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Dr. Curtis L. Parker Student Research Symposium_Oral Abstracts

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ORAL PRESENTATIONS

O-01 Title: Retinal Ganglion Cell Degeneration Linked to Pathogenic Tau Accumulation in Early and Late Stages

of Alzheimer’s Disease

Authors: Edward Robinson1, Miyah R. Davis1, Dieu-Trang Fuchs1 , Yosef Koronyo1 , Elena SalobrarGarcia2, Altan Rentsendorj1, Bhakta P. Gaire1, Rakez Kayed3, Lon S. Schneider4, Keith L. Black1, Alfredo A. Sadun5, Maya Koronyo-Hamaoui1

1Department of Neurosurgery, Maxine Dunitz Neurosurgical Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA

2Institute of Ophthalmologic Research Ramón Castroviejo, Complutense University of Madrid, Spain.

3Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch at Galveston, TX, USA

4Alzheimer’s Disease Research Center, Keck School of Medicine, University of Southern California, Los Angeles, California, USA

5Department of Ophthalmology, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA, USA.

Background/Significance: Histological and imaging studies indicate that retinal ganglion cell (RGC) loss occurs in Alzheimer’s disease (AD), potentially contributing to visual and circadian dysfunctions. We previously identified elevated pathogenic tau isoforms, hyperphosphorylated tau at serine 396 (pS396-tau) and tau oligomers (oligo-tau), in the retinas of patients with mild cognitive impairment (MCI, due to AD) and AD dementia compared to cognitively normal (CN) individuals. Whether these tau species localize within RGCs and contribute to neurodegeneration remains unknown.

Methods: Postmortem retinal cross-sections from 25 MCI/AD patients and 16 age- and sex-matched CN controls were examined. Immunofluorescence and Nissl staining were performed using the RGC marker RBPMS alongside antibodies for pS396-tau, T22+ oligo-tau, apoptosis, granulovacuolar degeneration (GVD) bodies, and necroptosis markers. Stereological quantification, RGC morphometry, and spatial distribution analyses were correlated with corresponding brain pathology and cognitive status.

Results: We provide first evidence of pS396-tau and oligo-tau inclusions within RBPMS+ RGCs in MCI and AD retinas. These retinas exhibited a 46–56% reduction in RBPMS+-RGCs and Nissl+ neurons, accompanied by marked soma hypertrophy (10–50%), nuclear displacement, and increased apoptosis (30–50%). CHMP2B+ GVD bodies and pMLKL+ necroptotic markers were prominent in affected RGCs. Tauopathy-laden RGCs were 2.1–3.5-fold more abundant in MCI and AD compared to CN, strongly intercorrelated (r = 0.85, P < 0.0001), and inversely associated with RGC density (r = −0.40 to −0.64, P < 0.05–0.01). Their accumulation correlated with advanced Braak stage (V–VI) and worse cognition (CDR 3, MMSE < 26).

Conclusion and Implications: Abnormal tau isoforms accumulate within RBPMS+ RGCs in MCI and AD, driving substantial RGC loss through apoptotic and GVD-necroptotic mechanisms. These findings implicate retinal tauopathy as a potential early and quantifiable biomarker of AD progression, warranting validation in larger cohorts.

Funding: Studies have been supported by the following NIH/NIA grants: R01 AG055865, R01 AG056478, R41 AG044897, and R01 G075998, by the Hertz Innovation Fund, the Gordon, Jona Goldrich, and Haim Saban Private Foundations. Ray Charles scholar foundation.

O-02

Title: Direct RNA sequencing reveals complex patterns of epi-transcriptomic modification following stroke

Authors: Zulma L. Reyes-Benitez, 1,2 Elham Amini Ph.D., 1 Andrea Pearson1,2, Robert Meller D.Phil.1,2., Michael Frankel, MD.3,4.

