Moderated Poster Discussions - T0 Research/Science

Monday, April 13, 2026
4:30 pm - 6:15 pm

T0 Research/Science: Basic biomedical research, including preclinical and animal studies, not including interventions with human subjects.

EXPLORING THE DIAGNOSTIC AND THERAPEUTIC ROLE OF PROTOPORPHYRIN IX PRODUCTION IN RELEVANT MODELS OF BURN INJURY (Dermatology)
Bailey Donahue, BS, University of Wisconsin-Madison School of Medicine and Public Health
Clinical visual assessment, the current standard for burn injury assessment, is prone to errors, with inaccuracies occurring in 25-30% of cases. Real-time fluorescence imaging may be an objective and reliable non-contact method of identifying burn wound characteristics. Protoporphyrin IX (PpIX) is a common photosensitizer produced in the heme pathway from its precursor 5-aminolevulinic acid (5-ALA) and additionally represents a potential novel therapeutic approach for burns using Photodynamic Therapy (PDT).
 

AGING AND LOW INTRINSIC FITNESS EXACERBATES PULMONARY INFLAMMATION AND INJURY IN RESPONSE TO INHALED MICROCYSTIN-LR IN RATS (Environmental Factors Affecting Health)
Upasana Shrestha, BS, University of Toledo College of Medicine and Life Sciences
Cyanobacterial harmful algal blooms release cyanotoxins such as microcystin-leucine arginine (MC-LR), one of the most prevalent and toxic variants, posing risks to human and animal health. While ingestion has been the primary exposure pathway studied, increasing evidence indicates that inhalation of MC-LR—contaminated aerosols can cause significant lung injury. These aerosols can travel long distances from their source, potentially exposing large populations, including vulnerable elderly individuals. Aging and low intrinsic aerobic fitness may increase susceptibility to environmental toxicants.
 

HYDROPHILIC STATIN USE IS ASSOCIATED WITH IMPROVED OUTCOMES IN MELANOMA PATIENTS UNDERGOING IMMUNOTHERAPY (Hematology and Oncology / Bone Marrow Transplant)
Peyton Roth, MS, University of Toledo College of Medicine and Life Science
Immunotherapy is a budding field in cancer therapy that has displayed significant improved outcomes for patients with melanoma and other forms of malignancy. Statins are a widely use class of lipid-lowering medications with emerging evidence supporting immunomodulatory effects that may influence cancer outcomes. Specific analysis to suggest improved patient outcomes for patients undergoing immunotherapy with concomitant statin use are limited. Statins exert distinct and differential effects depending on their chemical properties and are commonly subdivided as lipophilic or hydrophillic. We investigated the impact of stain use, and statin subtype (lipophilic vs hydrophilic) on clinical outcomes in melanoma patients treated with immunotherapy.
 

TRANSCRIPTOMIC ANALYSIS OF ALLERGEN-CHALLENGED CD4+ T-CELL SIGNATURES USING 3PODR (Immunology / Allergy)
Leo Roberts, University of Toledo Department of Neurosciences and Psychiatry
Seasonal allergic rhinitis (SAR) is a common, type 2—skewed inflammatory disease in which allergen exposure drives CD4+ T-cell activation and downstream cytokine signaling.  Epigenetic regulation is increasingly recognized as a contributor to allergic disease heterogeneity, including symptom severity and immune-cell state.
 

