Moderated Poster Discussions - T0 Research/Science

Tuesday, April 14, 2026
4:45 pm - 6:15 pm

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

MICROCYSTIN ACCELERATES CARDIAC INFLAMMATORY FIBROTIC SIGNALING IN AGED RATS WITH LOW AEROBIC CAPACITY (Environmental Factors Affecting Health)
Sonia Garg, The University of Toledo College of Medicine and Life Sciences
Cyanobacterial harmful algal blooms (cHABs) release cyanotoxins such as microcystins (MCs). MCs may injure the cardiovascular system and worsen hypertension and heart failure via pro-inflammatory and pro-fibrotic signaling. However, susceptibility to these toxins is poorly defined, and factors such as aerobic fitness and aging may be key modifiers.
 

KINOME ARRAY PROFILING OF GLIOBLASTOMA PATIENT-DERIVED CELL LINES: PRIMARY VS RECURRENT TUMOR PROFILES (Genetic and Molecular Medicine)
Jacob Wood, University of Toledo College of Medicine
Glioblastoma (GBM), a high-grade glioma, is an aggressive primary brain tumor characterized by near-universal recurrence despite aggressive multimodal therapy. Although advances in neurosurgical and molecular approaches have improved understanding of GBM biology, these advances have resulted in only modest survival benefits, underscoring the need for novel therapeutic strategies. Intracellular signaling networks, modulated by serine/threonine kinases (STKs) and tyrosine kinases (TKs), play key roles in tumor proliferation, invasion, and treatment resistance and represent actionable therapeutic targets. In this study, we performed kinome array profiling on patient-matched primary and recurrent GBM cell line pairs (pat29 and pat31) to identify signaling alterations associated specifically with tumor recurrence.
 

ASSOCIATION OF ANTI-ASTHMATICS WITH METASTASIS RISK IN BREAST CANCER PATIENTS WITH ASTHMA (Hematology and Oncology / Bone Marrow Transplant)
Yusuf Alam, BS, University of Toledo College of Medicine and Life Sciences
Asthma medications exert systemic immunomodulatory effects that extend beyond the pulmonary system, influencing inflammatory signaling, immune surveillance, and cytokine pathways implicated in cancer progression. Prior studies have suggested associations between certain asthma therapies and cancer incidence; however, these studies have not systematically compared individual asthma medication classes with respect to their impact on breast cancer metastases. Given the prevalence of asthma among breast cancer patients, clarifying whether specific anti-asthmatic medications influence metastatic risk represents an important and understudied clinical question. We integrated real-world clinical outcomes with class specific exposure analyses to evaluate associations between asthma maintenance therapies and breast cancer metastasis.
 

MULTIOMIC INTEGRATION IN INCREASING MENINGIOMA TUMOR GRADE REVEALS NER AND PLASMA MEMBRANE DYSREGULATION (Hematology and Oncology / Bone Marrow Transplant)
John Vergis, BS, The University of Toledo
The most common non-malignant histopathology for intracranial tumors is meningioma. The tumor’s clinical grade (WHO Grades 1,2, and 3) can help inform treatment plans and survival rates. Despite information being available on what molecular subgroups exist, especially in the context of multi-omics, to date there has never been a network-based multi-omic study involving the transcriptome and the proteome. Thus, this study analyzes transcriptomic (WHO grade 3 vs. grade 1) and proteomic (grade 2/3 vs. grade 1) results in a network-aware fashion to find the major categories of biological variability across grade.
 

OXIDATIVE MODIFICATION ALTERS IL-33 SIGNALING BY SHIFTING RECEPTOR ENGAGEMENT (Immunology / Allergy)
Ethan Luo,,Washington University in St. Louis
IL-33 is a cytokine that drives type-2 inflammation and tissue remodeling in the airway epithelium, implicated in diseases such as chronic obstructive pulmonary disease and asthma. IL-33 undergoes rapid oxidation in the extracellular space, becoming unable to bind and signal via its canonical receptor ST2. An alternative pathway has recently been identified for oxidized IL-33 to form a complex with the receptor for advanced glycation end products (RAGE) and promote inflammatory pathogenesis. However, the receptor specificity and molecular determinants of this interaction are still undefined. Studying how oxidative modification of IL-33 alters signaling through RAGE and ST2 is key to understanding how IL-33-driven inflammation is regulated in oxidative airway disease environments and to inform therapeutic treatments.
 

TAUOPATHY DISRUPTS GUT AND BRAIN BARRIERS AND SUPPRESSES B-CATENIN IN ALZHEIMER'S DISEASE (Neurology)
Yueqing An, University of Illinois Chicago
Tauopathy is a hallmark of neurodegenerative diseases, yet its systemic effects on peripheral organ integrity and barrier function remain poorly characterized. Our study investigates the systemic pathological and behavioral consequences of tauopathy in Alzheimer's disease (AD), focusing on its impact on tight junction and adhesion molecule expression in cerebral and intestinal tissues through the gut-brain axis.
 

