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  • Undergraduate Poster Abstracts
  • Medicine (E.G., Dentistry Surgery Optometry Veterinary)

    FRI-100 MATERNAL TOBACCO SMOKE EXPOSURE AFFECTS ELASTIN ISOFORM EXPRESSION IN RAT LUNGS

    • Brent Locklear ;
    • Lisa Joss-Moore ;

    FRI-100

    MATERNAL TOBACCO SMOKE EXPOSURE AFFECTS ELASTIN ISOFORM EXPRESSION IN RAT LUNGS

    Brent Locklear, Lisa Joss-Moore.

    The University of Utah, Salt Lake City, UT.

    Maternal smoking while pregnant is a significant problem. Fetal exposure to maternal tobacco smoke (MTS) alters lung function in human and animal models. We showed that MTS increases lung compliance in female, but not male, rat pups. Lung compliance depends on expression of elastin isoforms during lung development. We hypothesize that MTS exposure, sex, and lung development effect elastin isoform expression in offspring rat lungs. Pregnant rats were exposed to room air (control) or tobacco smoke (MTS) from gestational day 11 to term. Offspring were studied at term birth (d0-immature lung), and day 21 (d21-mature lung). Female and male pups were studied as separate groups (n = 6/group). Western blot was used to identify and quantify elastin isoforms. We identified full-length elastin (elastin) and a second isoform (elastinALT). Protein levels of elastin and elastinALT decreased with increasing lung development in male control rat lungs. In contrast, protein levels of elastin and elastinALT increased with increasing lung development in female control lungs. MTS decreased elastin and elastinALT levels at d0 in male rat lung compared to d0 male control. MTS increased elastinALT at d21 with no effect on elastin in female rat lungs relative to d21 female controls. MTS exposure, sex, and lung development affect elastin isoform expression in the rat lung. We speculate that increased elastinALT in d21 females contributes to the increase in compliance in the previous model.

    FRI-101 COMP-ANGIOPOIETIN 1 AS A POTENTIAL TREATMENT FOR CENTRAL RETINAL ARTERY OCCLUSION

    • Chalmer Gambler ;
    • Balamurali Ambati ;

    FRI-101

    COMP-ANGIOPOIETIN 1 AS A POTENTIAL TREATMENT FOR CENTRAL RETINAL ARTERY OCCLUSION

    Chalmer Gambler1, Balamurali Ambati2.

    1The University of Utah, Salt Lake City, UT, 2Moran Eye Center, University of Utah Hospital, Salt Lake City, UT.

    In the U. S., central retinal artery occlusion (CRAO) affects approximately 1 in 10,000 outpatients. CRAO results in permanent blindness among 65-79% of those affected. Although there are various treatments for CRAO, a combination of minimal results and negative side effects create a need for alternative therapies. Many cells within the inner retina are necessary to maintain normal vision but are damaged by CRAO due to less oxygen. However, COMP-Ang1 is a synthetic protein analog of angiopoietin 1 that may protect the retinal vasculature preventing neuronal cell loss. Our research involves experimenting with COMP-Ang1 to determine if it preserves the structure and thickness of the inner retina and rescues retinal neurons. We test the therapeutic effects of COMP-Ang1 in a mouse model of CRAO. First, CRAO is induced via laser within one eye, while the other eye serves as a control. Then, the eye with induced CRAO undergoes treatment with either COMP-Ang1 or a saline. Finally, the thickness of the CRAO treated eyes are compared to see if the group treated with COMP-Ang1 maintained retinal structure better than the group treated with saline. If the COMP-Ang1 treatment preserves structure, it suggests that it may also protect these cells from damage and lead to an effective alternative treatment for CRAO in humans to restore vision.

    THU-100 PRE-ILLNESS PULMONARY FUNCTION TESTING DOES NOT PREDICT CLINICAL OUTCOMES FROM THE ACUTE RESPIRATORY DISTRESS SYNDROME

    • Brianna Triplett ;
    • Rebecca Baron ;
    • Diana Barragan Bradford ;

    THU-100

    PRE-ILLNESS PULMONARY FUNCTION TESTING DOES NOT PREDICT CLINICAL OUTCOMES FROM THE ACUTE RESPIRATORY DISTRESS SYNDROME

    Brianna Triplett1, Rebecca Baron2, Diana Barragan Bradford2.

    1University of Alaska, Anchorage, Anchorage, AK, 2Harvard Medical School, Boston, MA.

