tbuckley/cabot-search huggingface dataset:
Abstract 16929: Propensity-matched Analysis of Triple Oral Antithrombotic Therapy versus Dual Antiplatelet Therapy Following Percutaneous Coronary Intervention
Authors: Daniel B Spoon, Ryan J Lennon, Joshua P Slusser, David R Holmes, Kent R Bailey, Verghese Mathew, Robert D McBane, Rajiv Gulati, Guri S Sandhu, Charanjit S Rihal
Journal: Circulation (2015)

Introduction: Triple oral antithrombotic therapy (TOAT) (aspirin, clopidogrel, and warfarin) is associated with an increased risk of bleeding. Despite this, the optimal management of patients with indications for warfarin following percutaneous coronary intervention (PCI) has not been established. We sought to compare long-term clinical outcomes between patients receiving TOAT with those receiving dual antiplatelet therapy (DAPT) (aspirin and clopidogrel) after PCI. Hypothesis: Patients with clinical indications for warfarin have higher baseline risk which is largely responsible for the observed differences in outcomes between patients receiving TOAT vs. DAPT. Methods: Retrospective analysis of prospectively collected data from 9,009 patients. The primary outcome was a composite of all-cause mortality, ischemic or embolic events (myocardial infarction or stroke), or bleeding. Secondary outcomes were death plus ischemic or embolic events, death plus bleeding, death, MI, stroke, and bleeding. A 2:1 propensity matched analysis was also performed. Results: In 9,009 patients, 812 received TOAT and 8,197 received DAPT. Median follow-up was 61 months. The primary end point occurred in 2,749 patients. At 1 year, 22% of patients treated with TOAT had the primary endpoint versus 11% of DAPT patients (p&lt;0.001). At 1 year, secondary end points of death or ischemic or embolic events (19% vs. 10%, p&lt;0.001), and death or bleeding events (15% vs. 5%, p&lt;0.001) also occurred with a higher frequency with TOAT. After propensity matched analysis the above differences were no longer significant with 1 year primary endpoint rates of 19% vs. 17% respectively (HR 1.95%, CI 0.88, 1.47; p = 0.33). Following propensity matching the only significant difference between TOAT and DAPT groups was minor bleeding (5% vs. 2%; HR 2.65, 95% CI 1.39, 5.03; p=0.003). Conclusions: In a large single center registry with comprehensive follow up, patients treated with TOAT had higher rates of ischemic and bleeding events. However, when baseline risks are accounted for event rates are similar, other than minor bleeding, indicating patient risk characteristics are largely responsible for the observed differences in outcomes.
MORPHOLOGY OF THE CULPRIT LESIONS OF ACUTE MYOCARDIAL INFARCTION ASSESSED BY OPTICAL COHERENCE TOMOGRAPHY IN PATIENTS WITH LOW DENSITY LIPOPROTEIN CHOLESTEROL LEVEL
Authors: Taishi Yonetsu, Masahiro Hoshino, Tetsumin Lee, Yoshihisa Kanaji, Akinori Sugano, Masao Yamaguchi, Masahiro Hada, Yohei Sumino, Yoshinori Kanno, Tomoki Horie, Shun Nakagama, Tomoyuki Umemoto, Tsunekazu Kakuta, Taro Sasaoka
