Dr. Curtis L. Parker Student Research Symposium_Poster Abstracts

POSTER ABSTRACTS

P-01 Title: Calcitriol Regulation of Interleukin 7 Receptor Expression in Non-malignant and Malignant Prostate Cell Lines

Authors: Blake Allen 1 , Chidinma Oguejiofor 2, Amani Gaddy 1, Rachel N. Martini, Ph.D.3, Leanne Woods-Burnham, Ph.D.4, Melissa B. Davis, Ph.D.3, Sean K. Kimbro, Ph.D.3, Rick A. Kittles, Ph.D.5, and Jabril R. Johnson, Ph.D.3

Mentor: Jabril R. Johnson, Ph. D., Morehouse School of Medicine

Background/Significance: Vitamin D3 metabolite (e.g., calcitriol) is a steroid hormone essential for optimal cell function and eliciting anti-tumorigenic effects in normal and malignant prostate cells. Serum vitamin D3 deficiency has been associated with increased prostate cancer (PCa) aggression in African American (AA) men. The incidence and mortality rate of PCa is higher in AA men in the U.S. than in their European American (EA) counterparts. Recent studies have reported differences between AA and EA prostate tumor microenvironments (TME) related to immune and inflammatory signals, which might contribute to the increased aggression in AA men. Interleukins, pro-inflammatory cytokines, are important regulators of inflammation in the TME and influence immune pathways underpinning prostate carcinogenesis. However, vitamin D regulation of immune and inflammation signaling is poorly understood. We hypothesize vitamin D regulates inflammatory signatures by suppressing innate immune cascades that underpin prostate carcinogenesis. This study aims to elucidate calcitriol-mediated suppression of immune and inflammatory genes impacting pathways underlying prostate carcinogenesis, thus identifying potential drug targets to mitigate disparate outcomes for AA men with PCa.

Methods: Whole-transcriptome analysis with RNA sequencing was performed on AA prostate cell line, RC-77N/E. We compared untreated RC-77N/E cells with cells treated with calcitriol. We designed a differential expressed gene (DEG) selection algorithm that filtered DEGs by FDR padj < 0.05, |Log2Fold Change|> 1, and pathway enrichment analysis focusing on immune/inflammatory pathways. RT-qPCR was used for validation on the RC-77N/E.

Results: Our DEG selection algorithm identified IL7R (Interleukin 7 Receptor) to be significantly suppressed via calcitriol treatment in RC-77N/E (FDR p adj < 0.05). Ingenuity Pathway gene-gene interaction revealed significant suppression of IL7R, which led to the predicted repression of leukocyte cell movement (p < 0.05; z score > 2). Gene network analysis revealed that calcitriol-mediated suppression of IL7R indirectly regulates the formation of malignant genitourinary solid tumors (p < 0.05). Preliminary findings from bioinformatic analysis suggest differences in IL7R expression between AA and EA men.

Conclusion and Implications: Our data revealed calcitriol’s potential regulation of IL7R expression and signaling, which is essential in innate immune signaling (e.g., leukocyte cell movement) in the TME. This study revealed the potential use of calcitriol regulation of IL7R expression and signaling involved in tumorigenesis for AA and EA PCa.

Acknowledgement of Funding: This research was supported by the NIH/NCI U54CA118638 HDREP pilot funding. In addition, the MSM Summer Research and Public Health Experience.

P-02 Title: Chemokine Ligand Promiscuity and Its Role in Lung Cancer Disparities

Authors: Briana A. Brock1,2,3; Murugesh Eswaran2,3, Hina Mir2,3, and Shailesh Singh2,3

1 Morehouse School of Medicine Ph.D. in Biomedical Sciences Program

2 Department of Microbiology, Biochemistry, and Immunology, Morehouse School of Medicine

3 Cancer Health Equity Institute, Morehouse School of Medicine

Mentor: Shailesh Singh, Ph.D.

Background/Significance: Lung cancer (LuCa) is the leading cause of cancer-related deaths in the U.S., with a five-year survival rate of 28%. African Americans (AAs) experience higher incidence and lower survival than European Americans (EAs), suggesting racial differences in molecular footprint contribute to disparities. Chemokine signaling, particularly via CCR5 and its ligand CCL5, is linked to tumor progression and are differently expressed in AAs compared to EAs. Which provided rational to hypothesize that differential CCR5/CCL5 signaling contributes to LuCa disparity.

Methods: Transcriptomic profiling was performed on AA- and EA-derived lung cancer cell lines. RNA sequencing (~50M reads/strand, 300 bp paired-end, Illumina) was analyzed using HISAT2 and Salmon. DESeq2 identified differential gene expression. Functional relevance of CCR5 was assessed via migration and proliferation assays (trans-well, MTT, BrdU), with or without CCR5 activation. Statistical comparisons used t-tests and Kruskal-Wallis analysis in GraphPad Prism.

Results: Expression of CCR3, CCR5, GPR75, and other cancer-related genes varied between AA and EA cell lines. Unexpectedly, CCR3 showed higher baseline expression than CCR5. Upon CCL5 stimulation, AA-derived cells exhibited distinct migratory patterns compared to EA. Maraviroc (MVC) significantly reduced proliferation (p < 0.0001) across all lines. Reintroduction of CCL5 restored proliferation, indicating CCL5 may engage multiple receptors to sustain tumor growth and motility.

Conclusions and Implications: Chemokine signaling in LuCa is complex, with ligand promiscuity and receptor redundancy supporting proliferation and migration. Differences in CCR3, CCR5, and GPR75 expression and migratory behavior between AA and EA cells suggest receptor usage may influence disparities in outcomes. Molecular interventions to modify CCL5related receptor expression or block their signaling, may reduce aggressive migratory behavior and reshape the tumor microenvironment, potentially improving treatment outcomes across racial groups.

Acknowledgment of Funding: This research was supported by 1R01CA256724-01 and partially by T32GM152760, 5U54CA118638-19, and 5U54MD007602-37.

P-03 Title: Disparities in Cervical Cancer Screening Among Adult Women in the United States: Insights from the 2021 Behavioral Risk Factor Surveillance System

Authors: Victoria E. Brown1; Naomi Campbell, MPH1; Anny Rodriguez, PhD, MPH1; Gemechu B. Gerbi, PhD, MSc1

1 Morehouse School of Medicine Master of Public Health Program

Mentor: Gemechu B.

Gerbi, PhD, MSc, Morehouse School of Medicine

Background/Significance: Cervical cancer is the second leading cause of death for women ages 2039 in the United States (US). We hypothesize that there are key socio-demographic factors may have negative implications regarding the utilization of cervical cancer screening services. Therefore, the objective of this study was to use the 2021 Behavioral Risk Factor Surveillance System (BRFSS) data to identify those factors among women aged ≥ 18 years in the US, with a purpose of reducing the prevalence of cervical cancer.

Methods: This study examined the research question: What factors are associated with cervical cancer screening among adult women in the US? The data were obtained from the 2021 BRFSS (N=6,459 women). Bivariate and multivariable logistic regression analyses, conducted using SAS version 9.4, were performed to assess factors associated with self-reported cervical cancer screening such as age, race, income, education, and health insurance status.

Results: In 2021, 42% of women who responded to the survey reported not being screened for cervical cancer. After adjusting for socio-demographic variables, several factors were associated with significantly higher odds of not reporting cervical cancer screening. These factors included being Black (AOR = 0.64 ; 95% CI, 0.56-0.72), Hispanic (AOR = 0.64 ; 95% CI, 0.52-0.78) or Asian (AOR = 0.26 ; 95% CI, 0.17-0.38); 18 to 24 (AOR = 0.16 ; 95% CI, 0.11-0.22), 25 to 34 (AOR = 0.46 ; 95% CI, 0.370.57), 65 or older (AOR = 0.54 ; 95% CI, 0.45-0.63); women with an education level of 8th grade (AOR = 0.31 ; 95% CI, 0.19-0.49), some high school (AOR = 0.45 ; 95% CI, 0.34-0.58), high school diploma or GED (AOR = 0.52 ; 95% CI, 0.45-0.60), some college (AOR = 0.77; 95% CI, 0.86-0.89); a household income of less than $24,999 (AOR = 0.56 ; 95% CI, 0.44-0.72), $25,000 to $49,999 (AOR = 0.54 ; 95% CI, 0.43-0.68), $50,000 to $74,999 (AOR = 0.77 ; 95% CI, 0.61-0.98); without insurance (AOR = 0.78 ; 95% CI, 0.62-0.98) were less likely to screen for cervical cancer.

Conclusion/Implications: Socio-demographic factors, inclusive of age, race, household income, education level, and health insurance status were predictor of self-reported lack of cervical cancer screening. These findings underscore the need to explore and address barriers in these groups to improve equitable access to cervical cancer screening. The self-reported data and administration of the survey by telephone increases the likelihood of recall bias and limits accessibility, reducing the overall generalizability of the data collected.

Acknowledgment of Funding: This research was supported by the Summer Cancer Research Education Program in collaboration with Morehouse School of Medicine, Tuskegee University, and the University of Alabama at Birmingham

P-04

Authors: Jamirah Chevrin, M.P.H. 1,2; Rachel Martini, Ph.D.1,2; Stefan Ambs Ph.D., MPH3, Alexandra R. Harris, Ph.D., M.P.H., M.S.3, Melissa Davis, Ph.D.1,2

1Institute of Translational Genomic Medicine, Morehouse School of Medicine

2Department of Microbiology, Biochemistry, and Immunology, Morehouse School of Medicine

3National Cancer Institute, Bethesda, MD

Mentor: Melissa Davis, Ph.D., Morehouse School of Medicine

Background/Significance: Chronic psychosocial stress contributes to cancer progression by altering immune function through neuroendocrine and inflammatory pathways. African American populations, disproportionately affected by systemic stressors such as racism and socioeconomic disadvantage, exhibit elevated inflammatory profiles and cancer disparities. Additionally, the Duffy Antigen Receptor for Chemokines (DARC/ACKR1) plays a key role in immune regulation through sequestration of proinflammatory chemokines. However, individuals with Duffy-null status, common among those of African descent, lack this regulatory mechanism on red blood cells, influencing circulating inflammatory profiles. The joint influence of psychosocial stress and Duffy-null status on immune response and cancer outcomes remains unclear.

Methods: We analyzed data from 121 women enrolled in the NCI Maryland Breast Cancer Stress Study (2012–2023). Participants completed the Cohen 10-item Perceived Stress Scale (PSS-10), and serum cytokines and chemokines (n= 92) were quantified using the Olink Proteomics Inflammation Panel. Duffynull genotype (rs2814778, CC) was determined by single-plex genotyping. Group differences were assessed by t-tests, and multivariable linear regression models adjusted for age, BMI, ER status, and race evaluated associations between genotype, stress, and inflammatory profiles.

Results: Duffy-null (CC) carriers exhibited distinct inflammatory signatures compared to non-null (TC/TT) genotypes. CC individuals showed significantly higher levels of CXCL1, CXCL5, and CXCL11 and lower levels of CXCL12 and CCL23 (all p < 0.05). Cytokine analyses revealed reduced IL-8 and IL-2 in CC versus TT carriers. Stratified analyses demonstrated that African American participants had higher CXCL5, CXCL1, and CXCL11 but lower IL-8, IL-18, IL-12, and IL-13 compared to European Americans. Stress stratification revealed that stress exposure in CC carriers may impact alterations in select chemokines (e.g., CCL4, CCL20, CCL3) and cytokines (e.g., IL-6, IL-8).

Conclusions and Implications: Our findings highlight a potential mechanism linking genetic ancestry, chronic stress, and immune dysregulation in breast cancer. The Duffy-null genotype may amplify the proinflammatory effects of psychosocial stress, contributing to racially patterned differences in immune profiles and tumor microenvironmental signaling. These results underscore the need for ancestryinformed, biopsychosocial frameworks in cancer disparities research and suggest that chemokine signatures could serve as biomarkers of stress-induced immune vulnerability in Duffy-null populations.

Funding Acknowledgement: This research was supported in part by the National Cancer Institute Summer Internship Program. This research was supported in part by the Polyethnic 1000, Breast Cancer Research Foundation, and the NIH (R01-CA259396).

P-05

Title: Isolation and Comparative Characterization of Exosomes from Cancerous and Noncancerous Breast Epithelial Cell Lines

Authors: Bethany Daniels1, Kevin Dickerson1, Nori Henley1, Audrey Quenneh1, Xavier Street2

1. Morehouse School of Medicine Master of Biomedical Research

2. Morehouse of School of Medicine Doctor of Philosophy in Biomedical Sciences

Mentors: Vincent C. Bond, Ph.D. and Ming Bo Huang, M.D., Morehouse School of Medicine

Background/Significance: Exosomes are small extracellular vesicles (30–150 nm) that mediate intercellular communication by transporting proteins, RNAs, and lipids. In breast cancer, tumorderived exosomes influence the tumor microenvironment by promoting angiogenesis, immune evasion, and metastasis. Cancer cells release more exosomes than normal cells, carrying oncogenic factors that support tumor growth and transfer malignant traits. Exosomal microRNAs (miRNAs) play critical roles in cell proliferation, migration, and epithelial-mesenchymal transition (EMT). Characterizing exosomes from normal and cancerous breast epithelial cells is essential for understanding their roles in tumorigenesis and resistance. Identifying exosomal biomarkers may enable non-invasive cancer diagnostics and inform therapeutic strategies. We hypothesize that cancerous breast epithelial cells secrete more exosomes than noncancerous cells. This study aims to isolate and compare exosome abundance between these cell types.

Methods: We analyzed two breast epithelial cell lines: MDA-MB-231 (triple-negative breast cancer) and MCF-10A (non-tumorigenic control). Cells were cultured to 70–80% confluence, and supernatants were collected. Cells were detached, pelleted, and counted. Exosomes were isolated from culture media via differential centrifugation and characterized using nanoparticle tracking analysis (NTA) to assess size, concentration, and fluorescence.

Results: The findings imply that the cancerous and non-cancerous lines differ in the particle concentration per cell. In line with their highly invasive phenotype, the aggressive triple-negative MDA-MB-231 cells produced the highest number of exosomes. This supports the idea that more cancerous cells rely on extracellular vesicle signaling to maintain their ability to proliferate and spread. MCF-10A cells, on the other hand, produced fewer vesicles, which may be indicative of their role in maintaining regular physiological signaling.

Conclusions and Implications: The experiment's findings show that exosome production is substantially higher in breast cancer cells than in noncancerous breast epithelial cells. The aggressive MDA-MB-231 cell line producing the most exosomes. These results imply that exosome secretion is associated with cancer and may contribute to the spread and communication of cancer cells. Although more research is required to fully understand the molecular cargo and functional effects of these vesicles, our findings demonstrate the potential of exosome profiling as a therapeutic target and diagnostic tool in the study of breast cancer.

Acknowledgment of Funding: This research was supported by Institutional Development Grant 885016. NIH NIMHD/U54/MD007602-38/PI: Dr. Sean Kimbro. MSM Cancer Health Equity Institute/Director: Dr. Brian Rivers. The American Cancer Society Diversity in Cancer Research. ACS Grant DICRIDG-21-072-01-DICRIDG/PI: Dr. Ming Bo Huang.

P-06

Title: Proteomic Signatures Reveal New Genetic and Biological Pathways Altered by Anti-HER2 Therapy in Prostate Cancer Cell Lines

Authors: Jazlyn Farlough, M.B.E.1; Nicole Mavingire, Ph.D.1; Janelle Moore1; Joy Solomon2 , Moyinoluwa Adeniyi2 , Odunayo Oluokun2 , Jabril R. Johnson, Ph.D.3; Mya Walker4; Clayton C. Yates, Ph.D.5; Rick A. Kittles, Ph.D.6; Firas Kobeissy, Ph.D.7; Yehia Mechref, Ph.D.2; Leanne Woods-Burnham, Ph.D.1

1Morehouse School of Medicine, Department of Surgery

2Texas Tech University

3Morehouse School of Medicine, Department of Microbiology, Biochemistry & Immunology

4City of Hope

5Johns Hopkins University

6Morehouse School of Medicine, Department of Community Health & Preventive Medicine

7Morehouse School of Medicine, Department of Neurobiology

Mentor: Leanne Woods-Burnham, Ph.D., Morehouse School of Medicine

Background/Significance: Human epidermal growth factor receptor 2 (HER2) overexpression in prostate cancer (PC) correlates with worse prognosis. Elevated HER2 activity drives tumor growth, therapy resistance, and metastatic potential by amplifying oncogenic signaling pathways and increasing cancer cell survival. We hypothesize that anti-HER2 treatment in PC cell lines alters the genetic expression of MYC and TP63, transcription factors. This study aims to validate MYC and TP63 expression in a Black, AR+ cell line (RC-77T/E) versus a White, AR- cell line (PC3), following anti-HER2 treatment, uncovering possible untargeted biomarkers and pathways, especially in Black men.

Methods: PC cell lines, RC-77T/E and PC3, were treated with 20 nM trastuzumab to target HER2 or vehicle control for 72 hrs. Multi-omic analyses, using liquid chromatography-tandem mass spectrometry and liquid chromatography with parallel reaction monitoring mass spectrometry, were used. To identify protein and metabolite associations and assess the enrichment of diseaserelated and functional pathways within the dataset, biological pathway and network analysis was performed using Qiagen’s Ingenuity Pathway Analysis software. Top gene hits MYC and TP63 were validated with qPCR.

Results: HER2/ERBB2 was detected in PC cells by qPCR, basally and in response to trastuzumab treatment. HER2 targeting with trastuzumab resulted in differential pathway and network expression in PC cells from a Black compared to a white man treated with anti-HER2 drug. RC-77T/E revealed multiple enriched pathways, associated with growth factor signaling and cell cycle regulation. PC3 exhibited lower viability response to trastuzumab, reflecting IPA results. Enriched pathways included lipid metabolism, hypoxia-inducible factor (HIF) signaling, and protein ubiquitination. Additionally, qPCR validation confirmed MYC and TP63 as significantly modulated genes in response to HER2 targeting in PC cells.

Conclusion/Implications: Leveraging HER2+ features in Black men enables novel therapy, potentially cutting metastasis and lowering death rates in high-risk PC patients. Utilizing multiomic paradigms, paired with qPCR, we identified possible PC untargeted approaches and candidate biomarkers that may be assessed in future pre-clinical and clinical investigations of HER2-targeted therapy in PC.

Funding Acknowledgement: NIH (KL2TR002381), NIH (UL1TR002378), PCF (20YOUN04), DoD Prostate Cancer Research Program (W81XWH2110038), NIH (TL1TR002382), NIH/NCI (U54CA118638), and NIH/NIMHD (2U54MD007602)

P-07 Title: Uncovering

Drug-Associated Skin Cancer Patterns Through Machine Learning

Authors: Gajelli, Tarini 1; Eswaran, Murugesh 1,2; Brock, Briana1,2; Mir, Hina1,2; Singh, Shailesh1,2

1 Cancer Health Equity Institute, Morehouse School of Medicine.

2 Department of Microbiology, Biochemistry, and Immunology, Morehouse School of Medicine.

Background/significance: Skin cancer is one of the most common and most treatable cancers in the United States. According to the Georgetown Health Policy Institute, approximately 66% of adults in the US rely on prescription medications, with many of them being senior citizens. Longterm use of these medications, especially those with photosensitizing or vasoactive effects, may be associated with an increased risk of skin cancer. Understanding how these medications, particularly in combination, may contribute to skin cancer risk is vital to reducing the incidence of this disease.

Methods: All of Us Database v8 was used to establish the association of frequently prescribed drugs with skin cancer risk. We examined combinations of up to 6 drugs to assess cumulative cancer risk, calculating cancer rates, photosensitivity ratios, and composite scores from aggregate data. Molecular docking and molecular dynamics simulations identified stable, highaffinity interactions between high-risk drugs and UV-response proteins (COX-2, TP53, MC1R, AHR). Random Forest and Gradient Boosting machine learning (ML) models were trained on derived features, optimized via grid search and 5-fold cross-validation, and evaluated using Area Under Curve (AUC), accuracy, and F1-score. SHapley Additive exPlanations (SHAP) analysis is used to interpret model outputs

Results: Among individuals who reported using these medications, patients with skin cancer were higher users of Hydrochlorothiazide (9.7%) and Prednisone (8.4%). While Acetaminophen (7.1%) is widely used, the relative risk of developing skin cancer is relatively lower. Corticosteroids [Fluticasone (8.6%)] and Proton Pump Inhibitors (PPIs) [Omeprazole (9.6%); Pantoprazole (8.0%)] were significantly associated with skin cancer. ML models achieved an AUC of 0.89, identifying photosensitivity rate, drug class, and vasodilator status as key predictors. SHAP analysis identified the combination of prednisone, omeprazole, atorvastatin, and hydrochlorothiazide as posing the highest predicted skin cancer risk.

Conclusion: Drug combinations, including corticosteroids, PPIs, and cardiovascular agents, may elevate skin cancer risk, mainly due to combined photosensitizing and vasodilatory effects. ML has identified synergistic interactions, finding the importance of monitoring cumulative drug exposure. These findings advocate enhanced dermatological screening and personalized medication planning for long-term users. This approach provides clinicians with a crucial personalized risk assessment tool, enabling proactive patient counseling and tailored prevention strategies, ultimately reducing the risk of skin cancer.

Acknowledgement of Funding: The project described was supported by the MSM/TU/UAB Comprehensive Cancer Center Partnership Grant U54 CA118638 and 5R01CA256724-03 from NCI. The content is solely the authors' responsibility and does not necessarily represent the official views of the National Cancer Institute or the National Institutes of Health.

P-08 Title: Pancreatic Adenocarcinoma: Examining the Intersection of Cancer, Diabetes, and Health Equity in Marginalized Communities

Authors: Gerald, Janae; Isac, John, MD, MS; Dawson, Justyn Spelman College; Morehouse School of Medicine

Background: Pancreatic ductal adenocarcinoma, PDAC, represents approximately 90 percent of pancreatic cancer cases and remains one of the deadliest malignancies, with a five-year survival rate of 13.3 percent. Late diagnosis drives poor outcomes. New onset diabetes in adults over 50 has emerged as an early clinical indicator of PDAC. PDAC and diabetes both disproportionately affect African American individuals and people living in low income or rural communities. Structural barriers such as underinsured, delayed referrals, limited specialty access, and provider bias contribute to these disparities.

Objectives: The study examined how diabetes and social determinants of health influence PDAC diagnosis, treatment access, and survival in marginalized communities. The hypothesis was that delayed recognition of new onset diabetes and systemic care inequities lead to later stage diagnosis and lower treatment rates among Black and underserved populations.

Methods: A structured literature review was conducted using peer reviewed journals, national cancer surveillance data, and public health reports. Data sources included the Surveillance, Epidemiology, and End Results Program (SEER). Center for Disease Control and Prevention (CDC) publications, and reports from the Pancreatic Cancer Action Network (PCAN), and the American Diabetes Association. The review evaluated biological links between diabetes and PDAC, racial and socioeconomic disparities in screening and treatment, and public health interventions focused on equity and early detection.

Results: Evidence showed that Black patients experience later stage DPAC diagnosis and are approximately 25% less likely to receive surgical treatment compared to white patients, contributing to lower survival rates. New onset diabetes frequently precedes PDAC diagnosis, yet clinical recognition remains inconsistent. National initiatives such as the National Comprehensive Cancer Control Program and the REACH program have expanded education and screening efforts. Emerging tools such as continuous glucose monitoring, AI based diagnostics, and telemedicine show potential for early detection, though access gaps persist in marginalized communities.

Conclusion: This review highlights the need for targeted screening strategies for older adults with new onset diabetes and stronger integration of equity focused care models. Improving provider awareness, expanding culturally responsive care, and increasing minority representation in clinical research are critical steps towards reducing diagnostic delays. This work reinforced the importance of health equity driven research in addressing cancer disparities and informs future efforts to improve outcomes for underserved populations through earlier detection.

Acknowledgements: The research was supported by the Undergraduate Cancer Health Equity Research and Training Program (UCHERTP) at Morehouse School of Medicine, whose resources and structured mentorship provided guidance in exploring the intersection of diabetes mellitus, pancreatic cancer, and innovative access to care.

P-09 Title: Isolation and Identification of Exosomes from Multiple Breast Cancer Cell lines.

Authors: Brianna Graham, Ki’Vanna Craft, Darrell Braithwaite, Megara Shepperson

Mentors:

Vincent C. Bond, Ph.D., and Huang, Ming Bo M.S., Morehouse School of Medicine

Morehouse School of Medicine

Background/Significance: Exosomes are minute, nanoscale membranous bodies that facilitate cell-to-cell communication by transporting proteins, nucleic acids, and lipids, playing key roles in cellular signaling, organ homeostasis, and disease processes. Originating from endosomes, exosomes derived from tumor cells carry oncogenic molecules that promote cancer progression, metastasis, immune evasion, and therapy resistance. In breast cancer, these vesicles can transform normal epithelial cells, stimulate tumor invasion, and modulate the tumor microenvironment. Several exosome proteins and nucleic acids have been identified as potential biomarkers and therapeutic targets for breast cancer. Based on these findings, we hypothesized that exosomes isolated from different breast cancer cell lines exhibit distinct molecular profiles and concentrations compared to non-tumorigenic breast cells, reflecting their role in disease progression and their potential as biomarkers.

Methods/ Materials: Human breast epithelial cell lines MDA-MB-231, MCF-7 (cancerous), and MCF-10A (non-tumorigenic) were cultured in RPMI 1640 media and maintained under standard conditions until reaching optimal confluency. Exosomes were isolated from conditioned media sequentially using differential centrifugation and ultracentrifugation. The resulting exosome pellets were resuspended in PBS and stored at 4°C. Exosome size and concentration were measured with nanoparticle tracking analysis using the Nano Sight LM10 instrument, providing quantitative and qualitative analysis of the exosomes produced by each cell line.

Results: Across all three breast cell lines MDA-MB-231, MCF-7, and MCF-10A total protein concentrations were similar, ranging from 41 to 44 mg/mL, with minimal differences between cancerous (MDA-MB-231, MCF-7) and non-cancerous (MCF-10A) lines. However, exosome particle concentrations were markedly higher in the cancerous cell lines: MDA-MB-231 exhibited the highest concentration (329.34 mg/mL), followed by MCF-7 (219.04 mg/mL), while the noncancerous MCF-10A had much lower levels (107.91 mg/mL). This indicates that breast cancer cell lines secrete significantly more exosome particles than non-tumorigenic breast cells, despite similar overall protein production, suggesting an association between malignancy and increased exosome output.

Conclusion/Implications: The marked increase in particle concentration in the cancerous cell lines is consistent with previous findings indicating higher extracellular vesicle secretion or increased cellular complexity in malignant cells versus normal epithelial cells. The similar total protein concentration suggests that bulk protein content may not differentiate between cancerous and non-cancerous cell lines, highlighting the importance of examining specific subcellular components or secreted particles.

Acknowledgement of Funding: This research was supported by Institutional Development Grant 885016. NIH NIMHD/U54/MD007602-38/PI: Dr. Sean Kimbro. MSM Cancer Health Equity Institute/Director: Dr. Brian Rivers. The American Cancer Society Diversity in Cancer Research. ACS Grant DICRIDG-21-072-01-DICRIDG/PI: Dr. Ming Bo Huang

P-10 Title: Care Gaps and Barriers in Access to Care for BRCA-Positive Patients

Authors: Kyla Griggs, Dr. Pamela Ganschow, MD, Vivian Pan, MS, CGC; Angelina Izguerra, BPH

University of Illinois Chicago

Cancer Department

DICR- Diversity in Cancer Research

Mentors: Vivian Pan, MS, CGC; Angelina Izguerra, BPH

Background: The BRCA1 and BRCA2 genes are major tumor suppressors; their mutations predispose individuals to a high lifetime risk for breast, ovarian, pancreatic, prostate cancers, and melanoma. Hereditary Breast and Ovarian Cancer (HBOC) syndrome requires frequent screenings and preventive interventions. However, care gaps significantly impact access to essential services, most profoundly in minority populations. This study examines specific barriers BRCA-diagnosed patients face, with an emphasis on disparities among minority groups. Data from twenty scholarly papers and thirty medical charts from UI Health’s hereditary cancer program were analyzed to assess demographic factors, family history, genetic testing, procedures, medications, and screenings. Results show extensive care disparities, often fueled by financial strain, lack of education, and distrust of the medical field.

Methods: This study investigates care gaps among BRCApatients using medical chart data from UI Health and twenty scholarly sources. Data were collected through Epic and stored in REDCap, including demographics, genetic testing, procedures, personal and family history, medications, and screenings. Information such as mammograms, MRIs, mastectomies, and oophorectomies were extracted to assess compliance based on NCCN recommendations. Each patient’s data was analyzed to identify barriers and disparities, particularly among minority groups.

Results: Thirty-five BRCApatients were examined. The average age was 41.4. Most were female (88%), minority (73%), insured (90%), non-Hispanic (58%), and single (60%). Most were diagnosed with BRCA2 (51.5%) compared to BRCA1 (48.5%). Patients met with a genetic counselor to discuss BRCA and should have a follow-up meeting after testing positive. More women received screenings and procedures (40%) than men (0%). Most patients had a family history of breast and/or ovarian cancer. Most were not yet diagnosed with cancer (72.8% not diagnosed). Overall, 54.5% had irregular screenings and procedures according to NCCN guidelines. Eight of nine White, non-Hispanic patients consistently maintained screenings and procedures. Eleven of twenty-four minority patients were inconsistent, with some never seen again after diagnosis and others missing or not scheduling appointments.

Conclusions and Implications: Many minority patients with BRCA mutations experience inadequate healthcare access, contributing to higher rates of irregular care. Increased attention to care gaps is essential to improving HBOC survival rates. Findings highlight the need for improved provider engagement, expanded patient education, and targeted outreach to underserved groups.

Acknowledgments: This project was completed as part of the Diversity in Cancer Research (DICR) program funded by the American Cancer Society. I would like to thank the CRTEC team, Dr. Ganschow, Angelina, and Vivian for their support and guidance

P-11 Title: Integrative Variant Annotation and Functional Prediction of DNA Repair Genes in the African American Hereditary Prostate Cancer Cohort

Authors: Sydni Kimble, B.S. 1; Kenyiata Hodge, Ph.D., MPH2; Deyana Lewis, Ph.D., MPH3 ; Cheryl D. Cropp, Pharm.D., Ph.D.2

1 Graduate Education in Biomedical Sciences (GEBS) Program, Morehouse School of Medicine 2 Department of Pharmacology & Toxicology,Morehouse School of Medicine3 Department of Community Health & Preventive Medicine, Morehouse School of Medicine

Mentor: Dr. Cheryl Cropp, Pharm.D., Ph.D, Morehouse School of Medicine

Background/Significance: Prostate cancer disproportionately affects African American men, who face higher incidence, aggressiveness, and mortality rates. However, African Americans remain underrepresented in genomic studies, limiting discovery of ancestry-specific risk variants. The African American Hereditary Prostate Cancer (AAHPC) cohort, 77 families with strong hereditary patterns, addresses this gap by enabling tracing of inherited variants and linking genetic changes to clinical outcomes. DNA repair genes in African American genomes are enriched with functional variants, making them crucial to understanding disease progression and treatment response. We hypothesize that the discovery of high-impact variants in the AAHPC cohort may contribute to prostate cancer risk in African American men.

Methods: Whole-exome sequencing was performed for 97 individuals from the AAHPC cohort. Variants were annotated using Ensembl VEP (GRCh38) and assessed across conservationbased (GERP++, phyloP, PrimateAI), established (CADD, PolyPhen, SIFT), and dbNSFP-based predictors (MetaLR, MutationTaster, MutationAssessor, etc.). The Evolutionary Action (EA) algorithm quantifies functional impact. Population allele frequencies were compared using gnomAD, 1000 Genomes, and AllofUs, while ClinVar and All of Us data supported clinical interpretation. Protein modeling with AlphaFold and FoldX examined structural changes, and drug response simulations explored therapeutic implications.

Results: A total of 931 DNA repair variants were detected, including 518 identified by VEP and five novel findings. A newly discovered SDHA variant showed the highest damaging scores across all 25 prediction tools, alongside two nearby SDHA variants within 20 kb, suggesting a functional hotspot. EA identified 926 variants, providing broader detection than VEP. Of 254 nonsynonymous variants, several showed strong predicted functional impact. Upcoming analyses will cross-validate findings using AllofUs data to identify ancestry-specific high-impact variants and evaluate drug–gene interactions.

Conclusion: This integrative analysis enhances understanding of hereditary prostate cancer in African Americans. The identification of clustered SDHA variants and their predicted pathogenicity highlights ancestry-linked molecular mechanisms that may inform personalized therapy.

Acknowledgements: Conducted at Morehouse School of Medicine within the Graduate Education in Biomedical Sciences (GEBS) program, supported by the Chan Zuckerberg Initiative (CZI2002-007045) and NIH diversity-focused genomic research initiatives.

P-12

Title: "Evaluation

of ancestry-associated HER2 and androgen receptor expression in prostate cancer patients using liquid biopsy"

Authors: Diana LeVasseur, M.S.1 , Jordan Ciuro, M.D.2,3, Shahid Ahmed, M.B.B.S.2,3, Sri Kollepara, M.D.1,3, Soroush-Rais Bahrami, M.D.4,5, Pamela Cooper1, Abdulrahman M. Dwead, Ph.D.1, Jabril R. Johnson, Ph.D.1, Rick A. Kittles, Ph.D.1, Leanne Woods-Burnham, Ph.D.1

1 Morehouse School of Medicine, Atlanta, GA

2 Emory University, Atlanta, GA

3 Grady Health Systems, Atlanta, GA

4 The University of Alabama at Birmingham, Birmingham, AL

5Wake Forest University School of Medicine, Winston-Salem, NC

Background: Androgen receptor (AR) is a nuclear receptor that drives tumor progression and is associated with prostate cancer (PC) aggressiveness. Human epidermal growth factor 2 (HER2) is a tyrosine kinase receptor and currently has no known ligand but has been recently implicated to promote PC metastasis and is associated with disease recurrence. While overexpression of HER2 has been associated with poor prognosis, advanced disease, higher Gleason score, and increased cell proliferation in PC cells and patients, these indicators have not been sufficiently evaluated in men of WestAfrican genetic ancestry (WAA). We hypothesize that there is a positive correlation between HER2, AR, and WAA.

Methods: IRB approval from Morehouse School of Medicine (MSM), Grady Memorial Hospital, and the University of Alabama at Birmingham were obtained to prospectively collect sera from consented patients (n=56) within the genitourinary oncology multidisciplinary clinic. Additionally, participants were recruited at City of Hope (COH) in Los Angeles, California from 2018 – 2020 as part of the Community-Based Prostate Cancer Screening Program (n=40). We conducted enzyme linked immunosorbent assay (ELISA) to quantify circulating HER2 and AR. We quantified ancestry estimates using validated ancestry genotyping.

Results: Preliminary data of 40 samples obtained from participants at COH, consisting of 23 samples from participants who self-identified as white, and 17 who self-identified as Black revealed associations between HER2, AR, and WAA using ELISA and ancestry genotyping. Comparing circulating HER2 and circulating AR by race showed moderate correlation in both white men and Black men. When comparing circulating HER2 to WAA, Black men showed a positive correlation (0.2974). Due to our small sample size, we are currently evaluating correlations between HER, AR, and WAA in our expanded cohort of clinical samples (n=56).

Conclusions and Implications: Thorough evaluation of circulating HER2 has major clinical utility to pursue additional PC treatment options using a precision medicine approach.

Acknowledgements of Funding: This study has been supported by NIH (KL2TR002381), NIH (UL1TR002378), PCF (20YOUN04), DoD Prostate Cancer Research Program (W81XWH2110038), NIH (TL1TR002382), and NIH/NIMHD (2U54MD007602).

P-13

Title: The Role of Physical Activity and Mindfulness-Based Interventions in Health Outcomes of African American Women Diagnosed with Breast Cancer

Author: Neha Nasar1, Desiree Rivers PhD, MSPH 2

1 Morehouse School of Medicine, MD Program

2 Morehouse School of Medicine, Summer Scholars in the Community

Mentor: Desiree Rivers Ph.D., MSPH, Morehouse School of Medicine 2

Background: African American women with breast cancer are advised to eat healthier, stay physically active, and manage stress (Smith et al., 2015), yet their lived experiences are not well represented in current research. Chronic stress, abnormal cortisol levels, and inflammation disproportionately affect African American breast cancer survivors and are linked to worse survivorship outcomes. While physical activity and mindfulness practices may improve mental well-being and reduce biological stress responses, their culturally relevant use in this population remains understudied. The purpose of this literature review is to identify studies and measures of exercise and mindfulness-based methods including yoga, meditation, and religion and their influence on psychosocial outcomes, physical health outcomes, and biological markers related to stress and inflammation among African American women diagnosed with breast cancer.

Methods: This review examined 16 studies (14 were included after screening) using SCOPUS and citation tracking. The search focused on how exercise and mindfulness practices such as yoga, meditation, and faith-based activities impact health outcomes. Studies were screened with a primary focus on African American women and intervention type. The findings were synthesized using a narrative thematic approach.

Results: Nine studies focused directly on African American women, while others addressed psychosocial or biological outcomes in similar populations. Overall, movement programs improved self-efficacy, physical activity, and weight. Mind-body practices supported better mood, reduced fatigue, and enhanced spiritual well-being. Programs grounded in culture and community, especially those held in church settings, helped increase participation Stigma, cost, and religious concerns were presented as barriers. Across studies, biological outcomes such as cortisol and inflammatory markers were infrequently measured.

Discussion: Most studies were small, short-term, and lacked biological outcome measures. While there is growing research on the benefits of exercise and dietary changes in African American women with breast cancer and the interest among the population, few studies have implemented mindfulness-based interventions or tracked inflammatory markers. Future research should prioritize culturally tailored interventions that engage the women in physical activity and mindfulness practices to address survivorship disparities in African American women. Studies should also incorporate biomarker tracking such as cortisol and key inflammatory markers at various points to assess changes in stress and inflammation. Larger, longer-term trials are also needed, along with follow-up assessments to determine whether the interventions lead to sustained behavior change.

Acknowledgment of Funding: This research is supported by the MSM Summer Scholars in the Community Program

P-14

Title: A Case Report of

Renal Cyst Communication Involution Secondary to Hydroureteronephrosis Decompression in the Setting of Urothelial Carcinoma

Authors: Jerry Yue MD1, Nathan Zhang DO1 , Matthew Nwerem MS2, Jesse Kao BS3, Stuart Deaderick MD4, Hardeep SinghPhD5

1 Transitional Year; Northeast Georgia Medical Center, Gainesville, GA

2 Medical Student; Morehouse School of Medicine, Atlanta, GA

3 Medical Student; Philadelphia College of Osteopathic Medicine Georgia, Suwanee, GA

4 Interventional Radiology; Northeast Georgia Medical Center, Gainesville, GA

5 Graduate Medical Education Research; Northeast Georgia Medical Center, Gainesville, GA

Mentor: Jerry Yue, MD, Northeast Georgia Medical Center

Background/Significance: Renal cysts are commonly detected incidentally on imaging, with prevalence increasing with age and male sex. While most remain asymptomatic, a small percentage may develop complications such as hemorrhage, infection, or mass effect, potentially leading to obstructive uropathy and hydronephrosis. In rare cases, elevated intrapelvic pressure may result in renal calyceal rupture or cysts. This report presents the case of a 79-year-old male with a history of urothelial carcinoma who developed right-sided hydronephrosis secondary to obstructive malignancy. Renal cysts that communicate with the collecting system are rare. Additionally, our case is unique because the cyst communication regressed following aspiration.

Methods: Abdominal Computed tomography (CT) imaging with contrast was conducted throughout. Initially ordered to rule out abdominal abscess, CT scans continued for investigation of irregular mass adjacent to the bladder, the subsequent mass resection, and for understanding the communication between the renal cyst and urinoma. Hounsfield density of fluid was used to distinguish cystic fluid. Fluoroscopic contrast injection allowed for visualization of the renal calyxcyst communication, as well as ruling out all other locations for cyst communication. A 5 French Yueh needle was advanced into the contrast collection of the cyst, and the collection was aspirated completely.

Results: Imaging revealed a large urinoma, possibly from calyceal rupture, along with inflammatory changes of abnormal communication between the collecting system and adjacent renal cyst. Notably, fluoroscopic imaging demonstrated contrast within the cyst, which was no longer present following nephrostomy tube decompression. Although rare, spontaneous or iatrogenic communication between a renal cyst and the collecting system can complicate management and may alter treatment options.