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

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

3Grady Hospital, Marcus Stroke & Neuroscience Center, Atlanta, GA, USA

4Emory University School of Medicine, Department of Neurology, Atlanta, GA, USA

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

Background: In the United States nearly 1 million people suffer a stroke each year. The gold standard treatment for ischemic stroke is currently tPA. For patients to receive this treatment, a distinction between hemorrhagic and ischemic stroke must be made within the therapeutic time window for tPA (4.5 hours following stroke onset). Hemorrhage is identified using CT imaging, diagnostic delays result in only 5% of eligible stroke patients being treated with tPA. Therefore, a biomarker to distinguish hemorrhage from ischemic stroke would have a great effect on population health. In this project, we aim to identify epitranscriptomic biomarkers to distinguish hemorrhagic stroke from other stroke subtypes (specifically 5-methylcytosine (5mC), 6-methyladenosine (m6A), Inosine (I), and Pseudo-Uridine (PsU).

Methods: Whole blood samples were collected from patients at admission (Grady Memorial Hospital, ATL, GA). Following extraction of RNA, 1 ug of RNAwas prepared for direct Sequencing using the Oxford Nanopore workflow (RSK004). Libraries were sequenced on flow cells (P24), for 72h. Read data was aligned to GRCh38 using Dorado and modified bases called. Modkit software was used to extract modified base calls to a bed file, and these data were split by base modification. Data was filtered to only include bases with at least 10x coverage and called present in all samples. For each modification, we determined differential modification rates and corrected for age, sex and race.

Results: Results showed an increase of 5mC and m6A and a decrease in I and PsU RNA modifications. Differential modification of RNA was observed in targets across all chromosomes, some mitochondrial RNAs showed higher levels of differential modification relative to chromosome size. Some RNAs species showed multiple modifications per target RNA. Pathway analysis using cluster profiler suggested modifications occur in RNAs associated with ATP Synthesis, oxidative phosphorylation, and immune system function.

Conclusions and Implications: The large and statistically robust changes observed in our results, suggest RNA modifications may have utility as biomarkers for hemorrhagic stroke diagnosis. Future analysis will include defining stroke biomarkers for ischemic & mimic strokes, as well as how RNA modifications of interest correlate to both gene expression and splicing.

Acknowledgement of Funding:

• This research is supported in part by the following grants: HG012334 , CEGS HG013595, U54 MD007602-33S1, RCMI U54 and NS112422.

O-03 Uncovering Species-Specific Patterns of Antimicrobial Resistance in Klebsiella pneumoniae and Acinetobacter baumannii

Damani Andre¹*, Ali Aslam², Ubong Udoh³, Philip Nwajiobi-Princewill⁴ Muhammed Idris5 Kenneth I. Onyedibe¹

¹Department of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine, Atlanta, GA

²Bioinformatics Core, Morehouse School of Medicine, Atlanta, GA

³ Department of Medical Microbiology and Parasitology, College of Medical Sciences, University of Calabar, Nigeria

⁴National Hospital, Abuja, Nigeria

⁵Infectious Diseases Division, Department of Medicine, Mercer University School of Medicine, Macon, GA

⁶Department of Medicine, Morehouse School of Medicine, Atlanta, GA

Background and Significance: Antimicrobial resistance (AMR) is a growing global health crisis responsible for over one million deaths each year. Klebsiella pneumoniae and Acinetobacter baumannii are critical-priority pathogens due to their resistance to multiple antibiotic classes. Most genomic studies focus on which resistance genes are present, but few analyze how those genes change over time. I hypothesize that Klebsiella pneumoniae and Acinetobacter baumannii exhibit distinct species-specific temporal patterns in antimicrobial resistance gene sequence and amino acid composition.

Methods: Complete genome assemblies for both species were obtained from NCBI RefSeq and GenBank. Each genome was annotated with AMRFinderPlus to identify resistance genes by class, contig ID, and coordinates. Sourmash k-mer profiling was used to determine the presence or absence of mutations in each gene across multiple years. Amino acid composition differences in dominant resistance genes were evaluated by comparing the three most compositionally distinct and sequence rich groups using analysis of variance, while sourmash k-mer profiling was used to assess temporal sequence variation.