Journal: Journal of the American College of Cardiology (2019)
Glucose transporter 1-mediated vascular translocation of nanomedicines enhances accumulation and efficacy in solid tumors
Authors: Kazumi Suzuki, Yutaka Miura, Yuki Mochida, Takuya Miyazaki, Kazuko Toh, Yasutaka Anraku, Vinicio Melo, Xueying Liu, Takehiko Ishii, Osamu Nagano, Hideyuki Saya, Horacio Cabral, Kazunori Kataoka
Journal: Journal of Controlled Release (2019)
IMPORTANCE OF ABDOMINAL COMPRESSION VALSALVA MANEUVER AND MICROBUBBLE GRADING IN CONTRAST TRANSTHORACIC ECHOCARDIOGRAPHY FOR DETECTING PATENT FORAMEN OVALE
Authors: Yoichi Takaya, Teiji Akagi, Rie Nakayama, Koji Nakagawa, Hiroshi Ito
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF HYPERTENSION ON THE PREDICTIVE VALUE OF HEMOGLOBIN GLYCATION INDEX ON CARDIOVASCULAR OUTCOMES
Authors: Jing-Lu Jin, Di Sun, Ye-Xuan Cao, Hui-Wen Zhang, Yuan-Lin Guo, Na-Qiong Wu, Cheng-Gang Zhu, Ying Gao, Qiu-Ting Dong, Geng Liu, Qian Dong, Jian-Jun Li
Journal: Journal of the American College of Cardiology (2019)
PERIARTERIAL NEOVASCULARIZATION AND ATTENUATED-SIGNAL PLAQUE PREDICT LONG-TERM MORTALITY AFTER HEART TRANSPLANTATION: RISK STRATIFICATION WITH IVUS-DETERMINED CORONARY INFLAMMATORY FINDINGS
Authors: Kuninobu Kashiyama, Kozo Okada, Hideki Kitahara, Ryo Kameda, M. Brooke Hollak, Helen Luikart, Paul Yock, Alan Yeung, Peter Fitzgerald, Kiran Khush, William Fearon, Yasuhiro Honda
Journal: Journal of the American College of Cardiology (2019)
Abstract 490: Enhanced Therapeutic Effects of MSC-derived Exosomes with an Injectable Hydrogel for Hindlimb Ischemia Treatment
Authors: Zongjin Li, Kaiyue Zhang, Xiangnan Zhao, Deling Kong, Qiang Zhao, Na Liu, Fengxia Ma
Journal: Circulation Research (2018)

Mesenchymal stem cell (MSC)-derived exosomes have been recognized as new candidates for cell-free treatment of various diseases. However, maintaining the retention and stability of exosomes over time in vivo after transplantation is a major challenge in clinical application of MSC-derived exosomes. Here, we investigated if human placenta-derived MSCs (hP-MSCs) derived exosomes incorporated with chitosan hydrogel could boost the retention and stability of exosomes and further enhance their therapeutic effect. Our results demonstrated that chitosan hydrogel notably increased the stability of proteins and microRNAs in exosomes, as well as augmented the retention of exosomes in vivo as confirmed by Gaussia luciferase imaging. In addition, we evaluated the therapeutic function of hP-MSCs derived exosomes incorporated with chitosan hydrogel in a murine model of hindlimb ischemia. Our data demonstrated that chitosan hydrogel could enhance the retention of exosomes and further augment the therapeutic effects for hindlimb ischemia as revealed by firefly luciferase imaging of angiogenesis. The strategy used in this study may facilitate the development of easy and effective approaches for assessing and enhancing the therapeutic effects of stem cell-derived exosomes.