BIOPHYSICAL CHARACTERIZATION OF TREM2 INTERACTIONS WITH APOE AD RISK VARIANTS (Immunology / Allergy)
Cynthia Zhi, Washington University in St. Louis School of Medicine
TREM2 is a scavenger receptor expressed on microglia that has emerged as an important drug target for Alzheimer’s disease (AD) and other neurodegenerative diseases. Ligands bind to TREM2 on microglia which triggers anti-inflammatory signaling, phagocytosis of amyloid beta, and proliferation. Apolipoprotein E (apoE) is a ligand for TREM2, and is also an AD risk factor. ApoE has three isoforms which vary in AD risk: apoE2 (protective), apoE3 (normal), and apoE4 (increased risk). In previous studies we found that apoE affinity for TREM2 potentially correlated with AD risk. Apoe2 showed the lowest affinity for TREM2 (KD =  590 nM), apoE3 was intermediate (KD = 440 nM) and apoE4, the high risk variant, had highest affinity (KD = 281 nM). New variants in apoE  isoforms have been reported that correlate with increased or decreased risk of developing AD. Therefore, we undertook biophysical study of TREM2 interactions with apoE variants to investigate a possible correlation between receptor-ligand interactions and risk of developing AD.
 

CYSTITIS AND SUBSEQUENT RISK OF GENITOURINARY MALIGNANCIES AND DYSURIA: A SEX-SPECIFIC RETROSPECTIVE TRINETX STUDY (Nephrology)
Emily Warden, The University of Toledo College of Medicine and Life Sciences
Inflammation of the bladder, termed cystitis, is most commonly caused by ascending bacterial infection. Its development and severity are influenced by multiple risk factors, including genitourinary anatomy, systemic comorbidities, and behavioral exposures such as sexual activity and tobacco use. Clinically, cystitis presents with symptoms including dysuria and urinary urgency and may progress to chronic conditions such as recurrent bacterial cystitis or interstitial cystitis. Although cystitis is associated with long-term urologic complications, the sex-specific risk of subsequent bladder and kidney malignancy, as well as persistent dysuria, following a first-time cystitis diagnosis in adults aged 50 years and older, remains incompletely characterized.
 

EXPLORING THE RNA-LEVEL EXPRESSION OF KINASES IN ALZHEIMER'S DISEASE (Neurology)
Ruqaya Kareem, MD, PhD, The University of Toledo College of Medicine
Alzheimer’s disease (AD), the most common neurodegenerative disease, involves the accumulation of neurofibrillary tangles composed of hyperphosphorylated tau protein and senile plaques of aggregated β-amyloid peptides. Since phosphorylation is central to tau pathology and signaling pathways implicated in Aβ production, protein kinases have been widely studied in AD pathogenesis. Kinase activity in AD has been examined primary at the level of protein expression through immunohistological studies. Although several kinases show altered expression in Alzheimer’s patients, it is critical to explore the expression patterns at the stages preceding protein formation. The Seattle Alzheimer’s Disease Brain Cell Atlas (SEA-AD) provides extensive single-cell profiling data, including single-nucleus RNA sequencing (snRNA-seq) and bulk RNA-seq, spanning the spectrum of Alzheimer’s disease severity, as well as neurotypical data for comparison. Using this extensive resource, we aim to provide a comprehensive analysis of gene expression at the RNA-level to better understand the molecular pathways impacted in Alzheimer’s disease and to inform the identification of potential therapeutic targets.
 

CD36 LINKS ARTERIOLAR ANGIOGENESIS TO ENDOTHELIAL CELL IMMUNITY IN DEVELOPMENT OF ALZHEIMERS DISEASE (Neurology)
Jada Harvey, University of Alabama at Birmingham
Alzheimer's disease (AD) displays profound cerebromicrovascular abnormalities, irregular arterioles, and potential abnormal immunity. CD36 is an antiangiogenic receptor in endothelial cells (ECs), which may regulate arteriolar angiogenesis. As an innate immunity receptor, CD36 may also be critical for the regulation of the immune property of vascular ECs. Ours and other studies suggest that abnormal CD36 expression may contribute to the development of AD.
 

CHARACTERIZATION AND INHIBITION OF LRP1-MEDIATED TAU SPREAD TO SLOW ALZHEIMER'S PROGRESSION (Neurology)
Daniel Paszkowski, BS, Washington University in St. Louis
Alzheimer’s disease is a neurodegenerative disorder characterized by neuronal cell death and deterioration of executive function. The amyloid cascade hypothesis posits that the accumulation of amyloid-beta plaques precedes and accelerates the deposition of tau neurofibrillary tangles. The low density lipoprotein receptor-related protein 1 (LRP1) has been identified as a major receptor for tau in the brain. However, the minimal determinants of binding of LRP1 and tau have not been identified.
 