Results: A total of 120,000 K. pneumoniae and 50,000 A. baumannii genomes were annotated. Pairwise sequence comparisons revealed variation within the same gene across years, confirming resistance genes are not static. When aggregated by drug class, K. pneumoniae was dominated by β-lactam ARGs, while A. baumannii was dominated by aminoglycoside ARGs. The aminoglycoside-resistant gene aac(6’) showed distinct temporal patterns: K. pneumoniae residues such as leucine, alanine, and glycine remained stable from 2007–2023, whereas A. baumannii displayed fluctuations in asparagine, threonine, and valine between 2010–2018 before stabilizing. These results indicate A. baumannii undergoes greater amino acid plasticity and faster sequence diversification.

Conclusion and Implications: K. pneumoniae and A. baumannii show clear differences in how their resistance genes evolve. K. pneumoniae tends to preserve existing structures, while A. baumannii adapts more rapidly to selective pressures. Understanding these dynamics may guide predictive strategies for tracking and managing antimicrobial resistance.

O-04

Title: Perceived Causes of Fertility Challenges and Utilization of Infertility Treatment

Modalities: Insights from U.S. Black Women

Authors: Isabel Morgan, PhD, MSPH1; Christine Tucker, PhD, MPH2 Aunchalee E.L. Palmquist, PhD, MA, IBCLC3, Stephanie Baker, PhD, MS, PT4, Larissa Jennings Mayo-Wilson, PhD, MHS2, Chantel L. Martin, PhD2, Natalie D. Hernandez, PhD, MPH1, Lasha S. Clarke, PhD, MPH1

1Morehouse School of Medicine Center for Maternal Health Equity; 2University of North Carolina at Chapel Hill Gillings School of Global Public Health; 3Duke University Global Institute of Health; 4Elon University Department of Public Health Studies

Mentor: Lasha Clarke, PhD, MPH, Morehouse School of Medicine

Background/Significance: Black women are underrepresented among infertility clinic patient populations, despite having the greatest prevalence of infertility. Prior research has focused on access to care based on assumptions regarding how Black women conceptualize infertility and perceive the usefulness of biomedical interventions. The purpose of this study was to explore what Black women themselves perceive as the causes of their fertility challenges and to examine the treatment modalities they use to address infertility

Methods: The study included 40 Black women ages 18-45 years, with a history of fertility challenges, recruited from medical practices and online fertility support groups, who participated in the Fertility Equity Study between 2021-2023. Participants completed a demographic survey, and up to two semi-structured interviews to discuss their fertility journeys and perceived causes of infertility. We used a thematic analytic approach to examine participant perceptions of infertility causes. Frequencies and percentages were calculated for each commonly reported cause of fertility challenges and for treatment modalities used.

Results: Most participants were 35-45 years, married or cohabitating, and had advanced educational degrees (e.g., PhD), with household incomes >$100,000, and some or full health insurance coverage with fertility benefits. Black women described five common perceived causes of their fertility challenges: 1) reproductive health conditions (n=27; e.g., fibroids); 2) age (n=7); 3) unknown causes (n=6); 4) structural conditions (n=4; e.g., medical neglect); and 5) stress (n=4). Thirty-two participants (78.0%) had initiated medically assisted reproduction (MAR), including medicated timed intercourse, intrauterine insemination, or in vitro fertilization. Nearly half of participants (n=19) only used MAR, while one-third (n=13) had used both MAR and holistic approaches (e.g., acupuncture, herbal teas). None of the participants who only used holistic approaches attributed their fertility challenges to reproductive health conditions.

Conclusions and Implications: While reproductive health conditions were the predominant perceived cause, nearly half of participants leveraged holistic approaches to address their fertility challenges, including those that also used MAR. These findings may inform how reproductive medicine specialists counsel Black women about their fertility challenges and underscore the importance of acknowledging and integrating the diverse ways patients engage both biomedical and holistic treatments in their fertility journeys.