Conclusions and Implications: This case raises the possibility that prior conditions may weaken the renal or ureter parenchyma from chronic irritation and inflammation. Atypical causes of urinoma formation, especially in patients with a history of malignancy, prior instrumentation, or obstructive uropathy, are important to patient outcomes as early recognition and multidisciplinary management of renal cyst variants can guide management and prevent treatment complications. This case also highlights the critical role of diagnostic imaging in identifying rare genitourinary anomalies and supports current limited evidence relating to this uncommon renal cyst presentation.

Acknowledgement of Funding: None

P-15

Title: Kaposi’s Sarcoma-Associated Herpesvirus: A Genomic Analysis

Authors: Briana Osei1,2 , Elena M Cornejo Castro1, Vickie Marshall1, Nazzarena M Labo1 , Isabella Liu1, Ananthakrishnan Nair1, Denise Whitby1

1Viral Oncology Section, AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Frederick, MD

2Morehouse School of Medicine Doctor of Medicine Program

Mentor: Elena M Cornejo Castro Ph.D., Viral Oncology Section, Frederick National Laboratory for Cancer Research

Background/Significance: Kaposi sarcoma (KS) is an endothelial cell tumor caused by the human gammaherpesvirus herpesvirus-8, or Kaposi sarcoma-associated herpesvirus (KSHV/HHV-8). KS remains amongst the most common malignancies in HIV positive individuals, particularly in sub-Saharan Africa and among men who have sex with men. Previous studies have hypothesized that distinct genomic variations may contribute to differences seen in virulence, transmission, and clinical presentation among KSHV-associated diseases (KAD) most referencing the variable K1 gene representing less than < 1% of the total viral genome. The purpose of this study was to compile and analyze the largest collection of KSHV near-full length genomes > 135K genomes to investigate patterns of viral diversity and evolution.

Methods: Publicly available sequencing and genome datasets related to KSHV were retrieved from the European Nucleotide Archive and the National Center for Biotechnology Information. Search terms included: Kaposi sarcoma, Human gammaherpesvirus 8, KSHV, taxid: 37296, 20000 > Sequence length < 200000. Fifty-two additional genomes were isolated from tissue biopsies, effusions, PBMC and oral fluid samples. Metadata including country of origin, isolation date and KSHV subtype information were collected. All data were assessed by two independent reviewers.

Results:Our initial search identified 6574 publicly available records of which 5,960 were excluded before screening due to genome length discrepancies (n=4606), duplicated records (n=608), no public data available (n=432), epigenomic datasets (n=197), and not containing KSHV sequences (n=118). After screening the remaining 613 datasets, 255 were excluded due to low coverage (n=235) or being synthetic constructs (n=20). This study reports the compilation of the largest KSHV genomic dataset to date, comprising 424 near full-length genome sequences. Further analyses will focus on the phylogenomic structure of the KSHV genome, including recombination, selection and molecular epidemiology.

Conclusions and Implications: This study establishes an essential genomic resource for understanding KSHV evolution and pathogenesis. Insights gained from this dataset may inform future diagnostic, therapeutic, and prevention strategies targeting KAD, particularly among populations with HIV.

Acknowledgement of Funding: This project was funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. 75N91019D00024. The content of this publication doesn’t necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations simply endorsement by the U.S. Government

P-16 Title: Combined treatment with agonists for CXCR4 and CB2 receptors reduces prostate cancer growth and metastasis

Authors: Nakea M. Pennant1; Alifiani B. Hartono, Ph.D.2; Shiqin Liu, M.D., Ph.D.2; Sidharth Paparaju2, Chung Lee2; Christopher Massey2; Tanya Stoyanova, Ph.D.2,3; Cimona V. Hinton, Ph.D.4

1. Center for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, GA, USA

2. Department of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, USA

3. Department of Urology, University of California, Los Angeles, CA, USA

4. Department of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine

Mentor: Cimona V. Hinton, Ph.D., Morehouse School of Medicine

Background/Significance: CXCR4, a G-protein-coupled receptor (GPCR) widely expressed in tumors regulates migration, survival, and immune responses through its interaction with SDF-1α, playing a crucial role in metastasis and tumor aggressiveness. We previously demonstrated that CXCR4 forms heterodimers with the GPCR cannabinoid receptor 2 (CB2) in human breast and prostate cancer cell lines in vitro. The combined treatment of CXCR4 and CB2 with SDF-1α and the CB2 agonist AM1241 induced a physical heterodimer, resulting in significantly inhibited CXCR4-mediated pro-tumor signaling, reduced migration, disrupted cytoskeletal organization, and downregulation of proteins involved in motility. Given the reported anti-metastatic effects of cannabinoids, targeting a CXCR4–CB2 heterodimer may offer a novel therapeutic approach. Based on the foregoing, we hypothesize that the combined treatment with agonists will minimize CXCR4-mediated tumor progression, specifically tumor growth, metastasis, and overall residual tumor survival in vivo.

Method: We created human prostate tumor xenografts in a spontaneous metastasis mouse model. Luciferase-containing human prostate cancer cells (DU145 RFP/Luc or PC3 GFP/Luc) were implanted subcutaneously. Once tumors reached 40 mm³, mice were randomized into four treatment groups: vehicle, SDF1α, AM124, and SDF1α/AM124(combo). Thereafter, primary tumors were resected at 400 mm³, and treatment continued prior to visualizing metastasis for residual or recurrent tumors.

Results: Xenografts treated with combined agonists displayed no local tumor recurrence posttumor excision, a significant reduction in tumor volume, and a lower incidence of metastasis to distal organs compared to the other treatment groups.

Conclusions and Implications: Combined agonist treatment presents a novel approach to managing CXCR4-driven tumor metastasis and potentially offers an alternative strategy to current CXCR4 antagonists for managing metastasis.

Acknowledgment of Funding:

• This research is funded in part by the Kessler Foundation Endowment at Morehouse School of Medicine (CVH)

• Fine Fettle, Inc. (CVH)

• National Institute on Minority Health and Health Disparities (CVH)

• National Institute of General Medical Sciences’ Biomedical Research Initiative for Doctoral Graduate Education B.R.I.D.G.E. Program (Clark Atlanta University); 5T32GM148395-03) (NMP)

P-17 Title: Exploring the Impact of Psychological Distress in African American Women Breast and Endometrial Cancer Patients

Authors: Analiese A. Poe¹, Gabrielle Ford, MPH2, Zakirah L. Abdul-Hameed2, Amirah Burton2 , Brian Rivers, PhD, MPH², Desiree Rivers, PhD, MPH² ¹Spelman College, UCHERTP ²Morehouse School of Medicine

Background/Significance: African American/Black women experience disproportionately higher rates of breast and endometrial cancer recurrence compared to White women. While biological determinants play a role, psychological factors such as chronic stress and anxiety are underexplored contributors to this disparity. Heightened psychological distress disproportionately increases the risk of reproductive cancer through dysregulated cortisol signaling and immunity suppression. Understanding the intersection between psychological distress and cancer recurrence is essential for improving survivorship and promoting health equity among this population.

Methods/Approach: An in-depth review of 25 articles published between 2014-2024 explored the effectiveness of culturally appropriate stress, anxiety, and reproductive cancer recurrence in African American women. The review thoroughly evaluated the linkage between psychological stress, anxiety, and reproductive cancer recurrence in African American women through the analysis of patient stress markers and patient outcomes. Additionally, this review focused on culturally responsive intervention mechanisms. This included stress management techniques, nutritional guidance, social support systems, and exercise-based programs tailored to the unique cultural and socioeconomic needs of African American women.

Results: The findings revealed a distinct association between psychological stressors and cancer recurrence amongst African American women. High stress and anxiety were linked to increased cortisol levels and immune suppression, both biological processes known to exacerbate tumor growth and recurrence. The evidence also demonstrated that culturally inclusive interventions such as community-based exercise were effective techniques for mitigating these effects and improving overall well-being.

Conclusion and Implications: The overall literature review highlights the importance of addressing psychological stress as risk factors in African American women’s reproductive cancer survivorship. To mitigate the risk of recurrence, incorporating culturally sensitive psychosocial intervention strategies has the potential to improve cancer survivorship and address healthcare disparities, ultimately promoting healthcare equity. Further research can be conducted to evaluate the longevity of these interventions in effectively reducing risk and increasing survivorship.

Acknowledgement of Funding: This research was supported by the American Cancer Society through the Undergraduate Cancer Health Equity Research and Training Program (UCHERTP). Additional support was provided by the Morehouse School of Medicine Cancer Health Equity Institute.

P-18

Title: Investigating Impact

of IL4R Ancestral Variants on Triple Negative Breast Cancer

Authors: Haseena Polk, Sean Kimbro

Institutional Affiliations:

Morehouse School of Medicine

Background/Significance: Studies have shown African Americans (AA) experience high levels of circulating cytokines in relation to various disease; furthermore, differences in serum levels of IL-4 based on race have been reported. Within cancer microenvironments IL-4 influences pathways involved in cell survival, proliferation and metastasis while also impacting cancer cell invasion and metabolism. IL-4 induces hepcidin, an essential peptide hormone in iron homeostasis. Hepcidin binds to ferroportin resulting in its degradation, leading to an increase in labile iron in breast cells. Iron plays a crucial role in cancer biology through its involvement in a form of iron-dependent regulated cell death characterized by lipid peroxidation, ferroptosis. Ferroptosis plays a dual role in cancer by suppressing tumor growth and enhancing therapeutic efficacy, while also possibly promoting tumor progression via inflammation-associated immunosuppression.Additionally, AAwomen are disproportionally affected by breast cancer, with a mortality rate 42% higher than that of white women within the U.S. Given this health disparity along with elevated IL-4 levels among this population an understanding of IL-4 and its impact on breast cancer is needed. Additionally, many variants within the IL-4 receptor (IL-4R) have been observed and correlated to various diseases. However, no investigation has been pursued on the effects these variants may have in relation to iron levels and anemia within individuals with increased IL-4. We hypothesize that IL-4 promotes ferroptosis in breast cancer cells and WestAfrican ancestral IL-4R variants influence ferroptosis through altered IL-4R signaling.

Methods: This study used TaqMan Genotyping assay to identify IL-4R variant status among selected cell lines (HCC-1806, MDA-MB-231 and MDA-MB-468). Western blot was used to observe protein concentrations of study related proteins among the specified cell lines.

Results: TaqMan SNP Genotyping assay determined rs1805015 to be homozygous for the alternative allelic sequence (CC) in all cell lines. While rs1801275 was found to be heterozygous in HCC-1806 and homozygous for the alternative allele in MDA-MB-231 and MDA-MB-468. Differences among study related protein concentrations were observed in cell lines.

Conclusion: This study aims to reveal the role IL-4 and IL-4R ancestral variants play cancer and to highlight the importance of investigating ancestral variants and their impact on diseases. Our current findings indicate the prevalence of IL-4R variants within breast cancer cell lines. Additionally, the differences in protein concentration suggest functional consequences associated with these variants. We aim to unpack this even further by examining how IL-4R variants influence downstream signaling and cellular behavior. Future work will integrate functional assays, inhibitor studies and evaluate clinical data to better understand how evolutionary immunogenetic diversity contributes to cancer risk.

P-19

Title: Association Between Medicaid Expansion and Colorectal Cancer Mortality Among Men in the Southern U.S., 2012–2021

Authors: Robinson, Jalen, BS; Bayer, Carey Roth, EdD; Choi, Hwanseok, PhD Morehouse School of Medicine, Atlanta, GA

Background/Significance: Colorectal cancer (CRC) is a leading cause of cancer-related death among U.S. men, with Non-Hispanic Black men experiencing the highest incidence and mortality rates. The Affordable Care Act (ACA) aimed to reduce disparities in preventive and treatment access through Medicaid expansion for low-income adults under age 65. However, the Southern United States home to the nation’s highest CRC mortality rates has shown uneven adoption of Medicaid expansion, potentially perpetuating racial and geographic inequities. Given that CRC screening now begins at age 45, this study examines whether Medicaid expansion is associated with changes in CRC mortality among Southern men aged 45–64 from 2012–2021, overall and by race. We hypothesized that expansion would be associated with lower CRC mortality, particularly among Non-Hispanic Black men.

Methods: A secondary, longitudinal analysis was conducted using age-adjusted CRC mortality rates (per 100,000 population) obtained from the CDC WONDER database. Sixteen Southern states plus the District of Columbia were categorized by Medicaid expansion status and year of implementation per the Kaiser Family Foundation Medicaid Expansion Tracker. Annual CRC mortality rates for Non-Hispanic Black and Non-Hispanic White men aged 45–64 were analyzed using a difference-in-differences (DiD) design, comparing pre- and post-expansion trends across expansion and non-expansion states, stratified by race.

Results: Between 2012 and 2021, Southern Medicaid expansion states exhibited modest but consistent declines in CRC mortality, whereas non-expansion states experienced stagnant or fluctuating rates. For instance, Arkansas (expansion in 2014) declined from 32.2 to 26.4 deaths per 100,000, while Georgia (non-expansion) remained nearly unchanged (21.0 to 21.1). Despite these improvements, Non-Hispanic Black men continued to experience higher CRC mortality across all states and time periods.

Conclusion and Implications: Medicaid expansion in the Southern United States was associated with modest reductions in CRC mortality among men aged 45–64, suggesting improved access to early detection and treatment. However, persistent racial disparities indicate that insurance expansion alone is insufficient to eliminate inequities rooted in structural determinants of health. Strengthening Federally Qualified Health Centers (FQHCs), supporting culturally tailored screening programs, and addressing systemic barriers to specialty care are essential policy and practice strategies to further reduce CRC mortality among high-risk populations in the South.

Acknowledgement of Funding: This project was conducted under the MSM/TU/UAB O’Neal Comprehensive Cancer Partnership. Supported by Award Number U54 CA118638 from the NIH National Cancer Institute. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

P-20

Title: Integrating Deprivation Index with Mutational Signatures and Circulating Biomarkers of Inflammation to Explore Breast Cancer Disparities

Author: Tia Sadler

Institution: Morehouse

Mentor:

School of Medicine, Department of Biomedical Research

Melissa Davis, PhD

Background/Significance: Breast cancer is the most frequently diagnosed malignancy among women in the United States and a leading cause of cancer-related mortality. While tumor-intrinsic biology is a major driver of disease progression, social determinants of health particularly neighborhood-level socioeconomic disadvantage also contribute to persistent disparities in outcomes. Recent studies indicate that social disadvantage correlates with altered tumor methylation, gene expression, and immune signaling. Biobehavioral research suggests neighborhood stressors activate pathways that heighten inflammation and impair DNA repair, potentially driving genomic instability. Because genetic ancestry also influences immune signaling, it is essential to distinguish these inherited factors from social and environmental exposures. In this study, neighborhood disadvantage is quantified using a Neighborhood Deprivation Index (NDI) incorporating census tract–level measures of income, education, employment, housing crowding, and household composition, constructed separately for the New York City and Detroit metropolitan areas to capture comparable urban structural conditions. We hypothesize that higher neighborhood deprivation is associated with tumor mutational signatures reflecting genomic instability and impaired DNA repair, as well as elevated circulating inflammatory and immune dysregulation biomarkers, representing complementary biological pathways through which social disadvantage becomes biologically embedded in breast cancer.

Methods: Data were sourced from the International Center for the Study of Breast Cancer Subtypes. Whole-genome sequencing from 139 patients was analyzed using the MuSiCal pipeline to quantify single base substitution, doublet base substitution, and indel signatures linked to genomic instability or DNA repair defects. Multivariable regression will assess associations between NDI quartiles and signature load, adjusting for age, race/ethnicity, subtype, and smoking status. Additionally, plasma levels of 50 cytokines/chemokines were measured in 905 patients via multiplexed Luminex® assays. Regression and mediation analyses will assess associations between NDI and biomarker levels, adjusting for BMI and stage.

Anticipated Results: We expect that higher NDI will correlate with signatures of homologous recombination deficiency and increased systemic inflammatory markers, supporting the concept that social disadvantage may become biologically embedded and promote tumor progression.

Conclusion/Implications: By integrating genomic and biomarker data with neighborhood-level social metrics, this project aims to reveal how structural inequities influence breast cancer biology. Findings may inform precision medicine and public health interventions designed to reduce disparities and improve outcomes for patients from socially disadvantaged communities.

Acknowledgements: This research is supported by grants OT2-CA297574 and R01-CA259396 from the NIH; the New York Community Trust; and the Breast Cancer Research Foundation.

P-21 Title: Exploring the Connection of Dysbiosis in Cancer and Neurodegeneration

Authors: Estella Smith, Nayya Khafri Jamison, MPH

Spelman College, Morehouse School of Medicine Cancer Health Equity Institute

Background/Significance: Neurodegenerative diseases such as Alzheimer’s disease are leading causes of disability, while cancers including colorectal cancer remain major causes of mortality worldwide. Epidemiological studies report an inverse relationship between Alzheimer’s disease and certain cancers, in which the presence of one condition is associated with a reduced risk of the other. However, inverse disease patterns at the population level do not exclude shared biological mechanisms that influence disease development. Emerging evidence suggests that gut dysbiosis, defined as an imbalance in the gut microbiome often shaped by diet, contributes to systemic inflammation, immune dysregulation, and metabolic dysfunction implicated in both tumor development and neurodegeneration. Gut dysbiosis has been associated with colorectal cancer through chronic inflammation and impaired cellular repair, while altered gut brain axis signaling has been linked to neuroinflammatory pathways involved in neurodegeneration. The objective of this study was to examine whether gut dysbiosis represents a shared mechanistic link between cancer and neurodegeneration while acknowledging their inverse relationship.

Methods: A targeted literature review was conducted using PubMed to identify peer reviewed studies published between 2015 and 2025 examining mechanistic links between gut dysbiosis, cancer, and neurodegeneration. This time frame was selected to capture advances in sequencing technologies, microbiome profiling, and gut brain axis research that were not consistently available prior to 2015. Studies were selected based on their focus on inflammation, immune modulation, metabolic dysfunction, and diet related changes in the gut microbiome.

Results: The reviewed literature demonstrated that gut dysbiosis contributes to colorectal cancer development through immune mediated inflammation and metabolic imbalance that support tumor progression. Findings also indicated that dysbiosis alters gut brain axis signaling, promoting neuroinflammation and neuronal damage associated with neurodegenerative disease. Studies addressing the inverse relationship between cancer and dementia suggest that although disease incidence differs, overlapping biological processes such as chronic inflammation and immune disruption remain involved in both conditions. These findings support gut dysbiosis as a convergent biological factor influencing cancer and neurodegeneration through shared mechanisms rather than shared disease outcomes.

Conclusion and Implications: Gut dysbiosis may connect cancer and neurodegeneration through immune disruption, chronic inflammation, and metabolic imbalance even in the presence of inverse disease risk. Because diet and environmental exposure strongly influence gut microbiome composition, disruptions in these systems may disproportionately affect underserved populations. Understanding gut dysbiosis as a shared mechanistic contributor underscores the importance of equitable access to nutrition, preventive screening, and gut health education in addressing disparities in cancer outcomes and neurodegenerative disease burden.

P-22 Title: Vitamin D (calcitriol) potentiates CB2-mediated anti-tumor responses in prostate cancer cell lines: molecular mechanisms and therapeutic potential

Authors: W. Blake Speed 1,2; Nakea Pennant3; Cimona V. Hinton, Ph.D.2

¹Morehouse School of Medicine, Master of Biomedical Research Program

²Morehouse School of Medicine, Department of Microbiology, Biochemistry, and Immunology

³Clark Atlanta University, Department of Biological Sciences

Mentor: Cimona V. Hinton, Ph.D., Morehouse School of Medicine

Background/Significance: Prostate cancer (PCa) stands as a significant public health concern, being the most frequently diagnosed non-skin cancer among men in the United States, and secondly, the leading cause of mortality in cancer-related deaths in this population. Vitamin D receptor (VDR) has anti-proliferative and pro-differentiation effects in several cancers.

Cannabinoid Receptor 2 (CB2) is a G-protein coupled receptor implicated in immune modulation and anti-tumor activity. We hypothesize that combined activation of VDR and CB2 reduces proliferation, migration, and survival of prostate cancer cells more than either receptor alone.

Methods: Experiments were conducted in human prostate cancer cell lines PC3 (highly metastatic, androgen-independent/hormone-resistant cancer) and DU145 (moderately metastatic, androgen-independent/hormone-resistant cancer). Cells were plated in complete media for 24 hours then serum-starved overnight. Cell lines with vitamin D (10nm) and AM1241 (1nm and 2nm) for 24 hrs. Protein lysates were collected and used to analyze expression.

Results: In PC3 cells, increasing concentrations of AM1241 (1nm vs. 2nm) demonstrated an increase in VDR expression, similar to expression of VDR in PC3 cells treated with calcitriol. However, expression of VDR did not change in DU145 cells upon treatment with AM1241.

Conclusions and Implications: VDR and CB2 independently have antitumor effects. Cannabinoid receptor 2 could potentially regulate expression of Vitamin D receptor via a synergistic effect to manage tumor growth. In the future, we will determine whether expression of Vitamin D receptor will be enhanced when the two agonists are treated in combination. We will also identify key signaling pathways that may be modulated by this interaction.

Acknowledgment of Funding: This research is funded in part by the Kessler Foundation Endowment at Morehouse School of Medicine (CVH) and Fine Fettle, Inc. (CVH)

P-23 Title: Obesity-Associated Leptin Chemoresistance in Prostate Cancer Cell Lines Attenuated Through Inhibition of ERK1/2 Signaling Pathway

Authors: Daniel Walters1, Justin Bromell2, Kofi Khamit-Kush3, Karen Russell Randall, Ph.D1 ., Jeffrey Handy, Ph.D2

1Morehouse School of Medicine, Pharmacology/Toxicology, 2Morehouse College, Biology Department, 3Clark Atlanta University, Biology Department

Background: Prostate cancer is the most common form of cancer for men in the United States, accounting for 30% of all cancer diagnoses in 2025. Obesity was determined to be a risk factor for prostate cancer onset and progression, with several studies correlating lower overall survival to body mass index (BMI). For obese individuals, leptin, an adipokine produced by adipose tissue, has been shown to induce chemoresistance through sustained proliferative signaling while inhibiting apoptosis and cell cycle arrest. Our lab and others have identified the ERK1/2 pathways as a likely candidate for leptin-induced chemoresistance. Our preliminary data indicate that ERK1/2 inhibition restores drug sensitivity in prostate cancer cell lines by overcoming chemoresistance induced by leptin.

Methods: Prostate epithelial cell line (RWPE-1) and prostate cancer cell lines LNCaP and PC3 were exposed to increasing concentrations of leptin (6ng/mL, 45ng/mL, 60ng/mL), a fixed concentration of therapeutics bortezomib (a 26S proteasome inhibitor (620nM))/docetaxel (a taxane that prevents microtubule disassembling (1.36nM)), or select inhibitor (SCH772984, an ERK1/2 inhibitor (10 µM)) for 24 hours. One-way ANOVA statistical analyses were performed using GraphPad Prism. Western Blot analyses were also performed to confirm ERK1/2 inhibition, as well as apoptosis via PARP activity. Experimental manipulations were compared to vehicle controls (Phosphate Buffered Saline (PBS; 1x) or dimethyl sulfide oxide (DMSO)).

Results: Elevated ERK1/2 signaling induced by high serum leptin resulted in increased cell proliferation and cytoprotection in prostate cells, inhibiting therapeutic-induced apoptosis in both epithelial and cancerous cell lines. PARP activity was significantly lower in conditions with elevated leptin compared to control and conditions with less leptin. Inhibition of ERK1/2 signaling resulted in restoration of sensitivity in the presence of excess leptin, reducing cell survival. Western blot analysis revealed reduced ERK and phosphorylated-ERK activity in combined conditions compared to control, along with increased PARP activity for apoptosis.

Conclusions and Implications: ERK1/2 signaling plays a crucial role in cancer cell proliferation and survival. In the event of therapeutically induced apoptosis, ERK signaling antagonizes apoptosis signaling, resulting in reduced therapeutic efficacy. If inhibiting ERK signaling assists therapeutic activity in vivo, then targeting ERK signaling in prostate cancer patients may serve as a potential aid in treatment and overall survival for obese prostate cancer patients.

Acknowledgement of Funding:

• This research was supported in part by the Graduate Student Initiative for Student Enhancement (G-RISE) program, Morehouse School of Medicine (360031 RISE).

• This research is supported in part by a grant from the Sherman Fair Child Foundation, Morehouse College.

P-24 Title: Characteristics

Associated with Disparities in Colorectal Cancer Screening Among Adults Aged 18 Years and Older in the United States: Findings From the 2021 Behavioral Risk Factor Surveillance System

Authors: Taylor Ware, Naomi Campbell, MPH, Anny Rodriguez, PhD, MPH, Gemechu Gerbi, PhD, MSc

Morehouse School of Medicine | 720 Westview Dr. SW| Atlanta, GA 30310

Purpose: Colorectal Cancer is ranked as the third most diagnosed cancer and the second leading cause of cancer-related deaths among both men and women. In 2025, there are an estimated 154,000 new cases of colorectal cancer in the United States. The objective of this study is to identify socio-demographic factors associated with self-reported colorectal cancer screening among adults in the U.S. aged 18 years and older using 2021 Behavioral Risk Factor Surveillance System (BRFSS) data.

Methods: Data was analyzed from the 2021 Behavioral Risk Factor Surveillance System (N = 6,030). Bivariate and multivariable logistic regression analyses were conducted to assess factors associated with self-reported screening for colorectal cancer. Analyses were conducted using SAS version 9.4.

Results: In 2021, 27.2% of U.S. adults reported having not being screened for colorectal cancer. After adjusting for socio-demographic variables, several factors significantly influenced a lower odd of not reporting a history of colorectal cancer screening. These included being aged 45 to 54 years (AOR = 0.13; 95% CI: 0.11–0.16), being aged 55 to 64 years (AOR = 0.63; 95% CI: 0.520.75), having an highest education level of elementary school (AOR = 0.53; 95% CI: 0.33-0.87), having an highest education level of some high school (AOR = 0.52; 95% CI: 0.38-0.72), having an highest education level of high school diploma or GED (AOR = 0.84; 95% CI: 0.71-0.99), having an highest education level of some college (AOR = 0.80; 95% CI: 0.68-0.94), having an household income of less than $24,999 (AOR = 0.63; 95% CI: 0.48-0.85) and having no insurance (AOR = 0.36; 95% CI = 0.25-0.51) were less likely to screen for colorectal cancer.

Discussion/ Conclusion: In 2021, 27% of surveyed adults reported not being screened for colorectal cancer. Adults who were 45-64 years old, all levels of education, had a household income of less than $24,999 or uninsured were significantly less likely to have been screened for colorectal cancer. These findings underscore the need to explore and address barriers in these groups to improve equitable access to colorectal cancer screening.

Keywords: Colorectal cancer, Screening, Adults, United States

P-25

Title: Effect of perilipin 2 on fatty acid-induced ferroptosis in Caki-1 cells

Authors: Linda Williams

Mentor:

Xueying Zhao, Ph.D., Department of Physiology, Morehouse School of Medicine

Background/Significance: Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cell carcinoma (RCC) in adults and is characterized by the accumulation of intracellular lipids. The lipid droplet-associated protein PLIN2 is significantly upregulated in ccRCC, contributing to tumor growth and disease progression. Advanced RCC treatments focus on slowing the progression of kidney damage, but remain largely resistant to chemotherapy. Recent studies have identified ferroptosis as a potential contributor to RCC pathogenesis. We hypothesize that PLIN2 may modulate key regulators of ferroptosis. The purpose of this analysis was to understand ferroptosis regulation and reveal new molecular targets in RCC treatment.

Methods: Caki-1 cells were transfected with siRNA negative control (siNC) or siRNA targeting PLIN2 (siPLIN2) and treated with high-dose palmitic acid to mimic hyperlipidemic conditions. Western blot analysis was performed to determine the expression levels of key ferroptosis marker proteins, including GPX4, ACSL3, and ACSL4. Treated Caki-1 cells were stained with Ethidium homodimer-1 red and Bodipy green, and fluorescence imaging was used to visualize lipid content and quantify cell death.

Results: Fluorescence imaging revealed that PLIN2 knockdown enhanced palmitic-acid-induced cell death in Caki-1 cells. Additionally, PLIN2 knockdown led to upregulation of GPX4, a ferroptosis-suppressing enzyme, and downregulated ACSL3 and ACSL4, enzymes necessary for fatty acid metabolism and ferroptosis sensitivity. High-dose Palmitic acid treatment significantly increased ACSL4 in siRNA negative control cells.

Conclusions and Implications: The findings of this study suggest that PLIN2 may modulate key regulators of ferroptosis. Further investigation is needed to understand the mechanisms by which PLIN2 influences regulated cell death under pathological conditions.

Acknowledgement of Funding: This research was supported by the National Institute of Health, the National Center for Research Resources, and the Research Centers in Minority Institutions Program under grants R16GM149499, 8G12MD007602, and U54MD007602. This research was supported in part by the MSM Summer Research and Public Health Experience.

P-26 Title: Microbial Shifts Following the Spiny Water Flea Invasion in Lake Mendota: Firmicutes Decline

Authors: Montana Williams-Johnson; Tiffany Oliver Ph.D.²

¹Spelman College Department of Biology

²Spelman College Department of Biology, Research Mentor

Mentor: Dr. Tiffany Oliver, Spelman College Department of Biology

Background/Significance: Invasive species, such as spiny water fleas, are known to disrupt freshwater ecosystems by altering food chains and the microbial community. Microbial communities respond rapidly to ecological disturbances, serving as indicators of environmental change. Firmicutes are one of the most abundant and significant bacterial phyla across diverse ecosystems. Changes in the abundance of firmicutes are often used to assess microbial community shifts from ecological stressors. In host-associated environments, the abundance of Firmicutes is often evaluated relative to that of Bacteroidetes using the Firmicutes/Bacteroidetes (F/B) ratio, a commonly used metric for describing microbial community structure. Alterations in this ratio have been associated with changes in gut health and metabolic status and have been explored in the context of certain diseases, including breast cancer. Lake Mendota, a freshwater lake, underwent a major ecological disturbance when spiny water fleas were introduced in 2014. However, the extent to which this invasion corresponded with long-term changes in Firmicutes abundance within the lake’s microbial community remains unclear. This study examines temporal patterns in Firmicutes abundance before and after the invasion to better understand microbial responses to ecological disturbance.

Methods: Microbial community data from Lake Mendota were analyzed to assess temporal changes in the bacterial phylum Firmicutes before and after the 2014 invasion of the spiny water flea. A long-term microbial dataset was examined, with analyses focused on samples collected between 2012 and 2019. All analyses were conducted in RStudio. Weekly relative abundance values for Firmicutes were grouped by year, and annual mean abundance values were calculated by averaging all weekly measurements within each year. This method allowed for comparison of Firmicutes abundance across years while accounting for seasonal sampling variation. Annual mean values were visualized using bar graphs to compare Firmicutes abundance across preinvasion (2012–2013), invasion (2014), and post-invasion (2015–2019) periods. These visualizations were used to identify temporal trends in Firmicutes abundance associated with the invasion event.

Results: Average annual Firmicutes abundance varied across the study period (2012–2019) (Figure 1). Firmicutes abundance was relatively high prior to the spiny water flea invasion, with elevated levels observed in 2012 and a peak in 2013. Following the invasion year (2014), the abundance of Firmicutes declined in 2015, indicating an initial postinvasion decrease. A temporary increase in Firmicutes abundance occurred in 2016; however, this increase was not sustained over time. From 2017 through 2019, Firmicutes abundance remained consistently low compared to pre-invasion levels. This trend of reduced abundance suggests a long-term shift in the microbial community linked to the introduction of spiny water fleas.

Conclusions/Implications: This study demonstrates that the 2014 spiny water flea invasion in Lake Mendota was associated with a sustained shift in microbial community, characterized by reduced abundance of Firmicutes in the years following the invasion. Although a temporary increase was observed in 2016, this fluctuation was not maintained, supporting the presence of a longer-term post-invasion shift rather than short-term variability. The observed ecological patterns of abundance fluctuation parallel microbial shifts commonly discussed in host-associated microbiome research, where changes in Firmicutes are frequently used as indicators of altered community structure.

P-27 Title: Palmitate-Induced Lipotoxicity is Prevented by Oleate Co-Treatment through Enhanced Lipid Droplet Formation in Human

Renal Tubular Epithelial Cells

Authors: Dana Battle, Salim Stewart, Xueying Zhao

Department of Physiology, Morehouse School of Medicine, Atlanta, GA, United States

Mentor: Xueying Zhao, Ph.D., Morehouse School of Medicine

Background/Significance: Saturated fatty acid-induced lipotoxicity, particularly from palmitate, contributes to the development of kidney injury, especially in individuals with obesity and metabolic disorders. In contrast, unsaturated fatty acids, such as oleate, promote the formation of lipid droplets (LDs), which sequester excess fatty acids and reduce cellular stress. LDs are key indicators of a cell’s capacity to buffer lipotoxicity, and the lipid droplet–associated protein Perilipin 2 (PLIN2) plays a central role in stabilizing and regulating these structures. This study investigated whether oleate co-treatment reduces palmitate-induced lipotoxicity in renal tubular epithelial cells (HK-2) and whether this effect is associated with increased PLIN2 expression and lipid droplet accumulation.

Methods: HK-2 cells were treated with bovine serum albumin (BSA)-conjugated palmitate (0, 150 µM, 300 µM, or 450 µM) with or without oleate (150 µM) for 24 h. Palmitate-induced lipotoxicity was first evaluated by measuring the levels of extracellular and total ATP, using the RealTimeGloTM Extracellular ATP and CellTiter-GloTM Luminescent Cell Viability assay kits. Western blot analysis was performed to further evaluate the protein levels of mitochondrial markers of fusion (mitofusin 2, MFN2) and fission (dynamin-related protein 1, DRP1), cell apoptotic markers [cleaved poly (ADP-ribose) polymerase-1 (PARP1) and C/EBP homologous protein (CHOP)], and lipid accumulation marker PLIN2. Immunofluorescence staining was used to visualize lipid droplet accumulation.

Results: Exposure of HK-2 cells to palmitate at high concentrations (300–450 µM) triggered a robust release of extracellular ATP (eATP), a damage-associated molecular pattern signal, which was detectable as early as 8 hours and peaked at 16 hours, in a dose-dependent manner. Additionally, a dose-dependent decrease in ATP production was detected in palmitate-treated cells at 24 hours. This cytotoxic response was accompanied by disrupted mitochondrial dynamics, characterized by a marked reduction in MFN2 and the accumulation of small, fragmented mitochondria. Consistently, palmitate also elevated the expression of cytotoxicity markers, cleaved PARP-1, and CHOP. Notably, palmitate-induced eATP increase and total ATP reduction were abolished in the presence of oleate co-treatment. Additionally, co-treatment attenuated palmitate-induced mitochondrial fragmentation, PARP-1 cleavage, and CHOP upregulation, which was accompanied by a significant upregulation of PLIN2 protein and pronounced accumulation of larger lipid droplets.

Conclusions and Implications: These findings suggest that oleate mitigates palmitate-induced mitochondrial dysfunction and lipotoxicity in human renal tubular epithelial cells through PLIN2mediated lipid droplet formation, highlighting lipid droplet remodeling as a therapeutic strategy to protect renal tubules from metabolic stress.

Acknowledgment of Funding: Supported by NIH, ATLANTIS and RCMI grants 1R16GM149499-01, TL1DK136047, U2CDK129501, and U54MD007602.

P-28 Title: Early Childhood Lead Exposure and Systemic Inflammation: Links to Metabolic and Hepatic Dysfunction — A Literature Review.

Authors: Akolbia Biggers-Rowland, MPH¹; Carmen Dickinson-Copeland, Ph.D.,

MSCR²

Mentor: Carmen Dickinson-Copeland, Ph.D., MSCR, Morehouse School of Medicine

Background/Significance: Early childhood lead (Pb²⁺) exposure remains a critical public health concern, affecting millions. Although neurodevelopmental effects of Pb are well-established, emerging evidence suggests systemic inflammation may mediate Pb²⁺'s metabolic and hepatic impacts. Complete blood count (CBC)-derived inflammatory ratios: neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and lymphocyte-to-monocyte ratio (LMR), represent accessible biomarkers of Pb²⁺-induced inflammation; however, their role in metabolic dysfunction remains poorly characterized. We hypothesize chronic pediatric Pb²⁺ exposure induces systemic inflammation, as measured by CBC parameters, which subsequently drives metabolic dysregulation, including alterations in body mass index (BMI), components of metabolic syndrome, and hepatotoxicity. This literature review synthesizes current evidence on Pb²⁺inflammation-metabolism pathways and identifies critical knowledge gaps requiring further investigation.

Methods: A comprehensive literature review was conducted using PubMed, Web of Science, and Scopus databases (2000-2025). Search terms included: Pb²⁺ exposure, pediatric/childhood Pb²⁺ poisoning, blood Pb²⁺ level, systemic inflammation, neutrophil-to-lymphocyte ratio, complete blood count, BMI/obesity, metabolic syndrome, and hepatotoxicity. Studies examining the effects of Pb²⁺ on inflammatory biomarkers, anthropometric measures, metabolic parameters, and hepatic function in pediatric populations were prioritized.

Expected Results: Previous evidence reveals consistent inverse associations between Pb²⁺ exposure and BMI in children, with studies documenting 20-43% reductions in the risk of overweight/ obesity among exposed populations. Lead significantly elevates inflammatory markers through various pathways, with occupational studies demonstrating dose-dependent increases in NLR and documentation that NLR mediates approximately 15% of Pb²⁺'s genotoxic effects. However, the mechanistic role of CBC-derived inflammatory ratios in mediating Pb²⁺'s metabolic effects remains unexplored. Lead exposure is associated with components of metabolic syndrome, including elevated fasting glucose, triglycerides, and insulin resistance. Multiple studies have demonstrated Pb²⁺-induced hepatotoxicity through inflammatory mechanisms involving the activation of TNF-α and IL-6. Epidemiological evidence shows significant variation in Pb²⁺ exposure across demographic groups: Black children experience 2-3-fold higher elevated blood Pb²⁺ levels compared to White children, even within similar socioeconomic categories. Lower socioeconomic status correlates with higher Pb²⁺ exposure and stronger associations with adverse health outcomes.

Conclusions and Implications: This review reveals while Pb²⁺'s inflammatory and metabolic effects are documented separately, critical gaps remain, including: (1) whether CBC-derived inflammatory ratios mediate the Pb²⁺-BMI relationship, (2) how inflammatory status modifies Pb²⁺'s metabolic effects across different populations, and (3)the interplay between Pb²⁺ exposure, inflammation, and demographic factors (socioeconomic status and race/ethnicity) as potential confounders and effect modifiers. The use of routine CBC parameters for inflammatory assessment provides a pragmatic and cost-effective approach for clinical risk stratification. Future research should employ mediation analyses of inflammatory ratios, test for effect modification by inflammatory status and socioeconomic position and develop integrated risk models, combining environmental exposures with readily available clinical biomarkers.

P-29 Title: Epigenetic Reprogramming in Poor Cardiovascular Health Black Adults

Authors: 1,2Harriet NA Blankson, 1Rashi Verma, 1,3Emine Guven, 2,4Kimberly Rooney, 1Andrea Pearson, 5Herman Taylor, 1Robert Meller, 2,4Charles D. Searles

1Neuroscience Institute,Morehouse School of Medicine, Atlanta, GA 30310, USA

2Atlanta VA Health Care System, Decatur, GA 30033, USA

3Department of Biomedical Engineering, Duzce University, Duzce 81000, TURKIYE

4Division of Cardiology, Emory University School of Medicine, Atlanta, GA 30322, USA

5Cardiovascular Research Institute, Morehouse School of Medicine, Atlanta, GA 30310, USA

Mentors: Charles Searles, MD, Emory University School of Medicine, and Robert Meller, DPhil, Morehouse School of Medicine

Background: Epigenetic remodeling through DNA methylation may underlie cardiovascular health (CVH) disparities by regulating protective and maladaptive molecular pathways. We aimed to characterize genome-wide DNA methylation differences associated with CVH status in Black adults.

