A5103146350- Sphingolipid Metabolism and Signaling
- Antiplatelet Therapy and Cardiovascular Diseases
- Platelet Disorders and Treatments
- Venous Thromboembolism Diagnosis and Management
- Lipid metabolism and biosynthesis
- Cell Adhesion Molecules Research
- Endoplasmic Reticulum Stress and Disease
- Acute Myocardial Infarction Research
- Atrial Fibrillation Management and Outcomes
- Cardiac Fibrosis and Remodeling
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Blood Coagulation and Thrombosis Mechanisms
- ATP Synthase and ATPases Research
- Atherosclerosis and Cardiovascular Diseases
- Inflammasome and immune disorders
- Lipid metabolism and disorders
- Peroxisome Proliferator-Activated Receptors
- Lipid Membrane Structure and Behavior
- Protease and Inhibitor Mechanisms
- Mechanical Circulatory Support Devices
- Erythrocyte Function and Pathophysiology
- Acute Ischemic Stroke Management
- Coronary Interventions and Diagnostics
- Cardiac Structural Anomalies and Repair
- Heparin-Induced Thrombocytopenia and Thrombosis
University of Kentucky
2013-2022
Lexington VA Health Care System
2012-2022
University of Arkansas for Medical Sciences
2022
Central Arkansas Veterans Healthcare System
2022
Great Ormond Street Hospital
2021
University College London
2021
Veterans Health Administration
2012-2020
University of Kentucky HealthCare
2019
University of Cincinnati Medical Center
2018
Rochester General Hospital
2018
Digoxin is frequently used for rate control of atrial fibrillation (AF). It has, however, been associated with increased mortality. remains unclear whether digoxin itself responsible the mortality (toxic drug effect) or it prescribed to sicker patients inherently higher due comorbidities. The goal our study was determine relationship between and in AF. association assessed enrolled AF Follow-Up Investigation Rhythm Management (AFFIRM) trial using multivariate Cox proportional hazards models....
Myocardial infarction (MI) triggers myelopoiesis, resulting in heightened production of neutrophils. However, the mechanisms that sustain their and recruitment to injured heart are unclear. Using a mouse model permanent ligation left anterior descending artery flow cytometry, we first characterized temporal spatial effects MI on different myeloid cell types. We next performed global transcriptome analysis cardiac types within infarct identify drivers acute inflammatory response underlying...
Autotaxin (ATX) is a secreted nucleotide pyrophosphatase/phosphodiesterase that functions as lysophospholipase D to produce the lipid mediator lysophosphatidic acid (LPA), mitogen, chemoattractant, and survival factor for many cell types. The ATX-LPA signaling axis has been implicated in angiogenesis, chronic inflammation, fibrotic diseases tumor progression, making this system an attractive target therapy. However, potent selective nonlipid inhibitors of ATX are currently not available. By...
The lipid mediator lysophosphatidic acid (LPA) is a potent regulator of vascular cell function in vitro, but its physiologic role the cardiovasculature largely unexplored. To address LPA regulating platelet and thrombosis, we investigated effects on isolated murine platelets. Although activates platelets from majority human donors, found that treatment with concentrations attenuated agonist-induced aggregation. Transgenic overexpression autotaxin/lysophospholipase D (Enpp2), enzyme necessary...
Rationale: Bioactive lipid mediators, derived from membrane precursors, are released into the airway and airspace where they bind high-affinity cognate receptors may mediate asthma pathogenesis. Lysophosphatidic acid (LPA), a bioactive mediator generated by enzymatic activity of extracellular autotaxin (ATX), binds LPA receptors, resulting in an array biological actions on cell proliferation, migration, survival, differentiation, motility, therefore could pathogenesis.Objectives: To define...
Despite treatment advances for sepsis and pneumonia, significant improvements in outcome have not been realized. Antiplatelet therapy may improve pneumonia sepsis. In this study, the authors show that ticagrelor reduced leukocytes with attached platelets as well inflammatory biomarker interleukin (IL)-6. Pneumonia patients receiving required less supplemental oxygen lung function tests trended toward improvement. Disruption of P2Y12 receptor a murine model protected against response,...
Background —Intimal hyperplasia contributes to restenosis after percutaneous vascular interventions. Both β 3 -integrins, α V and IIb (glycoprotein IIb/IIIa), leukocytes have been implicated in neointimal formation, based part on the results obtained using antagonists 1 or both receptors animal models. Methods Results —The responses wild-type mice, -integrin–deficient P-selectin–deficient mice were studied a model of transluminal endothelial injury femoral artery. At 4 weeks, not protected...
Ex vivo data suggest that a pharmacokinetic interaction may exist between proton pump inhibitors (PPIs) and clopidogrel, decreasing the antiplatelet effect of latter. We assessed baseline PPI use would increase 28-day 1-year composite endpoints in patients undergoing, or at high likelihood PCI randomized to loading dose clopidogrel versus just 4 weeks addition daily aspirin, CREDO trial. Twenty-eight day (Death/MI/UTVR) (Death/MI/Stroke) primary were analyzed based on study entry. For each...
Left ventricular hypertrophy (LVH), a risk factor for cardiovascular morbidity and mortality, is commonly caused by essential hypertension. Three geometric patterns of LVH can be induced hypertension: concentric remodeling, hypertrophy, eccentric hypertrophy. Clinical studies suggest that different underlying etiologies, genetic modifiers, mortality are associated with patterns. Since pressure overload-induced modeled experimentally using transverse aortic constriction (TAC) since C57BL/6J...