    Acute respiratory distress syndrome (ARDS) results in respiratory failure characterized by bilateral lung infiltrates that cause hypoxemia. We looked at whether underlying lung dysfunction predicts clinical outcomes from ARDS. Patients were selected from the Brigham and Women’s Registry of Critical Illness (ROCI). All ARDS subjects were screened (as well as matched controls) for pre-existing pulmonary function tests (PFTs) obtained prior to medical intensive care unit (MICU) admission and for clinical information. This information was used to determine correlations between pre-existing pulmonary comorbidities with the success of extubation and rates of re-intubation. Of the 560 patients in the ROCI, 102 were designated as ARDS and of those, 21 subjects had pre-existing PFTs. The ARDS subjects had a forced expiratory volume in 1-second (FEV1) range of 0.68 to 3.85 L (33 to 85% of predicted), a total lung capacity (TLC) range of 1.36 to 7.13 L (27 to 135% of predicted), and a diffusing capacity (DLCO) of 0.94 to 21.76 L (4 to 68% of predicted). We similarly examined subjects without ARDS who required mechanical ventilation and identified 18 subjects who had pre-existing PFTs performed. The non-ARDS subjects had a FEV1 range of 0.48 and 3.07 L (17 to 80% of predicted), TLC range of 2.77 to 4.96 L (50 to 82% of predicted) and DLCO range of 5.19 to 15.48 (19 to 65% of predicted). There was no correlation between PFT results and mortality in both the ARDS and non-ARDS cohorts. While underlying lung disease leads one to worry about ARDS prognosis, our data does not support using pre-existing pulmonary function data to predict clinical outcomes.

    FRI-110 PROGNOSTIC IMMUNOHISTOCHEMICAL BIOMARKERS IN THE DEVELOPMENT OF ESOPHAGEAL ADENOCARCINOMA IN BARRETT ESOPHAGUS

    • Estefania Perez Luna ;
    • Grace Guzman ;

    FRI-110

    PROGNOSTIC IMMUNOHISTOCHEMICAL BIOMARKERS IN THE DEVELOPMENT OF ESOPHAGEAL ADENOCARCINOMA IN BARRETT ESOPHAGUS

    Estefania Perez Luna1, Grace Guzman2.

    1College of Medicine, University of Illinois at Chicago, Chicago, IL, 2University of Illinois at Chicago, Chicago, IL.

    Barrett esophagus (BE) is one of the major risk factors in esophageal adenocarcinoma (EAC). In 2012, there were approximately 52,000 incident cases of EAC worldwide. Endoscopic surveillance is the main method of detection of EAC. Due to the silent nature of EAC, current technology is unable to accurately detect clinical signs during early stages of the cancer. Consequently, late stage diagnosis has led to dismal outcomes for patients with EAC, with 5-year survival rates between 3.7% and 15.6%. Molecular biomarkers useful in improving sensitivity and specificity of cancer detection have become an increased area of research in an effort to improve the prognosis of patients diagnosed with EAC. Currently, no ideal biomarkers in routine clinical practice exist that show promising prognostic potential indicative of overall survival in EAC patients. Given recent findings suggesting a role of the Akt signaling pathway in esophageal carcinogenesis, the aim of this literature review is to evaluate the prognostic utility of 5 potential biomarkers involved in the Akt signaling pathway. The biomarkers reviewed include: transcription factor FoxM1, cell cycle regulator Cyclin D1, nuclear β-Catenin, mitosis marker phosphohistone-H3, and tumor suppressor regulator MDM2. Review of these biomarkers will consider their immunohistochemical ability to aid in prognosis throughout the various stages leading up to EAC in patients with BE.

    FRI-103 EFFECT OF PERIODONTITIS ON OBESITY AND PLASMINOGEN ACTIVATOR INHIBITOR 1

    • Hugo Hidrogo ;
    • Keiko Watanabe ;

    FRI-103

    EFFECT OF PERIODONTITIS ON OBESITY AND PLASMINOGEN ACTIVATOR INHIBITOR 1

    Hugo Hidrogo1, Keiko Watanabe2.

    1University of Illinois at Chicago, Chicago, IL 2University of Illinois at Chicago College of Dentistry, Chicago, IL.

