Moderated Poster Discussions - T0 Research/Science

Monday, April 14, 2025
5:30 pm - 6:45 pm

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

NOVEL PHARMACOLOGICAL TREATMENT FOR PREECLAMPSIA: IN VITRO AND IN VIVO STUDY (Diagnosis or Treatment of a Disease Process or Clinical Syndromes)
Mehruba Zaman, BS, Virginia Commonwealth University SOM
Preeclampsia (PreE) is a hypertensive pregnancy disorder, which occurs in approximately 10% of all gestations. The literature hints at a potential therapeutic role of H2 relaxin in PreE. Due to the complex insulin-like structure of relaxin (A- and B- chains, 53 amino acids, 3 disulfide bonds), a novel H2 relaxin B-chain-only peptide variant B7-33 (27 amino acids without any disulfide bonds) has recently been developed.
 

ALLEVIATING STZ-DIABETIC FEMALE MICE BODY WEIGHT LOSS WITH ORAL GAVAGE OF HIPPOCRAETA VELUTINA EXTRACT (Endocrinology / Metabolism)
Maricica Pacurari, PhD, Jackson State University

Streptozotocin-induced diabetic mouse model is a widely used model to study cardiomyopathy in diabetes. However, STZ induces also body weight loss thus limiting studies progression.
 

EXPOSURE TO AEROSOLIZED MICROCYSTIN IMPACTS THE EXPRESSION AND RELEASE OF PRO-INFLAMMATORY SIGNALING MOLECULES FROM HEALTHY AND ASTHMATIC HUMAN AIRWAY EPITHELIAL CELLS IN A CONGENER DEPENDENT MANNER (Environmental Factors Affecting Health)
Bivek Timalsina, MS, The University of Toledo

Cyanobacterial harmful algal blooms (cHABs) are increasing in frequency, releasing toxic microcystins (MCs) into the environment, including airborne aerosols. MC-LR, MC-RR, and MC-LA are among the primary congeners detected in significant concentrations within cHAB aerosols. While MCs are known to induce inflammation, their effects on the human airway following inhalation remain poorly understood.
 

QUALITATIVELY ASSESSING THE IMPACT OF DE-FRAGMENTED CARE ON ADVANCE CARE PLANNING AND END OF LIFE CARE AMONG HIGH-UTILIZERS OF HEALTHCARE (Geriatrics and Aging)
Omar Marin, BS, University of Chicago

Advance care planning is defined as the process used to identify, comprehend, and implement the medical preferences and goals of patients near the end of life, particularly in preparation for limited decision-making capabilities. As the U.S. population continues to get older, Americans are projected to consume more healthcare than ever before, making advance care planning essential to delivering patient-centered care aligned with wishes and values, particularly for high healthcare utilizers who have multiple comorbidities.
 

POST-TRANSLATIONAL MODIFICATION OF HUMAN IL-33 IMPACTS CYTOKINE INFLAMMATORY ACTIVITY (Immunology / Allergy)
Morgan Payne, BS, Washington University in St. Louis

IL-33 is a proinflammatory cytokine upregulated in airway epithelium that propagates type-2 inflammation in chronic airway diseases such as chronic obstructive pulmonary disease (COPD) and asthma. While the abundance of IL-33 expression in airway epithelial cells is established, mechanisms that regulate cytokine release and activity are not fully understood. We have previously described a role for alternative splicing in regulated cytokine secretion in COPD that results in tonic cytokine secretion from airway cells. Upon release, IL-33 interacts with its primary receptor ST2 and IL-1RAcP forming a ternary complex, allowing for the propagation of type-2 immune signaling.
 

REVIVIFY GEL AND POWDER DRINK AS LOW AS ONE-THIRD CONCENTRATION ATTENUATED THE INFLAMMATORY AND ANTI-OXIDATIVE MARKERS IN LIPOPOLYSACCHARIDE-INDUCED JURKAT CELLS (Immunology / Allergy)
Waafi Awal, Missouri Southern State University

REVIVIFY pro-vitality antioxidant gel/powder is composed of primary antioxidant superoxide dismutase [SOD], prebiotic fibers, and diverse polyphenols from various fruit juices. SOD diminishes the superoxide free radicals produced during normal cellular processes. Dietary prebiotic fibers modulate beneficiary gut eco microbiomes and provide many health benefits including immunity. Polyphenols are phenolic compounds that act as antioxidants, anti-inflammatory, and antiviral agents that repair cells damaged from reactive oxygen and nitrogen species ROS/RNS. Combination of these three components stimulate immunity via T-cell activation and antioxidative and anti-inflammatory pathways. The Jurkat cell line is an immortalized T lymphocyte cell line that has most often been used as a prototypical T-cell line to study multiple events in T cell biology, including T cell signaling. In a previous study, we showed that both Revivify gel and powder attenuated the lipopolysaccharide-induced activation of Jurkat cells’ secretion of inflammatory and oxidative stress markers.
 