SEX-BASED GENE EXPRESSION DIFFERENCES IN ANEURYSMAL SUBARACHNOID HEMORRHAGE (Neurology)
Shawn Murphy, The University of Toledo Medical Center
Aneurysmal subarachnoid hemorrhage (aSAH) is associated with high morbidity and mortality, with accumulating clinical evidence indicating sex-specific differences in disease incidence and secondary complications such as delayed cerebral ischemia. However, the molecular basis underlying these sex-dependent differences remains poorly defined.
 

MULTI-REGION TRANSCRIPTOMIC ENRICHMENT ANALYSIS OF CYTOKINE PRODUCTION PATHWAY DYSREGULATION OF SCHIZOPHRENIA (Neurology)
Roshan Sirole, University of Toledo College of Medicine and Life Sciences
Schizophrenia is a complex neuropsychiatric disorder that significantly disrupts cognition, behavior, and emotional regulation and affects approximately 0.45% of adults worldwide. Increasing evidence suggests that immune and inflammatory processes, particularly cytokine signaling, play a central role in schizophrenia pathophysiology. While transcriptomic studies have identified immune-related gene expression changes in schizophrenia, the consistency of cytokine production pathway dysregulation across multiple brain regions remains poorly understood. Pathway-level analyses focused on cytokine-associated signaling provide an opportunity to identify shared immune mechanisms underlying pathway dysregulation in schizophrenia.
 

RECEPTOR TYROSINE KINASES AS A POTENTIAL THERAPEUTIC TARGET IN MULTIPLE SCLEROSIS USING DRUG REPURPOSING (Neurology)
Dawson Swicegood, The University of Toledo College of Medicine and Life Sciences
Multiple Sclerosis (MS) is a chronic immune-mediated inflammatory demyelinating disease of the central nervous system (CNS). It is characterized by destruction of myelin and oligodendrocytes, the myelin-producing cells of the CNS, leading to loss of the insulating sheath that is vital to proper neuronal communication and function. Demyelination, therefore, leads to the disruption of neuron signal propagation, resulting in clinical manifestations including cognitive dysfunction, vision loss, bowel and bladder dysfunction, and focal motor deficits. While remyelination can occur following CNS injury through oligodendrocyte-mediated repair, this process is dysregulated in MS, contributing to relapsing and/or progressive disease pathology.
 

MAPPING RSK4 ASSOCIATED SIGNALING IN ALZHEIMERS DISEASE USING PROXY BASED NETWORK AND MOTIF ANALYSES (Psychiatry)
Megha Subramanian, BA, University of Toledo College of Medicine and Life Sciences
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by early synaptic vulnerability and progressive disruption of protein kinase-regulated signaling networks. Kinome profiling of postmortem human brain tissue across AD progression has highlighted several well-characterized kinases, including ERK and Akt, as key contributors to disease pathology. However, the roles of numerous understudied “dark” kinases within these disrupted signaling networks remain largely unexplored. One such kinase is the p90 ribosomal S6 kinase isoform RSK4 (RPS6KA6) which was noted as a disease stage- and sex-associated signal in our previous work profiling the kinome throughout AD progression. RSK4 is less known in the context of AD than its closely related RSK family members. In this study, we examine RSK4’s unique role in brain physiology.
 

CARMIL1 PLAYS A CRITICAL ROLE IN ENDOTHELIAL BARRIER AND INFLAMMATION (Pulmonary / Critical Care)
Weiguo Chen, MD, University of Illinois Chicago
The acute respiratory distress syndrome (ARDS) results in alveolar edema, respiratory failure and high mortality. A dysfunctional pulmonary endothelial cell (EC) barrier is a key pathologic hallmark of ARDS. Protein regulation of the actin cytoskeleton is key to maintaining this barrier. We have previously identified a role for the cytoskeletal regulator capping protein Arp2/3 complex myosin-I linker (CARMIL1).
 

THE EFFECT OF PHYSIOLOGIC SHEAR STRESS ON THE PULMONARY ENDOTHELIAL BARRIER (Pulmonary / Critical Care)
Kelsey Holbert, MD, University of Illinois Chicago
Despite the pulmonary vasculature being exposed to constant flow, there is limited understanding of the effects of shear stress on the pulmonary endothelium and most in vitro work is performed under static conditions. Pathologic shear stress, through high cardiac output, contributes to several forms of pulmonary hypertension. By understanding critical cellular mechanisms associated with physiologic flow, in comparison to static conditions, we can better unravel pathologic flow conditions.
 