Acknowledgement of Funding: This research is supported by funding from Ferring Pharmaceuticals.

Authors: Ertha Sefu Omba, M.S., MP.H 1, Naomi Coles, M.S.2, Mari Chiles B.S.3, Jazmine Baylor, M.S.4, Berlandon Saint Julien, M.S.5

1 2 3 4 5

Morehouse School of Medicine Doctor of Medicine Program

Mentor: Ervin Christopher, MD, Morehouse School of Medicine, Director of Operations H.E.A.L Clinic

Background/Significance: Student-run free clinics (SRFCs) are vital in providing care to underserved populations while training future healthcare professionals. Despite their impact, SRFCs have faced recurring challenges with sustainability, resource allocation, and care continuity. We hypothesize that the development of a student-centered, evidence-based quality improvement (QI) framework emphasizing structured operations, interdisciplinary collaboration, and sustainable funding will enhance clinic efficiency and educational outcomes. Therefore, the purpose of this analysis was to examine 1) key operational challenges, 2) success factors, and 3) sustainability strategies to inform the development of a comprehensive QI model for SRFCs.

Methods: A structured literature review was conducted using peer-reviewed articles, national organizational reports, and published clinic evaluations identified through PubMed, Google Scholar, and organizational repositories focused on student-run clinics. An initial search identified 118 articles. After screening and exclusion of non–student-run clinic models, opinion-only articles, duplicates, and studies lacking operational or sustainability outcomes, 32 articles published between 2005 and 2024 were included. Recurring themes were qualitatively analyzed and organized into three domains: operational challenges, success factors, and evidence-informed interventions, which were used to develop a studentcentered QI framework.

Results: Analysis identified five major, recurring challenges across SRFCs: inconsistent volunteer staffing, limited and unstable funding sources, fragmented care coordination, insufficient health outcomes tracking, and gaps in interdisciplinary collaboration. Clinics with strong academic affiliations, faculty oversight, and curricular integration demonstrated improved continuity of care, expanded service scope, and greater operational stability. Based on these findings, the proposed QI framework includes structured volunteer recruitment and training models, diversified and sustainable funding strategies, standardized follow-up and outcome tracking systems, and intentional interprofessional engagement initiatives.

Conclusion/Implications: This student-led QI initiative introduces an adaptive and evidence-based framework to enhance the operational effectiveness and sustainability of SFRCs. By addressing persistent systemic challenges and empowering student leadership, the model aims to equip SRFCs with actionable tools to enhance healthcare delivery, advance interprofessional collaboration and uphold their educational mission of student-run care. Future work should evaluate implementation outcomes across diverse clinic settings to assess impact on patient care, learner outcomes, and long-term clinic sustainability.

Acknowledgment of Funding: This research was supported in part by the Johnson & Johnson/ National Medical Fellowship Alliance for Inclusion in Medicine Scholarship.

O-06 Title: Role of P311 in Diet Induced Obesity

Authors: Steven Moreton, MS1,2, Pavana Jyotsna Kasaram, PhD2, Kameswara Rao Badri, PhD1,2

1 Department of Pharmacology & Toxicology, 1Cardiovascular Research Institute, Morehouse School of Medicine, Atlanta, GA 30310

Mentor: Kameswara Badri, Ph.D., MB (ASCP)CM, Associate Professor, Morehouse School of Medicine

Background/Significance: The ubiquitous rise in obesity levels has had a pronounced impact on several metrics of metabolic health. The prevalence of associated disorders such as inflammation, insulin resistance, Type 2 diabetes mellitus, cardiovascular disease, and cancers has been linked to increased incidence of obesity. The complex and interconnected relationship between excessive body as well as white adipose tissue weight gain, and disease has initiated discussion on ways to curb the trend. However, the molecular factors that govern the accumulation of excessive adipose tissues (AT) have remained unknown. Based on our ongoing studies, A novel protein (small 8kDa intrinsically unstructured protein), P311 has been implicated as having a role in adipocyte biology, lipid metabolism and inflammation. However, young P311 knockout mice did not show any body weight and WAT weight differences compared with age matched C57BL/6 control mice. So, we hypothesized that secondary insults/factors like age and high-fat-diet might have a role in P311 mediated adipogenesis, lipid metabolisms and inflammatory status and associated mechanisms.

