tbuckley/cabot-search huggingface dataset:
Abstract 536: Increased O-linked Glycosylation in Diabetic Myocardium of Mice and Human
Authors: Vahid Agbortoko, Yuhong Liu, Guangbin Shi, Anny Usheva, Arun K Singh, Frank W Sellke, Jun Feng
Journal: Circulation Research (2018)

Objectives: The modification of serine and threonine residues of nuclear and cytoplasmic proteins by O-linked β-N-acetylglucosamine (O-GlcNAc) has emerged as a highly dynamic post-translational modification that plays a critical role in regulating numerous biological processes. Our focus was to establish the difference of O-linked glycosylation in diabetic (DM) and Non-diabetic (ND) heart of mouse and human in the presence or absence of cardioplegic ischemia and cardiopulmonary bypass (CP/CPB). Methods and results: Right atrial tissue was harvested pre- and post-CP/CPB from the ND patients and patients with type-2 DM undergoing cardiac surgery (n = 4/group).The post-CP/CPB tissue samples were from a atrial tissue segment exposed to cold, hyperkalemic blood cardioplegia (ischemia) and a brief period (10 minutes) of reperfusion. Ventricular tissue samples were also obtained from mice with and without type-2 DM (n =3/group). Thin Layer Chromatography (TLC) was used to measure the contents of acetyl coenzyme A (acetyl-CoA) in the tissue lysates of mouse and human myocardium. Western blotting and immunohistochemistry analysis were employed to determine the expression/localization of O-Linked β-N-acetylglucosamine (O-GlcNAc) in the tissue lysates and paraffin-embedded tissue sections. Diabetes tends to increase the amounts of acetyl-CoA and O-GlcNAc (20% increase vs. ND, P&lt;0.05) in the myocardium compared with ND. Post-CP/CPB further induced more acetyl-CoA and this effect was more pronounced in the diabetic atrial myocardium than that of ND. Immunofluorescence experiments with O-GlcNAc-specific antibody and paraffin-embedded tissue sections from human atria and mouse heart show a significant number of cells stain positively with the antibody in the diabetes sections (3 folds increases in optical density vs. ND, P &lt;0.01). The protein oxidation and ratio of NADH/NAD in the DM myocardium were significantly increased compared with ND (P&lt;0.05). Conclusion: Diabetes and cardioplegic ischemia are associated with an increase in O-linked glycosylation in the mouse and human myocardium, suggesting that diabetes and cardioplegic ischemia affect myocardial metabolism via hexosamine biosynthetic pathway.
RECURRENT GENOMIC COPY NUMBER VARIANTS IMPLICATE NEW CANDIDATE GENES FOR EARLY ONSET BICUSPID AORTIC VALVE DISEASE
Authors: Siddharth K. Prakash, Angela Yetman, Malenka M. Bissell, Yuli Y. Kim, Hector Michelena, Dawn S. Hui, Anthony Caffarelli, Maria G. Andreassi, Ilenia Foffa, Jacqueline Jennings, Rodolfo Citro, Dongchuan Guo, Margot De Marco, Justin T. Tretter, Simon C. Body
Journal: Journal of the American College of Cardiology (2019)
Direct reprogramming to human nephron progenitor-like cells using inducible piggyBac transposon expression of SNAI2-EYA1-SIX1
Authors: Jessica M. Vanslambrouck, Lauren E. Woodard, Norseha Suhaimi, Felisha M. Williams, Sara E. Howden, Sean B. Wilson, Andrew Lonsdale, Pei X. Er, Joan Li, Jovana Maksimovic, Alicia Oshlack, Matthew H. Wilson, Melissa H. Little
Journal: Kidney International (2019)
Empagliflozin Is Associated With a Lower Risk of Post-Acute Heart Failure Rehospitalization and Mortality
Authors: Gianluigi Savarese, Naveed Sattar, James Januzzi, Subodh Verma, Lars H. Lund, David Fitchett, Cordula Zeller, Jyothis T. George, Martina Brueckmann, Anne Pernille Ofstad, Silvio E. Inzucchi, Christoph Wanner, Bernard Zinman, Javed Butler
Journal: Circulation (2019)
Abstract 493: Serum Leptin and TNFa Levels in Relation to Systolic and Diastolic Heart Function in Obese and Normal-overweight Pregnant. First Trimester Data
Authors: Katherine Shreyder, Maira Carrillo, James Maher, Natalia Schlabritz-Lutsevich
Journal: Circulation Research (2018)