CATHEPSIN S MEDIATES MRSA-INDUCED LUNG ENDOTHELIAL DYSFUNCTION (Pulmonary / Critical Care)
Eleftheria Letsiou, PhD, University of Illinois Chicago
Acute lung injury (ALI) is characterized by severe disruption of vascular barrier integrity and exaggerated inflammation, often driven by pathogens like methicillin-resistant Staphylococcus aureus (MRSA). Endothelial cells (EC) play a pivotal role in controlling vascular permeability and coordinating inflammatory signaling. RNA-seq profiling of EC exposed to MRSA demonstrated marked transcriptomic alterations, identifying the gene CTSS among the most significantly upregulated genes. CTSS, which encodes the lysosomal protease cathepsin S, has been implicated in various inflammatory disorders, including ALI; however, its contribution to lung endothelial dysfunction remains undefined.
 

MODULATION AND MALIGNANT PROGRESSION OF RWPE-2 STEM-LIKE CELLS BY PFOA AND PFOS (Environmental Factors Affecting Health)
Duoling Xu, PhD, University of Illinois Chicago
Per- and polyfluoroalkyl substances (PFAS) are a class of widely used synthetic chemicals characterized by extreme environmental persistence and bioaccumulation. PFAS have been detected in numerous human tissues, and epidemiological evidence suggests that chronic occupational exposure is associated with an increased risk of prostate cancer. However, the role of PFAS in prostate carcinogenesis and the underlying cellular and molecular mechanisms remain poorly understood.
 

KAPOSI'S SARCOMA-ASSOCIATED HERPESVIRUS (KSHV) HIJACKS HOST WATER CHANNEL PROTEINS TO REGULATE KSHV REACTIVATION AND INDUCE AUTOPHAGY IN INFECTED CELLS (Immunology / Allergy)
Viridiana Guillen, Lake Forest College
Kaposi’s Sarcoma-associated Herpesvirus (KSHV) is a virus that has not yet been fully characterized within medical research. Identified in 1994, it continues to be studied for its mechanisms of transmission between hosts. KSHV is characterized by two distinct life cycles that contribute to its survival and propagation: the latent and lytic cycles. During latency, the virus remains inactive until it transitions to the lytic cycle, at which point viral replication and dissemination occur. KSHV relies on several host proliferation regulators, including water channel proteins called aquaporins (AQPs), especially AQP3. It is a protein found in most living organisms that facilitates the transport of water and glycerol. AQP3 is involved in microbial pathogenesis and inflammation-associated responses, which has led to interest in their potential as therapeutic targets.


MULTIOMICS ANALYSIS OF INTRACELLULAR SIGNALING DYSREGULATION IN GRIN1 CHANNELOPATHY (Psychiatry)
Priyanka Pulvender, BS, The University of Toledo College of Medicine and Life Sciences
The NMDA subtype glutamate receptor subunit 1 gene (GRIN1) encodes an obligatory subunit of the glutamatergic N-methyl-D-aspartate (NMDA) receptor. Pathogenic variants in GRIN1 cause GRIN1-related neurodevelopmental disorder, a rare and debilitating channelopathy characterized by intellectual disability, epilepsy, autism, movement disorders, and cortical visual impairment. A deeper understanding of molecular signaling changes in the brain is needed to facilitate the development of targeted therapies.
 

SPECIFIC POTENTIATION OF THE TMEM16A CHLORIDE CHANNEL CAN RESCUE IMPAIRED MUCOCILIARY TRANSPORT IN HUMAN AIRWAY MODELS OF CYSTIC FIBROSIS (Pulmonary / Critical Care)
Peihang Li, PhD candidate, Washington University in St. Louis
Cystic fibrosis is caused by loss-of-function mutations in the CFTR chloride channel, resulting in impaired airway defense mechanisms, including decreased mucociliary transport (MCT), which is required to remove infectious entities. Highly effective modulator therapies (HEMT) that target restoring the function of CFTR have been introduced in recent years,  but there are limitations: 1) they are not applicable to the 8% of patients that have class I mutations (early stop codons); 2) not all potentially appropriate CF patients respond to HEMTs; 3) long-term effectiveness is unknown; 4) persistent inflammation may be needed for HEMTs to function. In light of this, we investigated the possibility of selectively potentiating an alternative chloride channel in the airway in order to improve mucus function. We previously showed that a small protein, the Calcium Activated Chloride Channel Regulator 1 VWA domain (CLCA1 VWA), could selectively potentiate the TMEM16A chloride channel in cell lines. Here we investigate the ability of CLCA1 VWA to potentiate TMEM16A and modulate mucociliary transport (MCT) in human models of CF airway disease.