Methods: We profiled DNA methylation in whole blood from 351 Black individuals stratified into low versus high CVH groups using the American Heart Association’s Life’s Simple 7 metric (low < 10  high). Differentially methylated CpG sites (DMPs) were mapped across chromosomes, genomic features, and regulatory contexts. Gene ontology enrichment and EWAS analysis and included gene expression data to identify related genes.

Results: We identified 481 hypermethylated and 5,94 hypomethylated DMPs, enriched in DNASE-sensitive promoter regions. Epigenome wide association studies (EWAS) enrichment confirmed significant overlap with cardiometabolic and inflammatory phenotypes. Integration of methylation-expression analysis revealed 212 genes showing coordinated regulation, including PLIN5, ANO9, IGFBP1, HHEX, and BAFT. Hypermethylation of IGFBP3 coordinated with reduced gene expression suggests an epigenetic suppression of vascular protective signaling, consistent with endothelial dysfunction.

Conclusions and Implications: Poor CVH is marked by promoter and island based hypermethylation silencing stress response pathways, coupled with open-sea hypomethylation activating inflammatory genes.These findings highlight epigenetic reprogramming of vascular and immune regulations as key molecular features linking social and biological stress to cardiovascular risk.

Acknowledgement of Funding: This research work was made possible by funding from the NIH (R01NS112422, and RM1HG012334) and theAmerican HeartAssociation (15SFCRN23910003).

P-30 Title: Perceptions of Black Families on a Community-Engaged Diabetes Prevention Intervention: Qualitative

Findings from the FIGHT for Life Project

Authors: Jaiden Evans1; KaLeigh Pittman2; Kennedy Ingram1; Myla Bell1; Asia Rivers, MPH3; Shekwonya Samuel, PhD3; Sencarda Jordan4; Kenya Baker, MSPAS4; Rakale Quarells, PhD3

Albany State University, Department of Sociology and Psychology; 2. Albany State University, Department of Natural Sciences; 3. Morehouse School of Medicine; 4. Albany Area Primary Health Care

Mentor: Rakale Quarells, Ph.D.

Background/Significance: Black families in Albany, GA, experience higher rates of type 2 diabetes (T2D) compared to other race/ethnic groups, yet most prevention programs are not culturally tailored or practical for daily family life. Without relevance and engagement, lasting behavior change is difficult. This study will collect the perspectives of local Black families on adapting and culturally tailoring the Diabetes Prevention Program (DPP) to inform the development of the FIGHT for Life, family-centered, diabetes prevention intervention.

Methods: Families engaged in in-person focus group sessions discussing their perceptions of health behaviors, such as healthy food and physical activity habits, family togetherness, curriculum, and sustainability. Each session lasted two hours and was audio- and video-recorded with participant consent. Participants included families living in the same household, one parent/guardian (18+), self-identified as Black, and one child (8-15 years). The parent must have prediabetes or be at risk for prediabetes (CDC Pre-Diabetes Risk Test). Participants were recruited through local medical facilities, community events, and various media channels. Qualitative data collection was conducted using semi-structured interviews.

Results: A total of 19 families (N=38) participated in the focus groups. All parents were female (N=19, 100%), with an average age of 41.0 years (SD=9.5). Most children were male (N=11, 57.9%). Children had a mean age of 11.9 years (SD=2.1). Most parents had a college degree or higher (57.9%), and over half of adults were employed full-time (52.6%). Most parents never married (57.9%), and nearly half of families reported an annual household income of $20,000$39,999 (47.4%). Preliminary findings suggest that families value culturally relevant, familycentered approach to prevention of diabetes. Parents were interested in learning recipes, particularly making current meals healthier, but worried children might not like food. Overall, parents and children expressed wanting to try new food and the importance of a program that was considerate of location, time and weekday.

Conclusions and Implications: The findings from this study offer critical insight for refining diabetes prevention interventions among Black families in Albany, GA. Applying these results to program development will ensure that intervention strategies are culturally responsive, familycentered, and contextually appropriate. Future efforts will focus on operationalizing these adaptations into the intervention.

Acknowledgment of Funding: This research is supported in part by grant number 2U54MD007602-36 from the National Institutes of Minority Health and Health Disparities.

P-31 Title: Modeling Redox-Insensitive STING1 Variants via CRISPR/Cas9 Knock-In

Editing

Authors: Uswa Jadoon1,2, Adriana Harbuzariu3, Francisco J. Schopfer4, Luis Villacorta1,2

1 Department of Physiology, Morehouse School of Medicine

2 Cardiovascular Research Institute, Morehouse School of Medicine

3 Emory Stem Cell and Organoids Core

4 Department of Pharmacology and Chemical Biology, University of Pittsburgh

Mentor: Luis Villacorta, Ph.D., Morehouse School of Medicine

This project uses CRISPR/Cas9 to modify the STING1 gene's Exon 4, replacing cysteines at positions 88 and 91 with alanine (C88A, C91A). These variants aim to shed light on STING's role in inflammatory signaling and diseases like chronic inflammatory disorders.

Methods: Using the Benchling CRISPR design platform (based on the human genome reference GRCh38/hg38), we targeted Exon 4 of the TMEM173 gene (ENSG00000184584), located on chromosome 5 (chr5:139,475,534–139,482,935). Several guide RNAs (gRNAs) were evaluated for predicted efficiency and specificity, and a forward-strand gRNA located at position 1619 was selected based on its favorable on-target score (65.2) and acceptable off-target score (36.5).

To facilitate precise genome editing, we designed a single-stranded DNA (ssDNA) donor template containing homology arms of 200 base pairs (upstream) and 101 base pairs (downstream) from the specific edited point-mutations. The donor sequence incorporated two specific Cysteine-to-Alanine substitutions along with silent mutations in the protospacer adjacent motif (PAM) region to prevent re-cutting by Cas9. All nucleotide substitutions were designed to preserve the original amino acid sequence and maintain optimal codon usage.

Results: The optimized single-stranded oligodeoxynucleotide (ssODN) donor template incorporated targeted point mutations at nucleotide positions corresponding to Cys88Ala and Cys91Ala (resulting in amino acid substitutions C88A and C91A). Several silent mutations were added to the guide RNA target area to disrupt the PAM and prevent Cas9 re-cutting. For example, AGG was changed to AGA, and other PAMs like CGG to CGC were modified without changing the amino acids (synonymous mutations). This design enables precise genome editing via homology-directed repair (HDR) to create redox-insensitive cysteine variants of STING, serving as a valuable model to study how redox regulation influences inflammatory signaling.

Conclusions and Implications: This CRISPR editing strategy will serve as a foundational platform within our induced pluripotent stem cell (iPSC) pipeline for downstream differentiation into various relevant cardiovascular (e.g., cardiomyocytes, endothelial cells, and vascular smooth muscle cells) and endocrine (endometrial stromal and epithelial) cells. The overarching goal is to generate a library of iPSC lines carrying distinct gene variants, enabling the systematic study of how naturally occurring allelic differences influence cellular function, signaling, and disease phenotypes. This approach will support functional validation of human genetic variation and provide a resource for investigating variant-dependent mechanisms underlying health and pathology.

Acknowledgment of Funding:

• This research is supported in part by grant number R01HD115342-01A1 from NICHD, NIH.

P-32 Title: Genetic Ancestry and Socioeconomic Deprivation Affect the Accuracy of Type

2 Diabetes Polygenic Risk Estimation

Authors: Jennifer Jones, MS1

1Morehouse School of Medicine (MSM) Department of Microbiology, Biochemistry, and Immunology

Mentors: I. King Jordan, PhD, Georgia Institute of Technology (GT), James Lillard, PhD, MBA, Morehouse School of Medicine

Background/Significance: Type 2 Diabetes (T2D) is a complex disease with high prevalence in the United States (US) and disparate impacts across ancestry and socioeconomic strata. Polygenic risk scores (PRS) show great promise for estimating the genetic predisposition of complex diseases like T2D, supporting preventive medicine, but the context-dependence of PRS accuracy remains an open question. The objective of this study was to investigate how the predictive accuracy of T2D-PRS differs across ancestry and socioeconomic deprivation (SED) strata in a large, diverse cohort of US residents.

Methods: The study cohort was constructed from the All of Us Research Program, integrating health outcome, demographic, genomic, and socioeconomic data for 252,634 participants. Participants were characterized as T2D cases (1) or controls (0) using electronic health records (EHR). 1,259,150 T2D-associated variants were used to validate a multi-ancestry T2D-PRS, and five socioeconomic indicators [education, employment, income, health insurance, housing] were combined into a composite SED index. Self-identified race and ethnicity (SIRE) were harmonized with genetically inferred ancestry, and the cohort was stratified into three ancestry groups [AFR, AMR, EUR] and three SED strata [low, medium, high]. Logistic regression was used to measure PRS prediction accuracy across strata, controlling for age, sex, and genetic principal components, via odds ratio (OR) and incremental R2 values.

Results: SIRE and genetic ancestry groups corresponded for 98.8% of participants, yielding cohort strata that control both socioeconomic and genetic differences. The prevalence of T2D over the age of 50 was 20.92% for Black/AFR (n=52,608), 19.71% for Hispanic/AMR (n=41,747), and 13.37% for White/EUR (n=158,279) participants. PRS showed significant associations with T2D across all strata (ORs 4.79±4.02-5.70 to 21.31±18.52-24.52), consistent with its utility for patient risk stratification. PRS accuracy was highest for EUR (R2=0.045), followed by AMR (R2=0.042), and AFR (R2=0.017) ancestry groups. Low SED participants show the highest accuracy (R2=0.038), followed by medium SED (R2=0.036), and high SED (R2=0.029). Prediction accuracy varies 8x more across ancestry groups compared to SED strata.

Conclusions and Implications: Genetic and socioeconomic context bothmatter for the accuracy of T2D-PRS, with ancestry showing a stronger effect than SED. PRS perform poorly in high SED participants across all ancestry groups, indicating that T2D risk-increasing effects of socioeconomic deprivation render genetic risk differences less important. These findings underscore the need for integrative risk stratification methods that include genetic and socioeconomic data to ensure more equitable preventive medicine.

Acknowledgment of Funding: This research was supported by MSM and GT.

P-33 Title: P311 Modulates Adipocyte Plasticity and Adipose Tissue Inflammation through Mitochondrial Homeostasis and Macrophage Polarization

Authors: Pavana Jyotsna Kasaram, PhD1*, Steven Moreton, MS1, 2, Amrendra Pratap Singh, PhD1, Kameswara Rao Badri, PhD1, 2

1 Cardiovascular Research Institute, 2 Pharmacology and Toxicology, Morehouse School of Medicine, Atlanta, GA 30310

Mentor: Kameswara Rao Badri, PhD, Associate Professor, Morehouse School of Medicine.

Background/Significance: Obesity is a global pandemic characterized by excessive body fat accumulation affecting adult populations, about 20% globally and 42% in United States of America. Apart from the non-modifiable factors including genetics, ethnicity, race and age, modifiable factors like diet and lifestyle seem not very helpful in preventing this pandemic as evidenced by the recent rise in obesity (child and adult) incidences in the USA and worldwide. Chronic metabolic alterations mediated by mitochondrial homeostasis and inflammation are common in the pathogenesis of obesity and other metabolic diseases. Our laboratory recently showed the presence of P311 protein in white adipose tissue, brown adipose tissue and macrophages. Our ongoing studies indicate that P311 regulates adipocyte plasticity and macrophage polarity. So, we hypothesize that P311 regulates adipocyte plasticity through mitochondrial homeostasis and inflammation by macrophage polarity implicating P311’s role in a larger capacity regulating metabolism and inflammation.

Methods: We used 3T3-L1 preadipocytes, immortalized murine brown preadipocytes, L1 adipocyte and murine brown adipocytes along with macrophage cell lines (RAW264.7 cells and BV2 cells). Quantitative PCRs, immunoblots, immunofluorescence, mitochondrial (mt)-biogenesis assays, mt-membrane potential assays, reactive oxygen species (ROS) assays were performed along with macrophage polarity studies using lipopolysaccharide (LPS, M1 macrophage phenotype inducer) and interleukin-4 (IL4, M2 macrophage inducer).

Results: Our results showed that P311 induced mitochondrial biogenesis and improved mtmembrane polarity in white adipocytes, brown adipocytes and macrophages. P311 induced M2Macrophage phenotypeas observed in P311 overexpression studies and LPS/IL4 treated studies. Further, P311 protected adipocytes and macrophages (BV2) from endogenous and/or tert-butyl hydroperoxide (TBHP) induced ROS implicating the beneficial effects of P311 potentially mediated through mitochondria and macrophage functions.

Conclusions and Implications: P311 modulates adipocyte plasticity and adipose tissue inflammation mediated through mitochondrial homeostasis and macrophage polarization respectively implicating potential targeting of P311 pathways in reducing metabolic disorders.

Acknowledgement of Funding: This study was supported by SCORE/SC1 grant funding to KB (5SC1GM141937). SM is RISE Fellow supported by NIGMS, R25GM058268. We acknowledge the support to MSM Core Facility (RCMI grant, 5U54MD0076037). We thank Dr. Firas Kobaissy for kind gift of BV2 cells.

P-34 Title: Resuscitative Thoracotomy (RT) in Traumatic Cardiac Arrest

Authors: Simone Lester1, Lucy Deveaux-Hart2, Jonathan Nguyen1,3, Deepika Koganti2,3

1. Morehouse School of Medicine

2. Emory University School of Medicine

3. Grady Memorial Hospital

Mentor: Deepika Koganti, MD, Emory School of Medicine

Background/Significance: Resuscitative thoracotomy (RT) is a high-risk, resource-intensive intervention for patients in traumatic cardiac arrest (TCA). Existing guidelines vary: the Western Trauma Association emphasizes injury mechanism and transport time, whereas the Eastern Association for the Surgery of Trauma emphasizes mechanism and signs of life. This study evaluated blood transfusion requirements and survival outcomes following emergency department thoracotomy (EDT).

Methods: This retrospective study was conducted at a single American Level I trauma center between January 2014 and March 2025. The study included 467 patients who received emergency department (ED) thoracotomies. The primary variables collected included the volume and type of blood products transfused at key timepoints: in the ED, in the operating room, at 6 hours, and at 24 hours post-arrival. Data was abstracted from electronic medical records and recorded in a secure Excel spreadsheet. Statistical analysis was performed using JASP. Continuous variables were compared using a t-test, with a p-value of <0.05 considered statistically significant. Institutional Review Board (IRB) approval was obtained prior to data collection.

Results: Thus far, the results included are derived from 141 patients, 67 of whom survived to the OR. The blood products compared include whole blood, packed red blood cells (PRBC), and fresh frozen plasma (FFP) in both the OR and ED. Survivors to the OR received slightly higher mean units across most blood types. Statistical analysis reveals a significant difference in FFP administration (p = 0.018). When looking at OR blood transfusions patients who survived out of the OR received significantly more total units (p=0.006), PRBC (p=0.022), and FFP (p=0.011) compared to those that did not. Patients who survived to discharge received a higher average number of units; however, none of the outcomes reached statistical significance.

Conclusions and Implications: Higher blood product use was significantly associated with short-term survival, including survival to and out of the OR. However, the blood product use did not significantly differ between those who survived to discharge and those who did not. This highlights the need to further explore additional factors influencing patient survival in resuscitative thoracotomies. In the future, this data could be used to develop a predictive model of blood transfusion requirements and outcomes in resuscitative thoracotomies.

P-35 Title

: The Impact of West African Ancestral Variants on Per–Arnt–Sim Kinase (PASK)

Authors: AyomideOlayiwola, M.S; Kenisha Webb, M.S; Ashley Gayle, M.S; and Sean Kimbro, Ph.D.

1Morehouse School of Medicine, Ph.D. in Biomedical Sciences Program

2Morehouse School of Medicine, Department of Microbiology, Biochemistry, and Immunology

Mentor: Sean Kimbro, Ph.D., Morehouse School of Medicine

Background/Significance: Type II Diabetes is a chronic disease affecting over 27 million individuals in the United States. This condition often stems from the body’s inability to regulate blood glucose levels. African Americans are almost twice as likely to develop diabetes than European Americans. Genetic traits, obesity, and insulin resistance contribute to these disparities. However, little is known about how West African ancestral variants of genes play a role in this disparity. It is unknown how these variants may impact drug efficacy in patients of West African Ancestry. Per-Arnt-Sim Kinase (PASK) is a nutrient-sensitive protein kinase that regulates glucose metabolism. We have identified nucleotide variants (rs1131293, rs10167000, and rs3815305) in the PASK amino acid sequence observed in high frequencies in individuals of West African Ancestry (WAA) compared to European Ancestry (EA). We hypothesize that these variants significantly alter PASK protein structure, and these structural variations may impact glucose-related functions of PASK in individuals of WAA.

Methods: PASK variants were in the kinase domain of the protein with the highest allele frequencies in African Americans. These variants are rs3815305, rs10167000, and rs1131293. 3-Dimensional protein secondary structure prediction was conducted using PASK sequence data from the Protein Data Bank (PDB) and submitted to structural prediction software Robetta-Baker Lab. PSIRED Workbench was used to identify regions of altered secondary structure. Western blot detected the presence of PASK protein in cell lines HepARG, HepC3A, and HepG2. To identify if PASK WAA variants were present in cell lines, TaqMan Genotyping Assays were conducted using the above SNPs and following cancer cell lines: HepC3A, HepG2, Hep3B, MDA-MB-231, MDA-MB-468, and HCC-1806.

Results: Significant structural changes were present in each PASK variant when compared to wild-type PASK protein secondary structure. PASK protein was identified in the cell lines HepARG, HepC3A, and HepG2. As expected, the WAA variants were detected in selfidentified African American cell lines.

Conclusions and Implications: The findings of this experiment suggest that there are significant structural differences in PASK WAA variants. These differences could alter the docking abilities of known PASK effector molecules and glucose-related functions of PASK. Further research will be conducted to describe the impact of glucose on wild-type vs Ancestral Variant PASK activity. Additional research using the All of Us Database will explore the association between PASK WAA variants and clinical manifestations of T2D in African Americans.

Acknowledgement of Funding: NIH grant numbers 2U54MD007602-36 and R01MD01740

P-36 Title: Sleep Apnea and Cardiovascular Correlates in Female Collegiate Athletes (Sports & Exercise)

Authors:

Neeya Patel,¹ Austin J. Rim, MD,² J.T. Miller, MS,² Mekensie Jackson, MS,² Jonathan H. Kim, MD, MSc²

¹ Morehouse School of Medicine, Atlanta, Georgia, USA

² Emory Clinical Cardiovascular Research Institute, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia, USA

Mentor: Dr. Johnathan Kim, MD, Emory School of Medicine, Dr. Austin Rim, MD, Emory School of Medicine

Background/Significance: Obstructive sleep apnea (OSA) is an underdiagnosed condition associated with cardiometabolic disease and early cardiovascular risk. While OSA has been documented among male athletes, particularly American-style football players, its prevalence and clinical implications among female collegiate athletes remain unknown. Traditional risk factors such as obesity and daytime sleepiness may not fully capture sleep-disordered breathing risk in this population. Therefore, this study sought to comprehensively assess sleep health and vascular function in female collegiate athletes.

Methods: This cross-sectional, multi-center study enrolled female NCAA Division-I athletes from basketball, softball, and volleyball programs. Assessments included anthropometrics, blood pressure (BP), echocardiography, and vascular applanation tonometry. Sleep evaluations were performed using WatchPAT home sleep studies and Pittsburgh Sleep Quality Index (PSQI) surveys, with results verified by a sleep scientist. The prevalence and predictors of sleep apnea were analyzed, as well as associations with systolic BP (SBP), diastolic BP (DBP), pulse wave velocity (PWV), tissue Doppler E′ velocity, and left ventricular mass index.

Results: A total of 68 athletes (age 19.0±1.4 years; 63% freshmen; 25% basketball, 41% softball, 34% volleyball) were included. Sleep apnea (apnea-hypopnea index [AHI] ≥5) was present in 25% (n=17), and poor sleep quality (PSQI >5) in 36% (n=24). Athletes with sleep apnea were older (19.5±1.4 vs 18.8±1.3 years, p=0.04), had higher lean mass (61.6±7.0 vs 55.6±6.6 kg, p<0.01), and demonstrated increased arterial stiffness (PWV 5.6±0.8 vs 4.9±0.7 m/s, p<0.01). Lean mass independently predicted sleep apnea (OR 1.16, 95% CI: 1.04–1.30, p=0.01). Higher AHI predicted higher PWV (β=0.09, 95% CI: 0.04–0.15, p<0.01), although this association attenuated after adjusting for age, race, weight, and sport. Weight (β=0.07, p=0.03), lean mass (β=0.14, p=0.01), and age (β=0.55, p=0.03) independently predicted AHI, while body fat % and self-reported sleep quality did not.

Conclusions and Implications: Mild sleep apnea and poor sleep quality were common among female collegiate athletes. AHI was associated with increased arterial stiffness, suggesting potential early cardiovascular risk. Importantly, traditional markers such as body fat % and selfreported sleepiness were not predictive of sleep apnea in this population, highlighting the need for tailored screening approaches. Future longitudinal research should investigate sex-specific risk factors and long-term health outcomes of sleep-disordered breathing in athletes.

Acknowledgment of Funding:

• Funding: NIH / National Heart, Lung, and Blood Institute - R01HL162712 to Dr. Kim

P-37

Title: Evolution of Healthcare Spending: A Decade of Cardiovascular Disease Healthcare Spending Trends in the United States

Authors: Craig Terrell Robey, MS, Loretta Shields PhD DMin, Billie-Jean Martin MD PhD

Mentor Name:

Dr. Billie-Jean Martin, Stanford University

Institutional Affiliations:

Stanford University, Stanford Department of Cardiothoracic Surgery & Morehouse School of Medicine

Background/Significance: Heart disease has been the leading cause of death in the United States since the early twentieth century with associated cardiovascular diseases (CVD) (e.g., stroke) also topping the list. There are considerable racial-ethnic and location-based disparities in the all-cause mortality rate. Cause-specific mortality rates follow similar patterns. Despite the US spending more on health care than other high-income nations, it ranks lower than other highincome nations with regards to its health care access and quality scores. The purpose of this analysis was to identify trends in CVD healthcare spending at a state and region-level from 2010 to 2019.

Methods: Data was statistically analyzed from the health care spending datasets (2010 through 2019) provided by the International Health Metrics and Evaluation (IHME). Relevant state-level data from the large datasets was extracted and results were aggregated per type of care category. This was also done for the 10 regions as defined by the Centers for Medicare & Medicaid Services (CMS). All analyses were conducted using Stata.

Results: Statistical analyses revealed declines in CVD healthcare spending per beneficiary in ambulatory ($230.65 down to $222.95), in-patient ($414.46 down to $308.39), nursing facility ($42.85 down to $32.06), and pharmaceutical care ($81.89 down to $41.85) over the decade in all CMS regions. There was an increase in spending per beneficiary in emergency department care ($21.16 up to $26.59) and an increase in home health care for most regions ($22.13 up to $25.87). All 10 CMS regions followed similar trends with in-patient and ambulatory care accounting for the most spending per beneficiary, while other types being much lower. Region 2 (New York and New Jersey) generally had the highest spending per beneficiary per type of care, with other regions being variable. Overall, results indicate that per beneficiary spending decreased across most types of care in multiple regions.

Conclusions and Implications: The findings of this study indicate that further investigation is required to determine reasons for the overall decrease in cardiovascular healthcare spending. Regarding higher ambulatory and in-patient spending, it is important to determine if there are spending disparities between rural and urban areas with these two categories. There is also a need to investigate the increase in emergency and home health spending per beneficiary. Additionally, there is a need to assess correlations between spending and CVD mortality rates in these regions.

P-38 Title: Human P311

Missense Variants Demonstrate Significant Alterations in Protein Structure.

Authors: Makalah Saunders1, Pavana Jyotsna Kasaram1, Kameswara Badri1,2

1 Cardiovascular Research Institute, Morehouse School of Medicine, Atlanta, GA 30310

2 Pharmacology and Toxicology, Morehouse School of Medicine, Atlanta, GA 30310

Mentor: Kameswara Rao Badri, Ph.D., Associate Professor, Morehouse School of Medicine

Background/Significance: Obesity is a complex disease characterized by excessive body fat, affecting 42% of adults in the United States. Obesity is majorly associated with inflammation and increases the risk of developing chronic illnesses, including type II diabetes mellitus, hypertension, and cardiovascular disease. P311 is a small protein that is highly conserved across species and has roles in adipogenesis, blood pressure regulation, and macrophage polarization. However, little is known about the human P311 protein (hP311). We have previously shown the structure of murine P311 as an intrinsically unstructured protein with very small alpha helix secondary structure. P311 does not contain any known motifs and/or domains except a PEST domain, which acts as a rapid protein degradation signal. We hypothesize that missense variants within the major structural elements of hP311 alter its conformational stability and functionality, thereby modulating adipogenesis, adipocyte plasticity and possibly influencing susceptibility to obesity.

Methods: Amino acid (aa) sequences of three isoforms of human P311: isoform-a (68 aa), isoform-b (102 aa), and isoform-c (112 aa) were downloaded from the ncbi.nlm.nih.gov website. We predicted the structure of hP311 isoform-a, -b, and -c using multiple online tools, including ITASSER. Further, we identified over 150 missense variants out of ~100,000 known SNPs of P311 from the NCBI-SNPs database. Our evaluation of hP311-isoform-a demonstrated two alpha helices between amino acids 19-21 and amino acids 32-38. Evaluation of the aa sequence of hP311 isoform-a from NCBI demonstrated a PEST domain between amino acids 39-55. Among 150 missense variants, we focused on 15 SNPs that occur within the ��-helical secondary structure and PEST domain regions of hP311-isoform-a.

Results: The majority of hP311-isoform-a predictive models for all 15 SNPs demonstrated the complete loss of the helical structure between amino acids 19-21 and a shortened helical structure found between amino acids 32-38.

Conclusions and Implications: These significant structural changes to hP311 have the potential to alter its function. Our future work will focus on evaluating hP311 variants for their functionality in adipogenesis, macrophage polarity, and mitochondrial homeostasis.

Acknowledgement of Funding:

• MS is supported by the Morehouse School of Medicine Summer Research Experience for Medical Students Program.

• This study was supported by NIH/NIGMS grant funding to KB (5SC1GM141937).

P-39 Title: Tim-1 Deletion Amplifies Weight Gain and Steatosis in Metabolic DysfunctionAssociated Fatty Liver Disease

Authors: Salim Stewart, Dana Battle, Xueying Zhao

Department of Physiology, Morehouse School of Medicine

Mentor: Xueying Zhao,PhD, Department of Physiology, Morehouse School of Medicine

Background/Significance: Metabolic dysfunction-associated fatty liver disease (MAFLD) is commonly associated with obesity and characterized by excessive lipid accumulation and liver inflammation. The T cell immunoglobulin and mucin domain 1 (Tim-1) affects innate immunitydriven proinflammatory cascade in liver injury. This study was designed to further examine the role of Tim-1 in MAFLD development and progression.

Methods: Genetic background C57BL/6J male wildtype (WT) mice and Tim-1 knockout (KO) mice ages of 8-12 weeks old were fed with low-fat diet (LFD, 9% fat) or high fat diet (HFD, 42% fat) for 10 weeks. Body weight, liver weight, and liver index (Iiver weight/body weight) were recorded and compared among four groups: LFD-WT (n=8), HFD-WT (n=7), LFD-KO (n=6) and HFD-KO (n=6). The expression levels of ADRP (Adipose Differentiation-Related Protein), a lipid coating and lipid storage protein, and NGAL (neutrophil gelatinase-associated lipocalin protein), a biomarker for liver injury were further examined by Western blotting.

Results: 42% HFD feeding for 10 weeks significantly increased body weight in WT mice (HFDWT: 36.4 ± 1.7 g vs. LFD-WT: 30.4 ± 0.9 g, P<0.01). While Tim-1 deletion did not alter body weight in LFD-KO mice (30.6 ± 0.5 g), HFD-induced body weight increase was greatly enhanced in HFD-KO mice (44.4 ± 1.2 g, P<0.001 vs. HFD-WT). Moreover, Tim-1 deletion resulted in a substantial amplification of liver steatosis in HFD-fed mice. The livers of the HFD-KO mice were paler in color and heavier (liver weight: 3.24 ± 0.22 g and liver index: 7.49 ± 0.93, P<0.0001) compared with HFD-WT livers (liver weight: 1.66 ± 0.15 g and liver index: 4.54 ± 0.65). HFDinduced lipid accumulation was confirmed by a robust upregulation of the hepatic lipid storage protein, ADRP, which was increased by 11- and 24-fold in HFD-treated WT and KO livers, compared to their normal controls. In addition, HFD feeding greatly increased hepatic expression of pro-inflammatory factor NGAL by 3-fold in WT and 13-fold in KO mice.

Conclusions and Implications: Together, these results show that Tim-1 deficiency worsens HFD-induced body weight gain and steatosis, suggesting a regulatory role for Tim-1 in HFDinduced steatohepatitis. Tim-1 might be considered as a target for the prevention and treatment of MAFLD.

Acknowledgment of Funding: This research was supported by the National Institute of Health, the National Center for Research Resources, and the Research Centers in Minority Institutions Program under grants R16GM149499, 8G12MD007602, and U54MD007602. This work was supported by the Atlantis Training Program under grants TL1DK136047 and U2CDK129501.

P-40 Title: Neuregulin-1 Mitigates Malaria and Sickle Cell Disease-Associated HemeInduced Injury in iPSC-Derived Endothelial Cells

Authors: Cecilia Botchway, 1,2,3 Wesley Solomon, 2 William Agbozo, 2Adriana Harbuzariu,5 Kwadwo A. Kusi4, Alexander Quarshie, 6, Jonathan K Stiles 2

1 Morehouse School of Medicine Master of Science in Clinical Research Program

2 Department of Microbiology, Biochemistry & Immunology, Atlanta, GA

3 Department of Pathology, Korle-Bu Teaching Hospital, Accra, Ghana,

4 Noguchi Memorial Institute for Medical Research, Accra, Ghana

5 Emory Stem Cell Core, Atlanta, GA

6 Department of Community Health/Prev Med-Ch/PM MRC, Atlanta, GA

Mentor: Jonathan Stiles, Ph.D., Chair, Professor, MBI, Morehouse School of Medicine

Background/Significance: Intravascular hemolysis drives disease severity in malaria and sickle cell disease (SCD) by releasing toxic cell-free heme. Normally, scavengers like hemopexin (HPX), haptoglobin (HG), and heme oxygenase-1 (HO-1) neutralize heme, but these systems are depleted in SCD and malaria, leading to vascular dysfunction and inflammation. To study hemolysis-induced injury, we generated brain endothelial cells from induced pluripotent stem cells (iPSCs) reprogrammed from adult somatic cells. We hypothesize that heme exposure in iPSCderived endothelial cells from individuals with distinct hemoglobin genotypes triggers genotypespecific vascular inflammation. We also show that Neuregulin-1 (NRG-1), a cytoprotective peptide, mitigates this injury by promoting anti-inflammatory signaling and HO-1 expression. This study uses patient-derived iPSC-ECs to model vascular responses to hemolysis and assess NRG-1’s therapeutic potential.

Methods: In collaboration with Korle-BuTeaching Hospital (Accra,Ghana), hemoglobin genotype was determined via electrophoresis, and malaria/HIV status assessed using rapid tests. Clinical data were collected using standardized tools. Urine-derived epithelial cells (UDCs) and peripheral blood mononuclear cells (PBMCs) were isolated, cryopreserved, reprogrammed into iPSCs, and differentiated into endothelial cells. iPSC-ECs were exposed to heme (38 µM) to mimic hemolytic stress, followed by treatment with recombinant NRG-1 and CoPP (HO-1 inducer). Supernatants and lysates were analyzed for inflammatory markers and HMOX levels. Cellular responses, viability, proliferation, inflammation, and vascular integrity were evaluated.

Results: Heme exposure reduced cell proliferation and elevated inflammatory (CXCL10, IL-6, IL1β, TNF-α), angiogenic (Ang-2, VEGFA), and adhesion markers (VCAM-1, ICAM-1), as well as BDNF, most prominently in HbSS iPSC-ECs. NRG-1 treatment suppressed inflammation, restored endothelial integrity (VE-Cadherin, PECAM-1), and increased HO-1 expression.

Conclusion and Implications: Patient-derived iPSC-ECs offer a personalized ex vivo model to study vascular injury in hemolytic diseases like malaria and SCD. NRG-1 reduces heme-induced inflammation and restores endothelial structure, supporting its therapeutic potential. Genotypespecific endothelial responses to heme may underlie variability in disease outcomes, emphasizing the need for personalized treatment strategies.

Acknowledgment and Funding: Grant support: NIH/NINDS R01NS091616, GCTSA; NIH/NCATS, NIH/RCMI (2U54) MD007602-31, NIH/NIGMS R25AI164613, NIH/FIC 5R25TW009340, NIH/NCATS TL1TR002382. Funding for the study was provided by Fogarty Global Health (UJMT), Morehouse School of Medicine, Atlanta, Georgia.

P-41

Title: APOB and LDLR

Ancestry-Specific Variants and their role in Hypercholesterolemia

Authors:

Timothy Brantley Jr, Sean Kimbro Ph.D.

1. Morehouse School of Medicine Master of Science in Biomedical Research Program

2. Morehouse School of Medicine Department of Microbiology Biochemistry and Immunology

Mentor: Sean Kimbro, Ph.D., Morehouse School of Medicine

Background/Significance: Hypercholesterolemia also known commonly as high cholesterol, refers to a condition where there are elevated levels of low-density lipoprotein (LDL) within the blood circulation. The dysregulation of lipoprotein levels is correlated with increased risks in ASCVD (Atherosclerotic Cardiovascular Disease) and the management of cholesterol LDL levels are a common primary prevention method. Genetic contributions to high cholesterol are studied in conditions where genetic variants of either LDL receptors, or apolipoprotein B (ApoB) can produce difficulty in LDL cholesterol uptake and removal from the blood circulation. Our central hypothesis is that APOB and LDLR gene variants alter protein structure and reduce ApoB–LDLR binding affinity, impairing LDL uptake and raising serum cholesterol.

Methods: To investigate secondary structure changes inApolipoprotein B (ApoB) and its receptor LDLR, the protein prediction software AlphaFold2 will be utilized to model each structure based on their respective amino acid sequences. The models will include amino acid substitutions corresponding to the single nucleotide polymorphisms (SNPs) rs6752026 in APOB and rs11669576 in LDLR. AlphaFold2, predicts the three-dimensional structure of proteins from their amino acid sequences with accuracy comparable to experimental methods such as X ray crystallography and cryo electron microscopy. Subsequent analysis of protein-protein interactions will be performed using HADDOCK, an integrative modeling platform that combines experimental data with computational prediction to simulate biomolecular interactions.

Results: The SNP rs6752026 in APOB was found to be located within a prominent beta-barrel region of the ApoB protein, which is responsible for binding to LDLR. When overlaid with the wild type (WT), helical secondary structure changes were observed due to a proline-to-serine substitution in the amino acid sequence. Similar structural alterations were noted in LDLR containing the rs11669576 variant, resulting from an alanine-to-threonine substitution. Using HADDOCK, reduced binding complementarity was observed in variant-to-variant interactions compared to wild type–wild type binding.

Conclusions and Implications: The results of this study support the need for a more targeted and personalized approach to the treatment of hypercholesterolemia, with long-term implications for the prevention and management of heart disease. The observed structural variations in ApoB and LDLR suggest that genetic differences may influence protein function and receptor binding efficiency, potentially affecting individual responses to lipid-lowering therapies. Furthermore, these findings highlight the importance of considering genetic ancestry in cardiovascular research and clinical care, as genetic variation can differ not only between populations but also among individuals within the same racial ethnic group.

P-42 Title: sThy-1 Improves the Resolution of Lung Fibrosis

Authors:

Nevaeh Herndon, Jennifer Q Zhou, Sara Palega, Rachel Walker, Yan Y Sanders

VHS-EVMS Summer Scholars Program at ODU 2025, Macon & Joan Brock Virginia Health Sciences at Old Dominion University (ODU)

Background and Significance: Idiopathic pulmonary fibrosis (IPF) is a progressive, age-related, fatal disease with limited therapeutic options. It is the scarring of the lung tissue, which prevents gas exchange needed to maintain the blood oxygen level. Thy-1 is a cell surface marker that decreases with age and is decreased in patients with IPF. Published studies show that soluble Thy-1 (sThy-1) improves bleomycin-induced pulmonary fibrosis, which reduces some pro-fibrotic markers, such as α-smooth muscle actin and collagen. However, it is not clear whether sThy-1 would affect aging-related markers in lung fibrosis. We hypothesize that sThy1 will lead to reduced expression of biomarkers associated with aging (i.e., p21, IL-6, IL-1β) in aged murine lung tissues, which promotes the resolution of lung fibrosis in aged mice.

Methods: To determine the role of Thy1 in bleomycin-induced fibrosis, immunohistochemistry (IHC) was performed on lung tissues from aged mice (18 months) in the following groups (n=3/group): saline control, bleomycin-injury, and bleomycin with sThy-1 treatment. sThy1 was given starting week 3 after bleomycin injury, when the lung fibrosis is well-established, until week 6, when the mice were sacrificed, and the lung tissues were collected. Bleomycin was used as the well-established experimental model of pulmonary fibrosis that reliably induces a fibrotic model. Using aged mice enhances the persistence of the fibrosis and better reflects the agerelated mechanisms indicated in human IPF. The lung structures were examined using H&E and Trichrome stains. Aging-related biomarkers analyzed are p21, IL-6, IL-1β, and β-galactosidase. Brightfield microscopy on the Keyence BZ-X800 Series was used for imaging. The staining quantification was carried out using Image J.

Results: Biomarker distribution and expression levels were compared across groups to assess the effects of sThy-1 on lung fibrosis resolution. The Thy-1-treated group showed improved resolution of fibrosis and reduced aging-related markers. This was noted by the decrease in trichome stain for collagen, and aging biomarkers, i.e., p21, IL-6, IL-1β, and β-galactosidase.

Conclusion: Thy-1 treatment resulted in better resolution of bleomycin-induced pulmonary fibrosis in aged murine lung tissues. Compared to the bleomycin-only group, sThy-1 reduced the expression of biomarkers associated with aging and senescence, indicative of pro-fibrotic and inflammatory signaling pathways. These findings support the hypothesis that sThy-1 promotes lung fibrosis resolution, in part by modulating the expression of aging markers in fibrotic tissue. Because bleomycin-induced fibrosis in aged mice mirrors important pathological features that are relevant to IPF. The results provide evidence that sThy-1 may represent a hopeful therapeutic strategy to target IPF-relevant fibrotic and aging pathways.

P-43

Title: Circadian Rhythms in the Bladder and Kidney: A Cross-Species Transcriptomic Analysis

Authors: Zade Mahayni1; Ashu Mohammad, Ph.D.2;Amy D Dobberfuhl, M.D.2

1 Morehouse School of Medicine

2 Stanford Medicine Department of Urology

Mentor: Ashu Mohammad, Ph.D., Stanford University Department of Urology

Background/Significance: Circadian rhythms are ~24-hour cycles coordinating physiology with the light–dark cycle. Nearly all tissues have intrinsic clocks driven by BMAL1 and CLOCK, regulating 5–15% of organ transcripts. In the kidney and bladder, these clocks govern filtration, electrolyte handling, and bladder capacity; their disruption disturbs fluid balance and voiding, highlighting the therapeutic value of circadian alignment.

Methods: Dataset. To investigate how circadian timing is shared across tissues and species, we analyzed MetaCycle (meta2d, p≤0.05) phase calls from baboon bladder and kidney cortex (KIC) (Mure 2018), mouse KIC (Zhang 2014), and an unpublished mouse bladder dataset (Stanford Urology). Phases were wrapped to Zeitgeber Time (ZT∈[0,24)). For each contrast we examined only overlapping rhythmic genes and quantified phase similarity using the absolute circular difference Δ (0–12 ZT), circular–circular correlation (ρ), and Rayleigh tests on signed offsets. For cross-species visualization we also applied a +12 ZT shift to mouse.

Software. R (tidyverse, circular, patchwork); rhythmicity references: MetaCycle (Wu et al., 2016).