Introduction: Maternal obesity (MO) defined as pre-pregnancy body-mass index (BMI) &gt;30kg/m2, is the strongest risk factors for preeclampsia (PE). Information regarding cardiac changes in MO as well as the role of inflammatory biomarkers in PE pathogenesis is conflicting. The aim of this study was to evaluate echocardiography changes in normal/ overweight pregnant (NP) (BMI 18.0-30) and obese pregnant women (OP) (BMI&gt;30) and to correlate them to dynamics of biomarkers (leptin, TNFa, BNP, pentraxin-3, IL6) and mRNA. Material and methods: There were 11 OP (BMI 33.6±2.9) and 13 NP (BMI 25.5±2.3) enrolled into this study in the first trimester of pregnancy. All patients were nulliparous. There were no differences between OP and NP according to age and number of previous pregnancies. Patients with pre-pregnancy cardiovascular pathology were excluded. The 2D echocardiography with Doppler was performed in each pregnancy trimester. Echocardiography results, leptin and TNFa in the first trimester are available for now. Results: Left ventricular (LV) mass was significantly higher while ejection fraction (EF) and ratio of the early (E) to late (A) ventricular filling velocities (E/A ratio) appeared to be lower in OP, compared to NP (Table). Leptin was higher in OP. TNFa inversely correlated with stroke volume (SV), MO positively associated with leptin levels and negatively with E/A ratio (p&lt;0.05). Conclusion: Differences in systolic and diastolic heart function between OP and NW are being evident already in the first trimester. Involvement of leptin and TNFa; might be suggested. Identifying biochemical mechanisms driving cardiac changes in MO are crucial for PE prevention.
LONG-TERM SAFETY OF TICAGRELOR MONOTHERAPY IN PATIENTS UNDERGOING PCI FOR STABLE CORONARY ARTERY DISEASE IN THE GLOBAL LEADERS STUDY: IMPACT OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Authors: Mariusz Tomaniak, Ply Chichareon, Kuniaki Takahashi, Norihiro Kogame, Rodrigo Modolo, Chun Chin Chang, Yuki Katagiri, Ernest Spitzer Cano, Franz-Joseph Neumann, Sylvain Plante, Rosana Hernandez Antolin, Valeri Gelev, Philippe Brunel, Farzin Beygui, Krzysztof Filipiak, Robert van Geuns, Christian Hamm, Robert Storey, Osama Soliman, Yoshinobu Onuma, Pascal Vranckx, Stephan Windecker, Marco Valgimigli, Patrick Serruys
Journal: Journal of the American College of Cardiology (2019)
Abstract 119: Aberrant Caesin Kinase 2 Signalling Predisposes the Heart to an Apoptotic Phenotype in Type 2 Diabetes
Authors: Lauren E Smith, Desmond K Li, Stuart J Cordwell, Melanie Y White
Journal: Circulation Research (2018)

The clinical effects of myocardial ischemia/reperfusion injury (I/R) are typically significantly more adverse in patients with Type 2 Diabetes Mellitus (T2DM). We hypothesize that in T2DM hearts there are underlying molecular adaptations that, even in the absence of reduced functional output, can impact recovery if exposed to I/R. Given the likely rapid molecular response to I/R, we examined how T2DM alters basal myocardial protein phosphorylation to identify pathways associated with such adaptation. We employed a rat model that combined peripheral insulin resistance from energetic overload (high fat diet) and pancreatic insufficiency (streptozotocin), producing elevated blood glucose, serum triglycerides and reduced insulin sensitivity, consistent with a T2DM phenotype. Hearts were subjected to 60 mins ex vivo perfusion followed by protein extraction, trypsin digest, phosphopeptide enrichment and quantitative mass spectrometry. We identified abundance changes in &gt;5400 phosphopeptides despite no evidence of functional perturbation in LV pressure or heart rate between control and T2DM hearts. Differentially abundant phosphosites were mapped to signal pathways. This showed Akt contributed to 36% of pathways with reduced phosphorylation in T2DM hearts. Reduced phosphorylation of Akt at S124/S129 was consistent with the global pathway data (log2 ratio: -1.10). Given that S129 is a casein kinase 2 (CK2) target, we next examined CK2 and CK2 signaling. We observed significantly reduced CK2 abundance (CK2α: 0.41±0.08 and CK2β: 0.54±0.09; n -fold±SEM) and reduced phosphorylation of CK2 targets (CK2 substrate pS/pT-D/E: 0.84±0.01; n -fold±SEM) by Western blot. This was further confirmed by the over-representation of CK2 target sequences (pS/pT-D/E) in the negatively regulated phosphopeptide set (D, 10.45-fold; E 6.82-fold). Reduced phosphorylation at CK2 regulated sites on catenin β1, caspase 9 and eukaryotic translation initiation factor 3, suggests T2DM elicits a pro-apoptotic environment. Increased cleavage of caspases 3 and 9 (2.15±0.28 and 1.32±0.08; n fold±SEM, respectively) confirmed these data. In summary, changes in CK2 signaling may ‘prime’ a pro-apoptotic environment in T2DM hearts that subsequently limits recovery in I/R.
