tbuckley/cabot-search huggingface dataset:
Abstract 514: Focal Adhesion Kinase Inhibition Prevents Prolonged Nuclear Factor-κB Activation and Reduces Atherosclerosis in ApoE-/- Mice
Authors: James M Murphy, Steve Lim
Journal: Circulation Research (2018)

A key event in atherogenesis is the expression of cell adhesion molecules on endothelial cells (ECs) that recruit leukocytes to the vessel wall, where they accumulate over time and form atherosclerotic plaques filled with fatty lipids. Although lipid-lowering drugs have been beneficial in slowing down atherosclerosis, there is currently no treatment available to reduce the underlying triggers that promote EC activation. Focal adhesion kinase (FAK) is an integrin-associated protein tyrosine kinase that plays a key role in cytokine-induced pro-inflammatory molecule expression; however, the molecular mechanism has not been elucidated. We have revealed that a small molecule FAK inhibitor (PF-271) in human ECs reduces tumor necrosis factor-α (TNF-α)-induced sustained activation of nuclear factor-κB (NF-kB), a major inflammatory transcription factor. While NF-κB is normally bound to inhibitor of NF-κB α (IκBα) in the cytosol, TNF-α leads to rapid activation and nuclear localization of NF-κB after degradation of IκBα by activation of IκB kinase (IKK). Chronic exposure to cytokines leads to oscillations in NF-κB activation as IκBα is continually made by active NF-κB and degraded by active IKK. Surprisingly, we discovered that FAK inhibition blocks prolonged NF-κB activation through a time-dependent increase in IκBα protein stability, suggesting decreased IKK activity. By performing in vitro IKK kinase assays, we found that FAK inhibition did indeed reduce sustained IKK activity as seen by reduced serine phosphorylation of IκBα 3hr after TNF-α stimulation. Since both cell adhesion molecule expression and NF-κB in ECs is important for atherosclerotic lesion development, we tested the efficacy of FAK inhibition on atherogenesis in vivo . We found that oral delivery of PF-271 (twice daily, 8 weeks) significantly reduced atherosclerotic lesion area in ApoE-/- mice fed a western diet. Taken together, our data demonstrates that FAK inhibition potentially reduces atherogenesis by blocking sustained NF-κB signaling through decreased IKK activity.
LONG-TERM EVOLOCUMAB USE IN SUBJECTS WITH HOMOZYGOUS AND SEVERE HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA: PRIMARY RESULTS OF THE TAUSSIG TRIAL
Authors: Raul Santos, G. Kees Hovingh, Dirk Blom, Handrean Soran, Gerald Watts, J. Antonio Lopez, Sarah Bray, Christopher Kurtz, Andrew Hamer, Frederick Raal
Journal: Journal of the American College of Cardiology (2019)
REAL WORLD EXPERIENCE WITH LEADLESS CARDIAC PACING
Authors: Vaibhav Vaidya, Mingyan Dai, Samuel Asirvatham, Robert Rea, Trena Thome, Komandoor Srivathsan, Siva Mulpuru, Fred Kusumoto, K. Venkatachalam, James D. Ryan, Paul Friedman, Yong-Mei Cha
Journal: Journal of the American College of Cardiology (2019)
P055 CXCL13 as biomarker for histological involvement in sjogren’s syndrome
Authors: S Colafrancesco, R Priori, C Smith, A Minniti, V Iannizzotto, E Pipi, S Nayar, J Campos, D Lucchesi, F Arienzo, B Cerbelli, C Giordano, G Valesini, M Bombardieri, BA Fisher, F Barone
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Career situation of first and presenting author</h3> Post-doctoral fellow. <h3>Introduction</h3> Sjogren's syndrome (SS) is an autoimmune condition characterised by systemic B cell activation, autoantibody production and ectopic germinal centers (GC) formation within salivary gland (SG). The extent of SG infiltrate has been proposed as biomarker of disease severity. Plasma levels of CXCL13 correlate with GC activity in animal models and disease severity in SS, suggesting its potential use as a surrogate serum marker to monitor local B cell activation. <h3>Objectives</h3> To evaluate the potential role of CXCL13 as biomarker of SG pathology in two independent SS cohorts. <h3>Methods</h3> 109 patients with SS were recruited at Sapienza University of Rome (Italy) (n=60), or at Queen Elizabeth Hospital in Birmingham and Barts Health NHS Trust in London (n=49). Both sera and matched paraffin-embedded minor SG biopsy were available. Sicca (n=57) and healthy subjects (HS) (n=19) sera were used as control. CXCL13 gene expression was also assessed in 25 frozen SGs. <h3>Results</h3> CXCL13 serum levels were higher in SS patients [90.3 (84.2) pg/ml], compared to both sicca [61.9 (38.6) pg/ml), p=0.0005] and HS [36.5 (40.18) pg/ml, p&lt;0.0001]. No differences in average CXCL13 levels were detected between the two SS cohorts [83 (95.2) pg/ml and 103 (64.9) pg/ml, respectively]. In both Italian and British cohorts, serum levels of CXCL13 correlated with the percentage of SG infiltration (p=0.0008 and p=0.0004, respectively), FS (p=0.0010 and p=0.0103, respectively) and mean foci area (p=0.0167 and p=0.0054, respectively); higher serum levels were observed in patients with segregated foci (p=0.0553 and p=0.0019, respectively) and GCs (p=0.0147 and p=0.0044, respectively). Higher CXCL13 serum levels were also associated with anti-Ro/SSA antibodies (p=0.0007, Italian cohort and p=0.0294, British cohort) as well as rheumatoid factor (RF) (p=0.0037, Italian Cohort and p=0.0033, British Cohort). Tissue expression of CXCL13 was moderately correlate with the mean foci area and percentage of infiltration. Higher expression of CXCL13 transcripts was observed in SGs with segregated foci (p=0.0057) and GCs (p=0.0162). Serum levels of CXCL13 did not correlate with local mRNA levels of the same cytokine. <h3>Conclusions</h3> Our data foster the use of CXCL13 to monitor the extent of local pathology in SS and its validation in longitudinal clinical studies. Both serum and tissue expression of CXCL13 correlate with SS histological severity, suggesting a major role of this chemokine in SG lymphocytes recruitment and organization. <h3>Disclosure of Interest</h3> None declared.
OCCURRENCE OF RIGHT VENTRICULAR DYSFUNCTION IMMEDIATELY AFTER PERICARDIOCENTESIS
Authors: Yuki Obayashi, Masashi Amano, Chisato Izumi, Hibiki Mima, Hidenori Kojima, Seita Yamasaki, Masayuki Fuki, Miyako Imanaka, Maiko Kuroda, Takeshi Harita, Suguru Nishiuchi, Jiro Sakamoto, Yodo Tamaki, Soichiro Enomoto, Makoto Miyake, Hirokazu Kondo, Toshihiro Tamura, Yoshihisa Nakagawa
Journal: Journal of the American College of Cardiology (2019)
Abstract A02: Potential role of SMC6 downregulation as an indicator of tumor genetic instability in breast cancer
Authors: Flavia Rotea Mangone, Ana Cristina Victorino Krepischi, Suely Nonogaki, Dirce Maria Carraro, Maria Aparecida Nagai
Journal: Clinical Cancer Research (2018)

