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.

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.

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.

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.

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.

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.

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.

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. 

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.

Alzheimer's disease (AD) is the most common form of dementia. Improper cleavage of amyloid precursor protein by a complex containing presenilin 1 or presenilin 2 (PSEN2) can result in pathological amyloid beta plaques. Recent work from the Valdmanis group found novel PSEN2 RNA isoform variants in AD. Specifically, we identified two PSEN2 3'UTR isoforms - a short (507bp) and a long (3976bp) 3'UTR. The 3'UTR harbors essential regulatory elements such as microRNA binding sites and Alu elements that control transcript maturation, stability, and abundance. Here, we sought to elucidate the functional significance of the PSEN2 3'UTR isoforms. To accomplish this, we completed small RNA sequencing to identify microRNA levels in human AD and control frontal cortex brains and used TargetScan7 to map these reads to the PSEN2 3'UTR isoforms. Our analysis identified 53 miRNAs with significant differential regulation in AD frontal cortex bulk homogenate and 76 miRNAs in purified synaptosomes. One miRNA, miR-34c, was significantly downregulated in both fractions. We identified five different miRNAs with significant regulation changes in AD, including miR-326, miR-346, miR-548p, miR-890, and miR-217. Of note, the long PSEN2 3'UTR had nine miRNA binding sites and two Alu elements, while the short PSEN2 3'UTR only contained one miRNA binding site. We next tested PSEN2 3'UTR isoform localization in human AD and control frontal cortex brain tissue using BaseScope in-situ hybridization. We found a marked decrease in PSEN2 expression in AD samples. To develop in vitro PSEN2 3'UTR isoform models, we designed constructs containing the PSEN2 3'UTR isoforms to overexpress in either HMC3 human microglial or SH-SY5Y human neuroblastoma cell lines. In vitro validation results indicated increased long PSEN2 3'UTR isoform abundance to the short isoform. Determining the functional relevance of the short and long 3'UTR of the PSEN2 transcript will further our understanding of AD pathology.

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.

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.

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.

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.

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.

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.