Results: We found that core clock genes align tightly within species across bladder and kidney (median|Δ| ≈ 1.27 ZT in mouse; 0.52 ZT in baboon) and, after a +12 ZT inversion, also across species (median|Δ| ≈ 2.07 ZT for bladder; 2.37 ZT for KIC), indicating conservation of the oscillator’s timing. In contrast, total rhythmic genes showed tissue and species-specific phase programs: within species, mouse bladder–kidney differences were modest (median|Δ| 2.8 ZT), whereas baboon bladder peaked much later than baboon kidney (median|Δ| 5.78 ZT). Across species, conservation in the total set was weak (median|Δ| 4.81–6.14 ZT; ρ≈0) and was not rescued by a global +12 ZT shift (bladder worsened; kidney improved slightly yet remained weak).

Conclusions and Implications: Rhythmic-gene counts varied markedly across studies, likely driven by sampling density, power, and thresholding, so we emphasized a fixed core panel and overlap-based phase metrics to mitigate design effects. Together, these results support a model in which the core oscillator is conserved, while downstream, tissue and species-specific output programs reshape the broader rhythmic transcriptome.

Acknowledgment of Funding: This research was supported in part by the Stanford-HBMC Summer Research Program

P-44 Title: Germline and Somatic Variants Likely Share Mutational Hotspots in the Human Genome

Authors: Thais Silva Tavares¹˒⁴, Daniela Souza Lima Barbosa², Carolina Silva de Carvalho¹, Maycon Douglas de Oliveira¹, Luigi Marchionni³, Renan Pedra de Souza¹, Mateus Henrique Gouveia⁴, Francisco Pereira Lobo¹

¹ Institute of Biological Sciences, Universidade Federal de Minas Gerais (UFMG), Brazil

² Pontifícia Universidade Católica de Minas Gerais (PUC Minas), Brazil

³ Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, USA

⁴ Department of Public Health Education, Morehouse School of Medicine, USA

Mentor: Mateus Henrique Gouveia, Ph.D., M.Sc., Assistant Professor - Morehouse School of Medicine

Background/Significance: The evolution of the human genome and the emergence of genetic diseases are driven by mutations that, although originating from common mutagenic mechanisms, differ in their functional and selective consequences. Despite decades of research on mutation rate variability and contextual patterns, few studies have systematically compared the spatial distribution of germline and somatic variants across the human genome. We hypothesize that certain genomic regions intrinsically prone to recurrent mutations harbor both germline and somatic variants more frequently than expected by chance, which may result from common underlying mechanisms

Methods: In this study, We performed a large-scale integrative analysis of single nucleotide variants (SNVs) from HGDP (population-level germline), ClinVar (clinically relevant germline), and COSMIC (cancer-associated somatic) databases to investigate whether variants from different origins share genomic regions prone to recurrent mutation. SNVs were grouped by origin and classification (benign, pathogenic, rare, or common) and characterized through genomic annotation. Statistical significance of variant overlap was assessed using Fisher’s exact test. Shared loci underwent mutational signature (SBS) and functional enrichment analyses to identify overrepresented pathways and chromosomal regions.

Results: We observed a significant overlap between germline and somatic variants at specific loci, suggesting that certain genomic segments act as context-dependent mutational hotspots (regions that accumulate recurrent mutations under shared molecular or structural conditions), regardless of cell lineage. Five recurrent mutational signatures (SBS1, SBS5, SBS6, SBS54, and SBS87) were identified, among which SBS5 was notably widespread and of unknown etiology, potentially reflecting uncharacterized endogenous mutational processes involved in the formation of these hotspots. Enriched genomic loci, such as 13q12.12 and 19p13.3, which harbor genes involved in DNA repair and cell signaling, were identified along with key signaling pathways, including PI3K/AKT/mTOR and ECM–receptor interaction, both essential to tumor progression.

Conclusions and Implications: Altogether, our findings support the hypothesis that the human genome contains intrinsically vulnerable regions where recurrent mutations may bridge germline variation, somatic instability, and cancer evolution.

Acknowledgement of Funding: Supported by CAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brazil (Finance Code 001).

P-45 Title: Building an Imaging-to-Molecular Workflow on the EVOS M7000: Quantitative Analysis of TNBC and DARC/ACKR1-Linked Tumor Biology

Authors: Samiatu Yussuf 1; Rachel Martini, Ph.D2; Melissa Davis, Ph.D2 , Other Co-Author(s): Nourddine Djeddar2; Jamirah Chevrin, MPH2; Pascal Uchehara2

1 Spelman College, Atlanta GA, USA

2 Institute of Genomic Medicine, Morehouse School of Medicine, Atlanta GA, USA.

Mentor: Rachel Martini, Ph.D., and Melissa Davis, Ph.D, Morehouse School of Medicine

Background/Significance: Triple-negative breast cancer (TNBC) disproportionately affects women of African ancestry and is marked by more aggressive tumor biology and poorer outcomes. Ancestry-associated immune mechanisms, particularly those involving the Duffy Antigen Receptor for Chemokines (DARC/ACKR1), may contribute to these disparities. We hypothesize that this aggressiveness reflects distinct immunologic responses to tumor progression shaped by ancestry-specific genetic variation. However, standardized quantitative histopathologic data linking tissue morphology to molecular profiles remain limited, underscoring the need for integrative imaging-to-molecular approaches. This pilot study entails an establishment of microscopy-to-molecular analysis workflow using the EVOS™ M7000 Imaging System and a mouse mammary tumor model. We will (1) acquire high-quality histologic images, (2) perform quantitative analysis (i.e. cellular morphology and density), (3) develop and validate standardized imaging and cell-counting SOP, and (4) pilot integration of quantitative imaging with molecular assay outputs to support translational imaging studies focused on immune-modulated TNBC biology in African ancestry.

Methods: Formalin-fixed, paraffin-embedded (FFPE) mouse mammary tumor sections stained with hematoxylin and eosin (H&E). Imaging was performed using EVOS™ M7000 Automated Imaging System under standardized parameters. Regions of interest are annotated for tumor, stroma, and necrosis using on-board tools. Quantitative metrics including cell density and nuclear morphology using automated counting and segmentation functions. Images and metadata were exported for integration with downstream molecular datasets. This workflow will form basis for cross-validation in human TNBC samples, stratified by DARC/ACKR1 genotype.

Anticipated Results: We expect to generate a high-quality image dataset representing diverse tumor architectures within the mouse mammary model. Quantitative image analysis will yield reproducible cell density and morphology metrics, establishing performance thresholds for image QC and automated cell counting. These results inform SOP parameters for tissue imaging and support the development of ancestry-informed imaging biomarkers.

Conclusions and Implications: Creating foundation for future integration imaging-to-molecular pipeline at the Institute of Translational Genomic Medicine (ITGM). Standardizing imaging and quantitative analysis on the EVOS M7000 platform will enhance reproducibility and facilitate the linkage of histologic features with genomic and immunologic datasets. Ultimately, this approach supports ongoing efforts to elucidate ancestry-associated mechanisms underlying TNBC disparities and to develop precision imaging biomarkers for translational research.

Acknowledgment of Funding: This research is supported in part by grant number R01CA259396 from the NIH and the Student Research Training Program (SRTP) at MSM.

P-46 Title:

Neuregulin-1

Attenuates

Hemolysis-Mediated Kidney Injury in Humanized Sickle Cell Mice

Authors: William Agbozo, PhD1; Wesley Solomon, PhD1; Cecelia Botchway, PhD1; Oguljahan Babayewa, MD1; Alaijah Bashi, PhD1; Samuel Adjei, PhD2; Lily Paemka, PhD2; Solomon OforiAcquah1,2, PhD; Jonathan Stiles, PhD1

1 Morehouse School of Medicine, Atlanta, GA, USA.

2 University of Ghana, Legon, Ghana.

Mentor: Jonathan Stiles, PhD. Morehouse School of Medicine

Background: Sickle cell disease (SCD) is the most common inherited blood disorder predominantly affecting people of African ancestry. Kidney injury complications are three times higher among SCD patients compared to non-SCD individuals, significantly increasing their risk of kidney failure and early mortality. A major driver of kidney injury in SCD is intravascular hemolysis, which releases excess protein-free heme into circulation, triggering kidney injury through vascular inflammation, oxidative stress, and cytotoxicity. There is an urgent unmet need for targeted interventions against heme-driven kidney injury in SCD. Neuregulin-1 (NRG-1), a growth factor expressed by various cell types, has anti-inflammatory, antioxidant, and cytoprotective properties and holds therapeutic potential in SCD. We hypothesized that Neuregulin-1 reduces kidney injury in sickle cell mice by modulating hemolysis, inflammation and by inducing anti-heme cytoprotective factors. This study assessed the effects of NRG 1 on kidney injury and renal histopathologic changes in a humanized sickle cell mouse model that mimics clinical features of SCD.

Methods: Twelve week old Townes sickle cell (HbSS) and non sickle (HbAA) mice received NRG 1 (5 μg/kg/day) or vehicle via intraperitoneal infusion for two weeks. Hematological parameters, markers of hemolysis and inflammation, kidney injury and repair biomarkers, renal histopathology, and heme oxygenase-1 (HO-1) expression were evaluated.

Results: NRG-1 treatment significantly reduced white blood cell counts, total plasma heme, lactate dehydrogenase, and pro-inflammatory kidney injury mediators (IFN-γ, IL-6, CXCL10, VEGF-A, CCL19, MCP-5) in HbSS mice. Notably, higher dose NRG-1 (25 µg/kg/day), significantly increased circulating fetal hemoglobin containing red blood cells (F-cells). Urinary kidney injury biomarkers, neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C, were reduced, alongside a significant increase in renal repair biomarkers, clusterin and epidermal growth factor (EGF), after NRG-1 treatment. Additionally, NRG-1 reduced iron deposition in cortical tubules, glomerular congestion, Bowman’s membrane thickening, and glomerulosclerosis. NRG-1 also enhanced expression of the heme-degrading enzyme HO-1 in HbSS kidneys.

Conclusion: This work provides new insights supporting the exploration of NRG‑1 as a targeted therapeutic agent for kidney injury in SCD.

Acknowledgment of Funding:

• This research is supported in part by grants R01NS125775, U54HL141011, R43 HL149489 from the National Institutes of Health (NIH)

P-47 Title: The Invisible Controller: A Decade-Long Missed Diagnosis of HIV in a Socially Vulnerable Elite Controller

Authors: Hafiz Fadl, MD 1; Nicolas Bakinde, MD, Ph.D.1 ; Minnie Mitchell, MD 1,2 ; Keyera Ashe, MA, Medical Student 1,3

1 Morehouse School of Medicine Internal Medicine

2 Morehouse School of Medicine Neurology

3 Arizona State University Master of Sociology

Background/Significance: Elite controllers are a rare subset of individuals who are living with HIV while maintaining undetectable viral loads without antiretroviral therapy. Although their unique immune control provides valuable insight into potential HIV cure strategies, these cases can mask infection and delay diagnosis, particularly among socially vulnerable populations. This case illustrates how mental illness, homelessness, and fragmented healthcare access can lead to a decade long missed HIV diagnosis. This case emphasizes the need for vigilant screening, continuity of care, and equity focused approaches in managing atypical presentations of chronic diseases.

Methods: We conducted a retrospective case review of a single patient admitted to an inner-city safety net hospital in May of 2025. The patient provided informed consent for publication of anonymized details. Clinical information was obtained from direct patient interviews and review of electronic medical records for data spanning from 2015-2025. Data extracted included patient demographics, medical history, HIV-related laboratory results and relevant imaging studies. Descriptive analysis was used to summarize the patient’s immunological profile and course over time. There were no interventions performed.

Results: The patient’s CD4 count on admission in May 2025 was 1,267 cell/µL, and HIV-1 RNA was “undetectable”, despite no history of ART. Retrospective review confirmed a HIV positive serology from Jan 2015, but no subsequent documentation indicating care or treatment over the following decade. Additional lab data showed a CD4 count of 1,073 cell/ µL, 976 cell/µL, 1,131 cell/µL, and 1,105 cell/µL, spanning from 2017 to 2025 with continued “undetectable” HIV RNA. The non-contrast head CT and chest X-Ray revealed no acute intracranial pathology or opportunistic pulmonary infections.

Conclusions and Implications: The findings of the case demonstrate that even among rare elite HIV controllers, social and structural vulnerabilities can contribute to prolonged missed diagnosis. Clinical vigilance and integrated psychosocial assessment remain essential, regardless of laboratory findings. Elite control does not negate the need for routine HIV monitoring, counseling, and linkage to care. Addressing systemic barriers and strengthening equitable diagnostic practices are crucial to prevent similar oversights and ensure continuity of care for vulnerable populations.

P-48 Title: Global transcriptional reprogramming in iPSC-derived microglia exposed to malaria associated erythrocyte (RBC) hemolysis

Authors: Wesley Solomon1*, William Agbozo1, 2, Cecelia Botchway1,2, Adriana Harbuzariu3 , Jonathan K. Stiles1*

1Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, GA, USA.

2Department of Biochemistry, Cell and Molecular Biology, University of Ghana, Legon, Ghana.

3Emory Stem Cell Core, Emory University, Atlanta GA, USA.

Significance: Hemolytic disorders such as sickle cell disease and severe malaria are strongly associated with long-term neurocognitive deficits in children, yet the mechanisms driving CNS injury remain poorly understood. Recurrent hemolysis releases free heme and iron, destabilizing the blood–brain barrier (BBB), amplifying oxidative stress, and inducing maladaptive microglial activation that impairs neuronal connectivity and cognition. Under hemolytic stress, microglia adopt disease-associated phenotypes, secreting cytokines, chemokines, and angiogenic factors that further compromise BBB integrity. We hypothesized that heme exposure triggers global transcriptional reprogramming in microglia, reflecting pathogenic signatures of pediatric hemolytic disease and cognitive impairment, and that targeted interventions could preserve microglial function.

Methods: We employed pathway-level transcriptomics, secretome profiling, and viability assays in iPSC-derived microglia exposed to heme and assessed three candidate interventions.

Results: Heme induced broad transcriptional reprogramming, strongly activating Tissue Stress (GSS 61.5 / +61.5), Oxidative Stress (41.8 / +37.8), and IL-1 family signaling (62.3 / +62.3). Key gene-level changes included robust upregulation of HMOX1 (log₂FC = +5.15), indicating heme detoxification, and inflammatory mediators IL1B (+1.65) and CXCL8/IL-8 (+3.27). Homeostatic markers (CX3CR1, −1.13) and antigen-presentation genes (HLA-DRA, −0.75) were suppressed. Secretome analysis revealed elevated IL-1β, IL-6, IL-8, MCP-1, and VEGF, reinforcing BBB disruption and neuroinflammation. Disease signature scores aligned with Hemolytic Disorders (+33.4), Sickle Cell Pathogenesis (+31.1), and Severe Malaria (+28.5). Functionally, heme reduced microglial viability to ~52% of control. Among interventions:

• Cobalt Protoporphyrin (CoPP), a potent HO-1 inducer, improved survival (~69%) via stress adaptation but failed to restore cognitive pathways.

• Atorvastatin (ATV) modestly increased viability (~55%) yet most effectively reinstated microglial and cognition-related programs.

• Neuregulin-1 peptide (NRG1) enhanced viability (~58%) while amplifying neurogenesis and inflammatory signaling.

Conclusion: iPSC-derived microglia provide a translational platform for pediatric hemolytic disease. Our findings identify distinct therapeutic axes (stress adaptation, inflammatory control, and cognitive pathway preservation) that may guide adjunctive strategies to protect the developing brain.

Funding: This study was funded through the NIH/NINDS Institute (1 R01 NS125775-01).

P-49 Title: The role of Estrous cycle on Chlamydia pathogenesis using a SIAH2 KO mice model

Authors: Danielle Wright, M.S.¹ ; Yusuf Omosun, Ph.D.²

¹ Morehouse School of Medicine, Department of Microbiology, Biochemistry, and Immunology

² Morehouse School of Medicine, Department of Pharmacology and Toxicology

Mentor: Yusuf Omosun, Ph.D., Morehouse School of Medicine

Background/Significance: Chlamydia trachomatis is the most common bacterial sexually transmitted infection globally and a leading cause of preventable infertility in women. The pathogen can ascend through the upper reproductive tract, inducing inflammation, fibrosis, and long-term reproductive damage, even after antibiotic clearance. Host-pathogen interactions influencing these chronic outcomes remain poorly understood. SIAH2 (Seven in Absentia Homolog 2) is an E3 ubiquitin ligase that regulates inflammation, metabolism, and circadian rhythm via modulation of the core clock protein REV-ERBα. Notably, SIAH2 knockout (KO) female mice display sex-specific alterations in metabolic and rhythmic gene expression, suggesting an intersection between circadian and hormonal regulation in infection responses. Hypothesis: Disruption of SIAH2-dependent circadian regulation alters host susceptibility to C. trachomatis infection in a stage-dependent manner across the estrous cycle.

Methods: Female wild-type (WT) and SIAH2 KO mice were infected intravaginally with C. trachomatis during the estrous or diestrous phases, determined by vaginal cytology. Genital tract pathology was evaluated and photographed. Bacterial load was monitored longitudinally, and serum IgG2C and IgGA levels were measured using ELISA to assess systemic as well as local immune responses. Data were analyzed across genotypes and reproductive stages to determine how circadian and hormonal factors interact to modulate infection outcomes.

Results: Preliminary findings indicate that SIAH2 KO mice exhibit stage-specific differences in infection pathology relative to WT controls. KO mice infected during diestrous displayed reduced genital tract inflammation and tissue damage, whereas those infected during estrous exhibited heightened inflammatory responses. Conversely, WT mice infected during diestrous showed less pathology than KO counterparts, suggesting that SIAH2-dependent circadian signaling confers stage-specific protection. Serum IgG2C levels varied significantly across estrous stages and infection timepoints, indicating circadian influence on adaptive immunity.

Conclusions and Implications: These findings demonstrate that circadian regulation and reproductive stage jointly influence host responses to C. trachomatis. SIAH2 appears to act as a molecular integrator of circadian and hormonal cues, shaping immune and inflammatory dynamics during infection. Understanding how SIAH2-mediated pathways govern infection outcomes may improve strategies for managing chlamydial disease and optimizing treatment timing based on hormonal and circadian contexts.

Acknowledgment of Funding: This research was supported in part by the NIH

P-50 Title: Age and Sex

Differentially Influence Blood-Brain Barrier Dysfunction and Mortality Following Traumatic Brain Injury

Authors: Aliyah Anderson1, O’lisa Yaa Waithe, Amrendra Singh, Saravanakumar Muthusamy, Binu Tharakan.

Department of Surgery, Morehouse School of Medicine, Atlanta, GA1

Mentor: Binu Tharakan

Background: The blood-brain barrier (BBB) is a semi-permeable barrier, essential for maintaining brain homeostasis by regulating the movement of molecules between the blood and the brain. During traumatic brain injury (TBI), BBB structural integrity is compromised, leading to BBB hyperpermeability, cerebral edema, and neuroinflammation. The roles of age and sex in the context of BBB disruption following TBI remain poorly understood. This study aims to characterize the influence of sex on TBI-induced BBB hyperpermeability in aged mice, hypothesizing that BBB disruption varies between males and females.

Methods: Aged (20-22 month) male and female (C57BL/6) mice were subjected to sham or TBI procedures. Mice were anesthetized using isoflurane and injected with FITC-dextran (10-kDa) via jugular vein. Craniotomy was performed to expose the brain to intravital microscopy. Sham mice were subjected to craniotomy and loaded onto stereotaxic frame only. TBI mice were loaded onto stereotaxic controlled cortical impactor then subjected to a moderate TBI (1mm depth). Intravital imaging of the pial microvasculature and BBB permeability was measured.

Results: Significant BBB hyperpermeability was observed in both aged TBI male and female mice compared to sham. TBI in aged males resulted in significantly higher BBB hyperpermeability compared to TBI in aged females. TBI in aged female mice resulted in significantly higher postinjury mortality rate compared to TBI in aged males.

Conclusions: These findings indicate a sex-related susceptibility in BBB integrity following TBI; aged males experience a more notable BBB dysfunction following injury, while aged females exhibit increased mortality, potentially due to differential inflammatory mechanisms.

P-51 Title: Comparative Evaluation of Brain Trauma Biomarker Dynamics utilizing a novel Lateral Flow Device: An MSM-EMORY/Grady Collaboration

Authors: Khadija Boukholda, PhD1; Guangzheng Cai, MS1; Eman Elbayoumi, MD1; Mojtaba Golpich, PhD1; Nagla Massud, MD1; Yazan Bouchi, MD2; Jiepei Zhu, PhD1; Firas Kobaissy, PhD 1

¹Center for Neurotrauma, Multiomics and Biomarkers (CNMB), Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine, Atlanta, GA 30310, USA 2Morehouse School of Medicine, MD candidate

Mentor: Firas Kobaissy, Ph.D., Morehouse School of Medicine

Background/Significance: Traumatic brain injury (TBI) triggers a cascade of neuroinflammatory and structural changes that can be monitored through circulating biomarkers. Glial fibrillary acidic protein (GFAP) and its breakdown product (GBDP) are established indicators of astroglial damage and recovery. However, the concordance of biomarker quantification between wet and dried plasma matrices remains insufficiently investigated. Understanding these differences is essential for developing standardized, field-applicable biomarker assays.

Methods: Plasma samples were collected from patients enrolled at Emory University Hospital, including 27 wet, 29 dry, and 10 control subjects. GFAP and GBDP concentrations were quantified at Day 0 (D0) and Day 14 (D14) post-injury using high-sensitivity MSD ELISA immunoassays. Comparative and correlation analyses were performed to evaluate biomarker dynamics and matrix-related variability.

Results: Both GFAP and GBDP were significantly elevated at D0 compared with controls (p < 0.01–0.0001) and showed a marked decline by D14, reflecting partial recovery. Group analyses demonstrated strong discriminative effects across time points (R² = 0.23–0.70). Correlation between wet and dried plasma showed poor agreement, suggesting potential matrix-dependent influences on biomarker measurement.

Conclusions and Implications: GFAP and GBDP reliably reflect astroglial injury and subsequent recovery following TBI. Although correlation between wet and dried plasma matrices was limited, both demonstrated consistent biomarker trends. These findings support the potential of dried plasma as a practical, stable, and logistically favorable alternative for biomarker assessment in clinical and translational TBI research.

Acknowledgment of Funding: This research was supported in part by grant number [W81XWH2210740] from the Department of Defense (DOD],Also, this work is partially supported by the Research Centers in Minority Institutions (RCMI) Grant Number U54MD007602 from the National Institute of Minority Health and Health Disparities (NIMHD)

P-52

Title: The Role of TRPM7 in Microglia Activation and Microglia-Mediated Cerebral Vascular Endothelial Cell Injury

Authors: Kyra Brewer 1, 2, 3; Tao Yang 1; Zhigang Xiong, M.D., Ph.D 1; Tiandong Leng, M.D., Ph.D.1

1 Morehouse School of Medicine Department of Neurobiology

2 Morehouse School of Medicine Ph.D. in Biomedical Science Program

3 Morehouse School of Medicine Master of Science in Clinical Research

Mentor: Tiandong Leng, M.D., Ph.D., Morehouse School of Medicine

Background/Significance: Ischemic stroke is a major health burden in the U.S, affecting nearly a million people yearly. Current treatments, including thrombolysis and thrombectomy, are limited by efficacy and strict inclusion criteria, leaving most patients without effective treatment options. Evidence highlights TRPM7, a channel-kinase, as a promising neuroprotective target in stroke. However, the contribution of TRPM7 in non-neuronal cell types remains unknown. We propose to investigate TRPM7’s role in microglial activation and cerebral endothelial injury. We hypothesize that TRPM7 activation drives excessive pro-inflammatory response in microglia, leading to secondary injury of cerebral endothelial cells.

Methods: Lipopolysaccharide (LPS) was used to activate microglial cells. Immunocytochemical analyses of inducible nitric oxide synthase (iNOS), matrix metalloproteinase-9 (MMP-9), and arginase-1 (Arg-1) were performed to evaluate microglial activation. Transwell and scratch migration assays were conducted to assess the motility of microglial cells. Conditioned medium from microglial cultures was applied to endothelial cells, followed by wound-healing, viability, and ROS assays. All data are expressed as means ± SE. Statistical analyses were performed using one-way ANOVA on data collected from at least three independent experiments, with Dunnett’s post hoc test applied to correct for multiple comparisons.

Results: LPS markedly upregulated the levels of iNOS and MMP-9 in microglia, both of which were significantly decreased by TRPM7-channel inhibitor waixenicin A. In contrast, LPS reduced Arg-1 expression, whereas waixenicin A treatment significantly restored its levels (p<0.05). The TRPM7-kinase inhibitor TG100-115 did not alter the LPS-induced elevation of iNOS or MMP9 but significantly restored Arg-1 expression (p<0.05). Furthermore, both the TRPM7 channel and kinase inhibitors reduce the LPS-stimulated migration of microglia at 24 hours (p<0.01), but not at 48 hours (p>0.05). Conditioned medium from LPS-challenged microglia significantly reduced cerebral endothelial cell viability, an effect that was reversed by both TRPM7 channel inhibition (p<0.01) and kinase inhibition (p<0.05).

Conclusions and Implications: Our findings demonstrate that TRPM7 plays a pivotal role in regulating microglial activation and migration. Activated microglia induce cerebral endothelial cell injury, likely through the release of ROS and MMP-9. This mechanism may contribute to blood–brain barrier (BBB) disruption following stroke. TRPM7 inhibition significantly attenuates these pathological effects, suggesting that TRPM7 represents a promising therapeutic target for protecting BBB integrity and mitigating secondary vascular damage after ischemic stroke.

Acknowledgments of Funding: NIH R01NS128018, and R25GM058268

P-53 Title: Tailored Management of Pediatric CM-AVM Syndrome: Insights from a RASA-1 Positive AVM Case with Narrative Review

Authors: Leander Brooks1, Sandi Lam, MD2, Jonathan Scoville, MD2, Vaidehi Mahadev, MD1,2

1Department of Neurosurgery, Northwestern University Feinberg School of Medicine, Chicago, IL, USA 2Division of Pediatric Neurosurgery, Ann & Robert H. Lurie Children’s Hospital, Chicago, IL, USA

Introduction: (CM-AVM) syndrome, a rare, aggressive vascular disorder caused by pathogenic variants in the RAS p21 protein activator 1 (RASA1) gene.2 This genetic mutation disrupts normal vascular development, leading to high-flow anomalies; arteriovenous malformations (AVMs) and/or arteriovenous fistulas (AVFs), and accompanying multifocal capillary malformations 2. Due to the high recurrence of de novo AVMs and associated complications, patients with CM-AVM syndrome often require tailored, nuanced care approaches. 3 We hypothesize that, while structured management frameworks are documented for sporadic AVMs, the clinical approach to RASA1-positive CM-AVM remains highly variable, which has led to various challenges in practice. 3 Notably, there is a lack of standardized, evidence-based protocols for CM-AVM affected pediatric patients, particularly regarding intervention and modalities (e.g. radiosurgery, embolization, microsurgery), long-term surveillance and multidisciplinary clinical management. 3, 4, 5

Methods: A comprehensive literature review on CM-AVM management was conducted and synthesized with expert insights. These findings were compared to a retrospective chart review of a 14-year-old female with confirmed RASA1-positive CM-AVM, treated longitudinally at Lurie Children’s Hospital (2013–2025). This illustrative case helped explore whether RASA1-positive AVMs warrant distinct care frameworks from sporadic AVMs, emphasizing gaps in treatment, intervention, and long-term surveillance.

Illustrative case: Diagnosed with RASA1 mutation shortly after birth, the patient developed multiple de novo AVMs across a 12-year period, which were managed through a range of evolving and tailored interventions, including Gamma Knife radiosurgery, endovascular embolization and microsurgery. Following successful, well tolerated intervention, the patient transitioned to conservative monitoring with structured diagnostic intervals. This case emphasizes the clinical variability of CM-AVM and the need of individually tailored decision-making in the absence of evidence-based guidelines.

Conclusion/Clinical significance: This case highlights the evolving needs in managing RASA1positive, CM-AVM syndrome. While literature supports several effective interventions, there remains a lack of clarity around long-term surveillance, treatment outcomes and clinical decision making. In parallel, this illustrative case report contextualizes findings within the current literature, emphasizing the need for individualized protocols, integration of genetic screening, imperative of multidisciplinary care and broader advocacy for tailored management approaches in RASA1positive, CM-AVM syndrome.

Acknowledgement of Funding: This research was supported by the Alliance to Cure Cavernous Malformations (ACCM) through the Summer Alliance Program for Medical Student Research

P-54 Title: Assessing Neuroprotective Effects of Mitoquinone on H2O2 -Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells

Authors: Aubrey Brown 1, Mojtaba Golpich 1 , Khadija Boukholda ², Eman Elbayoumi ², Guangzheng Cai ³, Firas Kobeissy 1

1 Center for Neurotrauma, Multiomics & Biomarkers (CNMB), Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine, Atlanta, GA 30310, USA

2 Department of Biochemistry and Molecular Genetics, American University of Beirut, Beirut, Lebanon.

3 Department of Basic Medical Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar.

4 Department of Chemistry and Biochemistry, Texas Tech University, Lubbock, TX, USA

5 Department of Anatomy, Cell Biology, and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.

6 Neuromuscular Diagnostic Laboratory, Department of Pathology and Laboratory Medicine, American University of Beirut Medical Center, Beirut, Lebanon

Mentor: Firas Kobeissy, Ph.D., Morehouse School of Medicine

Background/Significance: Oxidative stress, a major contributor to secondary brain injury, promotes apoptosis, neuroinflammation, and mitochondrial dysfunction. Targeting the Nrf2–Keap1–ARE pathway using mitochondria-targeted antioxidants such as mitoquinone (MitoQ) has been proposed as a potential therapeutic strategy against neurotoxicity.

Methods: The neuroprotective effects of MitoQ on human neuroblastoma SH-SY5Y cells were assessed by MTT assay, SRB assay, and propidium iodide stain using MitoQ at concentrations of 0.03 and 0.05 µg/mL as pre-treatment or post-treatment for hydrogen peroxide (H2O2)-induced stress. Oxidative stress was evaluated by NBT assay and DHE staining while mitochondrial integrity was studied using MitotrackerGreen dye. The gene expression profile of the antioxidant genes Nrf2, SOD1, HOX1, and CAT and the inflammatory genes COX-2 and NFκB were investigated via RT-qPCR along with immunofluorescence imaging. Additional studies included LDH assays to assess cytotoxicity and immunohistochemistry with confocal imaging to examine NRF2 translocation from cytoplasm to nucleus.

Results: Pretreatment with MitoQ enhanced cell viability, preserved morphology, maintained mitochondrial phenotype, and reduced oxidative stress compared to H₂O₂-treated cells. MitoQ increased Nrf2 and HMOX1 expression, normalized SOD1 levels, and downregulated COX-2, supporting its antioxidant and anti-inflammatory effects. LDH release was significantly lower in MitoQ-pretreated cells, and NRF2 nuclear translocation was attenuated, suggesting mitigation of oxidative injury.

Conclusions and Implications: These findings demonstrate that MitoQ confers neuroprotection by modulating the Nrf2-mediated antioxidant response and reducing cellular oxidative damage, highlighting its therapeutic potential for oxidative stress-related neurodegenerative and traumatic brain injuries.

Acknowledgement of Funding: This work is partially funded by theAmerican University of Beirut (AUB); Medical Practice Plan (MPP) grant.

P-55 Title: Blood neurofilament light (NFL) levels as translational outcome biomarker for rat TBI models: a TOP-NT preclinical consortium study.

Authors: Cai, Guangzheng Troy1, Mendoza, E.2, Radabaugh, H.L.2, Wanner, IB.3, Zhu, J.P.1 , Febo, M.7, Wu, Z-Y.1, Apiliogullari, S.1, Harris, N.3, Koehler, R. Burns4, M. Zhou, JY.6, Huie, J.R., McCabe2, J. Richard Rubenstein8, Ferguson, A.R.3, Wang, K.K.1 Kobeissy, Firas1

1 Primary Neurobiology, Morehouse School of Medicine

2 University of California San Francisco, San Francisco, CA

3 University of California Los Angeles, Los Angeles, CA

4 Georgetown University, Washington, DC

5 Uniformed Services University of the Health Sciences, Bethesda, MD

6 Johns Hopkins University, Baltimore, MD

7 University of Florida, Gainesville, FL

8 SUNY Downstate Health Sciences University, Brooklyn, NY

Mentor: Kobeissy, Firas, PhD Morehouse School of Medicine

Background: Axonal injury-linked neurofilament light protein (NFL) has promise as blood-based biomarker for clinical TBI monitoring. However, preclinical TBI, its detectability, severity and temporal profiles are undefined. In this NIH-NINDS funded, five site, Translational Outcomes Project in Neurotrauma (TOP-NT) consortium, we measured blood-based NFL levels following controlled cortical impact (CCI at two compression depths) versus sham controls. There were four animal study sites (UCLA, Georgetown University, Morehouse School of Medicine/MSM, Johns Hopkins University). All samples were assayed centrally. The UCSF team conducted centralized statistical analysis.

Methods: Four-way repeated measures analysis of variance (Four-way RM ANOVA) was done on both untransformed and log transformed NFL concentrations on group (CCI versus Sham), sex, site, and time (post injury days 1, 3, 7, and 30).

Results: Untransformed NFL data show a robust and significant increase in CCI (at all timepoints) compared to sham (p-value < 0.001). There was a significant difference in injury NFL levels over time (p<0.001, partial eta square 0.109). Time by site interaction indicates a significant difference for NFL by time and group (p < 0.001, partial eta square 0.109). Four-way interaction between site, sex, injury, and time was not significant. Aggregated time plots of NFL levels separated for CCI and sham show the mean NFL levels at each time point for all four sites overlapped with each other with no significant differences.

Conclusions: These results indicate that the effect of CCI on NFL overtime can be successfully replicated across multiple research centers. These results show that brain injury-based neuropathologic markers such as NFL can be used as surrogate markers for TBI injury severity and as potential monitoring tools for advancing therapeutic treatment of TBI.

Acknowledgment of Funding: NINDS NS106945, NS10694, NS106937, NS106899 and NS106938 and Vivian Smith Foundation

P-56

Title: The effects of deferoxamine and iron on hydrogen peroxide mediated neuronal injury

Authors: Holland Hubert BS 1 , Ariana Colson, MS 3 and Kennie R. Shepherd, Ph.D 2

.

1. Spelman College and Morehouse School of Medicine, B.S./M.S. in Neuroscience Program.

2. Morehouse School of Medicine, Department of Pharmacology and Toxicology, and Neuroscience Institute.

3. Morehouse School of Medicine Master of Science in Biomedical Research Program

Mentor: Kennie Shepherd, PhD.

Morehouse School of Medicine

Background/Significance: An abundance of evidence demonstrates the involvement of oxidative stress and mitochondrial dysfunction in the pathophysiology of neurodegenerative diseases such as Parkinsons Disease (PD). The production of reactive oxygen species (ROS) has also been implicated in PD. Interestingly; increased iron content has been observed in several brain areas (particularly monoamine neuron containing areas) that degenerate in PD. It has been suggested that iron has a dual function, either aiding neuroprotection (serving as cofactor for antioxidant enzymes) or exacerbating neuronal injury (via reaction with hydrogen peroxide in Fenton reaction to generate ROS). Previously, the lab has demonstrated that hydrogen peroxide mediated neuronal injury, involves the production of ROS and mitochondria dysfunction. The role of iron during hydrogen peroxide mediated neuronal injury remains unresolved. The present study was undertaken to exam the effects of deferoxamine (iron chelator) and iron (at concentration that does not induce toxicity alone) on hydrogen peroxide mediated neuronal injury in SHSH-5Y cells (a monoamine containing cell line). We hypothesized that iron exacerbates hydrogen peroxide mediated neuronal injury.

Methods: To investigate hydrogen peroxide induced neurotoxicity, we assessed mitochondrial functioning/cell viability using MTT assays and assessed cell death using trypan blue exclusion assays. 2,7-Dichlorodihydrofluorescein diacetate (H2DCF-DA) assay was also utilized to quantify ROS production. To determine the effects on iron transport protein expression, western blotting along with densitometry analyses were used.

Results: Treatment of cells with 20M H2O2 significantly decreased the number of live cells by 83.5% when compared to controls. Pretreatment with deferoxamine (10M) alone, did not have any effect on mitochondria function and cell death. However, pretreatment of cells with 10M deferoxamine, significantly attenuated hydrogen peroxide induced cell death by 78.33%.

Conclusion & Implications: The result demonstrated that increased iron levels may play a role in hydrogen peroxide mediated neuronal injury, and may offer insight into the vulnerability of monoamine containing neurons affected in neurodegenerative diseases such as PD.

Acknowledgment of Funding: This research was done with the funding from NINDS grant #R25NS117365 and NIMHD grant #S21MD000101. The investigation was conducted in a facility constructed with support from Research Facilities Improvement Grant #C06 RR-07571 from the National Center for Research Resources, NIH.

P-57 Title: Detection of Autoantibody

Signatures in Traumatic Brain Injury Using a Novel High-Capacity Dried Plasma Lateral Flow Device

Authors: Eman Elbayoumi1, MD; Khadija Boukholda1, PhD; Guangzheng Cai1, MS; Mojtaba Golpich1, PhD; JiePei Zhu1, MD. PhD; Firas Kobaissy1, PhD.

1Center for Neurotrauma, Multiomics & Biomarkers (CNMB), Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine.

Mentor: Dr. Firas Kobaissy, PhD. Morehouse School of Medicine.

Background/Significance: Current diagnostic assays for traumatic brain injury (TBI), including GFAP, NfL, and Pituitary, rely on venous plasma. We evaluated a high-capacity dried plasma device that enables fingerstick sampling, ambient storage, minimal handling, and preservation of biomarker integrity. Analytical performance and stability were assessed using ELISA-based detection of antipituitary, GFAP, and NfL, and pituitary IgG and IgM autoantibodies following TBI.

Methods: Plasma samples were collected from TBI patients enrolled at Emory Hospital (27 wet plasma and 29 dried plasma samples) and from 10 healthy controls. Autoantibody concentrations were quantified at Day 0 (D0) and Day 14 (D14) post-injury using enzyme-linked immunosorbent assays (ELISA). Comparative and correlation between wet and dried plasma were performed to evaluate biomarker stability and the temporal dynamics of anti-pituitary, GFAP, and NfL IgG/IgM responses.

Results: Significant differences in post-TBI autoantibody levels were observed for anti-pituitary IgG in wet plasma (P = 0.0271), anti-pituitary IgM in dried plasma (P = 0.0143), anti-GFAP IgM in both wet (P = 0.0009) and dried plasma (P = 0.0024), and anti-NfL IgM in dried plasma (P = 0.0103), as revealed by ANOVA testing across Day 0 and Day 14 samples. Other autoantibody comparisons, including anti-GFAP and anti-NfL IgG in both matrices, did not reach statistical significance. Across all analytes and time points, correlations between wet and dried plasma measurements were weak (R² = 0.015-0.292), indicating moderate matrix-dependent variability and limited concordance in biomarker quantification between sample types.

Conclusion and Implications: Detection of pituitary, GFAP, and NfL autoantibodies post-TBI supports the feasibility of dried plasma formats for assessing TBI biomarkers. Even with modest matrix variability, the device demonstrated robust detection capability, highlighting its potential as a practical and stable alternative to current plasma collection methods for clinical and translational TBI research.

Acknowledgment of Funding:

• This work is funded from the grant from the Department of Defense (DOD)Award number W81XWH2210740.

• Also, this work is partially supported by the Research Centers in Minority Institutions (RCMI) Grant Number U54MD007602 from the National Institute of Minority Health and Health Disparities (NIMHD).

P-58 Title: Examining

the Association Between Behavioral Therapy and Social Outcomes in U.S. Children with Autism

Authors: Kiyanie Fedrick, MS¹; LaKesha Tables, MD, MPH, MS²; Peter Baltrus, PhD²

¹Master of Science in Medical Sciences, Morehouse School of Medicine

²Department of Community Health and Preventive Medicine, Morehouse School of Medicine

Mentor: LaKesha Tables, MD, MPH, MS, Morehouse School of Medicine

Background/Significance: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by persistent difficulties in social communication and behavioral regulation. Behavioral therapy, grounded in principles of applied behavior analysis (ABA), remains one of the most effective interventions for promoting positive social outcomes. However, disparities in treatment access and response persist across age, race, and gender. This study examined the association between behavioral therapy and social outcomes among U.S. children with ASD, while considering key demographic differences.

