2017 Cardiovascular Research Day Abstract Book

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3 Improving Patient Care on Left Ventricular Assist Device Support: Novel Outcome Predictors & Preventative Therapies Tara Shrout 1 • Travis Sexton, PhD 2 • Susan Smyth, MD, PhD 3 1College of Medicine, University of Kentucky • 2 Saha Cardiovascular Research Center, University of Kentucky • 3 Chief, Division of Cardiovascular Medicine, University of Kentucky Medical Student Background: Left ventricular assist device (LVAD) implantation is an increasingly common and important intervention for heart failure. Despite advancements, implantation introduces a foreign body across which blood experiences aberrant sheer stress. Clinical complications of bleeding and stroke develop secondary to an acquired coagulopathy, and patients’ quality of life is an important outcome to consider. This study uniquely correlates early platelet function and biomarkers alterations with clinical outcomes, as well as patient quality of life measures to help predict, address, and explore complications with LVAD support. Objectives: 1. Evaluate correlations between predictive measures of platelet function, biomarkers, laboratory trends with clinical complications outcomes and LVAD types. 2. Characterize the role of a novel hemostatic agent as a preventative therapy for bleeding. 3. Understand patients’ quality of life on LVAD support. Design: March 2014-August 2016, 68 enrolled patients underwent implantation of Heartmate II (n= 48), Heartmate III (n=2), Heartware (n=18). Blood collections: 24-hours preoperatively and 1-, 24-, 72-, and 168-hours postoperatively. Follow-up collections: between 30-90-days postoperatively. Platelet function analyzed via impedance aggregometry, five agonists, and novel hemostatic agent. Biomarkers of coagulation, platelet activation, and inflammation analyzed. Daily clinical data collected. Participants: Consecutive-based sample. Sociodemographics: age, gender, ethnicity, co-existing conditions collected. Eligibility: First-time LVAD implant. Exclusion: Age
4 Identification of a Lipid Signature in Clear Cell Renal Carcinoma (ccRCC) Suggest a Role of Phosphatidylinositol Remodeling in Disease Progression Chase Neumann 1 • Renliang Zhang, PhD 1 • Christopher Przybicin, MD 2 • Brian Rini, MD 3 • Mark Brown, PhD 1 1Cellular and Molecular Medicine, Cleveland Clinic • 2 Robert J. Tomsich Pathology and Laboratory Medicine, Cleveland Clinic • 3 Hematology and Oncology Taussig Cancer Institute, Cleveland Clinic Graduate Student The most lethal urological cancer and third most common urological cancer in the United States is clear cell renal carcinoma (ccRCC). Approximately 64,000 individuals in the United States are diagnosed with ccRCC annually, and more than 140,000 individuals die worldwide of ccRCC every year. The “clear cell” characteristic of this deadly kidney cancer is due to abnormal deposition of lipids in a large unilocular lipid droplet in cancer cells, and urinary biomarker studies have identified lipid droplet-associated proteins as predictive markers of disease progression. However, the mechanisms by which lipid metabolism impacts ccRCC progression are not well understood. We hypothesized that a group of mitogenic lipids exist within the ccRCC microenvironment that promote proliferation and metastatic potential. A high throughput Triple Time-of-Flight (TOF) LC- MS/MS lipidomics screen of metastatic ccRCC tumor samples and matched non-tumor adjacent tissue identifies a highly reproducible lipid signature of ccRCC. In agreement with previous reports, cholesteryl esters are increased in the tumor vs non-tumor. We also found a striking increase in phosphatidylinositol (PI) 36:4 and 34:1 in tumors. Membrane bound O-acyltransferase domain containing 7 (MBOAT7) is a lysophosphatidylinositol (LPI) acyltransferase that preferentially utilizes arachidonyl-CoA and 16:0 LPI as substrates. To further investigate the formation of 36:4 PI, an MBOAT7 product, we used TCGA datasets to analyze stage-specific expression of MBOAT7. MBOAT7 expression was found to increase with staging. This potential increase in phosphatidylinositol production, coupled with decreases in known phosphatase activity like PTEN, SACM1L, and MTM1 may lead to increased activation of the PI3K/Akt signaling activity. The impact of this work may suggest mechanisms why some patients are refractory to PI3K/mTOR inhibitors, while a small percentage (
Page 1 and 2: Cardiovascular Research Day ABSTRAC
Page 3 and 4: SCHEDULE FOR THE DAY Friday, Novemb
Page 5 and 6: SCHEDULE FOR THE DAY continued Frid
Page 7 and 8: 2017 GILL HEART INSTITUTE YOUNG INV
Page 9 and 10: FEATURED SPEAKER Calum MacRae, M.D.