AGGRESSIVE SODIUM RESTRICTION IN CHRONIC HEART FAILURE: 6G VERSUS 3G A RANDOMIZED STUDY
Authors: Haruki Sekiguchi, Ken Kobayashi, Makiko Kimura, Tatsuya Fukushima, Atsushi Suzuki, Tsuyoshi Shiga, Nobuhisa Hagiwara
Journal: Journal of the American College of Cardiology (2019)
THE ELEPHANT IN THE CONDUIT: BACTEREMIA IN A PATIENT WITH TETRALOGY OF FALLOT AND A TRANSCATHETER PULMONARY VALVE REPLACEMENT
Authors: Ada C. Stefanescu Schmidt, Nicola Maschietto, Sitaram Emani, Disty Pearson, William Kerr, James H. Maguire, Michael Landzberg
Journal: Journal of the American College of Cardiology (2019)
Abstract 21413: Molecular Basis of Maternal Obesity Induced Fetal Cardiac Contractile Dysfunction
Authors: Qiurong Wang, John F Odhiambo, Chris Pankey, Adel Ghnenis, Peter W Nathanielsz, Stephen P Ford, Wei Guo
Journal: Circulation (2017)

One third of the women at reproductive age are overweight or obese in US. Epidemiological studies in humans and studies on animals have shown that obesity during pregnancy ( i.e. maternal obesity, MO) increases incidences of cardiovascular diseases in offspring. Uterus environment is essential for fetal cardiac development and MO as a stress condition in uterus could program cardiovascular disease in prenatal and postnatal offspring. However, the mechanisms of the origin and development of MO-induced cardiovascular disease later in life remain unclear. For this purpose, we use sheep (sharing many similarities with human pregnancy) as a model to study the impact of MO on fetal heart contractile function. Previously, we have demonstrated that MO impaired fetal sheep cardiomyocyte contractility by reducing the peak shortening and velocity of shortening/relengthening and prolonged the time to peak shortening/relengthening. We also found that MO disrupted the calcium homeostasis in fetal cardiomyocytes by increasing intracellular Ca 2+ level and inducing the calcium insensitivity in the cell. In current study, we found that MO increased the phosphorylation of protein kinase A (PKA) as well as the phosphorylation of Ca 2+ /calmodulin-dependent protein kinase II (CaMKII), which further promoted phosphorylation level of ryanodine receptor type 2 (Ryr2) at Ser2808 and Ser2814 respectively. Expression level of FKBP12.6, a key protein interacting with Ryr2 for calcium releasing, was upregulated in MO fetal myocardium. On the other hand, MO reduced expression of myosin heavy chain in fetal myocardium. Moreover, the cardiac troponin T and troponin I expression level was upregulated in MO fetuses, whereas MO downregulated the expression of troponin C in fetal myocardium. Taken together, our findings suggest that increased CaMKII and PKA phosphorylation of Ryr2 plays a critical role in the development of MO-induced sarcoplasmic reticulum Ca 2+ leak in fetal cardiomyocytes. Furthermore, our data indicate that the change in expression levels of myosin heavy chain and troponin C, I and T is the cause of calcium insensitivity and contractile dysfunction in MO fetal cardiomyocytes. Our studies have provided a fundamental molecular basis of MO programmed heart disease.
Relationships of Overt and Silent Brain Lesions With Cognitive Function in Patients With Atrial Fibrillation
Authors: David Conen, Nicolas Rodondi, Andreas Müller, Juerg H. Beer, Peter Ammann, Giorgio Moschovitis, Angelo Auricchio, Daniel Hayoz, Richard Kobza, Dipen Shah, Jan Novak, Jürg Schläpfer, Marcello Di Valentino, Stefanie Aeschbacher, Steffen Blum, Pascal Meyre, Christian Sticherling, Leo H. Bonati, Georg Ehret, Elisavet Moutzouri, Urs Fischer, Andreas U. Monsch, Christoph Stippich, Jens Wuerfel, Tim Sinnecker, Michael Coslovsky, Matthias Schwenkglenks, Michael Kühne, Stefan Osswald, Sebastian Berger, Raffaele Bernasconi, Lorin Fröhlich, Tobias Göldi, Rebecca Gugganig, Thomas Kofler, Philipp Krisai, Michel Mongiat, Christiane Pudenz, Javier Ruperti Repilado, Aleksandra Schweizer, Anne Springer, Samuel