Methods: A cross-sectional analysis was conducted using data from the 2022–2023 National Survey of Children’s Health. The analytic sample included 1,531 children aged 6–17 years with parent-reported ASD diagnoses. Behavioral therapy status (receiving vs. not receiving) was the primary predictor. Social outcomes were assessed using the following variables difficulty staying calm when challenged, making friends, showing sensitivity, sharing ideas, and working to finish tasks. Complex-sample logistic regression models, adjusted for age, race, and gender, were used to estimate odds ratios (OR) and 95% confidence intervals (CI).

Results: Children who received behavioral therapy had significantly lower odds of difficulty staying calm when challenged (OR = 0.40, 95% CI [0.24–0.65], p < 0.001) and of difficulty making friends (OR = 0.81, 95% CI [0.43–0.95], p = 0.026). Other outcomes, including difficulty showing sensitivity and sharing ideas, trended positively but did not reach statistical significance.

Additionally, younger children had 72% lower odds of difficulty staying calm when challenged compared to older peers (OR = 0.28, p < 0.001), suggestingthat earlier intervention during key developmental stages may yield greater emotional regulation benefits. Race and gender were not significant predictors. These findings align with prior research demonstrating stronger treatment effects in early developmental stages (Reichow et al., 2018; Smith et al., 2020).

Conclusions and Implications: Behavioral therapy is strongly associated with improved emotional regulation and peer relationships among children with ASD, particularly when implemented early. These results emphasize the need for timely access to behavioral health services and equitable care delivery across populations. Expanding culturally competent behavioral health services and ensuring early developmental screening may help optimize outcomes and reduce disparities in care for children with ASD.

Acknowledgment of Funding: This research was supported in part by the Master of Science in Medical Sciences Program at Morehouse School of Medicine.

P-59

Title: Myelin Basic Protein (MBP)-Based Blood Diagnosis of Traumatic Brain Injury: Comparative Assessment of Dry Plasma Collected by a Novel Lateral Flow Device Versus Traditional Venous Plasma

Authors: Mojtaba Golpich1, Guangzheng Cai1, Khadija Boukholda1, Eman Elbayoumi1, JiePei Zhu1, Firas Kobeissy1

1 Center for Neurotrauma, Multiomics & Biomarkers (CNMB), Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine, Atlanta, GA 30310, USA

Mentor: Firas Kobeissy, Ph.D., Morehouse School of Medicine

Background/Significance: Rapid, accurate, and non-invasive diagnosis of traumatic brain injury (TBI) is essential in emergency settings such as battlefields and traffic accidents, where access to standard blood processing and transport facilities may be limited. Current diagnostic biomarkers for TBI rely on venous plasma, with no FDA-cleared options for capillary or dried formats. We evaluated a high-capacity dried plasma device enabling fingerstick sampling, ambient storage, minimal handling, and preserved biomarker integrity. This study aims to assess and compare the analytical performance and stability of a novel lateral flow (LF) device for blood plasma separation ("dry plasma") against conventional centrifugation-based plasma ("wet plasma") for measurement of Myelin Basic Protein (MBP) as a promising TBI biomarker.

Methods: Plasma samples were collected from healthy individuals (control) and TBI patients (day of injury [D0] and 14 days post-injury [D14]) enrolled at Emory University Hospital. To characterize biomarker stability, inter-matrix variability, and temporal dynamics of MBP response, comparative measurements were performed using ELISA-based detection in both wet (n=26) and dry (n=13) plasma samples per each time point and controls (n=10). Statistical differences among groups were evaluated using one-way ANOVA.

Results: MBP levels were significantly elevated in both plasma samples from TBI patients compared to controls at D0 and D14 (p<0.05). In both plasma types, MBP concentrations allowed clear stratification of controls, acute TBI (D0), and subacute TBI (D14). Notably, the dry plasma samples processed by the LF device exhibited robust discrimination between groups and demonstrated consistency and sensitivity equal to or greater than wet plasma. The dry plasma technique showed less variability of MBP values within each group, supporting its high efficiency and quality.

Conclusions and Implications: The LF device for dry plasma separation enables rapid, easy collection of high-quality plasma for MBP biomarker analysis in TBI, even under resource-limited or transport-restrictive conditions. Comparative data reveal that the device performs as well as or better than wet plasma methods for discriminating TBI groups, providing an effective and scalable option for clinical and field diagnostics. This device has the potential to improve TBI management through timely, accurate biomarker-based detection.

Acknowledgement of Funding: This work was supported by grants from the Department of Defense (Award W81XWH2210740), the National Institute of Neurological Disorders and Stroke (R01 NS110944), and in part by the Research Centers in Minority Institutions (NIMHD U54MD007602).

P-60 Title: Millimeter-Wave Directed Energy-Mediated Neural Cell Injury: Insights into Protein Degradation and Cell Injury Mechanisms

Authors: Mojtaba Golpich1* , Hamad Yadikar2,3, Sherifdeen Onigbinde4, Joy Solomon4, Vishal Sandilya4, Moyinoluwa Adeniyi4, Jiepei Zhu1, Yehia Mechref4 Firas Kobeissy1,5

1 Center for Neurotrauma, Multiomics & Biomarkers (CNMB), Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine, Atlanta, GA 30310, USA

2 Department of Biological Sciences, Faculty of Science, Kuwait University, Sabah Al Salem University City, Kuwait City 13060, Kuwait

3 OMICS Research Unit, Research Core Facility, Faculty of Medicine, Kuwait University, Kuwait City 13110, Kuwait

4 Chemistry and Biochemistry Department, Texas Tech University, Lubbock, TX 79409, USA

5 Center for Visual & Neurocognitive Rehabilitation (CVNR), Atlanta VAHealth Care System 1670 Clairmont Rd, Decatur, GA 30033, USA

Mentor: Firas Kobeissy, Ph.D., Morehouse School of Medicine

Background/Significance: Millimeter-wave directed energy (mmWave DE) is increasingly used in telecommunications and military applications, yet its biological effects on neuronal systems remain unclear. To characterize the spatially dependent cellular and molecular impacts of 34.14 GHz mmWave DE exposure on mouse neuroblastoma (N2A) cells as a model system.

Methods: N2Acells were exposed to mmWave DE for 48 hours, generating three defined zones: Center (direct exposure), Penumbra (peripheral exposure), and Control. Morphological changes were evaluated by microscopy; viability and membrane integrity were assessed via MTT and LDH assays. Cytoskeletal protein degradation (αII-Spectrin, Vimentin) was measured by Western blot. Label-free LC-MS/MS proteomics, Gene Ontology (GO), Ingenuity Pathway Analysis (IPA), and Pathway Studio were used to define global molecular responses.

Results: Center-exposed cells showed severe morphological disruption, reduced viability (p < 0.0001), and elevated LDH release, consistent with necrosis. Western blot revealed increased proteolysis of αII-Spectrin and Vimentin. Proteomic profiling identified >180 dysregulated proteins in the Center and 34 in the Penumbra, affecting cytoskeleton organization, mitochondrial function, and RNA processing. GO and IPA indicated activation of apoptosis, ER stress, and necrosis pathways, with inhibition of translation and cell movement. Pathway mapping linked DE-altered proteins to neurodegenerative and injury-relevant processes.

Conclusion and Implications: mmWave DE exposure induces graded cellular injury, ranging from stress adaptation in peripheral regions to proteostasis collapse and structural failure in directhit zones. These findings support reconsideration of mmWave safety standards and highlight parallels with neurodegenerative mechanisms.

Acknowledgement of Funding: This work is partially supported by the Research Centers in Minority Institutions (RCMI) Grant Number U54MD007602 from the National Institute of Minority Health and Health Disparities (NIMHD).

P-61 Title: Does

Low-Dose Acetylsalicylic Acid Influence Sleep Architecture of Habitual Sleep During Experimental Sleep Restriction and Recovery Sleep in Healthy Adults?

Authors: Juan A. Gomez1,2,3, Larissa C. Engert1,2, Rammy Dang1, Janet Mullington1,2, Monika Haack1,2

1Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, USA;

2Division of Sleep Medicine, Harvard Medical School, Boston, MA, USA;

3Morehouse School of Medicine, Atlanta, GA, USA

BACKGROUND & AIMS: Sleep deficiency, including insufficient sleep and sleep disturbance, is prevalent in the U.S. and promotes a pro-inflammatory state that increases the risk of cardiovascular, neurocognitive, and metabolic diseases. One way to mitigate these health outcomes is to target inflammation. Using low-dose acetylsalicylic acid (ASA, aspirin) as a probe, our lab has shown that low-dose ASA reduces inflammation and improves actigraphy-estimated wake after sleep onset (WASO), and sleep efficiency (SE). The aim of the present study is to evaluate the effects of low-dose ASA on sleep architecture as assessed with polysomnography (PSG) during baseline sleep, experimental sleep restriction, and recovery sleep in healthy adults.

METHODS: This double-blind, placebo-controlled, crossover trial included 46 participants (19F/27M; age range: 18-65 years). The protocol consisted of a 14-day at-home sleep monitoring phase followed by an 11-day in-laboratory stay, including a control sleep condition with placebo intake and two sleep restriction conditions with either placebo or low-dose ASA intake. Sleep was assessed at baseline on Day 3, on Day 8 (after 5 nights of sleep restriction or control sleep), and Day 10 (after 2 nights of recovery sleep or control sleep) using PSG. Sleep characteristics, including amount of stage N1, N2, N3, rapid-eye movement (REM) sleep, WASO, SE, sleep onset latency (SOL), and sleep fragmentation were evaluated using generalized linear mixed models (GLMM).

RESULTS: Data is available from 46 participants (19F/27M), including 113 stays in total (39 stays for sleep restriction/ASA, 37 stays for sleep restriction/placebo, and 37 stays for control sleep/placebo). Analysis is currently ongoing and will be presented at the meeting.

CONCLUSIONS: This study offers clarification on the role of low-dose ASA in modulating sleep architecture of habitual sleep during experimental sleep restriction and recovery sleep. By extending prior findings to PSG-derived sleep characteristics, our findings may reveal whether aspirin’s anti-inflammatory effects influence alterations in sleep architecture and sleep stage distributions. These findings will support further investigation into anti-inflammatory strategies for mitigating negative health consequences associated with sleep deficiencies.

P-62

Title: The effects of deferoxamine and iron on hydrogen peroxide mediated neuronal injury

Authors: Holland Hubert BS 1, Ariana Colson, MS 3 and Kennie R. Shepherd, Ph.D 2

1. Spelman College and Morehouse School of Medicine, B.S./M.S. in Neuroscience Program.

2. Morehouse School of Medicine, Department of Pharmacology and Toxicology, and Neuroscience Institute.

3. Morehouse School of Medicine Master of Science in Biomedical Research Program

Mentor: Kennie Shepherd, PhD.

Morehouse School of Medicine

Background/Significance: An abundance of evidence demonstrates the involvement of oxidative stress and mitochondrial dysfunction in the pathophysiology of neurodegenerative diseases such as Parkinsons Disease (PD). The production of reactive oxygen species (ROS) has also been implicated in PD. Interestingly; increased iron content has been observed in several brain areas (particularly monoamine neuron containing areas) that degenerate in PD. It has been suggested that iron has a dual function, either aiding neuroprotection (serving as cofactor for antioxidant enzymes) or exacerbating neuronal injury (via reaction with hydrogen peroxide in Fenton reaction to generate ROS). Previously, the lab has demonstrated that hydrogen peroxide mediated neuronal injury, involves the production of ROS and mitochondria dysfunction. The role of iron during hydrogen peroxide mediated neuronal injury remains unresolved. The present study was undertaken to exam the effects of deferoxamine (iron chelator) and iron (at concentration that does not induce toxicity alone) on hydrogen peroxide mediated neuronal injury in SHSH-5Y cells (a monoamine containing cell line). We hypothesized that iron exacerbates hydrogen peroxide mediated neuronal injury.

Methods: To investigate hydrogen peroxide induced neurotoxicity, we assessed mitochondrial functioning/cell viability using MTT assays and assessed cell death using trypan blue exclusion assays. 2,7-Dichlorodihydrofluorescein diacetate (H2DCF-DA) assay was also utilized to quantify ROS production. To determine the effects on iron transport protein expression, western blotting along with densitometry analyses were used.

Results: Treatment of cells with 20M H2O2 significantly decreased the number of live cells by 83.5% when compared to controls. Pretreatment with deferoxamine (10M) alone, did not have any effect on mitochondria function and cell death. However, pretreatment of cells with 10M deferoxamine, significantly attenuated hydrogen peroxide induced cell death by 78.33%.

Conclusion & Implications: The result demonstrated that increased iron levels may play a role in hydrogen peroxide mediated neuronal injury, and may offer insight into the vulnerability of monoamine containing neurons affected in neurodegenerative diseases such as PD.

Acknowledgment of Funding: This research was done with the funding from NINDS grant #R25NS117365 and NIMHD grant #S21MD000101.The investigation was conducted in a facility constructed with support from Research Facilities Improvement Grant #C06 RR-07571 from the National Center for Research Resources, NIH.

P-63 Title: Temporal

Organization of SCN Networks: Circadian and Light-Driven Reorganization

Author: Brianna Manning

Mentor: Alec Davidson, Ph.D., Morehouse School of Medicine

Background/Significance: We frequently experience circadian disruption due to exposure to irregular light–dark cycles. One of the most prevalent examples of this today is shift work –working long hours and overnight shifts. These frequent disruptions lead to adverse physiological and behavioral outcomes such as metabolic and mood disorders. The suprachiasmatic nucleus (SCN) serves as the master circadian clock, synchronizing internal rhythms to environmental light cues. While previous work has characterized molecular and cellular mechanisms within individual SCN neurons, how network-level dynamics govern circadian rhythmicity and light responses remains unclear. Understanding these network mechanisms is essential for linking cellular function to systemic circadian regulation and for addressing circadian misalignment in human health.

Methods: Using in vivo calcium imaging in NMS-icre::Ai162 mice expressing the GCaMP6s calcium indicator, SCN network activity was recorded every three hours across a 48-hour period under both constant darkness and 12:12 light/dark conditions. Imaging stacks were processed using Inscopix and Igor Pro software to generate correlation maps quantifying cell-to-cell synchrony and network coherence across time. Fluorescence intensity data were analyzed using cosinor and correlation analyses to assess rhythmicity, phase relationships, and temporal reorganization of SCN activity. Additional behavioral and physiological data, including locomotor activity and body temperature, were used to validate functional rhythmicity. Comparisons of baseline network organization with responses to acute light pulses at distinct circadian phases further assessed how environmental light cues modulate SCN topology and coherence.

Results: Preliminary data reveal time of day dependent changes in SCN network coherence, with variability across individual animals possibly linked to lens placement and intrinsic network properties. Ongoing analyses aim to clarify whether rhythmicity at the single-cell level predicts network synchrony and whether pre-existing network states shape SCN responses to light stimuli.

Conclusions and Implications: These findings are expected to illuminate how network-level synchronization within the SCN underlies circadian stability and responsiveness to light. By linking cellular activity to network topology, this research will refine experimental methodologies and contribute to understanding of how environmental light cues reorganize SCN circuits, a mechanism potentially underlying circadian disruption in shift workers.

Acknowledgment of Funding: This work is supported by the Simons Foundation, Davidson Laboratory, Morehouse School of Medicine.

P-64

Title: GPR37 Regulates Granule Cell Maturation and Affective Behavior in the Hippocampus via Sex-Dependent Mechanisms

Authors: Kaylor Mondaizie, M.S.1,2,3; Sharon Owino, Ph.D.2,3

1 Doctor of Philosophy in Biomedical Sciences Program, Morehouse School of Medicine

2 Department of Pharmacology & Toxicology, Morehouse School of Medicine

3 Neuroscience Institute, Morehouse School of Medicine

Mentor: Sharon Owino, Ph.D., Morehouse School of Medicine

Background/Significance: Hippocampal neurogenesis is a lifelong form of neural plasticity in which newly generated granule neurons mature and integrate into circuits supporting cognition and emotional regulation. Although essential for these functions, the molecular mechanisms governing late-stage granule cell maturation remain poorly understood. Wnt/β-catenin signaling regulates dendritic maturation and synaptic integration, yet upstream modulators particularly those acting through the Wnt co-receptor LRP6 are unclear. Evidence suggests the orphan G protein-coupled receptor GPR37 interacts with LRP6 and may potentialize Wnt signaling as an endoplasmic reticulum chaperone; however, its direct functional role in adult neurogenesis is unknown. As the ventral hippocampus regulates emotion, late-stage maturation here is closely linked to anxiety outcomes. We hypothesize that the GPR37–LRP6–Wnt/β-catenin axis represents a novel regulatory network promoting late-stage granule cell maturation, and that its disruption alters anxiety-related behavior.

Methods: Male and female C57BL/6 wild-type and Gpr37 / mice (2–4 months old) were used to assess hippocampal morphology and anxiety-related behaviors. Dentate gyrus cell populations were quantified using immunohistochemistry, RNAscope in situ hybridization, and IMARIS to assess total nuclei, neuronal density (NeuN), and markers of immature (DCX, calretinin) and mature (calbindin) granule cells. Confocal imaging and CellProfiler software quantified soma size and neuronal eccentricity. Anxiety-related behavior was assessed using the Light/Dark Box and Elevated Plus Maze paradigms, with DeepLabCut, a deep neural-network–based markerless pose-estimation tool, providing high-resolution tracking. Analyses were sex-balanced, blinded, and completed in RStudio and GraphPad Prism.

Results: The loss of GPR37 did not alter total nuclei or neuronal number in the dentate gyrus; however, female Gpr37 / mice exhibited increased neuronal eccentricity and larger soma size. In the light/dark box, Gpr37 / mice spent significantly less time in the light compartment and produced more boli than wild-type controls, indicating increased anxiety-related behavior. DeepLabCut analyses further revealed sex-influenced affective responses in the elevated plus maze, with Gpr37 / males showing reduced open- and outside-arm exploration, whereas females trended toward increased exploration.

Conclusions and Implications: These findings indicate that GPR37 positively regulates granule cell maturation and anxiety-related behavior, with emerging sex-influenced effects potentially mediated through LRP6-dependent Wnt/β-catenin signaling. Ongoing studies will delineate hippocampal contributions and employ lineage-tracing and Wnt-reporters to define direct GPR37–LRP6 regulation of neurogenesis and affective outcomes, ultimately informing the development of novel anxiety treatments.

Acknowledgement of Funding:

▪ Supported by NSF grant BRC-BIO 2334983.

P-65 Title: Zinc Chelation and H₂O₂-Mediated Cell Injury

Authors: Anthony J. Nicholson Jr1, Dexi

Chen2, Tiandong Leng2,

and Zhigang Xiong2

1. Morehouse School of Medicine B.S.-M.S. Neuroscience Dual Degree Program

2. Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine

Mentor: Zhigang Xiong, MD, PhD, Morehouse School of Medicine

Background and Significance: Neuronal cell death caused by oxidative damage is a key feature of stroke, traumatic brain injury and other neurological disorders. Hydrogen peroxide (H₂O₂), a major form of endogenous oxidant, can kill neurons by damaging molecules such as proteins, DNA and lipids. Zinc is a trace element which has a complex role in neurons; too much Zinc can worsen injury, while too little can disrupt normal cell function. This study investigates how H₂O₂induced injury is affected by Zinc chelation with TPEN in NS20Y cells, a neuronal cell line. Hypothesis: Zinc chelation has a significant influence on oxidative stress-mediated cell injury.

Methods: H2O2 -mediated cell toxicity was analyzed using LDH assay and live/dead (FDA/PI) staining in NS20Y cells. Cells were initially cultured in 24-well plates in DMEM for 48-72 h to reach a confluence of ~80%. The medium was then changed to those containing different concentrations of H2O2 (100 or 300 µM) in the absence or presence of 10 or 30 µM of TPEN. 50 µL medium sample was withdrawn from each well at 4 and 24 h for LDH assays. LDH assay was performed by measuring the absorbance at 492 nm with background readings at 620 nm subtracted. Maximal LDH release in each well was obtained by treating cells with 50 µL of 5% Triton X-100. Statistical analysis was performed using ANOVA.

Results: Incubation with H₂O₂ (100 or 300 µM) alone increased LDH levels at 4 and 24 hours (n=12, p<0.05), with higher H₂O₂ concentration and longer exposure showing more injury. Incubation with TPEN (30 μM or 10 μM) alone also produced high levels of LDH release (n=8, p<0.01), indicating that zinc removal can cause cell damage on its own. At 4 hours, H₂O₂+TPEN showed slightly lower LDH level than TPEN alone, but at 24 hours the combination of both either produced the same or higher values than TPEN alone, indicating complex interaction between Zinc chelation and H2O2-mediated neuronal cell injury. Further testing with lower doses of TPEN and H2O2 and analysis of cell morphology changes are ongoing.

Conclusion and Implications: Findings suggest that both H₂O₂ andTPEN can produce neuronal cell injury. TPEN alone causes cell death, indicating that removing Zinc affects cell survival. When TPEN was combined with H₂O₂, the degree of injury changed depending on the exposure time and the concentrations.

Acknowledgment of Funding: This research is supported in part by NIH R21AI185572, R01NS128018, and NSF 2401892.

P-66 Title: Proteomic and Behavioral Alterations in the Brain Following Repetitive Mild Traumatic Brain Injury

Authors: Nebechi Okpala; Khadija Boukhoda; Yaza Bouchi; Jiepei Zhu Ph.D.; Firas Kobiassy Ph.D.

Institution: School of Medicine Neurobiology

Mentor: Firas Kobiassy Ph.D., Morehouse School of Medicine

Background/Significance: Repetitive mild traumatic brain injury (rmTBI) has been linked to chronic neurological dysfunction and a heightened risk for developing neurodegenerative disorders like Alzheimer’s and Parkinson’s disease. The hippocampus, a region crucial for learning and memory, appears particularly susceptible to injury. Although studies have identified widespread proteomic alterations following TBI, the specific molecular and cellular responses to repeated mild trauma remain incompletely understood. This research investigates the early behavioral and proteomic changes in the hippocampus and cortex in a mouse model of rmTBI.

Methods: Male C57BL/6 mice (6–8 weeks old) were randomly assigned to sham, single mild TBI (smTBI), or repetitive mild TBI (rmTBI) groups. Proteomic analyses were conducted on tissue samples from both hemispheres (ipsilateral and contralateral) at 48 hours and 1-week post-injury to detect changes in protein expression. Differential expression analysis was used to identify significant proteins, and Gene Ontology (GO) enrichment was applied to explore related biological processes. Behavioral Morris Water Maze was used to evaluate spatial learning, memory.

Results: Proteomic profiling revealed numerous differentially expressed proteins (DEPs) in the hippocampus following rmTBI. Bar graph analysis demonstrated a marked increase in both upand downregulated proteins in the rmTBI group compared to sham and smTBI controls. GO analysis highlighted 20 significantly altered biological processes, particularly those related to oxidative stress, synaptic transmission, and cellular energy pathways. Behaviorally, rmTBI mice showed deficits in spatial learning and memory.

Conclusions and Implications: Repetitive mild TBI triggers early disturbances in protein expression within the hippocampus, especially in pathways linked to mitochondrial activity, oxidative stress, and synaptic communication. These proteomic shifts may underlie the cognitive and behavioral impairments observed in this model.

Acknowledgment of Funding: This work is partially supported by the Research Centers in Minority Institutions (RCMI) Grant Number U54MD007602 from the National Institute of Minority Health and Health Disparities (NIMHD), Institut National de la Sanété et de la Recherche Biomédicale, Région Hauts de France, Université de Lille, Agence Nationale de la recherche (Click & Detect, CE29, 2024).

P-67 Title: Edaravone Protects Human Brain Microvascular Cells Against Oxidative Stressinduced Barrier Dysfunction and Hyperpermeability

Authors: Gabriela Seplovich, MS, MPH1, Mojtaba Golpich, Ph. D2, Yehia Mechref. Ph. D3, Firas, Kobeissy, Ph. D2, Binu Tharakan, Ph. D1

1Morehouse School of Medicine, Department of Surgery

2Morehouse School of Medicine, Department of Neurobiology

3Texas Tech University Department of Chemistry and Biochemistry

Mentor: Binu Tharakan, Ph. D, Morehouse School of Medicine

Background/Significance: Traumatic brain injury (TBI) is a leading cause of morbidity worldwide and a major risk factor for neurological disease. Blood-brain barrier (BBB) dysfunction following TBI results in microvascular hyperpermeability, cerebral edema, and elevation of intracranial pressure. TBI triggers overproduction of reactive oxygen species (ROS) including hydrogen peroxide (H202), leading to mitochondrial damage in microvascular endothelial cells, the innermost monolayer of the BBB, and is associated with BBB disruption and the resulting microvascular hyperpermeability. The objective of this study was to characterize the effects of edaravone on human brain microvascular endothelial cells (HBMEC) in the context of TBI-induced oxidative stress and BBB disruption. Edaravone is an FDA- approved free radical scavenger approved for delaying motor neuron degeneration in Amyotrophic Lateral Sclerosis and has been shown to protect the BBB in diabetic stroke models. The role of edaravone as a BBB protectant in the context of TBI is not yet known.

Design/Methods: Human brain microvascular endothelial cells were seeded in Transwell inserts, simulating a BBB monolayer. Cells were exposed to increasing concentrations of edaravone and challenged with H202, a known ROS generated during TBI. Microvascular permeability was measured using FITC-Dextran fluorescent tracer (10 kDa) in cells grown as a monolayer on Transwell inserts. Cell viability was measured using Calcein AM fluorescent cell viability assay and ROS formation was measured using 2',7'-dichlorofluorescin diacetate (DCFDA)-based cellular ROS detection assay.

Results: Results indicate that H202-challenged cells resulted in hyperpermeability across the microvascular monolayer. When cells were pretreated with edaravone at 1, 5, and 10 µM for 24 hours, microvascular permeability was restored. Edaravone treatment reduced H202- induced ROS formation and, on its own, did not significantly affect cell viability. However, edaravone did restore viability in challenged cells.

Conclusions and Implications: The antioxidant edaravone is a promising neurovascular protectant. Our results suggest that edaravone protects against oxidative stress-induced ROS formation and associated BBB hyperpermeability, in the context of traumatic brain injury.

Acknowledgment of Funding: This research is supported in part by grant number 1SC3NS127765 from the National Institute of Neurological Disorders and Stroke, NIH

P-

68

Title: Zinc Sensitizes Neuronal Cells to Oxidative Stress

Authors: Xavier Street1,2, Dexi Chen2, Tiandong Leng2 and Zhigang Xiong2, Institutional Affiliation(s):

1. Neurobiology PhD Program, Morehouse School of Medicine, Atlanta, GA, USA

2. Department of Neurobiology, Neuroscience Institute, Morehouse School of Medicine

Background/Significance: Oxidative stress and irregular zinc homeostasis are both implicated in neuronal injury associated with brain ischemia and other neurodegenerative disorders. Hydrogen peroxide (H2O2) is a common player in oxidative damage, and excess extracellular zinc can damage neurons by disrupting mitochondrial function. This study investigates the interaction between H2O2 and Zinc-mediated injury of NS-20Y cells, a neuronal cell line.

Hypothesis: Excess zinc exacerbates H₂O₂-induced cell injury.

Methods: NS-20Y cells were initially cultured in 24 well plates in DMEM for 48-72 h to reach a confluence of ~80%. The medium was then changed to those containing different concentrations of H2O2 (100, 300, or 500 μM) in the absence or presence of 30, 50, 100 or 300 μM Zinc. Cell death was quantified by lactate dehydrogenase (LDH) release into the culture medium at 4,18,24,48 hours after acute exposures. LDH was measured on a plate reader and normalized to the maximal releasable value in each well after treating with Triton X-100. Data were collected across replicate wells and repeated in 3 or more independent cultures. Statistical analysis was performed using ANOVA.

Results: H2O2 increased LDH release relative to control in a dose-dependent manner, with 300 μM producing a larger effect than 100 μM. Zinc at 30 or 50 μM alone produced little or no LDH elevation, whereas 100 or 300 μM zinc alone induced a large increase in LDH release over the baseline. Combining zinc with H2O2 yielded higher LDH level than either agent alone, indicating that zinc sensitizes cells to oxidative injury. This potentiation was evident at 30 μM zinc and more pronounced at 100-300 μM zinc.

Conclusion and Implications: These findings support the idea that zinc amplifies oxidative stress induced neuronal cell injury. The interaction between zinc and H2O2 suggests converging toxicity on membranes and mitochondria, which is relevant to conditions where synaptic zinc release and oxidative stress occur. Next steps include testing whether a zinc chelator such as TPEN or an antioxidant would attenuate the combined toxicity. Together, the data point to zinc homeostasis as a modifiable contributor to neuronal vulnerability under oxidative stress.

Acknowledgment of funding: This research is supported in part by NIH R21AI185572, R01NS128018, and NSF 2401892.

P-69

Title: Blood Tau and Phosphorylated Tau Dynamics Across Post-TBI Phases Measured with Three Ultra-Sensitive Assay Platforms

Authors: Ali Tejada1; Guangzheng Cai, MS2; Khadija Boukholda, PhD2; Eman Elbayoumi, MD2; Firas Kobaissy, PhD2 , Jiepei Zhu, MD, PhD2

1. Morehouse School of Medicine, MD candidate, 2. Morehouse School of Medicine, Department of Neurobiology

Mentor: Jiepei Zhu, MD, PhD., Department of Neurobiology, Morehouse School of Medicine

Background/Significance: Tau and phosphorylated tau (p-tau) are axonal proteins released after TBI, indicating neuronal injury. Using three advanced assay platforms, this study tracked plasma tau and p-tau changes over time and compared results across technologies to explore tau-related mechanisms similar to those seen in Alzheimer’s disease.

Methods: Plasma total tau and p-tau levels were measured using three ultra-sensitive assay platforms: Quanterix Simoa (Tau 2.0, pTau181), Meso Scale Discovery (MSD) S-Plex (Tau, pTau181), and the SOFIA platform (T-Tau, p-Tau). Healthy controls (n=50) were compared with TBI patients at Day 1 (n=169), 2 weeks (n=141), and 6 months (n=137) post-injury. Mean ± SD concentrations were used to characterize biomarker trajectories, and cross-platform agreement was evaluated using Pearson’s correlation, Fisher r-to-z transformations, and ztests for correlated correlations.

Results: Healthy controls showed the lowest tau and p-tau levels (Simoa Tau 2.0: 0.35 ± 0.65 pg/mL). At Day 1 post-injury, TBI patients showed marked total tau increases (Simoa Tau 2.0: 3.19 ± 3.93 pg/mL; MSD Tau: 18.83 ± 43.25 pg/mL; SOFIA T-Tau: 520.5 ± 808.6 fg/mL) with modest p-tau changes. By 2 weeks, total tau declined toward baseline, while ptau peaked (SOFIA p-Tau: 4126.4 ± 3771.9 fg/mL). At 6 months, total tau nearly normalized (MSD Tau: 0.14 ± 0.10 pg/mL), but p-tau remained elevated (60.8 ± 51.7 fg/mL). Stronger Simoa–MSD correlations than Simoa–SOFIA were seen for Day 1 p-tau (z = 2.38, p = 0.02) and 6-month total tau (z = 2.46, p = 0.014).

Conclusions: Tau and phosphorylated tau levels rose after TBI across all three assay platforms. Total tau peaked acutely, while p-tau stayed elevated for months, indicating ongoing tau-related activity. Simoa and MSD showed stronger agreement than SOFIA. Multi-assay tau profiling may improve monitoring of recovery and early detection of long-term neurodegenerative risk.

Acknowledgment of Funding: This research was supported in part by the National Institutes of Health (NIH) grant [U01NS111680], “Analytical Validation of Tau and P-Tau in Mild TBI with Persistent Symptoms.”

P-70 Title: Whole blood transcriptome profile can predict a CT based diagnosis of hemorrhagic stroke

Authors: Rashi Verma1; Andrea Pearson1; Emine Guven1; Michael Frankel2; Roger Simon1; Robert Meller1

1. Neuroscience Institute, Morehouse School of Medicine, Atlanta, Georgia, USA.

2. Department of Neurology, Emory School of Medicine, Atlanta, Georgia, USA.

Mentor: Dr. Robert Meller, D.Phil., Morehouse School of Medicine.

Background: Stroke is the fifth leading cause of death and disability in the U.S., yet only ~5% of patients receive timely thrombolytic therapy (tPA), primarily due to delays in CT imaging required to rule out hemorrhage, where tPA can cause fatal intracranial bleeding. To address this critical gap, we hypothesize that the peripheral blood transcriptome-based AI/ML model may be utilized to identify hemorrhagic stroke, aiming to enable point-of-care triage and improve access to lifesaving treatment.

Methods: Whole blood was collected in PaxGENE tubes from patients admitted to the ER at Grady Memorial Hospital (Atlanta, GA) with a suspected stroke. Two RNA-seq datasets (temporally separated into 2 batches of samples (modeling and validation)) were generated using the IonTorrent whole transcriptome workflow. Data were sequenced on S5 IonTorrent sequencers and aligned to GRCh38 reference genome using STAR and Bowtie2. Counts were quantified using Stringtie2, and differentially expressed transcripts were identified using Limma. Differentially expressed transcripts were used as features to train machine learning models. Models were optimized with ten-fold cross-validation and performance was evaluated on the validation dataset using accuracy, sensitivity, specificity, and ROC-AUC metrics.

Results: We used 90 patient samples in the training set and 25 in the validation set. Transcriptome analysis (p < 0.05, fold change ≥ 1.5) across group comparisons revealed differentially expressed 298 transcripts (Hemorrhage vs. Ischemic Stroke), 231 transcripts (Ischemic Stroke vs. Stroke Mimic), and 241 transcripts (Hemorrhage vs. Stroke Mimic). From these, the top 100 up- and downregulated transcripts were selected, identifying 79 transcripts uniquely associated with hemorrhage. These features were used to train ML models using the caret package in R to distinguish Hemorrhagic Stroke patients from Stroke Mimics and Ischemic Stroke patients. The Partial Least Squares (PLS) model achieved the best standalone performance: 95% accuracy in training and 84% in validation (sensitivity = 0.67, specificity = 0.86, ROC-AUC = 0.91). Ensemble models (CaretEnsemble) further improved performance: NNET+RPART achieved 96% accuracy (sensitivity = 0.67, specificity = 1.0), while PLS+RANGER reached 92% accuracy (sensitivity = 0.67, specificity = 0.95).

Conclusion: Here we show admission RNAprofiles can differentiate stroke patient subtypes with clear implications for thrombolytic therapy.

Funding: This research is supported in part by grant number R01NS112422 from the National Institute of Neurological Disorders and Stroke (NINDS) and U54HG013595-01 from National Human Genome Research Institute (NHGRI).

P-71

Title: A Role for the Endocannabinoid System in Regulating Sleep and Circadian Rhythms.

Authors: MacKenzie White 1, Luis Sanchez2, Christopher Ehlen2

1. Morehouse School of Medicine Bachelor of Science Master of Neuroscience Program

2. Morehouse School of Medicine Department of Neurobiology & Neuroscience institute

Mentor: Chirstopher Ehlen, Ph.D., Morehouse School of Medicine

Background/significance: Current research cannot support the use of cannabinoids for the treatment of sleep disorders and poor sleep quality. The role of the endocannabinoid system and its endogenous receptors in sleep and circadian rhythms is unknown. We hypothesize that the endocannabinoid receptors (CB1 and CB2) are involved in both sleep and circadian regulation. This study will investigate the role of CB1 receptor or CB2 receptor in regulating mouse sleep and circadian rhythms. Aiming to 1) determine the effect of CB1 receptor removal and 2) the effect of CB2 receptor removal on mouse sleep.

Methods: CB1 KO and CB2 KO mice with the entire coding region of the CB1 receptor gene (CNR1) or CB2 receptor gene (CNR2) deleted were bred in house and maintained on a 12h light:12h dark cycle. Electroencephalographic (EEG) and Electromyographic (EMG) electrodes were surgically implanted under isoflurane anesthesia and allowed two weeks to recover. After 24-hour baseline sleep recordings, mice were sleep restricted for 6 hours and sleep recording continued for 18 hours. EEG recordings were hand scored for non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Wheel running activity was then recorded during two weeks of constant darkness to assess circadian period.

Results: Our findings demonstrate significantly longer circadian periods in CB1 receptor KO mice compared to wild type mice in constant darkness. Mice lacking either receptor spent significantly more time in NREM when compared to WT controlmice. CB1 receptor KO mice spent significantly more time in REM when compared to CB2 receptor KO and WT mice. Examination of the homeostatic response to sleep deprivation, revealed significant differences in the amount of sleep recovered after sleep deprivation. Both wild type mice and mice lacking CB1R recovered NREM in the six hours following sleep deprivation. In contrast, CB2 receptor KO mice did not recover any of the NREM lost during sleep deprivation.

Conclusion and Implications: These findings reveal a potential role for endocannabinoid receptors in sleep regulation. The results suggest that the endocannabinoid system may affect sleep and the mammalian circadian system through mechanisms that involve both cannabinoid receptor subtypes. Results of this study provide supportive information for future studies investigating the use of cannabis in humans. Furthermore, these findings identify the cannabis receptor targets, that should be targeted, in sleep and circadian rhythm disorders.

Acknowledgement of Funding:

• This research was supported by funding from the Kessler Foundation.

P-72

Title: Epidemiology of Pediatric Traumatic Brain Injury: Sex- and Mechanism-Specific Patterns from a Systematic Review

Authors: Jessica Wright¹; Yazan Bouchi¹; Sarah Thomas¹; Brianna Hayden¹; Laura Blackwell⁴; Andrew Reisner³; Samar El Hajj²*; Firas Kobeissy¹, ²*; Joseph Tyndall¹

¹ Department of Medicine, Morehouse School of Medicine, Atlanta, GA, USA

² MENA Program for Advanced Injury Research (MENA PAIR), Department of Epidemiology and Population Health, Faculty of Health Sciences, American University of Beirut, Beirut, Lebanon

³ Department of Neurosurgery, Emory University, Atlanta, GA, USA; Children’s Healthcare of Atlanta, Atlanta, GA, USA

⁴ Department of Pediatrics, Emory University, Atlanta, GA, USA; Children’s Healthcare of Atlanta, Atlanta, GA, USA

Mentors: Samar El Hajj, PhD; Firas Kobeissy, PhD

Background/Significance: Pediatric traumatic brain injury (pTBI) is a leading cause of morbidity and mortality worldwide. Despite the substantial burden, heterogeneity in reporting by sex and mechanism limits synthesis across studies. We hypothesize that sex-based biological and behavioral differences modulate pTBI risk and outcomes, while specific injury mechanisms, such as sports, motor vehicle collisions, and falls, are associated with distinct severity profiles. This review aims to clarify these relationships using a standardized analytic framework.

Methods: A systematic review of studies from 1935 to 2022 using MEDLINE, Embase, and Scopus identified 652 eligible studies from 35,867 screened, totaling 134 million participants. Data were extracted into REDCap and stratified by sex, mechanism (sports, MVCs, falls, blunt/struck, other), severity, and outcomes. Both study-weighted and participant-weighted analyses were performed to assess distribution patterns and reporting quality.

Results: Sports-related injuries accounted for 26.4% of studies but 72.4% of participants, reflecting large administrative datasets. Non-sports mechanisms, particularly MVCs (8.2%) and falls (10.1%), disproportionately contributed to severe injuries and mortality. Males represented 46.0% of participants, females 28.7%, and 25.3% were unspecified. Severity reporting was inconsistent, with 58.1% of studies using unspecified or mixed classifications. Overall mortality was 0.055% but reached 28.4% in severe strata. Rehabilitation outcomes were reported in only 12.8% of studies, underscoring major gaps in longitudinal care data.

Conclusions and Implications: This review, spanning 652 U.S. studies, reveals clear sex- and mechanism-specific disparities in pTBI research and outcomes. Males predominate in sportsrelated mild injuries, while MVCs and falls drive the severe and fatal spectrum across both sexes. Significant underreporting of sex, severity, and rehabilitation outcomes limits comparability and hinders prevention efforts. Standardized sex-disaggregated and mechanism-specific reporting is urgently needed to advance pediatric TBI surveillance, guide clinical care, and inform targeted prevention strategies.

Acknowledgment of Funding: This work was supported by the Morehouse School of Medicine and the MENA Program for Advanced Injury Research, Faculty of Health Sciences, American University of Beirut.