Methods: We treated mice with high fat diet (45%kCal from lipids) and matched controlled diet for 13 weeks. Our results show that HFD feeding significantly increased body weights and white AT weights along with in vivo lipogenesis compared to WT C57BL6 counterparts. We used immunoblots, immunohistochemistry, immunofluorescence and quantitative PCR methods to verify these pathways.

Results: We observed a decrease in several critical adipogenesis regulators such Pparγ and Srebp1 in P311 -/- subcutaneous white adipose tissue (SCWAT) and increased expression of lipogenesis pathway markers such as Plin1, Fasn, and Fabp4. The results indicated that lack of P311 induces obesity upon HFD feeding.

Conclusions and Implications: Our studies indicate that P311 is a key component of adipose biology (adipogenesis, adipocyte plasticity and AT expansion) and a potential target to treatment of obesity and other metabolic diseases.

Acknowledgment 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).

O-07 Title: The Impact of Acidic Cannabinoids in Alzheimer’s Disease

Mentor

Corresponding

Background/Significance: The cannabis plant produces phytocannabinoids in their acidic form known as acidic cannabinoids. Some of the acidic cannabinoids produced most in the cannabis plant are cannabidiolic acid (CBDA), tetrahydrocannabinolic acid (THCA), cannabichromenic acid (CBCA) and cannabigerolic acid (CBGA). Despite being abundantly produced in cannabis, acidic cannabinoids are rarely studied compared to neutral cannabinoids. Additionally, the bioavailability of acidic cannabinoids is higher compared to neutral cannabinoids. Alzheimer’s Disease (AD) is an age-related neurodegenerative disease that currently has no treatment. The causes of AD are unclear, although several hypotheses include the amyloid-beta (β) hypothesis and the highly phosphorylated tau (p-tau) hypothesis. This comprehensive review aimed to take a more in depth look at studies over the past eight years on the biosynthesis of acidic cannabinoids and to answer what are the effects of acidic cannabinoids on the development and symptoms of AD?

Methods: A literature review using PubMed was conducted from January to May of 2025 using PubMed. The key terms and phrases included in the search for this review were cannabis, cannabinoids, acidic cannabinoids, biosynthesis of acidic cannabinoids, acidic cannabinoids and Alzheimer’s Disease, cannabinoids and Alzheimer’s Disease, cannabis and Alzheimer’s Disease. Articles eight years and older were excluded from the review.

Results: The review taking place using PubMed resulted in four articles that met the inclusion criteria. The key takeaways from this review were that acidic cannabinoids have the potential to prevent AD and assist with the symptoms of AD. CBGA has shown the potential to inhibit enzymes that lead to β‐amyloid production, inhibit store-operated calcium entry (SOCE), act as an anti-inflammatory and to be a peroxisome proliferator activated receptor (PPAR)γ/α agonist. Recent evidence has shown that CBDA may minimize β‐amyloid and p-tau hippocampus levels, act as an anti-inflammatory and to inhibit enzymes that lead to β‐amyloid production. CBDA also has the potential to be a PPARγ as well as a PPARα agonist. Like CBDA, THCA has the potential to minimize β‐amyloid and p-tau hippocampus levels, inhibit SOCE and act as an anti-inflammatory. THCA is also a PPARγ agonist with neuroprotective properties.