Functional and Genomic Characterization of the Interaction between Acute Lymphoblastic Leukemia Cells and the Microenvironment Identifies Pathways for Therapeutic Intervention
Authors: Hiroki Yoshihara, Michelle L. Churchman, Jennifer L. Peters, David B. Finkelstein, Elisabeth M. Paietta, Mark R. Litzow, Charles G. Mullighan
Journal: Blood (2018)
HIGH-INTENSITY SIGNALS IN CORONARY PLAQUES ON T1-WEIGHTED MAGNETIC RESONANCE IMAGING CORRESPONDING TO INTRAPLAQUE HEMORRHAGE IN ATHEROSCLEROSIS ON HISTOPATHOLOGY OF DIRECTIONAL CORONARY ATHERECTOMY SPECIMENS
Authors: Kenzo Uzu, Rika Kawakami, Takahiro Sawada, Tomofumi Takaya, Yasuyo Taniguchi, Seiichi Hirota, Kenichi Fujii, Yoshinori Yasaka
Journal: Journal of the American College of Cardiology (2019)
PHASE ANALYSIS USING LOW DOSE 99M TC GATED-SPECT DETECTS SIGNIFICANT LATE GADOLINIUM ENHANCEMENT IN PATIENTS WITH NON-ISCHEMIC DILATED CARDIOMYOPATHY
Authors: Sakura Nagumo, Yasuyuki Suzuki, Naoya Matsumoto, Yasuo Okumura
Journal: Journal of the American College of Cardiology (2019)
Sex-Based Differences in Outcomes After Mitral Valve Surgery for Severe Ischemic Mitral Regurgitation
Authors: Gennaro Giustino, Jessica Overbey, Doris Taylor, Gorav Ailawadi, Katherine Kirkwood, Joseph DeRose, Marc A. Gillinov, François Dagenais, Mary-Lou Mayer, Alan Moskowitz, Emilia Bagiella, Marissa Miller, Paul Grayburn, Peter K. Smith, Annetine Gelijns, Patrick O'Gara, Michael Acker, Anuradha Lala, Judy Hung
Journal: JACC Heart Failure (2019)
PLATELET ACTIVITY IS ASSOCIATED WITH INCIDENCE OF MAJOR BLEEDING IN PERIPHERAL ARTERY DISEASE PATIENTS UNDERGOING LOWER EXTREMITY REVASCULARIZATION
Authors: Gustavo Hernandez, Nathaniel Smilowitz, Crystalann Rodriguez, Angela Lee, Elliot Luttrell-Williams, Michael Nardi, Yajaria Suarez, Judith Hochman, Caron Rockman, Jeffrey Berger
Journal: Journal of the American College of Cardiology (2019)
INITIAL POST-RESUSCITATION PH AS A PREDICTOR OF NEUROLOGIC OUTCOME FOLLOWING OUT-OF-HOSPITAL CARDIAC ARREST: A PROPENSITY-ADJUSTED ANALYSIS
Authors: Erich L. Kiehl, Ram Amuthan, Kyle B. Enfield, Lawrence Gimple, Daniel Cantillon, Venu Menon
Journal: Journal of the American College of Cardiology (2019)
ARE US HOSPITALS GAMING THE HOSPITAL READMISSIONS REDUCTION PROGRAM? AN EVALUATION OF 30-DAY READMISSIONS AND MORTALITY FOR TARGET CARDIOVASCULAR CONDITIONS USING A REGRESSION-DISCONTINUITY FRAMEWORK
Authors: Rohan Khera, Yongfei Wang, Khurram Nasir, Zhenqiu Lin, Harlan M. Krumholz
Journal: Journal of the American College of Cardiology (2019)
Abstract 17876: BNP Ratio Can Predict Early Rehospitalization in Patients With Heart Failure
Authors: Hiroyuki Onishi, Ryu Shutta, Akihiro Tanaka, Naoki Mori, Takahiro Yoshimura, Daisuke Nakamura, Masayuki Taniike, Nobuhiko Makino, Yasuyuki Egami, Masami Nishino, Jun Tanouchi
Journal: Circulation (2013)

Background: It has been reported that B-type natriuretic peptide (BNP) guided heart failure therapy is effective in clinical practice. However, BNP level is affected by the underlying cardiac disea...