P-73 Title: Trends in Surgical Wait Times for Total Joint Arthroplasty, 2000-2025

Authors: Ibaad Khan, BS1,2; Neeku Salehi, BS2; Chad A. Krueger, MD2; P. Maxwell Courtney, MD2; Eric B. Smith, MD2; David N. Kugelman, MD2

¹Morehouse School of Medicine, Atlanta, GA²Rothman Orthopaedic Institute at Thomas Jefferson University, Philadelphia, PA

Background/Significance: Total joint arthroplasty (TJA) is among the most common elective procedures in the U.S., with utilization steadily rising. With concurrent shifts toward outpatient surgery and increasing migration of cases to ambulatory surgery centers (ASCs), the net effect on wait times remains unclear. We sought to evaluate temporal trends in surgical wait times for TJA and examine whether insurance type or facility type were associated with significant differences in wait times. We hypothesized that surgical wait times have decreased over time and differ by facility type.

Methods: A retrospective analysis was performed using our institutional database of all primary total hip and knee arthroplasties conducted from 2000 to 2025. Wait time was defined as the number of days between a patient’s final orthopedic clinic visit and the date of surgery. Patients with wait times exceeding 2 years were excluded, as these cases likely reflected non-routine delays. Insurance type was classified as Medicare, private, Medicaid, or other; facility type was classified as full-service hospital, specialty hospital, or ambulatory surgery center (ASC). Linear regression models assessed the association between procedure year and wait time. A multivariate model adjusted for insurance and facility type. Statistical significance was defined as p < 0.05.

Results: A total of 153,837 procedures were included. Mean ± SD wait time for all procedures was 62.5 ± 53.9 days. In unadjusted analysis, later year of surgery was associated with slightly shorter wait times (−0.10 days/year; 95% CI −0.15 to −0.04; p < 0.001). After adjusting for insurance and facility type, the association was no longer significant (−0.03 days/year; p = 0.23). Compared with full-service hospitals, specialty hospitals (−4.26 days; p < 0.001) and ASCs (−2.03 days; p < 0.001) had significantly shorter waits. Insurance type, including Medicare vs. private, was not significantly associated with wait time.

Conclusion and Implications: From 2000 to 2025, surgical wait times for TJA decreased modestly, with no significant differences observed by insurance type. However, shorter waits at specialty hospitals and ASCs suggest shifting access patterns as arthroplasty moves toward outpatient settings. Monitoring these trends is essential to ensure continued patient access as care delivery models continue to evolve.

Title: Custom Prosthesis for Recurrent Aseptic Loosening in Distal Femoral Replacement: A Case Study

Authors: Shadrach Ofoegbu1; Adwin Denasty, MD2; Christopher Dussik, MD3; Rishi Balkissoon, MD, MPH4

1. Morehouse School of Medicine, Atlanta, GA, USA

2. University of Rochester School of Medicine and Dentistry, Rochester, NY, USA

3. Nth Dimensions

Mentor: Rishi Balkissoon, MD, MPH, University of Rochester

Background: Distal femoral replacement (DFR) is a salvage procedure for addressing distal femoral tumors, advanced femoral bone loss after total knee arthroplasty (TKA), periprosthetic distal femoral fracture, or comminuted intra-articular distal native femoral fracture in osteoporotic bone. DFR is associated with a high rate of failure. This case study presents a novel custom DFR revision scenario.

Methods: An 82-year-old female with insulin-dependent type 2 diabetes, obesity, and hypertrophic cardiomyopathy underwent right TKA, which later failed due to aseptic loosening, requiring revision TKA. Ten years later, she developed acute hematogenous periprosthetic joint infection (PJI) unresponsive to debridement and implant retention (DAIR). Staged revision followed, beginning with explantation, debridement, and prolonged intravenous and oral antibiotics. Once the infection was eradicated, a DFR was implanted for excessive femoral bone loss. Approximately two years later, she experienced aseptic femoral component loosening. Revision was undertaken; however, loosening recurred within two years. Given recurrence, poor remaining osteoporotic bone, and refusal of total femoral replacement, a custom DFR was created with a side plate, locking interlocking screw, and cephalomedullary screw to enhance implant fixation.

Results: At nine months postoperatively, she was doing well with no reported complications.

Conclusions and Implications: To our knowledge, no other reports describe a custom DFR incorporating a side plate with locking interlocking screw and cephalomedullary screw. Additional research is warranted to evaluate outcomes and performance. We propose that the use of this design enhances mechanical stability over standard options and may prevent recurrent aseptic loosening in DFR patients with osteoporotic bone.

Acknowledgment of Funding:

• This study was funded by Nth Dimensions.

P-75 Title: Minimal Residual Disease Detection of Serum Monoclonal Proteins in Multiple Myeloma Patients utilizing Affinity Purification and High-Resolution Mass Spectrometry

Authors: Justin A. Barthel1,2, Danya Ortiz2, Chenyin (Dawnie) Lu, MS2, Farida Elgebaly2 , Priscilla S.-W. Yeung, MD/PhD2,3, and Ruben Y. Luo, PhD2,3

1. Morehouse School of Medicine, Atlanta, GA;

2. Department of Pathology, Stanford University, Stanford, CA, USA;

3. Clinical Laboratories, Stanford Health Care, Palo Alto, CA, USA;

Mentors: Priscilla S.-W. Yeung MD/PhD and Ruben Y. Luo PhD

Background and Significance: Multiple myeloma is a common hematologic malignancy caused by the overproduction of monoclonal proteins (M-proteins) from clonal plasma cells: intact immunoglobulins (IgGs) and free light chains (FLCs). Diagnosis requires serum protein electrophoresis (SPEP) for IgGs and immunoassays for FLCs. However, these tests lack the necessary sensitivity and specificity to detect low concentrations. We aim to improve M-protein detection by using High-Resolution Orbitrap Mass Spectrometry (HR-MS). Our objective is to detect M-proteins with high sensitivity and specificity at a concentration of 15 µg/mL or lower. This will provide a clinically relevant platform for assessing minimal residual disease (MRD) and detecting earlier relapses.

Methods: The limit of detection for M-proteins was assessed across fourteen samples seven with kappa light chains (four IgG-K and three FLC-K) and seven with lambda light chains (four IgG-L and three FLC-L) each with known M-protein concentrations tested in triplicate using HRMS. CaptureSelect KappaXP and Lambda XP Affinity Matrix resins were utilized to bind antibodies and FLCs. Captured immunoglobulins were eluted using 10 mM glycine, followed by 0.1% formic acid, then analyzed by HR-MS for detection. Additionally, the detection capabilities of HR-MS were quantified by identifying 12 lambda and 12 kappa FLCs in myeloma patient serum samples that were detected by FLC immunoassays but had absent/trace detection by SPEP.

Results: Of the 14 serum samples used (7 kappa and 7 lambda IgGs and FLCs), 10 showed detectable protein concentrations between 10 and 15 µg/mL. These results indicate that HR-MS provides strong sensitivity for detecting both IgG and free light chain monoclonal proteins and highlight the method's potential utility in monitoring low-abundance M-proteins during disease remission or MRD evaluation. Notably, HR-MS detected FLCs in 22 of the 24 samples analyzed.

Conclusion and Implications: Given its comparable M-protein detection levels, HR-MS may serve as an additional method that is a less invasive and more cost-effective approach for MRD detection compared to bone marrow biopsy methods like multiparameter flow cytometry and nextgeneration sequencing. With the ability to detect and differentiate monoclonal from polyclonal proteins, HR-MS can complement FLC Immunoassay by directly detecting monoclonal FLCs in samples for clonality determination. In summary, HR-MS offers an integrated, non-invasive, and highly sensitive strategy for myeloma diagnosis and MRD assessment.

P-76 Title: Assessing the Performance of an Adult-Trained Whole-Body MRI Segmentation Model on Pediatric Lung Anatomy

Authors: Darlene Okpokpo, MS1; Michael Barrow, PhD2; Heike Daldrup-Link, MD, PhD, 2,3

1. Morehouse School of Medicine, Atlanta, GA

2. Department of Radiology, Division of Pediatric Radiology, Stanford University School of Medicine, Stanford, CA

3. Department of Pediatrics - Hematology/Oncology, Lucile Packard Children’s Hospital, Stanford University, CA

Mentors: Michael Barrow, PhD2; Heike Daldrup-Link, MD, PhD2,3

Background: Accurate lung segmentation in magnetic resonance imaging (MRI) is critical in pediatric thoracic imaging, particularly for evaluating and staging lymphoma. The diaphragm serves as an essential anatomical landmark, with disease involvement above or below this boundary determining stage classification. Recent advances in artificial intelligence (AI) have enabled automated segmentation using models primarily trained on adult datasets. However, pediatric patients possess unique anatomical and physiological characteristics that may limit the accuracy of these models. We hypothesize that an adult-trained MRI segmentation model will demonstrate reduced accuracy when applied to pediatric whole-body MRI due to anatomical and developmental differences, resulting in predictable failure patterns. This study evaluates the model’s ability to delineate lung and diaphragm boundaries in pediatric scans, identify common error types, and assess whether inaccuracies could impact lymphoma staging.

Methods: A total of 206 pediatric whole-body MRI scans were analyzed. An adult-trained MRI segmentation model was applied to identify the lungs and diaphragm. Segmentation outputs were reviewed and manually corrected using 3D Slicer, an open-source medical imaging platform. Errors were categorized into five groups: minor lung adjustments, significant lung errors, segmentation outside the lungs, incorrect anatomy, and total failure. Errors were analyzed with attention to implications for lymphoma staging accuracy.

Results: Of 206 scans, 28.6% demonstrated acceptable segmentation without modification, and 11.2% required minor adjustments. Significant lung segmentation errors occurred in 20 scans 9.7%, while 52.4% exhibited segmentation extending outside the lungs, often including mediastinal or abdominal structures. Despite these issues, 88.9% of scans still contained correctly localized lung regions that could be refined through manual correction. Major errors were most common in scans with mediastinal tumors or distorted anatomy.

Conclusion: Adult-trained AI segmentation models show moderate success when applied to pediatric MRI, with about 40% of scans requiring minimal or no correction. However, over half exhibited over segmentation or misclassification due to pediatric anatomical variability and disease-related distortion. These findings highlight the need for pediatric-specific training datasets and refinement strategies to improve model reliability for clinical use in pediatric oncology imaging.

P-77 Title: Computational Analysis of CB1 Cannabinoid Receptor Ligand Binding Using Molecular Docking

Authors: Daleena Gebrehiwet1,2, Mary Jo Ondrechen2

1Department of Chemistry & Biochemistry, Spelman College, Atlanta, GA

2Department of Chemistry & Chemical Biology, Northeastern University, Boston, MA

Mentor: Mary Jo Ondrechen, Ph. D., Northeastern University

Background/Significance: The cannabinoid receptor CB1 is a G protein–coupled receptor (GPCR) involved in regulating pain, mood, and appetite, and is a major therapeutic target whose activation depends on ligand-specific binding interactions. This study examined the binding behavior of three pharmacologically distinct cannabinoid ligands- AM6538 (inverse agonist), Δ9THC (partial agonist), and AM8411 (full agonist)- to evaluate how differences in ligand efficacy relate to predicted binding affinity and interaction patterns at CB1.

Objective/Goals: The objective of this study was to investigate the correlation between ligand efficacy and predicted binding affinity and interaction patterns at the CB1 receptor.

Methods: Molecular docking simulations were conducted using the Schrödinger Suite, specifically Maestro and Glide. The active-state CB1 receptor (PDB ID: 5XR8) was prepared with the Protein Preparation Wizard to assign bond orders, add hydrogens, and minimize structural energy. The orthosteric binding site was defined around key residues (Phe177, Tyr275, Ser505, Leu193, Phe501, and Cys508). Ligands (AM6538, THC, and AM8411) were processed using LigPrep to ensure accurate stereochemistry and protonation. Docking was performed in Glide Standard Precision (SP) mode to compare relative binding affinity and interaction profiles among the ligands. Protein- ligand interactions- including hydrogen bonding, π–π stacking, and hydrophobic contacts- were analyzed to compare binding affinity and structural complementarity.

Results: To address this objective, molecular docking scores revealed distinct differences in binding affinity among three ligands. AM8411 demonstrated the strongest predicted binding affinity for the CB1 receptor with a glide score of -10.52 kcal/mol, compared to -10.61 kcal/ mol for AM6538 and -8.71 kcal/mol for THC. Interaction analysis revealed that AM8411 forms multiple stabilizing hydrogen bonds, π–π stacking interactions, and hydrophobic contacts with key activesite residues, including Phe177, Tyr275, Ser505, Leu193, and Cys508, thereby contributing to enhanced ligand stability within the binding pocket. These results support AM8411’s classification as a high-affinity ligand and highlight its potential as a reference scaffold in the design of CB1targeted therapeutics.

Conclusions and Implications: AM8411 showed strong predicted affinity for CB1, forming stable hydrogen bonds and hydrophobic interactions with key residues. These findings support its classification as a high-affinity full agonist and highlight the value of computational docking in predicting receptor–ligand behavior. This work provides a structural basis for designing CB1targeted therapeutics.

Acknowledgement of Funding: Chem RXN Program- Research Opportunity

P-78 Title: The Role of Bmal1 in Regulating Mitochondrial Calcium Levels in 661W Photoreceptor Cells

Authors:

Mikaili Senwah, B.S

1

, Kenkichi Baba, Ph.D.

2

1 Spelman College & Morehouse School of Medicine, Bachelor of Science/Master of Science in Neuroscience Program

2 Morehouse School of Medicine, Pharmacology/Toxicology Department

Mentor: Kenkichi Baba, Ph.D., Morehouse School of Medicine

Background/Significance: The circadian clock gene Bmal1 is a core component of the molecular circadian machinery and plays a crucial role in regulating cellular calcium homeostasis, including calcium transport, storage, signaling pathways, and circadian calcium oscillations. In addition, Bmal1 influences cellular rhythmicity and mitochondrial function. Several studies have demonstrated that Bmal1 regulates mitochondrial dynamics to accommodate day–night energy demands. More recently, our laboratory discovered that Bmal1 modulates mitochondrial innermembrane ultrastructure by regulating MIC60 in mouse photoreceptor cells. Photoreceptors in the retina are among the most metabolically demanding neurons in the body, heavily relying on the precise regulation of mitochondrial activity to sustain vision. Mitochondrial calcium plays a crucial role in controlling energy production, signaling, and cell survival. However, when mitochondrial calcium is not properly regulated, it can induce dysfunction and lead to photoreceptor degeneration. However, the role of Bmal1 in calcium handling within the mitochondria has not been clearly defined. Understanding how Bmal1 influences mitochondrial homeostasis could highlight new mechanisms by which circadian regulation supports retinal health and protects against degenerative diseases. We hypothesize that the loss of Bmal1 will disrupt any rhythmic expression of calcium-handling proteins, leading to mitochondrial calcium imbalance and impaired bioenergetic function.

Methods: Wildtype 661W photoreceptor-like cells and Bmal1 knockout (BKO) 661W cells will be used. Mitochondrial and cytosolic calcium will be measured using Rhod-2 AM and Fura-2 AM fluorescent indicators. The expression level of calcium regulator genes and proteins, VDAC1-3, MICU1, MICU2 and mitochondrial calcium uniporter (MCU), will be assessed through qPCR and Western blotting. Mitochondrial function and glycolysis capacity will be evaluated using Seahorse analysis.

Anticipated Results: It is expected that Bmal1-deficient cells will exhibit disrupted rhythmic calcium regulation, altered calcium-regulatory protein expression, and reduced mitochondrial respiration compared to the 661w wild type cells. Pharmacologically blocking the MCU is anticipated to reproduce the same deficits observed in the Bmal1 knockout cells, suggesting that Bmal1 maintains mitochondrial calcium balance and metabolic efficiency through the MCU pathway.

Conclusions and Implications: This research will provide insight into how Bmal1 supports mitochondrial calcium homeostasis in photoreceptor cells and may identify novel molecular targets for preventing retinal degeneration.

Acknowledgement of Funding: This research is supported by the following grants:

• “The BS/MS Program in Neuroscience at the Atlanta University Consortium” Grant number: R25NS117365

• “The retinal clock modulates cell viability, retinal circuitry and locomotor activity rhythm” Grant number: SC1 GM135112-01A1 (NIGMS)

P-79 Title: Trends in Racial and Ethnic Disparities in Retinal Procedures Over Two Decades

Authors: Kara Barclay1 , Raziyeh Mahmoudzadeh MD3, Adarsh Mallepally 2, Stephanie Pan2,Jessica Randolph, MD2

1. Morehouse School of Medicine

2. VCU School of Medicine

3. VCU Department of Ophthalmology

Mentor: Jessica Randolph, MD2,VCU Department of Ophthalmology

Background/Significance: Retinal diseases can lead to vision impairment, significantly altering individuals’ quality of life, mental wellbeing, and physical health. Implementing effective and timely interventions to lower the likelihood of vision loss is often multifactorial. Understanding racial trends in retinal procedures is crucial to address disparities and promote health equity. The purpose of this study is to assess disparities in the utilization of retinal procedures among racial and ethnic subgroups over two decades in commonly indicated retinal procedures.

Methods: This was a retrospective cohort study from January 2004 to January 2024 using the TriNetX Collaborative Network. Adults with any of the following retinal diseases: diabetic macular edema (DME), central retinal vein occlusion (CRVO), exudative age-related macular degeneration (AMD), proliferative diabetic retinopathy (PDR), tractional retinal detachment (TRD), rhegmatogenous retinal detachment (RRD), a diagnosis of RRD and proliferative vitreoretinopathy (PVR) or TRD, and endophthalmitis. Patients were stratified by race and ethnicity: White, Black, Hispanic, Asian, Native American, and Pacific Islander. Propensity score matching (PSM) of demographics, BMI, A1c, comorbidities, eGFR, and SES was performed. The outcome for DME, CRVO, and exudative AMD was incidence of intravitreal injections (IVIs), panretinal photocoagulation (PRP) was measured for PDR, pars plana vitrectomy (PPV) was measured for TRD, an outcome of either PPV, scleral buckle (SB) or pneumatic retinopexy (PR) was measured for RRD, and complex PPV was measured for RRD and PVR or TRD. The comparison of outcomes between matched subgroups was assessed using a risk ratio (RR) and 95% confidence interval (CI). All analyses were conducted using the TriNetX Platform Analytics tool.

Results: Black patients were significantly less likely to receive IVIs from 2004-2009 (RR: 0.64, CI: 0.43-0.95), 2009-2014 (RR: 0.71, CI: 0.64-0.80), and 2019-2024 (RR: 0.91, CI: 0.85-0.97) within 6 months of diagnosis of DME compared to White patients. Black patients with exudative AMD were also less likely to receive IVIs from 2019-2024 (RR: 0.70, CI: 0.55-0.88) within 6 months of diagnosis. Similarly, Black patients with TRD were less likely to be treated with PPV from 2014-2019 (RR: 0.89, CI: 0.82-0.97) and 2019-2024 (RR: 0.91, CI: 0.82-0.99).

Conclusion/implications: Our results highlight a multitude of health disparities that persist in retinal procedures, including access to timely care, utilization of proper management, and barriers to quality healthcare.

Acknowledgement: The research was supported by Virginia Commonwealth University

P-80 Title:

Meeting Moms Where They Are: A Qualitative Study on Food Assistance Preferences and Delivery for Families with Young Children

Authors: Naja Bostwick MS1; Rachel Gross, MD, MS2,3, Christina Kim, Ph. D 2,3, Mary Jo Messito, MD 2,3, Laura Palacio Mazo, BA 2,3, Carol Duh-Leong, MD, MPP 2,3

Mentor: Carol Duh-Leong, MD, MPP2,3

Institutional Affiliations:

1 Morehouse School of Medicine Doctor of Medicine Program

2 Department of Pediatrics at NYU Grossman School of Medicine

3 Bellevue Hospital

Background/ Significance: Food insecurity remains a persistent public health challenge, affecting 47.4 million individuals, including 7.2 million children in the U.S. (USDA, 2023). Early food insecurity has lasting implications for child health and development, including higher rates of asthma, depression, and developmental delays. Federal programs such as SNAP and WIC aim to reduce food insecurity, yet many working-poor households still face access barriers. Existing research mainly examines program participation rather thanfamilies’ lived experiences and preferences. This study explores how mothers of young children experience and navigate food access and assistance, and identifies preferences for improving food assistance delivery.

Methods: This qualitative study was nested within the Starting Early Program, a maternal health cohort at Bellevue Hospital. Purposive sampling recruited mothers (n=20) based on family size and parenting experience. Inclusion criteria were first-trimester pregnancy, age ≥18 years, English or Spanish fluency, and plans for prenatal and pediatric care at Bellevue. Semi-structured interviews used open-ended questions exploring affordability, food quality, and program experiences. Inductive thematic analysis guided coding and theme development, with sample size determined by thematic saturation.

Results: Preliminary analysis identified themes reflecting mothers’ experiences with food access and assistance. Most participants reported financial strain, with budgets depleted by month’s end. While food assistance participation was common (WIC = 6; SNAP = 4), several mothers described confusion about eligibility and dissatisfaction with culturally mismatched options. Some reported unused benefits due to unfamiliar or undesirable foods. A strong preference for fresh, high-quality, culturally familiar foods emerged, tied to autonomy and dignity in feeding families. Overall, findings suggest that although WIC and SNAP provide critical support, gaps in accessibility, cultural relevance, and food quality limit effectiveness in promoting sustained food security.

Conclusions and Implications: Mothers’ narratives highlight the need for food assistance programs that go beyond eligibility and quantity to reflect real-life family food practices and values. Programs must address affordability, cultural relevance, and food quality to enhance participation and reduce waste. Centering mothers’ voices in food policy can foster more equitable, flexible, and empowering models of food assistance that support family well-being and long-term food security.

Acknowledgment of Funding: Supported by: AFRI #2022-08688 (Mary Jo Messito); The Sala Elbaum Pediatric Research Scholars Program (Carol Duh-Leong); APA Young Investigator Award – Nutrition in Underserved Communities Pathway (Christina Kim).

P-81

Title: Measuring Efficacy of Community Outreach Expansion and Type 2 Diabetes Mellitus Detection in an Urban Student-Led Clinic Patient Population from 2023–2024

Author: Mari Chiles1

1 Morehouse School of Medicine MD Program

Mentor: Christopher Ervin, M.D., Morehouse School of Medicine H.E.A.L. Clinic

Background: The Morehouse School of Medicine Health Equity for All Lives (MSM H.E.A.L.) Clinic provides healthcare to underserved individuals in Georgia (GA). Existing public health literature on type 2 diabetes mellitus (T2DM) highlights disparities between rural and urban areas, with rural areas having a higher incidence of chronic disease. Further research should highlight health inequities of vulnerable communities in resource-rich urban centers. The study aim is to compare the efficacy of MSM H.E.A.L. between 2023 and 2024 in conducting health screenings in underserved metro-Atlanta locations and detecting T2DM risk. We hypothesize that MSM H.E.A.L. increased screening numbers in disadvantaged locations in 2024 and that these locations exhibit increased rates of random blood glucose values > 140 mg/dL.

Methods: This study is exempt from IRB review. The locations of CBO events between 01/01/2023-12/31/2024, and blood glucose values collected at each, were compiled from REDCap, excluding those not occurring in the five most populous counties in GA: Fulton, Dekalb, Clayton, Gwinnett, and Cobb. We utilized the Area Deprivation Index (ADI) to record the associated decile ranking of socioeconomic disadvantage for each CBO location. We grouped ADI deciles into three categories: 1-3 (socioeconomically stable), 4-6 (moderately disadvantaged), and 7-10 (severely disadvantaged).

Results: MSM H.E.A.L. increased the number of CBO events in metro-Atlanta from 21 in 2023 to 47 in 2024. The number of individuals screened increased from 855 to 1758. The percentage of CBO events conducted in severely disadvantaged tracts decreased from 52% to 23% However, MSM H.E.A.L. equally conducted 10 events in severely disadvantaged tracts both years and increased the number of individuals screened in those areas from 261 to 467. All events in severely disadvantaged census tracts occurred in South Fulton, Central Dekalb, and Clayton counties both years. Comparing MSM H.E.A.L. patient T2DM risk for one CBO event in a socioeconomically stable versus severely disadvantaged census tract showed the percentage of individuals with a random blood glucose > 140 mg/dL being 23% vs. 33% respectively in 2023, and 10% vs. 19% in 2024.

Conclusion: MSM H.E.A.L. expanded health screening services between 2023 and 2024, attributed to a more efficient screening model and addition of trained staff and volunteers. Distinct areas of Fulton, Dekalb, and Clayton counties in metro-Atlanta exhibit severe socioeconomic disadvantage and higher rates of abnormal blood glucose values compared to socioeconomically stable areas, indicating increased T2DM risk. Further MSM H.E.A.L. outreach must focus on increasing screenings, resources, and T2DM education in the vulnerable neighborhoods identified.

P-82

Title: An Analysis of the Relationship Between Soil Microbial Diversity and Tooth Loss Across Atlanta Neighborhoods

Authors: Tyliah Hall; Jessica Coates, Ph.D.

¹ Spelman College, Biology Department

Mentor: Jessica Coates, Ph.D., Spelman College

Background/Significance: The mouth is often called the “gateway to the body,” highlighting oral health as a key indicator of overall well-being. According to the CDC, one in six U.S. adults aged 65 and older has lost all natural teeth, with rates nearly twice as high among low-income and Black seniors. Tooth loss reflects oral disease and issues, such as nutrition, access to care, and chronic health conditions. Environmental factors such as air and water quality, income, pollution, and neighborhood infrastructure have been linked to oral health outcomes in under-resourced communities. However, the role of soil environments in oral health remains largely unexplored. We hypothesized that lower soil microbial diversity is associated with higher rates of complete tooth loss among seniors. This study examined whether reduced soil biodiversity is associated with poorer oral health outcomes across Atlanta neighborhoods.

Methods: Soil was collected from five Atlanta neighborhoods, including Atlanta University Center, Buckhead, Cascade, Sandy Springs, and Vine City. Sites were selected to represent differences in income, racial composition, population size, and land use. Cascade, Vine City, and Atlanta University Center were lower-income and predominantly Black areas, while Buckhead and Sandy Springs represented higher-income communities. Bacterial isolates were screened using selective plating to identify species and phyla. Species richness and colony forming units(CFUs) were used as indicators of soil microbial diversity. Tooth loss prevalence data from 2021 and neighborhood demographic data were obtained from publicly available sources. Pearson correlations and multiple regression evaluated associations between soil microbial diversity and community tooth loss, including demographic covariates such as income, population size, and percent Black population.

Results: Species richness and CFUs varied across neighborhoods. Buckhead and Sandy Springs exhibited the highest diversity with 5.70E6 and 4.40E6 CFU/g and richness values of 18 and 14, while Atlanta University Center showed the lowest at 2.10E5 CFU/g and a richness of 7. Species richness was strongly negatively correlated with complete tooth loss (r= -0.87). Higher microbial diversity was associated with lower tooth loss: Buckhead 6.1%, Cascade 27.0%, and Atlanta University Center 26.4%.

Conclusion and Implications: These findings suggest a strong association between soil microbial diversity and oral health outcomes without implying causation. Lower soil biodiversity may reflect broader environmental and structural conditions, such as reduced infrastructure investment or chronic environmental stressors that also influence access to oral health resources. Soil microbial diversity may serve as a useful environmental indicator for understanding and monitoring neighborhood health disparities. Future studies should investigate pathways linking environmental quality, demographic factors, and oral health.

P-83 Title: Development of a Cardiac Arrest Risk Stratification Model Incorporating

Social and Clinical Predictors

Authors: Brianna Hayden1, MS; Eleanor Clarke, MPH1; Ertha Sefu Omba, MS, MPH1; Mutsa Nyamuranga, MPH1; Reyonna Maloney, MS1; Breeana Snowball, MS1; Ernest Alema Mensah, PhD, DMin, MS, MDiv2; Firas Kobeissy, PhD3 ; J. Adrian Tyndall, MD, MPH, FACEP4

Affiliations:

1: Morehouse School of Medicine- Doctor of Medicine Program

2: Morehouse School of Medicine- Department of Community Health and Prevention

3: Morehouse School of Medicine- Department of Neurobiology

4: Morehouse School of Medicine- Office of the Dean

Background: Cardiac arrest remains a leading cause of mortality in the U.S., with disproportionately poor outcomes among minorities and low-income populations. While clinical risk factors such as heart failure and myocardial infarction are well established, the role of social determinants of health (SDoH) in predicting cardiac arrest, particularly in the context of the COVID-19 pandemic is not fully understood. We hypothesized that combining clinical and social predictors into a tiered model would improve identification of individuals at high risk for cardiac arrest.

Methods: We analyzed NHANES data (2017–2023), evaluating adults with self-reported cardiovascular diagnoses. Logistic regression models were used to examine associations between SDoH and clinical with three major cardiac conditions: congestive heart failure (CHF), myocardial infarction (MI), and heart disease (HD). These outcomes were treated as proxies or contributors to cardiac arrest risk. Models were stratified by pre- and post-pandemic periods to detect shifts in risk profiles. Significant predictors were incorporated into a multi-tiered risk stratification model estimating relative cardiac arrest susceptibility across population subgroups.

Results: Age was the strongest nonmodifiable predictor across all cardiac outcomes, with increasing age associated with higher risk (OR range: 1.12–1.13). Female gender was protective for MI and HD (OR = 0.66 for both) but was associated with slightly increased odds of CHF (OR = 1.12). Race was not a dominant predictor. Among modifiable factors, smoking (CHF OR = 2.58; MI and HD OR = 1.87), diabetes (CHF OR = 2.10; MI OR = 2.10), obesity (CHF OR = 1.68; MI and HD OR = 1.63), and hypertension (MI and HD OR = 1.85) demonstrated the strongest associations. Pre- and post-pandemic analyses showed largely stable effect sizes. Individuals in the high-risk tier (score ≥7) showed markedly higher burden indices for CHF (0.85), MI (0.90), and heart disease (0.88), compared to low-risk individuals (≤3) whose indices were <0.30 across all outcomes.

Conclusion: This study highlights the compounded influence of SDoH and clinical conditions in elevating cardiac arrest risk and the consistent risk patterns observed across the pandemic period. By integrating multiple social and clinical variables, our novel stratification model provides a framework for early identification of at-risk individuals, informing targeted interventions.

Acknowledgment of Funding: This work was conducted without external funding.

P-84 Title: Romantic Relationships during Recovery: Exploration of the Influence of Romantic Relationships on Harm Reduction during Pregnancy/Postpartum

Authors: Tierra Hollaway, PhD, LMFT

Institutional Affiliation:

Morehouse School of Medicine and Emory University

Background/Significance: Substance use disorder remains a growing public health concern in the United States, particularly during pregnancy and postpartum, when the stakes for maternal and fetal health are high. Roughly 5% of pregnant women use one or more addictive substances. Peer and social support are well-documented protective factors in recovery, shaping emotional stability and behavior change. This study examined the influence of romantic relationships on pregnant/postpartum women’s recovery from substance use disorder. It is hypothesized that women who feel supported by their romantic partner are more likely to incorporate harm reduction practices or discontinue substance use during pregnancy/postpartum.

Methods: Participants were recruited in the following areas: Rural Georgia’s “Black Belt”, Rural Appalachian North Georgia, and Urban Atlanta. In this mixed-methods study, participants were enrolled based on the following eligibility criteria: at least 18 years of age, identified as Black/African-American, White or Hispanic/Latinx or of Spanish origin, were currently pregnant or pregnant within the last 3 months, lived in specific Georgia counties for at least 6 of the last 12 months, and used an illegal substance ormisused prescription medications in the 3 months before they knew they were pregnant. Qualitative and quantitative data were collected through semistructured interviews and demographic assessments. Thematic analysis was applied to qualitative interview data.

Results: There were 39 participants (46% pregnant and 53% postpartum). Most were aged 2534 (59%) and identified as White (62%). 38% identified as Black or multi-racial. The substances frequently used during pregnancy/postpartum were cannabis (84%), methamphetamine (69%), and opiates (64%), In the past 30 days, participants reported using cannabis (41%), methadone (17%), buprenorphine (15%), and opiates (12%). Qualitative themes described how participants chose to decrease their substance use, change the way in which they consumed substances to opt for a healthier option, and quit using substances due to negative physical reactions. Participants described how their romantic relationship contributed to their substance recovery journey in the following ways: partners showed support by not using substances that could trigger the pregnant/postpartum person, partners began treatment for substance use disorder for themselves, or participants decided to end the relationship due to partners continued substance use.15% experienced change in relationship status, 85% didn’t.

Conclusions and Implications: Findings suggest that having a supportive romantic partner can facilitate the reduction of substance use and incorporation of harm reduction practices during pregnancy/postpartum. Future research should explore how harm reduction practices affect romantic relationships, specifically in relationships where both partners are using substances, and assess the potential benefits of engaging romantic partners in recovery interventions for pregnant/postpartum women.

P-85

Title: Mapping the Miles: Travel Time and Food Access Among Students at Morehouse School of Medicine

Author(s): Zahra Irfan1; Maya Dewey1

1 Morehouse School of Medicine MD Student

Mentors:

Robina Josiah Willock, PhD, MPH; Chaohua Li, MPH, Morehouse School of Medicine

Background/significance: Food insecurity (FI) affects approximately 26-50% of graduate students in the U.S. and is associated with adverse academic, mental, and wellness outcomes. Structural barriers like transportation, classes, and financial constraints may limit students’access to nutritious, affordable food within one mile of campus. Although the Atlanta University Center (AUC) is not a food desert by definition, food quality, affordability, and travel time substantially restrict access. This study hypothesized that Morehouse School of Medicine (MSM) students would report significant barriers to accessing nourishing, affordable food within one mile of the AUC. The “Real Routes” study aimed to: (1) describe transportation-related time investments and modalities as structural determinants of FI among AUC students; and (2) disseminate resources mitigating FI among MSM students.

Methods: We conducted an environmental scan (windshield survey and visual documentation) of zip codes 30310 and 30314 to assess food retailers within one mile of MSM. Geospatial and time-based QGIS mapping examined access to grocers within a five-mile radius of MSM via personal vehicle, public transportation, and walking. A convenience sample of MSM students (MD, GEBS, PA, and PhD programs) was recruited to complete the “Real Routes” survey, which assessed types of food retailers used, transportation options, and barriers to accessing healthy food. Three issues of the MSM Food Access Bulletin (FAB) were distributed to mitigate FI-related challenges among students.

Results: The FAB was electronically distributed to 681 MSM students. It received 44 views and 28 responses to the survey (19 MD students, 9 other students). Cost, limited time, and inadequate options were the most common barriers. Most students shopped at full-service grocery stores (88%) and used private vehicles (82%). Food options within a 10-minute walk of the AUC were predominantly lower quality and higher cost. Public transportation to a grocery store within one mile increased one-way travel time by 20-30 minutes.

Conclusion and Implications: Time and cost constraints on healthy food access compel students, especially those without private transportation or adequate finances, to trade nutrition for other priorities. Institutional interventions like subsidized grocery shuttles, partnerships with affordable retailers, on-campus food distribution programs, and dissemination of food access resources may reduce transportation-related disparities and promote equitable food access. Addressing these structural barriers is essential to supporting student well-being and success and may inform food access strategies for other AUC students.

Acknowledgement of Funding: This research was supported by the MSM Summer Research and Public Health Experience, Department of Community Health and Preventive Medicine, Cancer Health Equity Research Institute, and National Center for Primary Care.

P-86

Title: A

Scoping Review of Trauma Informed Language in the Care of Injured Patients

Authors: P. Kallepalli1,2 , L. Hart2,3 , M. White3 , C. Castater1,2 , J. Bliton5 , R. Smith1,2,3,4

1Morehouse School of Medicine, Atlanta, GA, USA

2Grady Memorial Hospital, Trauma Surgery, Atlanta, GA, USA

3Emory University School of Medicine, Surgery, Atlanta, GA, USA

4Rollins School of Public Health at Emory University, Atlanta, GA, USA

5Jamaica Hospital Medical Center, Surgery, Queens, NY, USA

Mentor: Dr. Randi Smith, MD, MPH, Emory School of Medicine

Research Question: What educational strategies, clinical applications, and measurable outcomes have been reported in the literature regarding trauma-informed language among healthcare providers treating victims of violent or traumatic injury?

Introduction: Trauma Informed care (TIC) is a set of principles that can be used as a framework for healthcare professionals to mitigate traumatic stress or re-traumatization of injured patients. Importantly, trauma-informed language (TIL) is a key concept of TIC that provides safety, empathy, and autonomy to patients and avoids revictimization and re-traumatization. The language that clinicians use in treating traumatically injured patients is integral in providing holistic, trauma-informed care. This study's objective is to evaluate the literature on the education, guidance and outcomes associated with TIL to provide a current framework that will help practitioners provide better care for this population.

Methods: Cochrane CENTRAL, CINAHL, Embase, PubMed, and Web of Science were searched on July 2, 2024. Terms and controlled vocabulary associated with TIC, gun, gunshot, violent injury, residency (education) and emergency department were used. Results were limited to English language, published since 2004. Case reports, comments, commentary, editorials, letters, meta-analyses, reviews and systematic reviews were excluded.

Results: The searches yielded 3,960 records. The results were uploaded to Covidence©, an online tool used for systematic and scoping reviews. After 1,599 duplicates were removed by Covidence©, 2401 studies, including one study which was not discovered during the searches, were reviewed for the initial title/abstract screening. Of the 20 studies selected for further full text review, 3 studies were deemed eligible for this study. The literature suggests that TIL is infrequently taught and rarely utilized in managing traumatically injured patients. This leads to significant challenges in communication between trauma patients and providers. When taught, TIL improvestrainee communication skills and confidence. When utilized in the healthcare setting, TIL improves patient satisfaction and may mitigate post-traumatic symptoms in patients and physicians alike.

Conclusion: Understanding the positive impact that trauma-informed, patient-centered language has on victims of firearm violence remains elusive due to the profound paucity of literature. Future studies should focus on evaluating pedagogical approaches to integrating trauma-informed language into trauma care with an end goal of increasing comprehensive empathy practices and enhancing patient outcomes.

P-87 Title: A

Descriptive Study of Childhood Adversity and Suicide Vulnerability in African American Women.

Authors: Alexandra Khalil, BA1 , Marshall Fleurant, MD MPH2

(1) Morehouse School of Medicine, MD Program

(2) Emory School of Medicine, Department of Internal Medicine

(3) Grady Memorial Hospital

Mentor: Marshall Fleurant, MD, Emory School of Medicine, Department of Internal Medicine

Background: Adverse Childhood Experiences (ACEs) including abuse, household dysfunction, and community adversity are associated with increased risks for chronic diseases and psychiatric disorders in a dose-dependent manner1,2. Although 82.7% of the U.S. population reports 0–3 ACEs, African American women more frequently report high ACE scores on both conventional and expanded surveys3,4. Elevated exposure to multiple ACEs, particularly in urban, low-income communities, compounds the risk for adverse mental health outcomes, including suicidality1,5

Methods: This descriptive correlational secondary analysis examined cross-sectional data from low-income African American women in their 30s recruited from emergency, outpatient, and psychiatric services at Grady Memorial Hospital. Participants completed validated surveys assessing suicidal ideation, ACEs (conventional and Philadelphia ACEs [PHL ACE]), depressive symptoms, post-traumatic stress disorder, racial microaggressions, and more. Correlation and frequency analyses explored associations among ACEs, risk and resilience factors, and suicidality.

Results: In our database, we describe a total of 61 low-income African American women in their 30s at risk for suicide. Participants reported an average of 5.5 conventional and 3 expanded (PHL) ACEs, both exceeding national norms. Psychiatric comorbidity was high: 79% had depression, 69% had an anxiety disorder, and 74% had at least two psychiatric diagnoses; 85% reported a history of psychiatric or substance use hospitalization. Suicide risk was pronounced, with 62% at moderate to high risk by the Beck Scale for Suicidal Ideation. Both conventional and PHL ACE scores were negatively correlated with perceived social support, and PTSD symptoms showed the strongest associations with other clinical measures.

Conclusions: This highly vulnerable population experiences pronounced childhood and community trauma, psychiatric disease, and suicide risk. Greater childhood adversity was associated with lower perceived social support, underscoring the intersection of poverty, trauma, and psychiatric illness. These findings highlight the need for targeted, culturally tailored interventions and further research on risk and resiliency factors to inform effective suicide prevention strategies for African American women.