PARAOXONASE-1 PROTECTON OF VASCULAR CALCIFIACTION AND BONE MINERAL DISORDER IN AN ADENINE INDUCED MODEL OF CHRONIC KIDNEY DISEASE (Nephrology)
Prabhatchandra Dube, PhD, University of Toledo

Chronic kidney disease (CKD) is associated with vascular calcification and low bone mineral density. Paraoxonase-1 (PON1) is a lactonase enzyme synthesized in the liver and associated with HDL particles. It plays a crucial role in enhancing HDL's antioxidant, anti-inflammatory, and anti-atherogenic properties. Decreased PON1 activity leads to increased oxidative stress and is linked to worse clinical outcomes in CKD. However, the role of PON-1 in vascular calcification and bone mineral disorder in the context of CKD remains largely unexplored.
 

TARGETING THE MICROGLIA RECEPTOR TREM2 IN ALZHEIMER'S DISEASE: STRUCTURAL AND FUNCTIONAL ANALYSIS OF TREM2-MEDIATED AMYLOID BETA PHAGOCYTOSIS (Neurology)
Jessica Greven, BA, Washington University in St. Louis

The development of new innovative treatments to prevent and ameliorate Alzheimer’s disease (AD) requires knowledge of molecular mechanisms that are critical to neuronal health. The receptor TREM2 is part of a signaling complex that modulates inflammatory responses, phagocytosis and cell survival in microglia– resident immune cells in the brain that play a critical role in clearing misfolded aggregates such as amyloid beta (Aβ). In recent years, TREM2 has emerged as a promising drug target for AD. Understanding the molecular mechanisms underlying TREM2 signaling in microglia will facilitate the development of specific, safe and efficacious therapies for AD that target TREM2.
 

COMPARISON OF URINARY LEVELS OF ANGIOGENIC FACTORS AND A CARDIOTONIC STEROID IN PREGNANT PATIENTS WITH AND WITHOUT PREECLAMPSIA (Pathophysiology / Pathology)
Waafi Awal, Missouri Southern State University

Preeclampsia (preE) is a disorder characterized by the de novo onset of hypertension and proteinuria at mid-gestation. Despite scientific advances, preE remains a leading cause of maternal and neonatal mortality, preterm birth, and morbidity, particularly in developing countries. Soluble endoglin (sEng), PlGF (Placental Growth Factor), TGF-β-1, VEGF, and marinobufagenin are all implicated in new blood vessel formation called angiogenesis. An imbalance of pro- and anti-angiogenic factors is thought to cause preE. Marinobufagenin (MBG) is an endogenous cardiotonic steroid (CTS) that is elevated in preE; PlGF and VEGF are pro-angiogenic factors; sEng is an anti-angiogenic factor.
 

METABOLIC REGULATION OF HEPATIC GENES IN METHIONINE AND HOMOCYSTEINE METABOLISM: ROLE OF PPARG (Pathophysiology / Pathology)
Izabela M. Hawro, University of Illinois at Chicago

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is the leading cause of chronic liver disease worldwide1, and it is associated with the dysregulation of methionine and homocysteine (Hcy) metabolism. Recently, we published that hepatocyte peroxisome proliferator-activated receptor gamma (Pparg) is positively associated with the progression of diet-induced MASLD and negatively with the regulation of methionine and Hcy metabolism2.
 

CARMIL1 EXPRESSION ALTERS ENDOTHELIAL CELL SHAPE AND BARRIER FUNCTION (Pulmonary / Critical Care)
Mohammed Yaman Al Matni, MD, Division of Pulmonary, Critical Care, Sleep and Allergy, University of Illinois Chicago, Chicago, IL, United States

The acute respiratory distress syndrome (ARDS) results in severely impaired gas exchange and high mortality. Loss of pulmonary endothelial cell (EC) barrier integrity is a common pathologic hallmark of ARDS. Cytoskeletal proteins are critical regulators of EC barrier function. Alterations in actin structure and membrane-associated actin polymerization change EC shape to determine barrier function. Variation in the gene encoding the cytoskeletal regulator capping protein Arp2/3 complex myosin-I linker (CARMIL1) results in an isoleucine substitution for valine at amino acid position 77 and is implicated in human ARDS (Wei, et al. AJRCCM 2017). CARMIL1 is known to function at the periphery of motile cells and regulate membrane protrusion. We have previously identified a role for CARMIL1 in pulmonary EC regulation.
 