THE IMPACT OF TRANSCATHETER AORTIC VALVE IMPLANTATION ON LEFT VENTRICULAR REMODELING AT ONE YEAR POST INTERVENTION
Authors: Abdalla Hassan, Ashraf Abugroun, Cecilia Wong, Anouch Matevossian, David Kearney, Gerard Aurigemma, Nikolaos Kakouros
Journal: Journal of the American College of Cardiology (2019)
CONSEQUENT USE OF AVAILABLE ORAL LIPID LOWERING AGENTS WOULD BRING THE MAJORITY OF HIGH-RISK PATIENTS WITH CHD TO RECOMMENDED TARGETS: AN ESTIMATE BASED ON THE DYSIS II STUDY POPULATION
Authors: Anselm K. Gitt, Gaetano De Ferrari, Dominik Lautsch, Martin Horack, Carl Baxter, Philippe Brudi, Jean Ferrières
Journal: Journal of the American College of Cardiology (2019)
A novel lncRNA MCM3AP-AS1 promotes the growth of hepatocellular carcinoma by targeting miR-194-5p/FOXA1 axis
Authors: Yufeng Wang, Liu Yang, Tianxiang Chen, Xin Liu, Yang Guo, Qiaojuan Zhu, Xiangmin Tong, Wei Yang, Qiuran Xu, Dongsheng Huang, Kangsheng Tu
Journal: Molecular Cancer (2019)

Hepatocellular carcinoma (HCC) is the most common malignant liver tumor with poor clinical outcomes. Increasing amount of long non-coding RNAs (lncRNAs) have been revealed to be implicated in the carcinogenesis and progression of HCC. However, the expressions, clinical significances, and roles of most lncRNAs in HCC are still unknown. The expression of lncRNA MCM3AP antisense RNA 1 (MCM3AP-AS1) in HCC tissues and cell lines was detected by qRT-PCR and fluorescence in situ hybridization. Immunoblotting, CCK-8, EdU, colony formation and flow cytometry were performed to investigate the role of MCM3AP-AS1 in HCC cell proliferation, cell cycle and apoptosis in vitro. A subcutaneous tumor mouse model was constructed to analyze in vivo growth of HCC cells after MCM3AP-AS1 knockdown. The interactions among MCM3AP-AS1, miR-194-5p and FOXA1 were measured by RNA pull-down, RNA immunoprecipitation and luciferase reporter assay. We revealed a novel oncogenic lncRNA MCM3AP-AS1, which is overexpressed in HCC and positively correlated with large tumor size, high tumor grade, advanced tumor stage and poor prognosis of HCC patients. MCM3AP-AS1 knockdown suppressed HCC cell proliferation, colony formation and cell cycle progression, and induced apoptosis in vitro, and depletion of MCM3AP-AS1 inhibited tumor growth of HCC in vivo. Mechanistically, MCM3AP-AS1 directly bound to miR-194-5p and acted as competing endogenous RNA (ceRNA), and subsequently facilitated miR-194-5p's target gene forkhead box A1 (FOXA1) expression in HCC cells. Interestingly, FOXA1 restoration rescued MCM3AP-AS1 knockdown induced proliferation inhibition, G1 arrest and apoptosis of HCC cells. Our results recognized MCM3AP-AS1 as a novel oncogenic lncRNA, which indicated poor clinical outcomes in patients with HCC. MCM3AP-AS1 exerted an oncogenic role in HCC via targeting miR-194-5p and subsequently promoted FOXA1 expression. Our findings suggested that MCM3AP-AS1 could be a potential prognostic biomarker and therapeutic target for HCC.