Conclusion: The results from this review show that the use of acidic cannabinoids could be used as a preventative measure against AD as well as a treatment for the symptoms of AD. One area of this research that needs further investigation is how CBCA can affect the development of AD as well as the symptoms of AD

O-08 Title: Primary Care Physicians’ Access to Antiracist Medical Education Curricula: A Scoping Review

Authors: Shaila Day, D.O., M.S.1; Adesoji Oderinde, M.D.1; Dokun Dairo, M.D.1; Emmanual Marfo, M.D.1; Vicki Oladoyin, M.D.1; Dimitri Johnson, M.D.3; Simone Cotton, B.S.4; Elisabeth White3; Kiara Huff3, Kyra Robinson3; Kyra Tito3; Kalkidan Handiso, B.S.5; Erica Nash, B.S.4; Gakeria Kirton3; Robina Josiah Willock, Ph.D.2

1 Department of Medicine, Morehouse School of Medicine

2 Department of Community Health and Preventive Medicine

3 Doctor of Medicine Degree Program, Morehouse School of Medicine

4 Spelman College

5 Georgia State University

Mentor: Robina Josiah Willock, Ph.D., Morehouse School of Medicine

Background/Significance: In 2021, the Centers for Disease Control and Prevention declared racism a serious public health threat. Medical racism drives inequitable care, erodes patient–physician relationships, and entrenches racial health disparities. While Undergraduate and Graduate Medical Education programs increasingly incorporate antiracist curricula, there is a clear lack of information about the availability of antiracist continuing medical education (CME) for practicing physicians, especially in primary care. Given the essential role of primary care in continuous, relationship-based care, ensuring access to antiracist CME is imperative for addressing clinical inequities.

Objective and Hypothesis: This scoping review directly assesses the availability and scope of antiracist CME curricula for primary care physicians. We assert that, despite widespread acknowledgment of racism as a driver of health inequities, antiracist CME offerings in primary care are limited, fragmented, and largely absent from professional development and certification requirements.

Methods: We conducted a scoping review following the methodological guidance of Susanne Mak and Aliki Thomas. We searched for terms related to antiracism, medical education, CME, and health disparities in SCOPUS, PubMed, ProQuest, and MEDLINE. Two reviewers rigorously screened articles at the title, abstract, and full-text levels using Covidence software. We excluded studies focused on non–primary care specialties, UME, GME, or non-medical disciplines. We analyzed relevant data using qualitative content analysis and descriptive statistics.

Results: Of 1,646 articles screened, 266 underwent full-text review, and 11 met the inclusion criteria. Five studies described CME-accredited professional development courses, and two reported curricula delivered at national specialty meetings. Course duration and format varied widely, ranging from fourhour workshops to programs lasting up to 12 months. Pediatrics was the only specialty to incorporate antiracist education into its board certification requirements.

Conclusion and Implications: Findings confirm that antiracist CME in primary care is both limited and inconsistently implemented. To catalyze meaningful progress toward health equity, urgent and coordinated action is needed to integrate robust antiracist CME into professional development and certification frameworks.

Acknowledgement of Funding:

o This research is funded by the GA-CTSA/CRECD award.

o This research is part of the degree requirements for Master’s in Clinical Research program.

O-09

Title: Acetyl-CoA synthetase 2 is a novel regulator of NREM sleep and stress resilience

Authors: Ashton Arocho 1, 2;

1 Morehouse School of Medicine Graduate Education of Biomedical Sciences

2 Brigham and Woman’s Research Training Program in Sleep, Circadian and Respiratory Neurobiology

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

Background/Significance: Sleep is fundamental for our brain’s ability to properly function. Disrupting sleep impairs neurological processes such as brain-wide gene expression and the ability to overcome stressful conditions (resilience), among others. Non-rapid eye movement (NREM) sleep is necessary for resilience to occur, yet mechanisms underlying sleep’s ability to alter resilience remain unclear. One mechanism may be through an epigenetic modification known as histone acetylation, specifically through Acetyl-CoA synthetase 2(ACSS2). ACSS2 provides the substrate for histone acetylation and is highly expressed in neurons; therefore, we hypothesized that ACSS2 is part of the mechanism through which NREM sleep alters resilience to stress. In the present study, we used a mouse social-defeat stress model to investigate the role of ACSS2 in stress resilience and sleep regulation.