Stempfel, Thomas Szucs, Jan van der Stouwe, Gian Voellmin, Leon Zwimpfer, Drahomir Aujesky, Juerg Fuhrer, Laurent Roten, Simon Jung, Heinrich Mattle, Luise Adam, Carole Elodie Aubert, Martin Feller, Claudio Schneider, Axel Loewe, Tanja Flückiger, Cindy Groen, Nathalie Schwab, Christopher Beynon, Roger Dillier, Franz Eberli, Simone Fontana, Christine Franzini, Isabel Juchli, Claudia Liedtke, Jacqueline Nadler, Thayze Obst, Xiaoye Schneider, Katrin Studerus, Dominik Weishaupt, Silke Kuest, Karin Scheuch, Denise Hischier, Nicole Bonetti, Corina Bello, Henriette Isberg, Alexandra Grau, Jonas Villinger, Mary-Monica Papaux, Philipp Baumgartner, Mark Filipovic, Marcel Frick, Adriana Anesini, Cristina Camporini, Giulio Conte, Maria Luce Caputo, Francois Regoli, Tiziano Moccetti, Roman Brenner, David Altmann, Manuela Forrer, Michaela Gemperle, Mathieu Firmann, Sandrine Foucras, Benjamin Berte, Andrea Kaeppeli, Brigitta Mehmann, Markus Pfeiffer, Ian Russi, Kai Schmidt, Vanessa Weberndoerfer, Mabelle Young, Melanie Zbinden, Luisa Vicari, Jane Frangi, Tatiana Terrot, Hervé Gallet, Elise Guillermet, Francois Lazeyras, Karl-Olof Lovblad, Patrick Perret, Cheryl Teres, Nathalie Lauriers, Marie Méan, Sandrine Salzmann, Nisha Arenja, Andrea Grêt, Sandra Vitelli, Jane Frangi, Augusto Gallino, Renate Schoenenberger-Berzins, Fabienne Witassek, Ernst-Wilhelm Radue, Pascal Benkert, Thomas Fabbro, Patrick Simon, Ramun Schmid
Journal: Journal of the American College of Cardiology (2019)
Abstract 315: Time-resolved Expression of Membrane-targeted Proteins During Ipsc-cardiomyocyte Differentiation
Authors: Edward Lau, Rajani Shrestha, Cody T Thomas, Damon R Williams, Joseph C Wu
Journal: Circulation Research (2018)

Background: The ability to create human cardiomyocytes from induced pluripotent stem cells (iPSCs) has spurred advances in disease modeling and drug testing, but there remains an ongoing need to improve the purity and functional maturity of derived cardiomyocytes. Membrane proteins are an integral component of cell signaling and specification. To better understand iPSC-cardiomyocyte differentiation and identify potential surface markers of cell maturity, we set out to examine how membrane-targeted proteins gradually remodel in differentiating cardiomyocytes. Methods: Human iPSCs from three donors were differentiated into cardiomyocytes in 40 independent differentiation plates. We sampled protein expression at independent time points at up to daily intervals during day 0 to day 14 post-differentiation, then sparsely up to 100 days. The extracted proteins were analyzed using a Q-Exactive HF Orbitrap high-resolution mass spectrometer to quantify how the relative quantity of membrane-targeted proteins changes over time in differentiating cells. Results: We identified 1095 annotated cell membrane proteins and quantified their temporal changes in abundance across 40 samples. Protein expression in the first two principal components recapitulated gradual differentiation of iPSCs into mesoderm, cardiac progenitors, and more mature cardiomyocytes. Membrane protein expression partitioned the samples into three discernible clusters, representing early (day 0-5), mid (day 6-10), and late (day 11+) differentiation time points. In total, 115 cell membrane proteins showed differential expression in late vs. early differentiation, including two popeye-domain-containing proteins (POPDC2 and BVES) known to be involved in cardiac development. In particular, we identified two proteins, dysferlin (DYSF) and alpha-1 syntrophin (SNTA1), which continued to show strong upward changes in late differentiation time points, nominating these proteins for investigation as markers for mature cells. Conclusion: We report the time-resolved expression profiles of over 1000 membrane-targeted proteins during iPSC-cardiomyocyte differentiation. Future work into the membrane proteome may lead to maturity markers to guide maturation efforts.