    Periodontitis is a chronic inflammatory disease that breaks down the tooth-supporting tissues caused by accumulation of bacteria on the surface of the tooth and under the gingiva. The results from epidemiological studies show that periodontitis is associated with negative impacts on general health. Some studies have found obesity to be statistically correlated to periodontitis, but currently the relationship between periodontitis and adipose cells has yet to be fully elucidated. The goal of this study is to determine the effects periodontitis has on obesity, particularly the expression of plasminogen activator inhibitor 1 (PAI-1) by macrophages using chimeric mice with toll-like receptor 2 and 4 (TLR2&4) expression in the setting of periodontitis. We hypothesize that PAI-1 expression in adipose tissue is upregulated via TLR2&4 expressed by macrophages in adipose tissue in the setting of periodontitis. To demonstrate the effect periodontitis has on adipose cells, we will perform immunohistochemistry and immunofluorescence microscopy to determine the expression of PAI-1 in adipose cells as well as in embedded macrophages in TLR2&4 chimeric mice and control mice with and without periodontitis. PAI-1 is expected to be expressed only in adipose tissue from wild type (WT) and WT:dKO mice induced with periodontitis. If it is determined that periodontitis induces PAI1 production via macrophages in adipose tissue, this will be the first study to demonstrate that periodontitis can lead to obese conditions. This study further suggests that by maintaining overall good oral health we can reduce overall health complications.

    THU-107 MULTI-GENE PANEL TESTING IN BREAST, OVARIAN, AND PANCREATIC CANCER CASES: PREVALENCE AND UNINTENDED SCREENING RECOMMENDATIONS

    • Antontrey Begaye ;
    • Erin Young ;
    • Sean Tavtigian ;

    THU-107

    MULTI-GENE PANEL TESTING IN BREAST, OVARIAN, AND PANCREATIC CANCER CASES: PREVALENCE AND UNINTENDED SCREENING RECOMMENDATIONS

    Antontrey Begaye, Erin Young, Sean Tavtigian.

    The University of Utah, Salt Lake City, UT.

    Multi-gene panels are currently used to test individuals with strong family histories of cancer for pathogenic variants in cancer susceptibility genes. Identification of pathogenic variants effects the medical management of the carrier and at-risk relatives can then be tested in order to qualify for earlier or more intensive preventive measures. Our study focuses on the population of hereditary breast and ovarian cancer (HBOC) and pancreatic cancer cases. The current eligibility criteria for testing, which controls whether insurance companies will pay for the testing, are based predominantly on family history; this limits the availability of testing for the population of women with limited or unknown family histories. The goal of our study is to expand the criteria for genetic testing for incident cancer cases. We tested breast (n = 55), ovarian (n = 25), and pancreatic (n = 66) cancer cases, unselected for family history, with a custom 34-gene panel test. Our results show 14% of the breast, 32% of the ovarian, and 18% of the pancreatic cancer cases carried either a known pathogenic variant or a variant of uncertain significance (VUS) with a relatively high probability to be pathogenic. Seventy-two percent of these variants were located in genes within established medical management recommendations. The next step in this analysis is to use the Utah Population Database to explore cancer incidence in first, second, and third degree relatives of our variant-carrying incident cases. The results will inform our understanding of variant carriers’ lifetime cancer risk, which may impact eligibility criteria for testing.

    THU-102 USE OF LIPID BILAYER COATED MESOPOROUS SILICA NANOPARTICLES FOR GEMCITABINE DERIVATIVE DELIVERY TO RESTORE DRUG SENSITIVITY IN PDAC TREATMENT

    • Yanan Kang ;
    • Xiangsheng Liu ;
    • Huan Meng ;

    THU-102

    USE OF LIPID BILAYER COATED MESOPOROUS SILICA NANOPARTICLES FOR GEMCITABINE DERIVATIVE DELIVERY TO RESTORE DRUG SENSITIVITY IN PDAC TREATMENT

    Yanan Kang, Xiangsheng Liu, Huan Meng.

    University of California, Los Angeles, Los Angeles, CA.