Acknowledgment of Funding: This research is supported in part by the MSM Summer Research and Public Health Experience and Emory School of Medicine, Department of Internal Medicine

P-88 Title: Prevalence, Treatment, and the Control of Depressive Symptoms in the

United States, 2017-2020

Authors: Colby Lindsay1; Chaohua Li, MPH2,3; Peter Baltrus, PhD2,3

1 Morehouse School of Medicine MD Program

2 Morehouse School of Medicine Department of Community Health and Preventive Medicine

3 National Center for Primary Care

Mentor: Dr. Peter Baltrus, Ph.D., Morehouse School of Medicine

Background/Significance: Depression affects 25.1% of U.S. adults (2017–2020) and remains a leading cause of disability. Despite guidelines recommending combined pharmacologic and behavioral therapy for moderate to severe cases, major treatment gaps persist. Using NHANES data, this study examined depression prevalence, treatment patterns, and disparities by demographic group and symptom severity. Among adults with PHQ-9 ≥15, only 26.6% received both medication and therapy, while 42.7% received no treatment. Women and younger adults reported higher symptom rates. Although evidence-based care improved slightly compared to prior data, access remains inadequate. This study evaluated national trends in depression prevalence, treatment, and symptom control using NHANES 2017–2020 data.

Methods: This cross-sectional study analyzed 8,304 NHANES participants aged ≥18 with complete PHQ-9 data. Depression severity was categorized as mild (5–9), moderate (10–14), moderately severe (15–19), or severe (≥20). Pharmacologic treatment was defined as antidepressant use in the past 30 days: behavioral treatment as consultation with a mental health professional in the past year. Treatment patterns were examined by severity, focusing on PHQ-9 ≥15.

Results: Overall, 25.1% of U.S. adults had depressive symptoms up from 21.6% in 2005–2008. Women consistently exhibited higher prevalence across all ages. Among those with PHQ-9 ≥15, only 26.6% (95% CI, 21.0–32.2) received both pharmacologic and behavioral care, while 42.7% (95% CI, 34.4–51.0) received none. Even among severe cases (PHQ-9 ≥20), 35.1% remained untreated, though combined treatment rose from 14.8% to 26.6% compared to 2005–2008.

Conclusions: Although combined treatment rates for severe depression have nearly doubled, nearly half of adults with significant symptoms remain untreated. Rising depression prevalence alongside persistent treatment gaps highlights an urgent need for system-level reforms, provider expansion, and policies addressing barriers to equitable mental health care.

Acknowledgment of Funding:

• This research was supported in part by Morehouse School of Medicine Summer Research and Public Health Experience

P-89 Title:

Surgical Risk Assessment for Adults with Sickle Cell Disease: A Literature Review Addressing Gaps in Perioperative Care

Authors: Bianca McAlister1 , John H. Stewart, IV, MD, MBA, FACS 1,2 , Anny Rodriguez, Ph.D., MPH1

1 Morehouse School of Medicine Master of Public Health Program

2 Grady Memorial Hospital

Mentor: Anny Rodriguez, Ph.D., MPH, Morehouse School of Medicine

Background/ Significance: Sickle Cell Disease (SCD) is one of the most prevalent inherited blood disorders globally, characterized by a point mutation in the β-globin gene resulting in the production of abnormal hemoglobin (HbS). The consequent vaso-occlusion, chronic anemia, and multi-organ dysfunction create unique clinical challenges, particularly in the surgical setting. Adults with SCD are at increased risk for postoperative complications such as acute chest syndrome, infection, and thromboembolic events. Widely used surgical risk calculators fail to incorporate disease-specific variables, such as baseline hemoglobin, hydroxyurea use, or history of vaso-occlusive crises, limiting predictive accuracy. This study seeks to evaluate perioperative outcomes among adults with SCD and to determine the need for a disease-specific surgical risk model. We hypothesize that a SCD specific surgical risk calculator will more accurately predict postoperative outcomes in adults with SCD than current general risk tools.

Methods: A comprehensive literature review was conducted to assess existing research on perioperative outcomes in adult patients with SCD. Sources included peer-reviewed articles, national datasets. The review examined complication rates across surgical subspecialties, demographic and clinical predictors of outcomes, and the limitations of current risk tools.

Results: Preliminary findings reveal a significant gap in risk prediction accuracy for adults with SCD undergoing surgery. Current models underestimate complication rates and fail to account for hematologic parameters and disease-specific comorbidities. Limited data disaggregation by surgical subspecialty further obscures the true burden of risk. Adults with SCD, particularly those treated at safety-net hospitals such as Grady, experience disproportionately high morbidity rates relative to the general surgical population.

Conclusions and Implications: The absence of a validated surgical risk model for SCD represents a critical gap in perioperative medicine and health equity. Developing a tailored risk calculator that integrates disease-specific clinical indicators can improve surgical planning, patient counseling, and postoperative management. This emphasizes the need for national and institutional collaboration to enhance perioperative outcomes for adults with SCD.

Acknowledgement of Funding:

• This research was supported the MSM Summer Research and Public Health Program

P-90 Title

: Is “Brain Rot” Real? The Perceived Impact of Short-Form Social Media on Brain Function and Mental Health

Authors: Naman Shah¹*, Truc Bui¹*, Toyaunna Hamm¹*, Jessica Alvarez¹*, Tylin Siwemuke¹, Nithya Rajanala¹, and E. Vanessa Spearman-McCarthy¹, MD

Institutional Affiliations: ¹Medical College of Georgia, Augusta University, Summer Educational Enrichment Program

Background/Significance: “Brain rot” is a popular internet term describing perceived cognitive decline associated with excessive short-form social media (SFSM) use. SFSM includes brief, attention-grabbing content from platforms like TikTok, Instagram Reels, and YouTube Shorts. Prior research suggests that these platforms may negatively affect attention, memory, and mental health. This study evaluated whether the concept of “brain rot” reflects measurable trends by examining associations between SFSM use and perceived cognitive and mental health consequences.

Methods: A cross-sectional survey to measure perceived “brain rot” was developed in Qualtrics and distributed electronically (e.g., email, social media, etc.). The nine-question survey was open to all respondents without age restrictions and collected demographic information, frequency and duration of SFSM use, Likert scale responses assessing agreement with statements about perceived effects of SFSM on procrastination, memory, attention span, and mental health, and open-ended qualitative responses about perceived experiences with “brain rot.” After ten days, 249 complete and valid responses were analyzed using single-factor ANOVA to assess correlation between SFSM use and perceived cognitive or behavioral effects.

Results: Respondents were predominantly female (65%) and aged 20-25 years (59%). The sample was primarily Asian (45%) and Black or African American (35%). Analysis revealed significant correlations between SFSM use and perceived negative effects on procrastination tendencies (r = 0.779, p = 0.0016) and attention span (r = 0.742, p = 0.0208). Increased SFSM use was also associated with perceived negative effects on memory (r = 0.694) and mental health (r = 0.666). Age had a significant association with SFSM use (r = -0.881, p = 0.0001) and with perceived mental health harm due to SFSM (r = -0.811, p = 0.0003), suggesting that younger participants tended to use SFSM more and perceived more adverse effects. Qualitative responses noted both detriments (e.g., cognitive fatigue and distraction) and benefits (e.g., stress relief and social connection).

Conclusions and Implications: Based on our study, perceived “brain rot” is a real phenomenon. While excessive SFSM use appears to be associated with perceived impairment in attention, procrastination, and mental health, SFSM may also serve positive social and psychological roles. These findings underscore the need for further research to clarify SFSM’s impact on cognitive well-being and inform public health recommendations for responsible use.

Acknowledgement of Funding: This research was supported by the Student Educational Enrichment Program (SEEP) at the Medical College of Georgia. Special thanks to Dr. Vanessa Spearman-McCarthy, TylinSiwemuke,andNithyaRajanalafortheirmentorshipandguidance.

P-91 Title:

Sociodemographic Disparities in Breast Cancer Screening Prevalence Among Women in the United States: Findings from the 2021 Behavioral Risk Factor Surveillance System

Authors: Shaylyn Sullivan, Naomi Campbell, MPH, Anny Rodriguez, PhD, MPH, Gemechu B. Gerbi, PhD, MSc

Morehouse School of Medicine | 720 Westview Dr. SW | Atlanta, GA 30310-1495

Introduction: Breast cancer remains one of the most commonly diagnosed malignancies among women in the United States and a leading cause of cancer-related mortality. Although mammography is a well-established tool for early detection, disparities in screening persist across sociodemographic groups, reflecting broader inequities in access to preventive care. Prior research has documented differences in screening by age, race and ethnicity, and socioeconomic status, yet contemporary national estimates examining these patterns across multiple dimensions of inequality remain limited. This study examines sociodemographic factors associated with selfreported history of breast cancer screening among U.S. women using nationally representative data.

Methods: We conducted a cross-sectional analysis using data from the 2021 Behavioral Risk Factor Surveillance System (BRFSS), including 9,080 women aged 18 years and older who responded to the breast cancer screening module. The primary outcome was self-reported history of having ever received a mammogram. Independent variables included age, race and ethnicity, household income, education level, health insurance status, and U.S. census region. Weighted bivariate analyses and multivariable logistic regression models were used to estimate adjusted odds ratios (AORs) and 95% confidence intervals (CIs). All analyses were conducted using SAS version 9.4.

Results: Overall, 79.0% of women reported having ever received a mammogram, while 21.0% reported no history of screening. After adjustment for covariates, age, race and ethnicity, and insurance status emerged as the strongest predictors of screening. Compared to women aged 65 years and older, those aged 18–24 (AOR = 0.006; 95% CI: 0.004–0.009), 25–34 (AOR = 0.01; 95% CI: 0.01–0.02), 35–44 (AOR = 0.05; 95% CI: 0.04–0.07), and 45–54 (AOR = 0.37; 95% CI: 0.27–0.50) had substantially lower odds of having ever been screened. Asian women had significantly lower odds of screening compared to White women (AOR = 0.65; 95% CI: 0.43–0.98), while Black women had higher odds (AOR = 1.50; 95% CI: 1.26–1.79). Uninsured women were approximately half as likely to report prior screening compared to those with employer-based insurance (AOR = 0.50; 95% CI: 0.39–0.63). Differences by income and education were observed descriptively but were attenuated in adjusted models.

Conclusion and Implications: This study reveals persistent sociodemographic inequities in breast cancer screening exposure among U.S. women, particularly among younger adults, uninsured populations, and certain racial and ethnic groups. These disparities reflect structural barriers to preventive care, including gaps in insurance coverage, culturally responsive outreach, and continuity of care. Future research should examine how health system navigation, providerlevel factors, and regional access patterns shape screening trajectories over the life course. Targeted, equity-centered interventions such as community-based outreach, patient navigation programs, and policy reforms that reduce financial and logistical barriers are essential for ensuring that all women have access to timely, life-saving breast cancer screening.

Keywords: Breast cancer screening, health disparities, women’s health, prevention, BRFSS

P-92 Title: Let’s Talk–PERIOD: Addressing Menstrual Health Inequity through Education and Community Engagement

Authors: Laini Tuboku-Metzger¹; Dr. Erica Walker¹; Katherine Egland² ¹Brown University, Providence, RI; ²Education, Economics, Environmental, Climate & Health Organization (EEECHO), Gulfport, MS

Mentor: Dr. Erica Walker, Brown University School of Public Health

Background and Significance: Young girls in underserved communities often lack access to accurate, age-appropriate menstrual health education, compounded by stigma, misinformation, and barriers to product access. To address these inequities, PERIOD., an interactive activity book for girls ages 8 to 12, was developed under the mentorship of Dr. Erica Walker through the Community Noise Lab at Brown University. A literature review and environmental scan informed the book’s development by identifying gaps in cultural relevance, accessibility, and engagement within existing menstrual health resources. The Let’s Talk PERIOD community event, held in collaboration with the EEECHO, a community-based organization focused on health education and equity, served as the initial implementation and evaluation setting.

Methods: Findings from the literature review and environmental scan directly informed the book’s content and design, emphasizing medically accurate information, stigma reduction, and confidence-building strategies. The PERIOD. activity book was launched at the Let’s Talk PERIOD event in Gulfport, Mississippi, which included expert-led panels, menstrual product distribution, and facilitated community dialogue. Girls ages 8 to 12 and their caregivers participated to support intergenerational communication. Pre- and post-event, multi-item surveys were administered in person to attendees (N = 51) to assess menstrual health knowledge, comfort discussing menstruation, confidence managing periods, and perceived stigma. Quantitative data were analyzed using percentage change, and qualitative responses were thematically coded.

Results: Post-event surveys showed improvements in menstrual health knowledge (“A lot”: 59.2% pre-event vs. 83.7% post-event) and comfort discussing menstruation (“Very comfortable”: 60.4% pre-event vs. 88% post-event). Qualitative analysis identified four key themes: Normalizing Periods (33.3%), Supporting Others (29.8%), Health Knowledge (26.3%), and Menstrual Hygiene (10.5%). Participants frequently described increased confidence, reduced stigma, and improved language for discussing menstruation. Additionally, 92% of respondents rated the PERIOD. activity book as “Extremely Helpful.”

Conclusions and Implications: These findings suggest that the PERIOD. activity book is an effective, community-informed resource that increases menstrual health knowledge, reduces stigma, and empowers participants to engage more confidently with their reproductive health. Pairing evidence-informed educational tools with community-based implementation represents a promising approach to advancing menstrual health equity. Based on participant feedback, an online interactive version of the PERIOD. Resources are currently being developed to expand accessibility beyond in-person events, with future efforts focused on broader dissemination and continued community input.

Acknowledgment of Funding: This project was supported by the Community Noise Lab at Brown University School of Public Health (Dr. Erica Walker, Principal Investigator) and the Education, Economics, Environmental, Climate & Health Organization (EEECHO).

P-93 Title

:

The Synergistic Effects of Faith-Based Engagement and Nurse Navigation in Increasing Prostate Cancer Screenings Among African American Men

Authors: Amaya Williams1; Jianni Braxton1; Keisa Mansfield, MPA1; Ursula Mathis, MBA1; Rick Kittles, Ph.D.2; Brian Rivers. Ph.D.2

1. Phoebe Putney Memorial Hospital, Albany, GA

2. Morehouse School of Medicine, Atlanta, GA

Mentor: Keisa Mansfield, Phoebe Putney Memorial Hospital

Background/Significance:AfricanAmerican (AA) men experience disproportionately high rates of late-stage prostate cancer (PCa) diagnoses, with incidence and mortality rates 70% to 110% higher than those of White men in the United States. Research from the American Cancer Society indicates that distrust of healthcare providers contributes to delayed screening among AA men. Faith-based organizations, which hold significant trust within the Black community, combined with nurse navigation, have the potential to reduce these disparities. This study examines the impact of faith-based engagement and nurse navigation in increasing prostate cancer screenings among AA men.

Methods: This initiative is a partnership between the Albany Coalition of Pastors, Morehouse School of Medicine, and Phoebe Putney Memorial Hospital. An eight-month training program was implemented for pastors, two church members, and local barbers. Health fairs were organized to provide free PSAand health screenings. Nurse navigators received health fair PSA results and provided guidance to participants with elevated PSA levels (>4.0). Additionally, through the Prostate Cancer Precision Prevention Program (PCP3), men aged 40 and older were consented for genetic risk assessment, and additional blood samples were collected for research.

Results: A total of 1,165 specimens were tested for prostate cancer, with 97% of participants identifying as African American. 7% of men tested had elevated PSA levels (≥4.0), and 18 were diagnosed with prostate cancer. Among men with elevated PSA, 32% had received a colorectal screening, 45% had received a PSA screening, and 14% had received a lung cancer screening in the past 12 months. 78% of those with an elevated PSA reported having a primary care provider, while 22% did not. For the PCP3 study, 281 of 336 men attending the health fairs consented to participate, representing an 83% consent rate, with 99% identifying as African American.

Conclusions and Implications: Targeted screenings combined with nurse navigation facilitated early detection and timely intervention for high-risk individuals. The involvement of faith-based organizations, including logistical support such as church transportation, highlights the importance of community engagement in overcoming healthcare barriers. These findings underscore the critical role of culturally informed, community-based interventions in reducing prostate cancer disparities among African American men.

Acknowledgment of Funding: This project was supported byAward NumberACS DICR IRG23-1026782-01-DICR IRG from the American Cancer Society. The content is solely the responsibility of the authors and does not necessarily represent the official views of the American Cancer Society.

P-94

Title: The Association Between Depression, Anxiety, and HIV/PrEP Adherence SelfEfficacy

Among People Incarcerated in Jail

Authors: Ayishat Yussuf1; Rhonda Holliday, Ph.D., MA2,; Anne Spaulding, Ph.D., MPH3

1 Spelman College Department of Psychology

2 Morehouse School of Medicine Department of Community Health and Preventive Medicine

3 Emory Rollins School of Public Health Department of Epidemiology

Mentor: Rhonda Holliday Ph.D., MA, Morehouse School of Medicine

Background/Significance: There are roughly 1.2 million people in the United States living with HIV. Roughly 13% of individuals living with HIV are not aware of their diagnosis and need treatment. Black and Hispanic communities experience higher HIV rates compared to other racial/ethnic groups. People who are incarcerated are also disproportionately affected by HIV, with a prevalence of 1.5%, which is higher compared to the general population. HIV risk is commonly underestimated by incarcerated men engaging in risky sexual behaviors, including unprotected sex and injection drug use. Pre-exposure prophylaxis (PrEP) is a medication utilized to prevent HIV, which has significantly helped in reducing HIV transmission risk when taken consistently. Several barriers impact access to HIV care, including stigma, transportation, medical mistrust, and mental health outcomes. Recent literature has examined the impact of mental health conditions and has found that rates of anxiety and depression are significantly higher in people living with or at risk of HIV compared to the general population. A research gap remains in identifying the connection between mental health outcomes and HIV/PrEP adherence selfefficacy within the incarcerated population. The purpose of this research study is to examine the association between depression, anxiety, and HIV/PrEP adherence self-efficacy among people incarcerated in jail.

Methods: The Emory and Morehouse School of Medicine Substance Use and HIV Action for Re-entry and Engagement (SHARE) Project, is a research study aimed at linking people in Fulton County Jail who use substances and who have HIV or are at risk for HIV to substance use treatment and HIV prevention and care, including PrEP, through a peer navigation intervention. Participants completed baseline surveys that assessed their depression (PHQ-9), anxiety (GAD7), and HIV/PreP adherence self-efficacy.

Results: To date there have been 82 participants enrolled in the pilot study with 84% being Black/African American, 92% cisgender men, and 28% living with HIV. A linear regression will be conducted to examine if depression and anxiety predict HIV/PrEP adherence self-efficacy among the study sample.

Conclusions and Implications: Data from this pilot study will be used to inform a larger implementation trial designed to increase PrEP uptake within jails in the Metro Atlanta Area.

Acknowledgment of Funding: This study is funded by the National Institute of DrugAbuse grant #1R61DA062365. This research was supported in part by the RCMI Student Research Training Program.

P-95 Title:

Endometriomas as a Marker of Disease Severity: Predictive Value on Preoperative MRI

Authors: Daniel Aka 1; Priyanka Jha2; Martina Francisco2;

1 Morehouse School of Medicine, Doctor of Medicine Program

2 Stanford School of Medicine

Mentors: Priyanka Jha, MD, Martina Francisco, MD

Background/Significance: Endometriosis is a chronic condition affecting 7–13% of women of reproductive age. It is defined by the presence of endometrial glands and stroma outside the uterus, commonly involving the bladder, bowel, ovaries, and other pelvic structures. This ectopic tissue often causes pelvic pain, dyspareunia, and infertility. Endometriosis is classified into three types: superficial peritoneal lesions, ovarian endometriomas, and deep infiltrating endometriosis (DIE). DIE consists of fibrotic lesions that invade pelvic tissues. Endometriomas are thick-walled, blood-filled cysts usually associated with more extensive disease and multifocal deep lesions. Our goal is to compare the deep endometriosis disease distribution in patients with and without endometriomas on preoperative MRI.

Methods: This IRB-approved, HIPAA-compliant retrospective study included patients with surgically confirmed endometriosis from two institutions who underwent preoperative MRI, over a three-year period. Patients underwent dedicated endometriosis protocol MRI. Radiology records were analyzed for the presence of disease in the anterior, middle, and posterior pelvic compartments following the reporting guidelines from Society of Abdominal Radiology (SAR) for endometriosis. Disease distribution was evaluated on both a compartment-specific and sitespecific basis and compared between patients with and without ovarian endometriomas. Statistical analysis was performed using Fisher’s exact test and odds ratios to determine statistical significance.

Results: A total of 353 patients with surgically confirmed endometriosis underwent MRI over a 3year period at the 2 institutions. Of these, 154/353 (43.6%) had visualized endometriomas, while 199/353 (56.4%) did not have endometriomas. Patients with endometriomas had three times more frequently encountered deep disease in the anterior compartment and ~ 6 times more frequently encountered disease in middle, and posterior compartments (p < 0.0001). Site-specific disease assessment also showed more frequent deep disease at all sites except the vagina, with the odds ratios (OR) being the highest for the ureters in anterior compartment (OR=9.43,p<0.05), uterine posterior serosal plaques (OR=9.97,p<0.0001) and rectosigmoid disease (OR=4.73,p<0.0001).

Conclusion /Clinical Relevance: Patients with endometriomas were significantly more likely to have disease in the anterior, middle, and posterior compartments compared to patients without endometriomas, suggesting that endometriomas are associated with greater disease severity and disease burden in patients with endometriosis. Patients with endometriomas also had higher frequencies of disease in all 3 compartments. Presence of endometriomas was associated with increased frequency of deep endometriosis involvement of the ureters, posterior uterine serosa and the rectosigmoid.

P-96 Title: Food Insecurity and Maternal Metabolic Health in the U.S. Southeast: An All of Us

Analysis

Authors: Alaijah Bashi, PhD, MSCR 1; Peter Baltrus, PhD2; CarlaMoore, PhD3; Erica L. Johnson, PhD 1

1 Morehouse School of Medicine Department of Microbiology, Biochemistry, and Immunology

2 Morehouse School of Medicine Community Health and Preventative Medicine

3 Morehouse School of Medicine Bionutrition Core

Mentor: Erica L. Johnson Ph.D., Morehouse School of Medicine

Background/ Significance: Food insecurity (FI), defined as limited or uncertain access to sufficient and nutritious food, remains a critical determinant of maternal and population health. Pregnant individuals are particularly vulnerable to inadequate nutrition and related metabolic risks. While geographic disparities in FI are shaped by socioeconomic (SES) and environmental conditions, this study examined urban–rural differences in FI and associated metabolic outcomes using data from the All of Us Research Program (AoU), a nationwide biobank designed to address gaps in populations that have been historically underrepresented in research. Understanding these relationships is essential for identifying populations at greatest risk and informing targeted interventions to improve nutritional access and maternal health outcomes.

Methods: Data from 12,191 participants who were pregnant at enrollment and resided in the U.S. Census–designated Southeastern region were analyzed using RStudio within the AoU platform. Self-reported measures included FI and SES. Geographic information system (GIS) mapping and descriptive analyses were used to assess spatial patterns of FI, metabolic indicators, and urbanization across the Southeast using aggregated Zip3. Multivariable models evaluated associations between FI and metabolic outcomes, including body mass index (BMI), C-reactive protein (CRP), and lipid profiles.

Results: Analyses revealed substantial variation in FI across the Southeastern United States, with higher prevalence observed in Tennessee and South Carolina compared with Georgia and North Carolina. Rural participants experienced greater FI than their urban counterparts; however, food insecurity in urban settings was associated with stronger metabolic effects. Specifically, FI was most strongly associated with higher body mass index (BMI; OR = 1.057), elevated C-reactive protein (CRP; OR = 1.038), and lower HDL cholesterol (OR = 0.973). No significant associations were observed for blood pressure, LDL cholesterol, or blood glucose.

Conclusions/Implications: FI disproportionately affects pregnant individuals in the Southeastern United States. Although FI is more prevalent in rural areas, food-insecure pregnant individuals in urban settings exhibit greater metabolic disruption. These findings indicate that FI during pregnancy in the Southeast represents both a social and biological risk factor. By integrating regional spatial data with metabolic measures from pregnant participants in AoU, this study provides a pilot framework for identifying geographic “hot spots” of nutritional risk. Future analyses will examine how access to public services, healthy food environments, and other contextual factors contribute to FI and maternal nutrition.

Acknowledgment of Funding: Supported by the National Center for Advancing Translational Sciences, NIH (UL1TR002378, TL1TR002382), and by R01MD017690 and U54HG013595.

Compliance Statement: Analyses were conducted within the All of Us Researcher Workbench in compliance with program data use policies. The content is solely the authors’ responsibility

and does not necessarily represent official NIH views.

P-97 Title: Emerging Therapeutic Approach with Dandelion Phytochemicals in Breast Cancer Treatment

Authors: Angel Champion, MSHI 1*; Sadia Kanwal, Ph.D.2; Rafat Ali Siddiqui, Ph.D.2

1 Morehouse School of Medicine, Master of Science in Health Informatics Program

2 Food and Nutrition Science Laboratory, College of Agriculture, Virginia State University

Mentor: Sadia Kanwal, Ph.D.

Background/Significance: Triple-negative (TNBC) remains one of the most aggressive and treatment-resistant breast cancer subtypes, disproportionately affecting Black women, underrecognized in men, and contributing to significant global health disparities. Conventional chemotherapy often fails to eliminate cancer stem cells that drive relapse and metastasis, highlighting an urgent need for targeted, low-toxicity alternatives. Dandelion (Taraxacum officinale), a medicinal plant rich in bioactive phytochemicals, presents a promising avenue for phytopharmaceutical intervention. Harnessing its anti-inflammatory, antioxidant, and apoptotic properties offers a potential for safer and more effective cancer therapeutics.

Methods: Ethanolic extracts of T. Officinale leaf and root were evaluated for antiproliferative efficacy against MDA-MB-231 TNBC cell lines. Phytochemical screening identified major bioactive compounds including flavonoids, triterpenes, sterols, and saponins. Building on these findings, a ligand functionalized phytosomal formulation is being developed through thin-film hydration and freeze drying to enhance bioavailability and targeted delivery. The formulation is being optimized for particle stability (target size 100-200 nm; zeta potential ±30mV) and sustained release under physiological conditions. Characterization studies will include dynamic light scattering, zeta potential analysis, and controlled-release profiling in vitro using organ-onchip and TNBC organoid models.

Results: Leaf and leaf cut-and-sifted extracts exhibited the strongest dose-dependent cytotoxic effects, reducing cell viability to 8-9% through apoptosis. Ongoing formulation studies aim to validate these effects through sustained-release nanoparticle systems designed for enhanced bioavailability and tumor specificity.

Conclusions and Implications: This translational research establishes a comprehensive preclinical framework for developing T. Officinale as a botanical drug candidate for TNBC therapy. Integrating natural product chemistry, nanotechnology, and advanced microphysiological modeling demonstrates the potential of dandelion-derived phytochemicals to advance precision oncology and improve accessibility to effective cancer care, particularly in underserved populations.

Acknowledgment of Funding:

• This work was supported by Evans-Allen grant and a Capacity Building grant to R.A.S. From NIFAUSDA (2018-38821-27756).

P-98 Title:

Genome-Wide Analysis of Genetic Variants Associated with Preterm Birth Across Continental Ancestries in the All of Us Biobank

Authors: Amber Dawning, MS1; Mateus Gouveia, PhD3; Melissa Davis, PhD4; Fengxia Yan, MD5; Erica L. Johnson, PhD2

1Morehouse School of Medicine PhD in Biomedical Sciences Program

2Morehouse School of Medicine Department of Microbiology, Biochemistry, & Immunology

3Morehouse School of Medicine Department of Public Health Education

4Morehouse School of Medicine Institute of Translational Genomic Medicine

5Morehouse School of Medicine Department of Community Health and Preventive Medicine

Mentor: Erica L. Johnson, Ph.D., Morehouse School of Medicine

Background/Significance: Preterm birth (PTB), delivery before 37 weeks of gestation, is the leading cause of neonatal morbidity and mortality and disproportionately affectsAfricanAmerican women. While PTB is influenced by complex genetic and environmental factors, the genetic mechanisms contributing to risk across ancestries remain insufficiently understood, in part due to the historical focus on European cohorts in genomic studies. The All of Us Biobank provides a unique opportunity to investigate ancestry-informed genetic contributions to PTB in a diverse U.S. population. We hypothesize that genetic variants influencing inflammatory and immune regulatory pathways contribute to PTB risk, and the prevalence of these variants differs by continental ancestry.

Methods: Data was obtained from the All of Us Biobank, where PTB cases were defined using the OMOP code for delivery before 37 weeks of gestation (n = 5,000) and full-term births served as controls (n = 2,339). VCF files were processed using Hail merged with phenotypic data, and quality control included filtering variants by call rate (>95%), minor allele frequency (>1%), and Hardy-Weinberg equilibrium (p > 1x10-6), as well as removing variants or individuals with genotype missingness (>5%) using Hail and PLINK. Population structure was evaluated using PCA, and continental ancestry was inferred with ADMIXTURE (K=13) using the 1000 Genomes reference. Genome-wide association analysis was performed in PLINK using logistic regression adjusted for demographic covariates and principal components, and results were visualized using Manhattan and QQ plots to identify ancestry-specific associations.

Results: Admixture analysis revealed diverse continental ancestry within the cohort, and PCA confirmed population structure consistent with these inferred groups. Self-reported race corresponded with genetic ancestry, though notable heterogeneity existed within categories. Several variants in inflammatory and immune regulatory pathways exhibited ancestry-specific allele frequency patterns, including enrichment among participants of African ancestry. Ancestry adjustment reduced confounding and highlighted ancestry-specific genetic effects on PTB risk.

Conclusion and Implications: Genetic variation and continental ancestry contribute to PTB susceptibility, highlighting the importance of accounting for population structure risk assessment. These findings emphasize the need to include ancestrally diverse populations in genomic studies to identify ancestry-specific determinants of PTB and inform equitable precision medicine strategies.

Acknowledgement of Funding: R01MD017690

P-99 Title: Chemical Toxins in the Placenta: PBDE-Induced Oxidative Stress and Inflammation in JEG-3 Trophoblast Cells

Authors: Keturah Eaves1; Dr. Carmen Dickinson-Copeland, Ph.D.1, MSCR; Dr. Erica L. Johnson, Ph.D.1-2

1 Morehouse School of Medicine Department of Microbiology, Biochemistry & Immunology

2 Morehouse School of Medicine Department of Obstetrics & Gynecology

Mentor(s): Dr. Carmen Dickinson-Copeland, Ph.D., MSCR; Dr. Erica L. Johnson, Ph.D.

Background/Significance: Polybrominated diphenyl ethers (PBDEs) are synthetic flame retardants detected in maternal blood, placental and fetal tissues despite regulatory restrictions. While epidemiological studies link PBDE exposure to adverse pregnancy outcomes, the molecular mechanisms underlying placental toxicity remain unclear. Specifically, the relationship between PBDE-induced oxidative stress, Nrf2 antioxidant pathway activation, and inflammatory signaling in trophoblast cells is poorly characterized. This study examines the impact of BDE-47 and BDE-99 exposure, two commonly detected congeners, on oxidative stress and immune responses in JEG-3 trophoblast cells, with a focus on Nrf2-mediated antioxidant defenses and downstream inflammatory signaling pathways.

Hypothesis: PBDE exposure will induce concentration-dependent ROS production in trophoblast cells, leading to the upregulation of antioxidant genes, Nrf2 and HMOX1, and activation of inflammatory pathways resulting in the upregulation of IL-6 and NF-kB.

Methods: JEG-3 trophoblast cells will be exposed to environmentally relevant concentrations of BDE-47 and BDE-99 (0.5, 1, 5, and 10 μM). Cell viability will be assessed following 24 hours of exposure through the MTTAssay. ROS production will be measured at 24 hours using the DCFHDAfluorescence assay. RT-qPCR will quantify the mRNAexpression of Nrf2 pathway genes (Nrf2, HMOX1) and inflammatory markers (IL-6, NF-κB), as well as STAT5A and STAT5B, at 24 hours. Western blot analysis will measure protein levels of total Nrf2, phosphorylated Nrf2 (Ser40), HO1, and phosphorylated NF-κB (p65) at 24 hours. All experiments will include positive controls (H2O2 or LPS) and will be performed with N=3 biological replicates, each with technical triplicates. Data will be analyzed by two-way ANOVA with Tukey post-hoc tests (α=0.05).

Expected Results: We expect no significant decrease in cell viability following BDE-47 and BDE99 treatments. We anticipate a significant increase in ROS production following 24-hour exposure of 10 uM, BDE-99. At 24 hours, we expect elevated IL-6 mRNA and protein secretion, accompanied by concurrent NF-κB activation. Protein expression of phosphorylated Nrf2 and HO1 should increase at 24 hours, indicating sustained antioxidant response.

Conclusions/Implications: This study will further elucidate molecular mechanisms linking PBDE exposure to placental oxidative stress and inflammation. Understanding these mechanisms may inform risk assessments for environmental toxicant exposure during pregnancy and identify potential therapeutic targets for protecting maternal-fetal health.

Acknowledgement of Funding: This research is supported in part by NSF2502800; R01MD017690; 2U24ES029490-06.

P-100

Title: Protective role of neuregulin 1 against prostaglandin F2 alpha-induced luteolysis.

Authors: Rayven Todd¹, Saswati Banerjee², Babayewa Oguljahan3 , , TKayhlia Cornish4, Winston E. Thompson², Indrajit Chowdhury5

¹Master of Biomedical Science Research, Graduate Education in Biomedical Sciences; ²Department of Physiology; 3Center for Laboratory Animal Resources, 4Doctor of Medicine Program, Graduate Education in Biomedical Sciences; 5Department of Obstetrics and Gynecology, Morehouse School of Medicine, Atlanta, Georgia 30310.

Background/Significance: The corpus luteum (CL) plays an important role in early pregnancy by producing progesterone (P4), a hormone essential for placental development and maintaining pregnancy. Dysregulation of CL function is a leading cause of early pregnancy loss in women. Therefore, understanding the regulation of CL function is crucial for improving pregnancy outcomes. Neuregulin 1 (NRG1), a member of the EGF family, is intensely expressed during mid CL and supports CL differentiation. NRG1 is well studied in the nervous and cardiovascular systems and in ovarian follicular functions. However, the exact role of NRG1 in late CL function remains poorly understood. We hypothesize that NRG1 modulates prostaglandin F2 alpha (PGF2a) activation and inflammatory responses in CL by contributing to the maintenance of CL function and promoting a healthy pregnancy.

Methods: The pregnant rats were treated with PGF2a alone as a luteolytic agent or along with different doses of NRG1 for 48 hours to understand the effects of NRG1 on CL protection.

Results: The PGF2a treatment of pregnant rats interferes with CL normal physiological state of CL, resulting in a decrease in P4 and estrogen (E2) synthesis and secretion, with the loss of fetus and a decrease in pregnant rat body weight (BW). Whereas treatment of exogenous NRG1 along with PGF2a of pregnant rats, NRG1 interferes with PGF2a action and protects the CL normal physiological state, resulting in maintenance of P4 and E2 synthesis and secretion, with protection of fetal death and maintenance of pregnancy.

Conclusion: These results suggest that NRG1 acts as a protective and pro-survival factor in the maintenance of CL functions.

Acknowledgements of Funding: This study waspartly supported by National Institutes of Health Grants 1 SC1 GM130544-01A1, 1SC3GM113751, and G12RR03034. This research was conducted in a facility constructed with support from the Research Facilities Improvement Grant C06RR018386 from the National Institutes of Health National Center for Research Resources.

P-101

Title: Apoptotic Engulfment Mutations in C. elegans Lead to Reduced Fertility

MaKyra Wilson¹, Chloe Alston², Regine Charles², Farzaneh Shahabi², and Anna K. Allen²

¹

Department of Biology, Spelman College, Amgen Scholars Program ² Department of Biology, Howard University

Background: Apoptosis, or programmed cell death, is vital for development and tissue homeostasis. In Caenorhabditis elegans, germline apoptosis removes excess or defective germ cells to ensure proper oocyte maturation, making it an ideal model for studying apoptotic regulation. The engulfment pathway, responsible for clearing dying cells, is crucial for maintaining fertility and germline integrity. This study examined how mutations in apoptotic engulfment genes affect fertility by comparing brood sizes of heterozygous and homozygous mutants. We hypothesized that homozygous mutants would show a greater reduction in brood size than heterozygotes due to loss of functional compensation from a wild-type allele. Understanding these effects provides insight into the genetic regulation of germline apoptosis and its role in reproductive health.

Methods: Caenorhabditis elegans strains were maintained at 20 °C on nematode growth medium (NGM) plates seeded with Escherichia coli OP50. Apoptotic engulfment mutants (ced mutants), which carry loss-of-function mutations in cell death abnormal (ced) genes required for the recognition and clearance of apoptotic cells, were analyzed alongside the wild-type N2 strain. Male worms were generated by heat shock of hermaphrodites at 30 °C to induce X-chromosome nondisjunction. Homozygous ced mutant strains were maintained as stable lines, while heterozygous mutants were generated by crossing N2 males with homozygous ced mutant hermaphrodites, producing offspring carrying one mutant and one wild-type allele. Fertility was assessed using brood size assays by counting the total number of viable progeny produced per hermaphrodite. Phenotypic analyses were additionally performed to evaluate germline morphology and reproductive development across genotypes.

Results: Homozygous ced mutants exhibited a marked decrease in brood size and reduced progeny viability compared to the wild-type (N2) strain, indicating that disruption of apoptotic engulfment pathway genes negatively impacts fertility and germline health. These mutants also displayed consistent phenotypic abnormalities, including reduced oocyte production and irregular germline morphology. In contrast, heterozygous ced mutants generated through crosses with N2 showed brood sizes and progeny viability comparable to wild type, indicating functional rescue of fertility defects.

Conclusion: These results demonstrate that mutations in apoptotic engulfment pathway genes negatively affect fertility and progeny viability in C. elegans, highlighting their essential role in maintaining germline homeostasis. The observation that heterozygous ced mutants crossed with N2 displayed normal brood sizes and viable offspring suggests that one functional wild-type allele is sufficient to rescue fertility defects caused by loss of engulfment function, consistent with genetic compensation. Future studies examining interactions between engulfment genes and additional apoptotic regulators involved in RNA processing and germline development, such as etr-1, will further clarify how coordinated apoptotic pathways preserve reproductive success and developmental integrity.

Acknowledgement of Funding: Dr. NIH NIGMS 1R15GM147865-01

P-102

Title: How effective are community-based interventions in lowering the risk of lung cancer in African American men between the ages of 50-70 years old in rural GA?

Authors: Adicia Maddox, Amara Shobe, and Rehgan Miller

1. Morehouse School of Medicine Master of Physician Assistant Studies Program

Mentor: Dr. Christopher Ervin, MD, Morehouse School of Medicine

Background/Significance: Lung cancer remains the leading cause of death among African American men between the ages of 50 and 70 in the United States. Despite improvements in detection and treatment, African American men continue to experience disproportionately higher incidence and mortality rates compared to other racial groups. We hypothesize that these disparities are influenced by structural barriers such as limited access to healthcare and socioeconomic challenges, particularly in rural areas. Therefore, the purpose of this review was to examine existing literature on lung cancer screening among African American men in rural areas and to identify strategies that can promote equity in early detection and prevention.

Methods: During our windshield survey we traveled toMeriwether County, Georgia which allowed us to assess community demographics, strengths, and weaknesses. We then collaborated with Community Spark Solutions, District 4 Public Health, and Dr. Christopher Ervin, MD to conduct key informant interviews to identify the community’s main health challenges. A literary review was conducted utilizing the following keywords: “lung cancer” AND "Black men or African American men" AND “smoking cessation”. We reviewed 20 peer-reviewed articles to evaluate the alignment with our PICO, identify gaps in knowledge, and determine strategies to improve patient outcomes. Studies utilized national datasets and mixed methods, though limitations included data variability and limited rural representation.

Results: The studies demonstrated that African Americans are less likely to meet lung cancer screening eligibility due to the structure of the criteria. Among U.S. lung cancer cases, 32% of African American men met screening criteria compared to 56% of white men. Social determinants of health, including transportation, insurance status, and access to care, were identified as contributors to inadequate screening. Implicit bias and communication barriers during clinical encounters were also noted.