HSP70 IS A CHAPERONE FOR IL-33 SECRETION AND FUNCTION IN CHRONIC AIRWAY DISEASE (Pulmonary / Critical Care)
Omar Osorio, Washington University in St. Louis

IL-33 is a key driver of type 2 inflammation and relevant to epithelial biology. However, the mechanisms for IL-33 secretion and regulation in the context of chronic airway disease is still not understood.
 

ELUCIDATING THE STRUCTURAL AND FUNCTIONAL BASIS OF TREM2/IL-34 SIGNALING IN INFLAMMATORY AIRWAY DISEASE (Pulmonary / Critical Care)
Joshua R. Wydra, Washington University in St. Louis

TREM2 is an extracellular receptor expressed on macrophages. Engagement of ligands by TREM2 triggers signaling that controls macrophage function and roles in disease. The cytokine IL-34 was recently identified as a novel ligand for TREM2. Given the role of activated macrophages in inflammatory airway diseases, we sought to investigate the potential role of TREM2/IL-34 in inflammatory signaling and elucidate the structural basis for this novel interaction.
 

FIBRONECTIN-TARGETING PEPTIDE PET PROBE UPTAKE DURING FIBROGENESIS CORRELATES WITH LUNG FUNCTION DECLINE DURING THE PHASE OF ESTABLISHED FIBROSIS IN THE MURINE MODEL OF THE DISEASE (Pulmonary / Critical Care)
Ksenija Bernau, PhD, University of Wisconsin-Madison

Idiopathic pulmonary fibrosis (IPF) is a devastating disease that leads to death in over 40,000 people in the U.S. each year due to relentless scar formation, lung stiffening and respiratory failure. Average survival from diagnosis is 3-5 years, with disease course varying drastically and unpredictably1, 2. A major barrier for effective clinical care of patients with this disease is the lack of non-invasive biomarkers for real-time assessment of disease activity3, 4. IPF is characterized by persistent deposition of extracellular matrix (ECM) proteins. This process is initiated in fibroblastic foci, the leading edge of new fibrosis5-7. Fibronectin is one of the most differentially upregulated ECM glycoproteins and plays a key role in fibrogenesis7. Fibronectin serves as a scaffold for deposition of other ECM and specifically localizes to fibroblastic foci, thus playing a key role during the early phases of disease progression7, 8.
 

FUNCTIONAL ROLE OF S1PR2 IN MRSA-INDUCED LUNG INJURY AND BARRIER DYSFUNCTION (Pulmonary / Critical Care)
Alison W. Ha, PhD, University of Illinois Chicago

Acute respiratory distress syndrome (ARDS) is a severe and often fatal form of respiratory failure. Sepsis is among the leading causes of ARDS, with Methicillin-resistant Staph aureus (MRSA) serving as a common pathogen that causes systemic inflammation and ARDS. The disruption of the alveolar-capillary membrane barrier is a hallmark of MRSA-induced acute lung injury (ALI) and leads to increased permeability and accumulation of fluid and proteins within the lung.  Understanding the mechanisms that preserve the alveolar-capillary membrane integrity is crucial for advancing therapeutic strategies to combat ARDS. Among key molecular players, sphingosine-1-phosphate receptors (S1PR) are recognized for their roles in modulating endothelial barrier function. While S1PR1 has been well established as barrier promoting, the role of S1PR2 in barrier regulation remains less clearly defined.
 

DOES ATORVASTATIN MITIGATE RENAL TRANSPLANT REJECTION? A DRUG REPURPOSING STUDY (Transplant Medicine)
Hunter M. Eby, university of toledo college of medicine

Renal transplant rejection occurs in approximately 20% of recipients, significantly reducing graft lifespan by up to 50%. This often necessitates re-listing patients for transplantation and returning them to dialysis. Development of medications to prevent renal rejection has been a priority in transplantation research. The most recent drug approved to combat rejection, belatacept, received FDA approval in 2011. Despite ongoing efforts, the development of new medications frequently falters during Phase 2 clinical trials (70-80%). This study seeks to overcome this challenge by leveraging an in silico approach to identify FDA-approved drugs that could be repurposed to mitigate rejection eventsvasculitis.