    Pancreatic ductal adenocarcinoma (PDAC) is the 4th leading cause of cancer-related mortality in the U. S., with an overall survival of less than 1 year. This is due to a subgroup of PDAC tumors that has been shown to be intrinsically resistant to chemotherapeutic agents including the 1st line treatment, gemcitabine (GEM). This resistance is partially due to low expression of deoxy-cytidine kinase (dCK), a rate-limiting enzyme that activates gemcitabine to gemcitabine monophosphate (GMP) for cell killing. Gemcitabine is also inefficient because of the unfavorable pharmacokinetic profiles and limited tumor perfusion in vivo. In order to overcome these problems, we hypothesized that the nanoparticle-enabled delivery of gemcitabine monophosphate could be used to more efficiently treat PDAC with low dCK expression. This gemcitabine derivative requires the use of a nanocarrier, which is otherwise inefficient for cellular uptake due to the electrostatic repelling effect. Given this background, a robust nanoplatform, i.e., lipid bilayer (LB) coated mesoporous silica nanoparticle (MSNP) was used for GMP loading, which contains porous spaces for high loading capacity and is also coated with a phospholipid bilayer (LB) for reducing premature drug release. After iterative optimization by tuning drug/particle ratio, solvents, and loading time, our results showed that 110 nm GMP-laden LB-MSNP exhibited a 20% loading capacity for GMP loading without premature release. Future investigation will include comparative analysis using GMP-laden LB-MSNP versus GEM-laden particle in PDAC cells with low/high dCK expression. We expect that GMP LB-MSNP will exhibit more efficient killing effects and, thus, provide a better treatment for GEM-resistant PDAC.

    THU-101 VARIATION OF HOSPITAL AND SURGEON COST FOR ADULT SEPTOPLASTY AND TURBINATE REDUCTION

    • Trevor Champagne ;

    THU-101

    VARIATION OF HOSPITAL AND SURGEON COST FOR ADULT SEPTOPLASTY AND TURBINATE REDUCTION

    Trevor Champagne1, Jeremy Meier2.

    1 University of North Dakota, Grand Forks, ND, 2The University of Utah, Salt Lake City, UT.

    This study reviews the differences in hospital and surgeon costs associated with septoplasty and turbinate reduction in adults. An observational cohort study was performed in a multi-hospital network using a standardized activity-based accounting system to determine costs associated with septoplasty and bilateral inferior turbinate reduction from January 2012 to May 2015. Adults (aged > 18) were included in this study. The hospital cost categories analyzed included: anesthesia, operating room (OR), pharmacy, post-anesthesia care unit (PACU), same-day-surgery (SDS). There were 88 surgeons included in the study. The study cohort initially included 3,874 patients. There were 1,342 patients with no OR cost (the greatest cost component); these were excluded from the total cost calculation. The mean total cost for the 2,532 patients studied was $3,011.84 (sd $1575.10, range $545.60 to $21,201.12). OR was the greatest average cost per case ($1,465.8), followed by SDS ($459.12), and pharmacy ($139.70). There was wide variation of average cost per case per surgeon ranging from $171.71 to $8,524.97. This study demonstrates a wide variation in cost associated with the common general otolaryngology procedure of septoplasty and inferior turbinate reduction. OR, SDS, and pharmacy costs represent the largest contribution to overall cost and potential areas for further investigation for cost reduction associated with these procedures. There also is wide variation among the average cost per case for surgeons performing these procedures. Further research is needed to identify factors contributing to the large variation in operative cost for these procedures.

    FRI-102 THE EFFECT OF AN EXPERIMENTAL MODEL OF HIGH GLUCOSE PLUS INSULIN ON PTEN

    • Noemi Rivera ;
    • Rody San Marti ;

    FRI-102

    THE EFFECT OF AN EXPERIMENTAL MODEL OF HIGH GLUCOSE PLUS INSULIN ON PTEN

    Noemi Rivera, Rody San Marti.

    1Universidad Metropolitana, Trujillo Alto, PR, 2University Austral of Chile, Valdivia, CL.

    Diabetes mellitus is one of the 10 most common causes of deaths worldwide. This chronic disease afflicts more than 437 million people around the world. The World Health Organization has estimated that this situation will continue to increase. Diabetes is characterized by chronically high levels of glucose in the blood. Over time, this disease brings severe conditions such as retinopathy, neuropathy, diabetic foot, and diabetic nephropathy (DN). DN is the principal cause of renal disease. Renal complications are present in 30-40% of diabetic individuals. The final stage of DN produces an advanced renal fibrosis. Proximal tubule epithelial cells (PTEC) have a mesenchymal origin, and are able to revert to a profibrotic phenotype through epithelial-mesenchymal transdifferentiation (EMT). EMT causes an accumulation of secretion into factors attached to the extracellular matrix, which results in renal fibrosis. PTEN is a tumor suppressor that dephosphorylates proteins to modulate the cell cycle progression. In this study, we evaluated the influence of an experimental model of high glucose plus insulin on PTEN in proximal tubule epithelial cells from humans. The results show that high glucose decreases the expression of PTEN. The results also show that the presence of insulin in HK-2 cells makes PTEN decrease, while with high glucose plus insulin PTEN expression is not altered.