Ibrutinib therapy downregulates AID enzyme and proliferative fractions in chronic lymphocytic leukemia
Authors: Pablo Elías Morande, Mariela Sivina, Angimar Uriepero, Noé Seija, Catalina Berca, Pablo Fresia, Ana Inés Landoni, Javier M. Di Noia, Jan A. Burger, Pablo Oppezzo
Journal: Blood (2019)
A LIFE SUPPORT-BASED COMPREHENSIVE TREATMENT REGIMEN DRAMATICALLY LOWERS THE IN-HOSPITAL MORTALITY OF PATIENTS WITH FULMINANT MYOCARDITIS: A MULTIPLE CENTER STUDY
Authors: Chen Chen, Sheng Li, Chenze Li, Xiao Ran, Guanglin Cui, Kun Miao, Chunxia Zhao, Yan Wang, Jiangang Jiang, Dao Wen Wang
Journal: Journal of the American College of Cardiology (2019)
DRUG RELATED PLATELET INHIBITION: IS THERE A ROLE FOR REDUCTION OF CEREBRAL MICROEMBOLI IN TRANSCATHETER AORTIC VALVE IMPLANTATION PATIENTS?
Authors: Charalampos Kalantzis, Michael Vavuranakis, Vassilis Voudris, Elias Kosmas, Konstantinos Toutouzas, Ioannis Iakovou, George Latsios, Konstantinos Kalogeras, Evangelia Bei, Carmen Maria Moldovan, Maria Kariori, Ourania Katsarou, Angelos-Michail Kolokathis, Dimitrios Vrachatis, Efstratios Katsianos, Gerasimos Siasos, Dimitris Tousoulis, Manolis Vavuranakis
Journal: Journal of the American College of Cardiology (2019)
Abstract 451: Impact of Resistant Starch Diet on Atherosclerosis in the Presence of Chronic Kidney Disease
Authors: Oleg Karaduta, Boris Zybaylov
Journal: Circulation Research (2018)

Chronic kidney disease (CKD) affects approximately 10% (1 of 10) of the worldwide population and is associated with a significantly increased risk of developing cardiovascular disease (CVD) due to the acceleration of atherosclerosis. In particular, a high incidence of atherosclerosis occurs in chronic renal failure patients with uremia, but the pathogenesis of the events that contribute to uremic atherosclerosis is poorly understood. Inflammation, vascular stiffness likely resulting from endothelial dysfunction, and accelerated atherosclerosis are considered prominent factors contributing to the high rates of CVD in CKD. Our lab aims to demonstrate structural and functional protection against atherosclerosis by resistant starch diet, will provide a rationale to evaluate its use in CKD patients. At the moment, our preliminary result shows significant increase in the bacteroidetes-to-firmicutes ratio. In addition, we observed an increase in the Ruminoccoccus genus upon RS supplementation. Next, we applied our metaproteomics analysis pipe-line to assess proteome changes between the four groups - healthy, healthy+RS, CKD, and CKD+RS. Our data shows that RS diet stimulates bacterial mass biosynthesis (characterized by highly abundant transcription/translation-related proteins) and increases bacterial proteins that may participate in host urea cycle. An understanding of the link between microbiota and development of atherosclerosis in presence of end stage renal failure is of considerable clinical relevance. Our further plans include implementing deeper statistical analysis to establish strong correlations between those changes and CKD/CVD outcome, as well as identifying a target agent for CVD treatment. In summary, our methodology results in data on both host and bacterial proteins and yields both peptide-level and protein-level information. Our studies provide a foundation for identification of peptide-level, protein-level, and organism-level biomarkers of advanced kidney disease and suggest novel therapeutic targets. There is significant potential for drugging the microbiome with dietary recommendations.
Abstract 489: Ex vivo Porcine Coronary Artery Remodeling With Seeded Endothelial Cells
Authors: Mehmet H Kural, Guangxin Li, Juan Wang, Guohao Dai, Laura E Niklason, Liqiong Gui
Journal: Circulation Research (2018)

Coronary heart disease is the most common cardiovascular problem that causes 370,000 deaths in America annually. Replacing the diseased coronary artery with a conduit obtained from another part of the patients’ body is the gold standard for the current surgical interventions. The great saphenous veins are widely preferred as coronary bypass grafts since they are easy to harvest and can replace multiple arteries due to their abundance. However, the endothelial cells in saphenous vein lose their venous characteristics and cannot function properly, which causes frequent graft failure. Conversely, arterial grafts have higher patency rate due to better function of endothelium. Yet, arterial grafts are not abundantly available as saphenous veins. Tissue engineered blood vessels can potentially serve as an ample source for bypass conduits. However, small-diameter engineered vessels are also tending to fail without a healthy endothelium. Here we propose to investigate the potential of Sox17-overexpressing endothelial cells in the vessel lumens to prevent intimal hyperplasia. Sox17 expression leads to upregulation of arterial, anti-thrombotic and anti-inflammatory markers in endothelial cells. We used an ex-vivo porcine coronary artery model where we cultured the vessels in perfusion bioreactors to mimic arterial flow conditions. Our preliminary results show that the vessel wall injury, seeded endothelial cells and arterial shear acted synergistically on smooth muscle cell death in the media layer (Fig. 1). The present ex vivo vessel culture platform is a promising tool to study remodeling by isolating factors like endothelial cells, soluble and mechanical factors.
