenal cells and assess their effect on steroidogenic capacity of the cells. Our findings suggest that PKIα and PKIγ play key roles in cortisol regulation and may have broader implications for gene regulation in adrenal cells.

Under acute genotoxic stress, such as chemoradiation, stem cells can undergo cell cycle arrest at the G1/S phase to avoid apoptosis. This protective state, called quiescence, is reversible once stress-free conditions allow re-entry into the cell cycle to regenerate daughter cells. We have previously demonstrated a common mechanism by which two types of stem cells—Drosophila germline stem cells (GSCs) and human-induced pluripotent stem cells (hiPSCs)—enter quiescence. Recently, we found Cyclin E (CycE) associated with the outer mitochondrial membrane (OMM) in both GSCs and hiPSCs. We are interested in studying the interaction between CycE mitochondrial localization domains and mitochondrial proteins responsible for CycE localization.To map the CycE mitochondrial localization domain, I have generated four CycE truncations tagged with GFP: ΔN-terminus, ΔCyclin Box_N terminus, ΔCyclin Box_C terminus, and ΔC-terminus. I have tested these constructs in various cell lines, including Rcc4, HCT116, MCF10A, HEK, and HeLa, and found that HCT116 exhibits mitochondrial localization of CycE. I will compare the localization of wild-type CycE-GFP versus mutant CycE using immunofluorescent staining of CycE and mitochondria in HCT116, as this cell line is well-suited for transfection studies. We have shown that mitochondrial CycE is degraded in quiescent stem cells through PINK1/PARKIN-mediated mitophagy. We propose that CycE degradation is necessary for quiescence entry. In Drosophila GSCs, we observe that upon irradiation, cells overexpressing non-degradable CycE continue cell division, whereas control cells undergo quiescence. Understanding the mechanism by which Cyclin E localizes to the OMM will enhance our knowledge of how it prevents quiescence entry, thereby contributing to the development of anti-cancer treatments.

Developing solutions to address social risk factors (SRF) in low- and middle- income countries (LMIC) can be difficult as many SRFs are a result of lacking financial support. SRFs are adverse living conditions that may impact the physical or mental well-being of an individual or community. Addressing SRFs in LMICs can increase implementation of evidence-based practices aimed at improving mental health outcomes. In this study, we focused on who is involved in proposed solutions that address SRFs and what specific roles those individuals undertake. Understanding what persons and roles are involved in a solution can help organize and facilitate action. We conducted a secondary inductive thematic analysis on qualitative data from a parent NIMH-funded study which aimed to develop strategies to address SRFs alongside a culturally adapted form of trauma-focused cognitive behavioral therapy (TF-CBT) for children who experienced parental death in Western Kenya. In the parent study, clinical supervisors conducted a workshop and training for TF-CBT lay-counselors to co-develop strategies to address SRFs. Most suggested strategies supported economic empowerment and a worksheet was designed to aid implementation of the strategies. This study uses data from worksheets filled out at 10 different schools in which lay-counselors designed economic empowerment strategies. The primary solutions included poultry rearing, vegetable gardening, and tree nurseries. Preliminary results show that most solutions tend to require school administration, teachers, children, for whom the solutions are for, and their guardians. Administrative roles tended to supply land required for solutions, teachers and guardians mostly supplied resources, while children were tasked with implementation of the solutions. Knowing who executes what roles can help inform what resources, skills, or knowledge a person can contribute to a solution, which may facilitate transferability between solutions. This can help researchers and communities individualize strategies to address SRFs where certain persons may be unavailable.

The NF-KB family of transcription factors regulates genes involved in immunity, inflammation, and other biological processes. Members of the NF-KB family can form homo- or heterodimers, which contribute to specific responses to various stimuli. The p50/c Rel heterodimer, an important player in adaptive immunity, regulates gene expression, but its DNA-binding specificity and regulatory mechanisms remain incompletely understood. This study investigates the expression and purification of recombinant p50/c Rel heterodimers. I expressed recombinant c Rel and p50 in Escherichia coli and purified the proteins using Ni²⁺ affinity chromatography. SDS-PAGE analysis confirmed the successful isolation of both proteins at the expected molecular weights. This work lays the foundation for further biochemical characterization, including the investigation of their DNA-binding properties and role in immune signaling. These findings contribute to the understanding of the p50/c Rel heterodimer's function in NF-KB mediated gene regulation. Future studies are needed to explore its DNA-binding specificity and how these interactions impact immune responses and diseases such as cancer and inflammatory disorders. 

Extracellular vesicles (EVs) play a crucial role in cell communication and may provide insights into improving care and outcomes for patients with pulmonary diseases. EVs have been studied as potential disease biomarkers to improve diagnosis of lung diseases. This study investigates medium (150-500 nm) and large (500-1000 nm) EVs in patients with Idiopathic Pulmonary Fibrosis (IPF) and Cystic Fibrosis (CF) to determine antibody presence and variation between these two patient groups and between larger sized extracellular vesicles. The characterization of macrophage populations, macrophage subsets, and T Cell phenotypes in IPF and CF patients is done through the analysis of immunophenotypic markers. The experimental findings contribute to understanding immune cell dynamics in IPF and CF patients, potentially informing targeted therapeutic strategies. 

The p50/RelA dimer is an essential part of the NF-ĸB signaling pathway, which is responsible for regulating inflammation and immune responses. Most prior biochemical research focused on the mouse version of the p50/RelA dimer. While the findings are useful, its implication to human health remains unclear. This raises the question, how effective do experiments involving mouse proteins reflect those involving humans? We used protocols to express and purify human and mouse p50/RelA dimers, aiming to generate proteins for structural and functional analysis. In the first stage, recombinant protein expression and affinity chromatography techniques were used for purification of both proteins, followed by an SDS-PAGE to assess molecular weight and stability. We found that mouse proteins showed higher intensity bands compared to human proteins, indicating a higher yield. This suggests stability factors as well as potential differences in degradation rates between species. In the second stage, ion exchange and size exclusion chromatography were used to further purify the proteins. During ion exchange chromatography, neither protein bounded as effectively as expected, highlighting the need for protocol optimization. Improving the chromatography conditions will help increase stability and yield of both proteins allowing for more accurate comparisons between the mouse and human p50/RelA dimers. These optimizations are important because it will improve our ability to compare NF-ĸB pathway functionality between species and ultimately make it easier to translate findings from mouse models to human health.