Methods: We generated a novel transgenic mouse model to knock out Acss2 specifically in Camk2a neurons utilizing Cre-LoxP technology. Acss2 fl/fl mice were crossed with a Cre-Camk2a driver to generate Acss2 fl/fl; CAMK2a-Cre knockout mice (Acss2KO). Acss2KO mice and littermate controls underwent ten consecutive days of social defeat stress using a resident-intruder paradigm. Social interaction with a caged conspecific and distance traveled in an empty arena was measured one and seven days after the last social defeat session. In another study, epidural electroencephalography (EEG) and electromyography (EMG) electrodes were used to examine the effects of Acss2KO on undisturbed sleep and sleep deprived conditions. Mice were allowed 24hs of undisturbed sleep followed by a day of 6h sleep deprivation (kept awake for the first 6hs of the sleep period, ZT 0–6) once and then allowed an18h recovery opportunity. EEG/EMG recordings were hand scored by a trained observer.

Results: Acss2KO mice exhibited resilience to social defeat stress and greater exploratory behaviors compared to littermate controls, that persisted 7 days after the last social defeat session. These Acss2KO mice also showed greater NREM sleep quantity and quality both during undisturbed and sleep deprived conditions compared to their littermate counterparts.

Conclusions: Acss2 knockout in CAMK2a neurons promoted resilience to social defeat stress and promoted NREM sleep both during undisturbed and sleep deprived conditions. These findings indicate that ACSS2 is a novel regulator of sleep homeostasis and stress resilience, suggesting that ACSS2 is part of the mechanism linking sleep changes to changes in resilience

Acknowledgment of Funding:

This work was supported by NIGMS 127260 to JCE; training grant NHLBI 007901 (AA), Czeisler PI; Research Centers in Minority Institutions (RCMI) grant NIMH 007602, Kimbro PI.

1 Department of Behavioral, Social, and Health Education Sciences, Rollins School of Public Health at Emory University

2 Doctor of Medicine Program at Morehouse School of Medicine

Mentor: N/A

Background/Significance: Pediatric otolaryngologic conditions, such as chronic otitis media, hearing loss, and obstructive sleep apnea, can significantly affect language development, academic performance, and long-term health. These conditions require timely diagnosis and specialized care, yet not all children have equitable access to such services. Racial/ethnic and socioeconomic disparities in pediatric healthcare are well-documented, but their specific impact on otolaryngologic care has received less focused attention. Understanding how structural and systemic barriers influence access, treatment, and outcomes is essential for developing targeted, equity-driven solutions in this specialty. This research will be guided by the following question:

How do multilevel factors across the Social Ecological Model contribute to racial/ethnic and socioeconomic disparities in pediatric otolaryngology care in the United States, and which interventions show promise in reducing these inequities?

Methods: This review presents a structured literature review of 45 peer-reviewed sources published between 2004 and 2024. Guided by the Social Ecological model, the analysis examines pediatric otolaryngology disparities across five levels: structural, organizational, community, interpersonal, and individual. Sources include national datasets, health policy reports, qualitative studies, and clinical outcome evaluations related to pediatric otolaryngology access and equity.

Results: Evidence from the literature demonstrates that children from historically marginalized backgrounds, particularly those who are publicly insured, low-income, or from racial/ethnic minority groups, experience disproportionately long wait times, lower referral completion rates, and delayed surgical care. Medicaid patients often face administrative burdens and live in regions with no pediatric otolaryngology providers. Barriers such as language discordance, transportation limitations, and low caregiver health literacy further compound disparities. Promising interventions include care coordination hubs, Medicaid fee parity, video interpreter services, mobile diagnostic vans, and onestop weekend clinics. However, many studies are small, single-site, and lack long-term outcome tracking or demographic stratification.