NEIGHBORHOOD DISADVANTAGE AND VARIATIONS IN CORONARY ARTERY DISEASE CARE AND OUTCOMES AMONG OUTPATIENT CARDIOLOGY PRACTICES
Authors: Rishi Wadhera, Yang Song, Amy Kind, Deepak L. Bhatt, Liyan Dong, Gheorghe Doros, Alexander Turchin, Thomas M. Maddox, Robert Yeh, Kim Allan Williams, Karen Joynt Maddox
Journal: Journal of the American College of Cardiology (2019)
Communicating, and Justifying, Nonefficacy Benefits for New Drugs Approved on the Basis of Noninferiority Trials
Authors: Joseph S. Ross, Christina C. Wee
Journal: JAMA Internal Medicine (2019)

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EPHA3 a novel tumour specific therapeutic target for medulloblastoma
Authors: Carolin Offenhauser, Benjamin Carrington, Kris Thurecht, Kathleen Ensbey, Zara Bruce, Paul Jamieson, Yi Chieh Lim, Seckin Akgul, Michelle Li, Brett Stringer, Simon Puttick, Adrian Fuchs, Daniel Picard, Wendy Ingram, Andrew Hallahan, Andrew Moore, Terrance Johns, Nicholas Gottardo, Marc Remke, Andrew Boyd, Bryan Day
Journal: Neuro-Oncology (2018)
ADENOSINE STRESS RESPONSE WITH NATIVE T1 MAPPING IS ASSOCIATED WITH CONTRASTED FIRST-PASS PERFUSION CARDIAC MAGNETIC RESONANCE IMAGING IN CANCER SURVIVORS TREATED WITH ANTHRACYCLINES: MEASURING CORONARY MICROVASCULAR DYSFUNCTION IN CARDIO-ONCOLOGY WITHOUT CONTRAST
Authors: Carolyn J. Park, Alexandra L. Thomas, W. Gregory Hundley, Jennifer H. Jordan
Journal: Journal of the American College of Cardiology (2019)
PET/MRI: A NOVEL IMAGING MODALITY TO GUIDE TAILORED IMMUNOTHERAPY IN EOSINOPHILIC MYOCARDITIS
Authors: Aditya Parikh, Maria Giovanna Trivieri, Anuradha (Anu) Lala, Sumeet Mitter, Tim Hinohara, Philip Robson, Zahi Fayad, Maya H. Barghash
Journal: Journal of the American College of Cardiology (2019)
COMPARISON BETWEEN CARDIOVASCULAR TRIAL OUTCOMES AND TREATMENT EFFECTS USING CLINICAL ENDPOINT COMMITTEE ADJUDICATION VERSUS ROUTINE HEALTH DATA: A SYSTEMATIC REVIEW
Authors: Craig Rodrigues, Ayodele Odutayo, Sagar Patel, Arnav Agarwal, Bruno Roza da Costa, Ethan Lin, Peter Juni, Shaun Goodman, Michael Farkouh, Jacob Udell
Journal: Journal of the American College of Cardiology (2019)
Abstract 291: The Type I Interferon Receptor Amplifies Innate Immune Responses After Myocardial Infarction
Authors: Richard P Ng, Kevin R King, Aaron D Aguirre, Sean P Arlauckas, Ralph Weissleder
Journal: Circulation Research (2018)

Ischemic heart disease (IHD), the leading cause of death in the world, begins with myocardial infarction (MI). Overly exuberant innate immune responses are detrimental to post-MI healing and repair. Efforts to achieve post-MI cardioprotection focused on blocking NFκB-mediated inflammation have been largely unsuccessful. We recently discovered that MI leads to cytosolic DNA sensing in leukocytes and triggers the interferon regulatory factor 3 (IRF3)-dependent expression of interferon stimulated genes (ISGs). We found that genetic inhibition of IRF3 after MI reduces inflammation, limits ventricular dilation and contractile dysfunction, and improves survival. In this work, we test two hypotheses. 1) Type I interferons (IFNs), secreted by a few DNA-sensing/IRF3-activated leukocytes, signal via type I interferon alpha/beta receptors (IFNARs), to amplify ISG expression after MI. 2) Pharmacologic inhibition of type I IFN/IFNAR signaling blocks response amplification and significantly reduces ISG expression. We established DNA-stimulated bone marrow derived macrophages (BMDMs) as an in vitro model of the post-MI type I IFN response and measured the expression of ISGs ( Cxcl10 , Irf7 , Ifit1 , and Ifit3 ) by qPCR. We quantified and compared changes in ISG expression caused by direct