Siglec-15 as an immune suppressor and potential target for normalization cancer immunotherapy
Authors: Jun Wang, Jingwei Sun, Linda N. Liu, Dallas B. Flies, Xinxin Nie, Maria Toki, Jianping Zhang, Chang Song, Melissa Zarr, Xu Zhou, Xue Han, Kristina A. Archer, Thomas O’Neill, Roy S. Herbst, Agedi N. Boto, Miguel F. Sanmamed, Solomon Langermann, David L. Rimm, Lieping Chen
Journal: Nature Medicine (2019)
COLD PRESSOR TESTING AND SYMPATHETIC NERVOUS SYSTEM CONTRIBUTION TO ISCHEMIA WITH NO OBSTRUCTIVE CORONARY ARTERY DISEASE: RESULTS FROM THE WOMEN'S ISCHEMIA SYNDROME EVALUATION-CORONARY VASCULAR DYSFUNCTION PROJECT
Authors: Janet Wei, Puja Mehta, Sawan Jalnapurkar, Parham Zarrini, Ahmed AlBadri, Galen Cook-Wiens, Daniel Berman, Louise Thomson, Balaji Tamarappoo, Behzad Sharif, John Petersen, R. David Anderson, Carl J. Pepine, C. Noel Bairey Merz
Journal: Journal of the American College of Cardiology (2019)
Abstract P381: Recruiting Young Adults Into Obesity Trials: Lessons From The Early Trials
Authors: Leslie Lytle, Catherine Loria, Laura Svetsky, John Jakicic, Karen Johnson, Christine Olson, Kevin Patrick, Rena Wing, Debra Tate, Diana Fernandez
Journal: Circulation (2012)

Early adulthood is a time of weight gain yet there is a paucity of evidence about how best to prevent weight gain or promote weight loss in this age group. Data from the Coronary Artery Risk Development in Young Adults (CARDIA) study show that young adults (18-40y) gain an average of 1-2 pounds per year with the largest weight gain (about 3 pounds a year) during the ages of 20-29. Excess weight gain in early adulthood is associated with later adverse levels of cardiovascular risk factors such as hypertension, dyslipidemia, and diabetes. To address this issue, in 2009 the National Heart, Lung, and Blood Institute, along with the Eunice Kennedy Shriver National Institute of Child Health and Human Development funded seven separate randomized controlled trials to refine and test behavioral approaches for weight control among young adults (18-35y) at high risk for weight gain. All studies focus on prevention of weight gain or weight loss among young adults, conduct formative research, conduct a two-year randomized controlled trial, and use innovative technologies (e.g.., social media, texting, smart phones). Recruitment issues for health-related interventions in this population group have been recognized as a significant challenge. Recruitment challenges include high mobility, competing demands (school, jobs, young families), low perceived risk of health consequences, and lack of investigator experience targeting this population, Each of the seven EARLY studies tests its own primary hypotheses, with a cumulative estimated sample size of 6063 young adults. To date with the trials approximately half way through the recruitment period, the 7 studies have had an initial contact with 12,669 participants and have screened 6425 participants. After prescreening, screening and the consent procedure, 1554 participants have been randomized, representing about 12% of those initially contacted about the study. The EARLY trials have recruitment targets for males, Hispanic and non-white participants and success with those goals has differed across the seven trials. The objective of this presentation is to present details on prescreening, screening, consent and randomization rates across the trials and to describe the recruitment process for the EARLY trials. We will describe recruitment methods and strategies that have been found to be most effective in recruiting young adults into the EARLY obesity trial. Strategies used to target Hispanic and non-White young adults as well as male participants will also be detailed.