DEVELOPING A DIFFUSION-WEIGHTED MRI-BASED ALGORITHM TO PROVIDE CLINICALLY SIGNIFICANT AUTOMATED MEASUREMENT OF ACUTE INFARCT VOLUME (Neurology)
Ada Tadeo, BS, Cedars Sinai Medical Center
Stroke is the leading cause and mostly cause medical disorder associated with permanent disability in adults in the United States. Developing more effective treatment options for stroke requires more accurate predictive imaging biomarkers of response to therapy that are readily available in the clinical setting. Treatment options for acute ischemic stroke patients are limited because rapid changes in tissue viability begin and persist during vascular occlusion, making them difficult to accurately predict on hyperacute computed tomography imaging. We have previously demonstrated that the change infarct volume is a more sensitive predictor of neurologic outcome than penumbral volume and early estimates of infarct volume, but this previous technique required perfusion-weighted (PW) imaging and gadolinium delivery. The development of an automated tool for measuring acute infarct volume using only diffusion-weighted (DW) imaging will simplify and streamline clinical workflows and provide a more accurate patient prognosis.
 

MARKERLESS POSE ESTIMATION USING DEEPLABCUT TO ANALYZE PRECIPITATED OPIOID WITHDRAWAL IN MICE (Psychiatry)
Diya Bhatia, The University of Texas at Austin
Opioid Use Disorder (OUD) is a chronic, relapsing condition in which repeated cycles of opioid use and withdrawal drive persistent drug-seeking behavior. Withdrawal produces intense negative affect, and the avoidance of these symptoms becomes a primary motivator for continued opioid use. Rodent models are widely used to study withdrawal-related behaviors, but traditional scoring methods are subjective, inconsistent, and labor-intensive. To address this limitation, we applied DeepLabCut (DLC), a markerless deep-learning pose estimation tool, to objectively quantify somatic signs of precipitated morphine withdrawal in mice with either intact or ablated calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus (CGRP PBN).
 

ACTIVATION OF USP30 IMPAIRS LUNG MICROVASCULAR INTEGRITY BY INCREASING DNA METHYLATION THROUGH DEUBIQUITINATING METHIONINE ADENOSYLTRANSFERASE (Pulmonary / Critical Care)
Baoyinna Baoyinna, The Ohio State University
Microvascular inflammation and barrier disruption play critical roles in the pathogenesis of acute inflammatory diseases (1-3), such as Pseudomonas aeruginosa- or SARS-CoV-2-induced acute respiratory distress syndrome (ARDS) and sepsis. In response to inflammatory stimulators, including bacterial endotoxin, ECs increase expression of chemokine and adhesion molecules, such as IL-8, VCAM1, and ICAM1, ultimately causing neutrophil accumulation transmigration to the site of inflammation, endothelial barrier disruption, and tissue damage (4-6). Hence, preservation of EC function is a novel therapeutic option for more effective treatment of acute inflammatory diseases. De-ubiquitinating enzymes remove mono-ubiquitin or polyubiquitin chains from ubiquitinated proteins to stabilize proteins or regulate enzyme activities (7-9). USP30 is a deubiquitinase localized on the mitochondrial outer membrane (10, 11). The canonical function of USP30 is to antagonize Parkin- and Pink1-mediated mitochondrial mitophagy (10, 12). USP30 inhibition has been shown to be beneficial for treatment of certain mitochondrial disorders, mostly focusing on neurodegeneration and cancers (12-16). The role of USP30 in EC inflammation and barrier integrity has not been reported.
 