DNA stimulation, incubation with conditioned media containing secreted factors from DNA-stimulated cells, and treatment with an IFNAR neutralizing antibody. Compared to unstimulated BMDMs, ISG expression was amplified by &gt;35-fold in BMDMs stimulated by either DNA or conditioned media. However, there was no significant amplification when the experiments were performed in the presence of an IFNAR neutralizing antibody. In a mouse model of MI, single cell RNA-Seq revealed that IFNAR-deficient mice have reduced numbers of ISG-expressing leukocytes compared to wild type controls, which indicates that IFNAR-dependent amplification of innate immune responses occurs after MI in vivo . Collectively, these results demonstrate that IFNAR ligands are important amplifiers of DNA-induced innate immune responses after MI and suggest that anti-interferon therapy should be further investigated in vivo to improve clinical outcomes after MI.
ASSOCIATION BETWEEN RIGHT VENTRICULAR TO PULMONARY CIRCULATION UNCOUPLING AND RENAL BLOOD FLOW IN HEART FAILURE
Authors: Valentina Labate, Francesco Bandera, Maurizio Losito, Michela Caracciolo, Marina Rovida, Monica Barki, Eleonora Alfonzetti, Marco Guazzi
Journal: Journal of the American College of Cardiology (2019)
Plasticity of Promoter-Core Sequences Allows Bacteria to Compensate for the Loss of a Key Global Regulatory Gene
Authors: Otmane Lamrabet, Jacqueline Plumbridge, Mikaël Martin, Richard E Lenski, Dominique Schneider, Thomas Hindré
Journal: Molecular Biology and Evolution (2019)

Transcription regulatory networks (TRNs) are of central importance for both short-term phenotypic adaptation in response to environmental fluctuations and long-term evolutionary adaptation, with global regulatory genes often being targets of natural selection in laboratory experiments. Here, we combined evolution experiments, whole-genome resequencing, and molecular genetics to investigate the driving forces, genetic constraints, and molecular mechanisms that dictate how bacteria can cope with a drastic perturbation of their TRNs. The crp gene, encoding a major global regulator in Escherichia coli, was deleted in four different genetic backgrounds, all derived from the Long-Term Evolution Experiment (LTEE) but with different TRN architectures. We confirmed that crp deletion had a more deleterious effect on growth rate in the LTEE-adapted genotypes; and we showed that the ptsG gene, which encodes the major glucose-PTS transporter, gained CRP (cyclic AMP receptor protein) dependence over time in the LTEE. We then further evolved the four crp-deleted genotypes in glucose minimal medium, and we found that they all quickly recovered from their growth defects by increasing glucose uptake. We showed that this recovery was specific to the selective environment and consistently relied on mutations in the cis-regulatory region of ptsG, regardless of the initial genotype. These mutations affected the interplay of transcription factors acting at the promoters, changed the intrinsic properties of the existing promoters, or produced new transcription initiation sites. Therefore, the plasticity of even a single promoter region can compensate by three different mechanisms for the loss of a key regulatory hub in the E. coli TRN.
GLOBAL LONGITUDINAL STRAIN AS A PREDICTOR OF OUTCOME IN PATIENTS UNDERGOING AUTOLOGOUS STEM CELL TRANSPLANTATION FOR MULTIPLE MYELOMA
Authors: Alexandra J. Ritts, Kendra Coonse, Maros Ferencik, Jessica Minnier, Miriam Elman, Emma Scott, Rebecca Silbermann, Sarah Nagle, Eva Medvedova, Richard Maziarz, Stephen Heitner
Journal: Journal of the American College of Cardiology (2019)