Page 11 and 12: SPECIAL PRESENTATION Mark Stoops He
Page 13 and 14: NOTES 12
Page 15 and 16: 2017 POSTER PARTICIPANTS 40 Mohamed
Page 17 and 18: 2017 ABSTRACTS 16
Page 19: 2 Inhibition of Megalin Reduces Ath
Page 23 and 24: 6 Serum Amyloid A Activates the NLR
Page 25 and 26: 8 Azithromycin Therapy Reduces Card
Page 27 and 28: 10 Evidence of Angiotensin II-depen
Page 29 and 30: 12 Auditory Entrainment of Respirat
Page 31 and 32: 14 Cardiac specific Rad knockout In
Page 33 and 34: 16 Hypercholesterolemia Induces Acu
Page 35 and 36: 18 A Novel Approach for Modifying I
Page 37 and 38: 20 Clinical Use of the Amplatzer Se
Page 39 and 40: 22 Regulation of Akt Signaling by N
Page 41 and 42: 24 Vascular Inflammatory Regulation
Page 43 and 44: 26 Vascular inflammation induced ex
Page 45 and 46: 28 Sexual Dimorphism of Angiotensin
Page 47 and 48: 30 Computational modeling of amylin
Page 49 and 50: 32 PCB 126 Exposure Increases Perip
Page 51 and 52: 34 Endothelial Mineralocorticoid Re
Page 53 and 54: 36 Optimization of immunomagnetic s
Page 55 and 56: 38 Gestational Diabetes Provokes Po
Page 57 and 58: 40 The Prognostic Role of Elevated
Page 59 and 60: 42 Lysophosphatidic Acid Receptor 4
Page 61 and 62: 44 Recapitulating In Vivo Fibroblas
Page 63 and 64: 46 Sex-Specific Differences in Card
Page 65 and 66: 48 Ticagrelor Reduces Inflammation
Page 67 and 68: 50 Association between Plasma Chole
Page 69 and 70: 52 Does Light Pollution Affect the
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54 Impact of miR-33 antagonism on m
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56 Isolation and characterization o
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58 The XY sex chromosome complement
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60 CHROME: a Long Non-coding RNA th
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62 Making Good: Secretory Quality C
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64 Thrombospondin 1 (TSP1) Deficien
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66 Serum Amyloid A3 is a High Densi
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68 Adipocyte deficiency of ACE2 inc
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70 Hypercholesterolemia-induced end
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72 Increased Circulating Trimethyla
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74 Circulating Bacterial Small RNA
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76 Pancreatic Beta Cell Export of m
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78 Understanding inhibition of lipo
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80 Insulin signaling regulates apol
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82 Protease-activated Receptor 2 De
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84 Reduced Low-Density Lipoprotein
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86 Pharmacological inhibition of Hu
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88 The Effects of Hypercholesterole
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90 Reduced HDL in mice overexpressi
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92 Human Antigen R (HuR) Regulates
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94 Impact of miR-33 antagonism on c
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96 HB-EGF is a Key Positive Regulat
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98 HDL-miR-223 Communication Pathwa
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100 Short-Term Exercise Training Di
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102 The Ral-Exocyst Pathway Regulat
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NOTES 120
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2017 Cardiovascular Research Day Abstract Book

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