Conclusions and Implications: Disparities in pediatric otolaryngology are pervasive yet modifiable. While innovative interventions have demonstrated success in improving access and timeliness of care, broader implementation and rigorous, equity-focused evaluation are needed. Future research should prioritize multi-site trials, community-informed program design, and metrics that measure not just improvement, but gap closure

O-11

Title: Ancestry modifies preeclampsia biology: integrated placenta bulk RNA-seq and PBMC scRNA-seq analyses reveal immunometabolic re-balancing with higher African ancestry

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

Mentor: Erica L. Johnson, PhD, Morehouse School of Medicine

Background/Significance: Preeclampsia (PE) disproportionately affects women with higher African ancestry, yet ancestry-specific biology remains poorly resolved. We hypothesized that genetic ancestry modulates PE biology and that ancestry-aware models would reveal coherent shifts across placenta and peripheral blood.

Methods: We re-analyzed five placental bulk RNA-seq cohorts (GSE186257, GSE234729, GSE203507, GSE114691, GSE204835) and one PBMC single-cell cohort (GSE266488). Genetic ancestry was inferred directly from RNA-seq: variants were called with nf-core/rnavar (GATK, GRCh38), harmonized to 1000 Genomes, LD-pruned, and ADMIXTURE yielded per-sample ancestry proportions. Placenta expression was modeled per study with limma–voom; study-level contrasts for the PE main effect (PE vs control) and the PE×African-ancestry interaction were combined by random-effects meta-analysis. Ranked statistics were tested by FGSEA (Hallmark/Reactome). For scRNA-seq, FASTQ files were processed with Cell Ranger and analysed in Seurat; cell labels were transferred using Azimuth. Two analyses were performed: (i) cell frequencies donor-level lineage proportions were fit with linear models percent ~ disease ×African ancestry; (ii) pseudobulk DE cell type–specific counts were aggregated per donor and tested with matching main and interaction models, followed by FGSEA. After standard QC, the dataset comprised placenta: 217 samples (5 cohorts) and PBMC: 48 donors, ~654k high-quality cells.

Results: Across placental cohorts, 822 genes were differentially expressed in PE (FDR≤0.05), enriched for Hypoxia, ER stress/UPR, TNFα/NF-κB, and Protein Secretion; canonical PE genes (FLT1, LEP, INHBA, PAPPA2) were up-regulated. Seventeen genes showed a significant PE×African-ancestry interaction (FDR≤0.05): with increasing African ancestry, Hypoxia, TNFα/NF-κB, and Complement were amplified, whereas MYC/E2F cell-cycle, Oxidative Phosphorylation, and fatty-acid/xenobiotic metabolism were attenuated. In PBMCs, five lineages displayed significant disease×ancestry interaction (FDR<0.05): NK_CD56bright, CD16_monocytes, B_naïve, CD4_naïve, and CD4_CTL. Europeans with PE showed decrease in NK_CD56bright and CD16_monocytes with increase in B_naïve; inAfrican-ancestry donors, CD4_naïve were increased with relative stability of NK_CD56bright and CD16_monocytes. Pseudobulk DE mirrored these trends: the PE main effect favored proliferative/metabolic programs (E2F, OxPhos, Glycolysis) with depletion of TNFα/Interferon; the interaction indicated that higher African ancestry strengthened TNFα/NF-κB/inflammatory modules and weakened IFN-α/γ. Together, placenta and PBMC results indicate that as African ancestry increases, PE shifts toward a hypoxia–NF-κB–complement axis with relatively reduced interferon and mitochondrial/cell-cycle programs an ancestry-modulated immunometabolic endotype.

Conclusion and Implications: An ancestry-aware framework reveals the biology of PE, which is masked in pooled cohorts, and motivates the discovery of ancestry-stratified biomarkers and the development of tailored immunometabolic interventions.

Acknowledgement of Funding: Supported by grant numbers R01HD97843, R01MD017690, and U54MD007602.

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