Conclusions and Implications: The findings of our research suggests that African American men remain disproportionately affected by lung cancer and are less likely to receive timely screening. Implementing risk-based lung cancer screening and encouraging smoking cessation could improve health outcomes and inclusivity by accounting for racial and socioeconomic risk factors. Understanding these disparities will enable healthcare workers to encourage and provide equitable, patient centered care and advocate for policies that address health inequities in early detection and prevention of lung cancer.

Acknowledgment of Funding: N/A

P-103

Title: Community-Based Lifestyle Interventions for Hypertension Control Among Low-Income African Americans: A Systematic Review

Authors:

Madeline Anastasi, Aksh Chhabra, Kyana Bradley, Carrin Matson

Morehouse School of Medicine, Physician Assistant Program

Mentor: Stephanie

Y. Banks, MPH, Morehouse School of Medicine

Background/Significance: Hypertension is a leading, modifiable contributor to cardiovascular morbidity and mortality in the United States. African American adults experience earlier onset, poorer blood pressure (BP) control, and higher rates of stroke, heart failure, and chronic kidney disease inequities that are intensified in low-income communities where food insecurity, limited access to healthy foods, and constrained healthcare access make sustained lifestyle change difficult. Because these barriers are shaped by local context, community-based interventions delivered through trusted community infrastructure can extend practical support for diet and selfmanagement beyond the clinic. This systematic review seeks to answer: What is the effectiveness of community-based lifestyle and self-management interventions in improving hypertensionrelated outcomes among low-income African American adults?

Methods: A systematic search of PubMed, Scopus, Galileo, and ScienceDirect identified studies published from January 2015 to December 2025. Eligible studies evaluated community-based lifestyle or self-management interventions delivered through trusted community settings or partners (e.g., community health workers, peer leaders, faith-based organizations, senior centers, or community clinics) among African American adults with hypertension or elevated BP. Extracted data included study design, population characteristics, intervention components, BP outcomes (change and/or control), self-management behaviors (including diet adherence and home BP monitoring), and statistical significance.

Results: Ten studies met inclusion criteria, including randomized and cluster randomized trials, quasi-experimental studies, and qualitative evaluations. Interventions commonly paired lifestyle counseling with self-management supports such as home BP monitoring, peer or community health worker involvement, and delivery through trusted community settings. Most studies reported improvements in BP and/or self-management behaviors. However, results varied: some studies showed modest or nonsignificant BP changes despite improvements in diet-related measures, particularly in shorter interventions or samples with controlled baseline BP. Several studies noted reduced effects after program completion, and heterogeneity in intervention design and outcomes limited comparability across studies.

Conclusion and Implications: Community-based lifestyle and self-management interventions show promise for improving hypertension-related outcomes among lowincome African American adults by extending practical, culturally relevant support beyond clinical settings. Findings support integrating trusted community partners and settings into hypertension management, alongside usual medical care, to strengthen engagement and self-management. Future research should prioritize standardized outcomes and longer follow-up to clarify durability, implementation, and scalability.

P-104 Title: Preventing Lower Extremity Amputations in Patients with Diabetes and Peripheral Artery Disease: Evidence-Based Interventions for Rural Populations

Authors: Chrishanity Jones¹, Nate Smith¹, Josephina Chapman¹, Chiamaka Nwokeocha¹

1. Morehouse School of Medicine, Master of Science in Physician Assistant Studies

Mentor: Christopher Ervin, MD, Morehouse School of Medicine

Background/Significance: Lower extremity amputations (LEAs) remain one of the most preventable yet devastating outcomes of diabetes mellitus and peripheral artery disease (PAD). Rural and underserved regions, such as Appalachia, continue to experience disproportionately high amputation rates due to limited access to preventive care, delayed diagnosis, and socioeconomic barriers. Our initial analysis identified race and geography as key contributors to these disparities. Building on that foundation, this project focuses on identifying the most effective prevention and intervention strategies to reduce LEA risk among adults with diabetes and/or PAD in rural communities.

Methods: A comprehensive literature review was conducted using SCOPUS and PubMed databases. Inclusion criteria encompassed adults with diabetes and/or PAD living in rural or medically underserved areas, with studies examining preventive or interventional strategies to reduce LEAs. Ten peer-reviewed articles published between 2018 and 2024 were analyzed. Extracted data included intervention type, target population, clinical outcomes, and implementation challenges.

Results: These findings suggest that early screening, multidisciplinary foot care teams, culturally competent education, mobile outreach, and telemedicine substantially reduce the risk of diabetic foot ulcers and amputations. Notably, patients managed with telemedicine experienced a significantly lower risk of amputation compared with those receiving standard care (RR 0.45, 95% CI 0.29–0.71; P = .001). Geographic mapping studies emphasized the value of targeting highincidence areas, while community-based podiatry programs and vascular interventions improved outcomes by enhancing access to timely care. The studies identify physician assistants and healthcare providers as integral to risk identification, patient education, and adherence support through the use of evidence-based interventions, including mobile outreach and telehealth, to promote chronic disease prevention and limb preservation.

Conclusions and Implications: Preventive and early-intervention strategies are vital to reduce diabetes-related amputations, especially in rural, resource-limited settings. Our research shows that accessible, barrier-free programs in trusted community spaces such as rural Southern churches effectively reach medically marginalized populations. Evidence highlights that equitable access, culturally sensitive care, and proactive screening improve limb preservation, underscoring the need for integrated, multidisciplinary approaches in rural healthcare that bridge the gap between prevention and access.

Acknowledgment of Funding: N/A

P-105

Title: Closing

the Pressure Gap: Reducing Hypertension Disparities Through Cultural Competence

Authors: Silsila Rahman, Shanila Huerta, Prisca

Oguike, Shah Rahman

Mentor: Stephanie Banks

Background/Significance: Hypertension is one of the leading preventable causes of cardiovascular morbidity contributing to heart failure, myocardial infarction, chronic kidney disease and premature death. Immigrant populations in the United States are even more at risk due to acculturation stressors, lack of education/knowledge of the healthcare system, lack of financial/work stability and lack of access to healthcare in general. Furthermore, standard clinic models often fail to meet cultural and linguistic needs of various immigrants, further increasing these disparities. We hypothesized that among adult immigrants with history of hypertension, culturally based community interventions will result in better blood pressure control, medication adherence compared to standard clinic-based models of care. Therefore, this analysis is created to synthesize supportive evidence on culturally tailored hypertension control interventions among the immigrant populations result in better patient outcomes.

Methods: A literature review was conducted using PubMed and Scopus to evaluate randomized controlled trials, and clinical trials that examined culturally informed, community-based hypertension interventions among immigrant adults published in English within the past five years. Search terms included “immigrant or migrants” “hypertension,” “community-based,” “culturally tailored,” and “interventions.” Studies were included if they described culturally tailored intervention strategies. Searches were conducted between June 13 and June 18, 2025, and articles were reviewed on June 26, 2025.

Results: Several studies highlight how social determinants influence cardiovascular health among immigrant populations. Community-based interventions, such as CHW-led programs for South Asian and Filipino Americans, improved hypertension and diabetes management through culturally tailored education. Qualitative research among Hispanic/Latino adults emphasized financial and cultural barriers to healthy eating. Pilot trials in older Chinese Canadian immigrants demonstrated the benefits and acceptance of culturally relevant dietary and exercise programs. These studies provide firm evidence that culturally tailored, community-based, and socially aware interventions are vital to improving chronic disease outcomes among immigrant and minority populations.

Conclusions and Implications: Hypertension remains a significant health concern, particularly among immigrant populations, and cultural, linguistic and systemic barriers often hinder effective diagnosis and treatment. Various research studies demonstrate how culturally tailored, community-based interventions that focus on efficient culturally competent communication strategies have been shown to work in improving blood pressure control through increased medication adherence and improved patient-provider trust. Improving social determinants of health through mitigating socioeconomic challenges in accessing care is crucial to reducing disparities in hypertension prevalence, management, and prevention. There should be more research focusing on the long-term benefits of culturally competent healthcare interventions. Acknowledgment of Funding: Morehouse School of Medicine.

P-106 Title: Unearthing Community-Defined Health Needs and Assets

Authors: Fatima Abu Bakr, Karimatu H. Kallon, Justin Ok, Judy Chong, Maliha Hasan, Alexia Yemat Burgos, Thierry Muchi Awah, Ronah Magembe, Marcus Marcelin, Raigan Traylor

Institutional Affiliations: Morehouse School of Medicine

Mentor: Gilberte Bastien, Ph.D., Morehouse School of Medicine

Background/Significance: The objective of this project is to identify community health needs and assets in Collier Heights, a neighborhood located in West Atlanta. Collier Heights is a community that is rich with history and culture as one of the first designated African American (AA) communities within Atlanta. In collaboration with The Study Hall, a non-profit after-school program serving local elementary school students, we conducted a multi-pronged assessment to illuminate opportunities to promote health equity within the community.

Methods: Data collection methods included a windshield survey, key informant interviews (n=5), and a focus group dialogue. The windshield survey involved driving through Collier Heights to assess community strengths as well as access gaps. Photography, videography, and written notes were utilized to capture key observations. Five key informants (three members of The Study Hall staff, a local church leader, and the city planner of the Collier-Heights Neighborhood Planning Unit) met with our group to share their perspectives on health and related needs within the community. A focus group dialogue (FGD) was conducted with seven parents of children served by the Study Hall. FGD questions focused on exploring the parents’ experiences with The Study Hall program and the Collier Heights community as a whole. The discussion also provided important insight into community needs and strengths. Data captured was analyzed to identify recurring themes and trends.

Results: Food insecurity, limited access to healthcare, availability of housing, and general safety concerns were noted across the windshield survey, key informant interviews, and the focus group. The availability of parks, recreational activities for children, active leadership from the church, and the rich AA cultural history were identified as community assets. Views on education seemed to vary based on each individual’s role within the community. Themes from key informant interviews and the focus group dialogue revealed there may be existing resources to address identified needs. However, access to those resources is limited by education, transportation, and bureaucratic red tape.

Conclusion and Implications: The results to date highlight important health access barriers, including challenges navigating the healthcare system, medical insurance, government bureaucracy, etc. Additional needs around access to adequate nutrition and food insecurity were also noted. In collaboration with trusted community leaders, we hope to implement an educationbased program to improve health literacy and increase accessibility of community resources. Successful implementation of such an intervention could improve health access, minimize health disparities, and advance the general well-being of the residents of Collier Heights.

P-107

Title: Assessing Community Assets, Needs, and Barriers to Youth Advancement and Success in NPU-T

Authors: Aramide Olorunfemi¹, Ashley Issak¹, Diamond Beckford¹, Fiza Hasta¹, Jelani Jarrett¹, M. Sanam Chaudhary¹, Natnael Hagos¹, Saahas Anandan¹, Zoe Andrews¹

¹Morehouse School of Medicine, Doctor of Medicine Program

Mentors: Jammie M. Hopkins, DrPH, MS, MSCR, and Maisha Standifer, PhD, MPH, Morehouse School of Medicine

Background/Significance: Neighborhood Planning Unit-T (NPU-T) encompasses the Atlanta communities of Ashview Heights, the Atlanta University Center, Harris Chiles, Just Us, The Villages at Castleberry Hill, West End, and Westview. The poverty rate within this neighborhood is approximately 27%, which is more than twice the state average of 13.6% and well above the national rate of 12.5%. These socioeconomic disparities contribute to limited health education and inadequate youth development resources. We hypothesize that while the Boys and Girls Club provides valuable support and resources, many teens still face structural barriers that limit access to career readiness and personal development, despite their close proximity to higher educational institutions in the Atlanta University Center.

Methods: A windshield survey was conducted within a three-mile radius of the Atlanta University Center, focusing on neighborhoods zoned to Booker T. Washington High School and KIPP schools. Qualitative data, including photographs and videos, were collected to document environmental and structural factors influencing community health. Nine semi-structured interviews were conducted among business owners, healthcare professionals, local employees, Boys and Girls Club staff, and an NPU-T representative to identify recurring themes related to structural barriers. Findings from these interviews informed the development of two focus groups with twelve teens at the John H. Harland Boys and Girls Club.

Results: Windshield survey results revealed numerous gaps in NPU-T, ranging from limited healthy food options and healthcare facilities to a lack of safe spaces for community engagement. Qualitative feedback from key informant interviews and focus groups highlighted disconnects between the NPU-T community and Atlanta University Center despite being within the same geographical area. Increased connection to the institutions could address their concerns by enhancing opportunities for mentorship, financial literacy education, and career training.

Conclusions and Implications: NPU-T community members expressed a strong desire for mentorship, practical skill-building, and engagement beyond existing after-school programs. The insights from this study aim to guide the development and implementation of future community engagement and educational interventions for local teens to access educational resources that can be provided by Atlanta University Center.

Acknowledgment of funding: This research was supported in part by Morehouse School of Medicine Faculty and Staff; Drs. Jammie M. Hopkins and Maisha Standifer and the John H. Harland Boys and Girls Club High School Program.

P-108 Title: Identifying the Needs of Dunbar Elementary School

Authors: Lawrence Bayin1; Ranya Benchaaboune1; Isha Gohel1; Katlynn Karwan1; Sean Mitchell1; Leticia Mosqueda1; Tyra Perkins1; Brevin Rose1; Annabelle Zekeri1

1Morehouse School of Medicine, Doctorate of Medicine Program

Mentors: Stephanie Banks, MPH2 ; Carey Roth Bayer, EdD., MEd, BSN, RN, CSE3; Martina Jackson Brown, MEd, EDS4

2 Morehouse School of Medicine, Department of Physician Assistant Studies

3 Morehouse School of Medicine, Department of Community Health and Preventive Medicine/Anatomy, Pathology, & Medical Education

4 Dunbar Elementary School, Instructional Coaching

Background/Significance: Dunbar Elementary is a pre-K through 5th-grade school located in the Mechanicsville neighborhood of Atlanta, Georgia, within NPU-V. Dunbar Elementary serves as a representative lens of the Mechanicsville community, as it is at the center of the geographical area and reveals the dynamics of its surroundings. The purpose of this project was to conduct a community needs assessment to identify resources, strengths, and potential needs of the neighborhood.

Methods: We conducted two windshield surveys, five key informant interviews, and one focus group. The windshield surveys included one driving team and one walking team. Both teams documented observations using photos, videos, and field notes. Next, we completed five key informant interviews with individuals that were instrumental to the community. Finally, we conducted one focus group with Dunbar Elementary teachers. Both the interviews and focus group utilized open-ended questions to elicit participants’ perspectives on community strengths and areas for improvement.

Results: The windshield survey revealed open green spaces fostering a community-oriented environment, but also safety concerns like missing school zone signs. Three of five key informants noted that many children lack resources at home – a concern echoed by 13 teachers in a focus group. Both the interview and focus group highlighted staff burnout linked to supporting families with limited resources and pressure to improve district rankings. Overall, the most prominent themes identified were limited access to home resources and increased burnout.

Conclusions and Implications: To address the two overarching themes, we have proposed a multifaceted approach: crafting a resource guide to improve awareness of services currently available at Dunbar Elementary; partnering with local organizations to provide nutritious meals to families over the weekends; and creating educational wellness infographics to promote teacher well-being. It is our hope that these actions will promote overall community well-being. The final implementation of ways to address these themes will be determined by the community. If we are successful with the proposed interventions, we hope to increase utilization of resources available and minimize stress on Dunbar staff.

Acknowledgment of Support: This project was supported in part by the MSM Community Health Course.

P-109 Title: Assessing Community Health and Safety Needs Among Students at Finch Elementary School

Authors: Tamilore Adeogun1; Chiemela Ananaba1; Tiarra Green1; Jada Grimes, MS1; Manaal Khalid1; Regina Kyei1; Vidyashree Manivannan1; Keon Nelson 1; Muraya Shekhey1; Vashaun Williams, MS1; Sherry Crump, MD., MPH, FACPM2; LaKesha A. Tables, MD., MPH, FACPM2

1 Morehouse School of Medicine Doctor of Medicine Program

2 Morehouse School of Medicine Department of Community Health and Preventive Medicine

Mentors: Sherry Crump, MD., MPH, Morehouse School of Medicine; LaKesha A. Tables, MD., MPH, FACPM, Morehouse School of Medicine

Background/Significance: Finch Elementary School, a predominantly Black Title I school in NPU-S, serves families with a median income of $50,000. Many students live in nearby neighborhoods where rising crime rates and the prevalence of assault and homicide pose growing safety concerns. According to data from the Atlanta Police Department, the assault rate in NPUS increased from 194 to 252 per 10,000 residents between 2024 and 2025. The purpose of this community needs assessment is to examine the health and safety needs of students at Finch Elementary School.

Methods: Qualitative data collection, including a windshield survey and key informant interviews, were used to initiate the needs-based assessment. The windshield survey documented neighborhood conditions in NPU-S. Interviews with community members focused on Social Determinants of Health, quality of life, behaviors, beliefs, and resources available to community members. Key informant interviews lasted 20–40 minutes and were recorded and transcribed. All procedures followed confidentiality and safety protocols. To further explore the key themes ascertained from the key informant interviews, two focus groups were planned and executed –one with students and one with teachers and administrators from Finch Elementary.

Results: The windshield survey revealed a large presence of deteriorating homes, neglected public spaces, and unregulated residential areas. Both key informant interviews and focus groups revealed themes of decreased safety of children in their neighborhoods. Focus group results further disclosed rising emotional distress and mental health concerns among students such as anger issues, anxiety, and depression. It was also found that students modeled harmful behaviors they saw in their neighborhoods, leading to discipline problems in school.

Conclusions and Implications: Preliminary findings from windshield surveys, key informant interviews, and focus groups highlight a significant need for community-based interventions that address both safety concerns and mental health among Finch Elementary School students. Poor housing and building conditions in these children’s neighborhoods could potentially create unsafe environments for children to live, play, and commute to school. Exposure to neighborhood crime may negatively impact children’s emotional well-being and behavioral development. Long-term solutions should emphasize emotional regulation, reframe perceptions of crime and harmful behaviors, and equip children with positive coping mechanisms and safety skills. By targeting how environmental stressors are managed, these interventions reduce the influence of unsafe neighborhood conditions on children’s emotional and behavioral health.

Acknowledgements ofFunding: This project is supported by theMorehouse School of Medicine Department of Community Health and Preventive Medicine.

P-110

Title: JAK/STAT Inhibitors Promote STAT Functional Cross-Regulation in Healthy

Placental Cells

Authors: Toidi Adekambi1 PhD, Tyana T. Joseph1* MS, Erica L. Johnson1, 2 PhD

1 Department of Microbiology, Biochemistry, and Immunology, Morehouse School of Medicine, Atlanta, GA 30310

2 Department of Obstetrics and Gynecology, Morehouse School of Medicine, Atlanta, GA 30310

Mentor: Erica L. Johnson, PhD

Background/Significance: The placenta is transitory but key organ with various immunological and endocrinological roles that modulate maternal and fetal physiology to promote maternal-fetal tolerance, pregnancy maintenance and parturition at term. In normal, healthy pregnancy a delicate balance of hormones and cytokines regulates JAK/STAT signaling in immune cells at the maternal-fetal interface. The signal transducer activator of transcription (STAT) proteins are a family of cytoplasmic transcription factors which share an overall general structure, organized into functional modular domains. The mammalian STAT family comprises STAT1, STAT2, STAT3, STAT4, STAT5a, STAT5b and STAT6 which have distinct tissue-specific expression patterns. Very little is known regarding the role of JAK/STAT signaling and JAK inhibitors in placental cells. For example, abnormal activation of STAT3 can result in elevated levels of proinflammatory cytokines which are linked to early parturition. We investigated the effect of the JAK inhibitors on JAK/STAT signaling pathway in decidual cells as well as the production of cytokines by decidual cells.

Methods: CD14+ cells were purified from placenta decidual tissues from healthy pregnancy women and treated with representative of JAK inhibitors (pimozide and ruxolitinib). We investigated STAT1, STAT2, STAT3, STAT5a and STAT5b expression in decidual cells via RTqPCR and western blotting assay and assessed whether JAK inhibition impacts cytokine production by decidual cells by ELISA.

Results: Pimozide and ruxolitinib reduced the expression of STAT1, STAT2, STAT5a and STAT5b but increased the expression of STAT3 suggesting functional cross-regulation. They also diminished the capacity to induce IL-6 and TNF-a production by decidual cells.

Conclusions and Implications: In the absence of STAT1, STAT2, STAT5a and STAT5b during the pimozide and ruxolitinib decidual cells treatment, sustained STAT3 activation can reduce the production of pro-inflammatory cytokines which may favor normal fetal development.

Acknowledgement of Funding: NSF 2502800, RO1 MD017690

P-111

Title: Knowledge Is Prevention: How Health Literacy Influences HIV rates amongst Black Women

Authors: Alexandria White1 ,

Armoni Moore1 , Brianna Parham1, Immanuelle Pongo

1

1 Morehouse School of Medicine Department of Physician Assistant Studies

Mentor: Sharon A. Rachel, MA, MPH, MS, Morehouse

School of Medicine

Background/Significance: Human Immunodeficiency Virus (HIV) affects over 39 million people worldwide. Research has shown that Black women are significantly more impacted by HIV. Socioeconomic factors, stigmas, discrimination, and lack of healthcare access contribute to this disparity. It is crucial to address these systemic issues to help reduce the incidence of HIV among Black women. This study aims to answer the question: How does health literacy influence HIV risk among Black Women compared to other demographics?

Methods: A systematic literature review was conducted using SCOPUS and PubMed. Key terms such as “HIV” or “AIDS” and “African American” or “Black” and “women” and “Health Literacy” were searched. Articles were limited from 2014-2024. The study had to be conducted in the United States and written in English. Reviews were excluded from the search. 673 articles were initially found. Individual searches further narrowed the number of articles returned.

Results: A total of ten articles were used in the review. To analyze the data collected, the studies used a variety of statistical analysis techniques. Such as, statistics and logistic regression, which showed significant associations (p < 0.05) between limited health literacy and poorer HIV knowledge, reduced PrEP awareness, and lower engagement in prevention and care services. Chi-squared analysis demonstrated significant improvements (p < 0.005) in HIV knowledge, preventive behaviors and self-efficacy among health literacy focused interventions. These articles provided both qualitative and numerical data that supports the idea that inadequate health literacy contributes to the heightened HIV risk among Black women by limiting access to necessary testing, prevention, and treatment services.

Conclusions and Implications: Although Black/African American women make up only about 13% of the female population, they account for nearly 50% of HIV diagnoses among women. This disparity reflects how limited health literacy and access to healthcare significantly impacts the prevention of HIV among African American women when compared to other demographics. Across reviewed studies, the results indicate that limited health literacy is associated with reduced PrEP awareness and lower engagement in prevention. Clinical recommendations include increasing awareness among the public and healthcare providers, establishing care models, and facilitating preventive services like PrEP and routine HIV screening are needed to reduce HIV transmission in this population.

Acknowledgement of Funding: N/A

P-112

Title: The impact of early family, school, and community-based interventions for childhood obesity: a systematic review

Authors: Lauren Parks1, Rifah Haque1, Edgar Alcantar1, DaSean Deshazer1

Mentor:

Sabrina Botts, DMin, MMSc., PA-C Morehouse School of Medicine

Background/Significance: Childhood obesity remains a major concern in the United States, affecting around 20% of children, with higher rates affecting nonHispanic black (20%) and Hispanic (26%) populations.1 These disparities are influenced by socioeconomic, behavioral, and environmental factors, even with national initiatives; effective prevention remains a challenge. There are inconsistent evaluations of the effectiveness of early family-based, school-based, and community-based interventions in reducing BMI and improving health behaviors. The purpose of this study evaluates these different approaches specifically: In children, are family-based interventions more effective than school or community-based interventions in reducing obesity risk and improving health behaviors?

Methods: A systematic literature review was conducted between June 13th and June 27th using PubMed and SCOPUS databases. The keywords used included childhood obesity, family, school, and community interventions. Inclusion criteria were peer reviewed U.S studies published within the last 10 years focusing on children ages 2-18. Of 133 identified articles, 12 met the criteria. Data from these articles were extracted and analyzed for study design, intervention type, participant characteristics, and outcomes related to BMI and health behaviors in children.

Results: Twelve studies were analyzed including randomized controlled trials, quasi experimental, and longitudinal studies. The strongest outcomes were seen with multiple components combining behavioral, nutritional and Physical activity. Programs that were culturally tailored to the populations they served integrating family, school, and community engagement, also had strong outcomes. Family based interventions significantly reduced children's BMI zscores (p<0.001). School-based interventions showed some improvement, especially when combined with family involvement or supportive policies. Programs that emphasize parent education, nutrition literacy, and physical activity showed improvements in diet, activity levels, and self-confidence. Digital and policy interventions had limited impact and sustainability due to engagement and environmental barriers. Across all studies, high family engagement, cultural adaptation, and consistency were key success indicators.

Conclusions and Implications: These findings support the implementation of obesity prevention programs primarily focused on family engagement within schools, primary care, and communitybased settings. Effectiveness increases with culturally tailored programs, sustained family engagement, and collaboration between schools, healthcare, and public health systems. However, many studies were limited by short follow up periods and challenges maintaining long-term participant engagement. Future research should prioritize longterm evaluation, objective behavioral measures, and targeted interventions in high-risk populations.

Acknowledgment of Funding: This research was supported in part by Morehouse School of Medicine Physician Assistant Studies.

P-113

Title:

Culturally Relevant Drug Education and Conflict Resolution Intervention at Carver STEAM Academy

Authors: Ariana Woods¹; Beven Jojo¹; Camille Shakir¹; Deneen Ekwueme¹; Erika Beasley¹; Miracle Gosier¹; Naomi Cargill¹; Taylor Jackson¹; Valentin Iaquinta¹; William Pemu¹

¹Morehouse School of Medicine, Excellence Learning Community, Community Health Course (CHC)

Mentors: Dr. Carey Bayer, Morehouse School of Medicine; Dr. Gail McCray, Morehouse School of Medicine; Dr. Ryan Clark, Morehouse School of Medicine

Background/Significance: Adolescent drug use remains a serious public health issue, with nearly 20% of high school students reporting illicit drug use in 2023 (CDC). Urban youth are especially vulnerable due to misinformation, peer pressure, and socioeconomic stress. To address this, the Excellence Learning Community at Morehouse School of Medicine developed a culturally tailored, interactive program for ninth graders through the Community Health Course. The project aimed to improve understanding of drug effects, strengthen conflict resolution skills, and enhance recognition of misinformation.

Methods: A three-part educational intervention was delivered by the Excellence LC as part of the CHC curriculum to 13 ninth-grade students at Carver STEAM Academy. Each 45-minute session focused on science-based learning, social media myth-busting, and cultural competency with conflict resolution. Pre- and post-surveys assessed knowledge, media literacy, and confidence, analyzed through descriptive statistics and qualitative feedback.

Results: Among 13 participants, post-intervention results showed consistent improvement across all questionnaire items, with overall increases in correct responses ranging from 28% to 40%. These findings indicate gains in understanding and engagement. Qualitative feedback highlighted the program’s relevance and interactive design. Qualitative responses emphasized the program’s relatability, cultural resonance, and interactive approach. Students reported that the sessions made health education “feel real” and “connected to everyday life.”

Conclusions and Implications: This pilot shows that combining culturally responsive education, media literacy, and conflict resolution skill training effectively engages adolescents and supports healthier decision-making. The Excellence LC model offers a replicable framework for schoolbased prevention that empowers youth through relevant, interactive learning. Future work will expand to additional grade levels and assess long-term impact.

Acknowledgements: Conducted by the Excellence LC as part of the Morehouse School of Medicine CHC. In collaboration with Carver STEAM Academy. The authors thank Carver STEAM faculty and staff for their partnership and support.

P-114

Title: Beyond Food Deserts: Analyzing Distance-Based Food Access Among Students at Morehouse School of Medicine

Authors: Maya Dewey1; Zahra Irfan1; Chaohua Li2, MPH; Robina Josiah Willock, PhD, MPH3,4

1 MD2 Morehouse School of Medicine

2 National Center for Primary Care, Morehouse School of Medicine

3 Faculty Mentor, Department of Community Health and Preventive Medicine, Morehouse School of Medicine

4 Cancer Health Equity Research Center, Morehouse School of Medicine

Background/Significance: Food insecurity represents a growing public health concern, affecting up to 40% of higher education students. Students face unique barriers including class schedules, lack of transportation, limited campus food options, and personal finances. Consequences include impacts on academic performance, mental health, and overall wellbeing, underscoring the importance of assessing FI in student populations. However, limited research has examined how distance and retail distribution impact access to food retailers. The USDA's food desert definition full-service grocer within 1 mile fails to capture navigating between convenience stores, limited-service markets, and full-service grocers. Therefore, we hypothesized that MSM students in zip codes 30310 and 30314 would report barriers to accessing nutritious and affordable food within one mile of the AUC.

Methods: This study employed an environmental scan (windshield survey and visual documentation) of food retailers within one-mile, geospatial mapping, and three issues of the MSM Food Access Bulletin (FAB), which included a quantitative survey assessing food access barriers. The purpose was to: 1) describe the time costs and modality profiles that characterize transportation as a structural determinant of FI among students in zip codes 30310 and 30314, and 2) use the FAB to increase awareness and accessibility to resources that mitigate FI. Food retailers were classified into three tiers: full-service grocers, food marts/convenience stores, and community gardens/ markets. A convenience sample of MSM students (N=681), were recruited via email and the FAB. The Real Routes survey assessed demographics, food security status, shopping preferences, travel distances, and transportation methods. QGIS and Google Maps analyses assessed travel times and distances.

Results: Within a 5-mile radius, we identified 17 full-service grocers, 58 food marts/convenience stores, and 29 community gardens/food markets. Survey respondents (N=28) MD (N=19), PA, GEBS, and PhD students (N=9) rely on full-service grocers (89.3%), with 77% traveling +1 mile for fresh produce. Nearly 36% travel 5+ miles to access fresh food. Travel time constraints emerged as primary barriers.

Conclusions and Implications: While one full-service store within 1 mile of the AUC may disqualify the area from formal food desert designation, this research shows that poor-quality food options within a 1-mile radius coupled with significant travel distances to access healthy and affordable food underscore the true disparities and challenges in food access for MSM students.

P-115

Title: Bridging Community Insight and Environmental Observation: A Windshield Survey and Key Informant Assessment of Health and Resource Inequities in Atlanta’s NPU-V

Authors: Angeliene Belnavis¹; Aaron Cooper¹; Emmanuel Emovon¹; Kiyanie Fedrick, MS ¹; Riesa Hoque¹; Caitlyn Johnson¹; Zipporah Kaffey, MS¹; Kaitlyn Taylor, MS¹, David Levine, MD, FAAP ²; Tandeca King Gordon, Ed.D., MEd

Mentors: David Levine, MD, FAAP, Morehouse School of Medicine; Tandeca King Gordon, Ed.D., MEd, Morehouse School of Medicine

Background: Access to healthcare services, nutritious food options, and safe recreational spaces plays a critical role in promoting positive health outcomes. Within Neighborhood Planning Unit V (NPU-V), comparisons between the east and west sides revealed notable differences in access to these essential resources. We hypothesize that the observable differences in the built environment across NPU-V would correspond with differences in access to healthcare services, food resources, and transportation infrastructure. The underling objective of this study was to assess neighborhood-level resource distribution and built environment characteristics within NPU-V to inform future health equity interventions

Methods: A qualitative, descriptive approach was used to assess the built environment and social dynamics. During the windshield survey, observations were documented on housing, transportation, healthcare access, public amenities, and indicators of gentrification. Team members also conducted a semi-structured key informant interview. Data were analyzed thematically to identify recurring patterns in community strengths, needs, and opportunities for intervention.

Results: Observations revealed stark contrasts across NPU-V. The east side showed greater development with grocery stores, urgent care centers, and public facilities. While the west side had fewer resources, limited grocery options, and only one pharmacy near a package store. Gentrification was apparent, with newly built homes adjacent to aging or foreclosed properties. The key informant echoed these themes, emphasizing persistent food insecurity, transportation limitations, and healthcare access issues. Many families live in multigenerational homes with limited mobility, hindering access to medical and mental health services.

Conclusion: Findings demonstrate that while NPU-V maintains a strong social network and collective resilience, systemic inequities persist in healthcare access, food security, and transportation infrastructure. Gentrification has intensified disparities between east and west sectors, threatening to displace long-term residents and erode community trust. Strengthening partnerships between schools, healthcare providers, and community-based organizations can address resource fragmentation. Future efforts should focus on improving transportation routes to medical centers, increasing availability of fresh foods, and expanding mental health education to sustain the community’s social fabric while advancing health equity.

Acknowledgement of Funding:

• This research was supported in part by the Morehouse School of Medicine Faculty and Staff.

• This research was supported in part by David Levine, MD, FAAP ² ; Tandeca King Gordon, Ed.D., Med

P-116

Title:

Evaluating the Impact of Family-Centered Asthma Education on Pediatric SelfManagement and Health Equity in Low-Income Urban Communities

Authors: Danielle Moore1 ,Koeba Plummer2,Domonic Williams3,Ke’Von Hamilton4

Mentor:

Sabrina Jackson Botts, DMin, MMSc., PA-C, Morehouse School of Medicine

Background/Significance:Asthma continues to be a leading chronic condition affecting children in the United States. The burden of disease is especially high among Black, Brown, and Latino children living in low-income communities, where barriers such as environmental triggers, limited healthcare access, and challenges with medication adherence often result in uncontrolled symptoms and frequent emergency room visits. Caregiver knowledge and confidence play a central role in pediatric asthma management, yet many families lack tailored education and support. This study examines does family-centered asthma education improve self-efficacy and clinical outcomes for children aged 6–12 in underserved urban communities?

Methods: Afocused literature review was conducted using public health and medical databases, targeting peer-reviewed studies published after 2000. Ten studies met inclusion criteria, encompassing randomized controlled trials, systematic reviews, and retrospective analyses. Articles were screened for themes related to pediatric asthma education, caregiver involvement, program setting, and outcomes related to symptom control, healthcare utilization, and selfmanagement of skills. Studies that lacked methodological clarity or did not include children in urban or low-income settings were excluded.

Results: Across the selected studies, asthma education programs that engaged both caregivers and children consistently demonstrated positive outcomes. Families who participated in structured education services reported greater confidence in managing asthma symptoms, and children showed improvement in symptom control and reduced emergency room visits. School and community-based interventions were particularly effective in reaching families with limited access to care. Additionally, environmental and social determinants such as air pollution and neighborhood-level disadvantages were frequently associated with poorer asthma control, underscoring the need for comprehensive support strategies.

Conclusions and Implications: Based on the evidence from the reports, there is an indication that family-centered asthma education can strengthen self-efficacy and clinical outcomes for children living in underserved communities. Culturally responsive and accessible programs embedded in schools or community settings may help reduce asthma-related disparities. Future efforts should focus on sustainable program delivery, long-term impact, and tailored support for caregivers facing environmental and socioeconomic challenges. Evidence provided by this review suggests family-centered asthma education programs incorporating community partnerships and tailored education may help advance health equity for pediatric patients in similar urban settings.

P-117

Title: Understanding Determinants of Family Healthy Weight Program Engagement Among African American Families

Authors: Hailey Ray1 , LaKesha Tables2, Latrice Rollins2, La Shawn Hoffman, ZahraShahin3 , Ebony Section3 ,

Morehouse School of Medicine Doctor of Medicine Program ¹, Morehouse School of Medicine Community Health and Preventive Medicine 2, Morehouse School of Medicine Prevention Research Center 3

Background: Childhood obesity remains a pressing public health concern, with prevalence rates in the U.S. rising from 13.9% in 2000 to 19.3% in 2018. In response to this growth, The Center for Disease Control (CDC) and the American Academy of Pediatrics (AAP) endorsed Family Healthy Weight Programs (FHWPs) as evidence-based interventions designed to promote healthy lifestyle behaviors through family-centered nutrition, physical activity, and behavioral counseling. However, African American families are less likely to engage in or benefit in these programs due to a range of systemic, cultural, and structural barriers. This study aimed to explore African American community perspectives to inform the selection and design of an equitable, culturally responsive FHWP by understanding determinants in participation for African American Families.

Methods: Data was collected through nine key informant interviews with local stakeholders from organizations including Morehouse Healthcare, Children’s Healthcare of Atlanta, Antioch Urban Ministry, YMCA, CHOICES, Urban Performance, and the Center for Black Women’s Wellness. Additionally, two focus groups were conducted: one with parents and one with children aged 9–15 who have been diagnosed with overweight or obesity. Recordings were transcribed and the transcripts were analyzed using thematic analysis to identify common themes across participant responses.

Results: Thematic analysis revealed key determinants impacting participation: (1) time constraints and scheduling conflicts, especially on weekdays, with strong preference for weekend, summer, or virtual options; (2) importance of inclusive, non-stigmatizing language, particularly given children's experiences with weight-related bullying; (3) need for support for non-participating siblings, to reduce family burden; and (4) discomfort with clinical settings, with many children preferring community-based environments.

Conclusion and Implications: These findings emphasize the value of community-informed program design. Recommendations include offering flexible scheduling, integrating virtual and inperson formats, incorporating family-based activities like cooking classes, and ensuring language and setting choices foster a supportive, inclusive atmosphere. Ultimately, tailoring FHWPs to reflect the lived experiences of African American families can improve engagement and promote more equitable health outcomes.

Acknowledgement of funding: This project is supported in part by grant 5NU58DP007572-0200. This research was supported in part by the MSM Summer Scholars in the Community.

P-118 Title: Ischemic Stroke Risk in Women Using Combined Oral Contraceptives vs Progestin-Only Contraceptives

Authors: Idara Ekong1

, Shakquanda Cepeda1, Ruthlynn Pierre1, Ainsley Seals1 1. Morehouse School of Medicine, Physician Assistant Studies Program

Mentor: Professor Sharon Rachel, MA, MPH, MS, Morehouse School of Medicine

Background/Significance: Although hormonal contraceptives are frequently used to prevent conception and treat hormone-related disorders, there is worry about their potential long-term association with cerebrovascular accidents. CVAs cause severe, irreversible deficits because of brain hemorrhage or infarction brought on by vascular injury. Progestin-only contraceptives have less impact on coagulation and vascular endothelium compared to combination oral contraceptives (estrogen & progesterone) which increase clotting factors in the liver, then thrombus formation. Important variables to consider include the dosage of estrogen, the length of use, and additional dangers (such as smoking, migraines, arrhythmia, hypertension or atherosclerosis). To assist well-informed decisions about reproductive health, this review of the literature attempts to investigate the relationship between long-term contraceptive usage and stroke risk, filling important gaps.

Methods: A systematic literature review was conducted to examine the relationship between ischemic stroke and oral contraceptive use, focusing on combined oral contraceptives (COCs) versus progestin-only contraceptives (POCs) in women. PubMed, Galileo, and SCOPUS were searched using keywords including “oral contraceptives,” “stroke,” “combined hormonal contraception,” and “progestin-only,” generating 102 articles. Inclusion criteria required original studies spanning the past 15 years with clear comparisons between COCs and POCs. To ensure relevance, our critical analysis selection required the application of exclusion criteria, which removed studies that did not differentiate between COCs and POCs or lacked outcome data on ischemic stroke. To further this, our application of inclusion criteria such as age range and study design curtailed additional studies, resulting in our final 15 results available for analysis. Core study components were extracted into Excel, including design, population, characteristics, outcomes, and confounding variables. Emphasis was placed on studies using national registry data for greater validity.

Results: Across 15 included studies the review found that women using combined oral contraceptives (COCs) had a higher risk of ischemic stroke compared to those using progestinonly contraceptives (POCs). Several studies showed a 1.5–2.5-fold increase in stroke risk with COCs, with one study reporting an adjusted OR of 1.75 (95% CI 1.45–2.10). POCs did not show a significant increase in risk (adjusted OR 1.02, 95% CI 0.85–1.23). Higher-dose estrogen formulations were linked to greater risk, although the overall absolute risk remained low.

Conclusion: Use of combined oral contraceptive was associated with a higher risk of ischemic stroke compared to progestin only contraceptives. Providers should thoroughly risk assess each patient while taking into consideration the confounding factors that could potentially increase the risk of ischemic stroke with COC before prescribing.

Acknowledgment of Funding: N/A