ELUCIDATING THE ROLE OF GASDERMIN ISOFORMS IN ASTHMA PATHOGENESIS (Pulmonary / Critical Care)
Asta Simonovic, BS, Washington University School of Medicine, St Louis
Chronic lower respiratory disease, including asthma and COPD, remain a leading cause of global morbidity, often characterized by persistent Type-2 inflammation and mucus hypersecretion. This inflammatory environment is often driven by the aberrant release of IL-1 family cytokines which function to propagate immune responses. Gasdermins (GSDMA-E) are a family of pore forming proteins involved in pyroptosis, a lytic cell death that facilitates cytokine release via large membrane pores. While Gasdermin D (GSDMD) is the canonical driver of pyroptosis, the functional roles of other family members, particularly GSDMB and GSDMC remain poorly understood in the context of the airway epithelium. The GSDMB gene is located at the asthma-associated 17q21 locus, the most replicated genetic risk factor for childhood-onset asthma. GSDMB is expressed as multiple spliced isoforms, suggesting evolved functions beyond cell death, with established roles in vesicular trafficking and wound healing. Similarly, GSDMC has been linked to non-lytic cytokine release, vesicular trafficking, and proliferation.
 

COMPARATIVE EFFECTS OF CYANOTOXINS ON HEPATOCYTES ACROSS SPECIES: IMPLICATIONS FOR HUMAN AND VETERINARY CARE (Environmental Factors Affecting Health)
Apurva Lad, PhD, University of Toledo
Cyanobacterial harmful algal blooms (cHABs) generate a diverse suite of bioactive cyanotoxins, including the hepatotoxins microcystin-LR (MC-LR) and cylindrospermopsin (CYN), and the neurotoxin anatoxin-a (ATX). In addition to human exposures, dogs are a well-recognized sentinel species for acute bloom-associated illness, and cattle are at risk through contaminated drinking water sources, making these species highly relevant to public health and veterinary practice. Although not all cyanotoxins primarily target the liver, the liver plays a central role in uptake, biotransformation, detoxification, and acute-phase signaling, making hepatocytes a practical model to capture both direct injury and systemic response pathways. Defining species-specific hepatocyte responses is critical for improving diagnostic interpretation and guiding management across human and animal exposures.
 

DEVELOPING ANTI-TREM2 SINGLE-CHAIN VARIABLE FRAGMENTS (SCFVS) THAT CAN BLOCK IL-34 BINDING AS POTENTIAL ASTHMA THERAPEUTICS (Pulmonary / Critical Care)
Cherish Amby-Okolo, Washington University School of Medicine
Chronic airway diseases such as asthma are driven by macrophage activation, which triggers inflammation in the lungs. One receptor essential to this process is Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), which is expressed on macrophages. The lab has shown that TREM2 expression is increased in mouse models of chronic inflammatory airway disease, leading to airway inflammation. We also identified the cytokine IL-34 as a ligand that binds to TREM2 to promote macrophage activation. Therefore, the biological question we ask is whether blocking the interaction between TREM2 and IL-34 reduces macrophage-driven inflammation in asthma.
 

TARGETING THE "UNDRUGGABBLE" ONCOGENIC TRANSCRIPTION FACTOR NUCLEAR FACTOR I/B IN PEDIATRIC MEDULLOBLASTOMAS (Hematology and Oncology / Bone Marrow Transplant)
Abhishek Bhattacharya, PhD, University of Nebraska Medical Center
Nebraska ranks in the top 10 states for pediatric brain tumors, the leading cause of cancer-related mortality in childhood. Medulloblastomas (MB) are the most common malignant brain tumors and divided into four primary subgroups amongst which group 3 tumors (G3MB) exhibit the highest aggressiveness. Nuclear Factor I/B (NFIB), a developmentally-active transcription factor enriched in G3MBs, plays a pivotal role in promoting tumorigenesis and metastasis in various cancers by inducing a change in chromatin structure that enhances accessibility to pro-tumorigenic and pro-metastatic programs.