Abstract Genetic instability is a common feature of cancer. Homologous recombination (HR) is involved in one of the major mechanisms of DNA double strand break repair (DSB) and depends on the formation of Holliday junctions (HJ) that should be solved for the maintenance of genomic stability. Deregulation of HR control mechanisms results in DNA damage. Data from the literature has shown that SMC6 complexed with SMC5 is involved in DSB repair. Previous sequencing data from our group showed the occurrence of some SMC6 genetic variants in sporadic breast cancer. In the present study, we sought to investigate a possible association between SMC6 expression level and genomic instability in breast cancer. SMC6 mRNA expression pattern determined by qRT-PCR and Copy Number Variation (CNV) data obtained by using whole-genome comparative genomic hybridization on microarrays, were determined in a cohort of 33 breast cancer samples of women who did not carry BRCA1/BRCA2 mutations. SMC6 protein expression was carried out in a tissue micro-array containing breast cancers samples. Statistical analyses were performed by using SPSS Software 20. Data comparison revealed that tumors with higher SMC6 mRNA expression showed a trend toward lower median numbers of total CNVs per genome, corroborating the role of SMC6 genomic stability maintenance. SMC6 protein expression was tested in a panel of 74 breast cancer tumors, and cases were classified into two groups: SMC6 negative (negative to weak nuclear staining) and SMC6 positive (moderate to strong nuclear staining). No association among SMC6 staining and clinic-pathologic features was observed. However, patients with SMC6 negative tumors had a trend to a shorter disease-free survival (DFS) and overall survival (OS) than those with SMC6 positive tumors (median DFS 29.0 vs. 172.0 months, Log Rank = 0.123 and median OS 30.47 vs. 153.30 months, Log Rank = 0.117). Although preliminary, our findings point to a possible association between SMC6 downregulation and poor outcome of patients, suggesting theatSMC6 may serve as an indicator of tumor genetic instability for patients with breast cancer. Supported by Fapesp and CNPq. Citation Format: Flavia Rotea Mangone, Ana Cristina Victorino Krepischi, Suely Nonogaki, Dirce Maria Carraro, Maria Aparecida Nagai. Potential role of SMC6 downregulation as an indicator of tumor genetic instability in breast cancer [abstract]. In: Proceedings of the AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. Philadelphia (PA): AACR; Clin Cancer Res 2018;24(1_Suppl):Abstract nr A02.
INTRAVASCULAR POLARIMETRY CHARACTERIZES PLAQUE COMPOSITION AND INSTABILITY IN PATIENTS WITH CORONARY ARTERY DISEASE
Authors: Kenichiro Otsuka, Martin Villiger, Antonios Karanasos, Laurens van Zandvoort, Pallavi Doradla, Jian Ren, Norman Lippok, Joost Daemen, Roberto Diletti, Robert-Jan van Geuns, Felix Zijlstra, Gijs van Soest, Jouke Dijkstra, Seemantini Nadkarni, Evelyn Regar, Brett Bouma
Journal: Journal of the American College of Cardiology (2019)
Chemotherapy and Supportive Care Agents as Essential Medicines for Children With Cancer
Authors: Yoram Unguru, Melanie Brooke Bernhardt, Stacey L. Berg, Liza-Marie Johnson, Kimberly Pyke-Grimm, Catherine Woodman, Conrad V. Fernandez
Journal: JAMA Pediatrics (2019)

In resource-rich countries, 5-year survival rates for children with cancer approach 85%. This impressive statistic is largely the result of integrating research with clinical care. At the core of this endeavor are multiagent combination chemotherapy and supportive care agents (CASCA). Most CASCAs belong to the class of sterile injectable drugs, which make up the backbone of many proven and life-saving pediatric oncology regimens. There are few if any alternative agents available to treat most life-threatening childhood cancers. In the United States, shortages of CASCAs are now commonplace. The consequences of drug shortages are far reaching. Beyond the economic costs, these shortages directly affect patients' lives, and this is especially true for children with cancer. Drug shortages in general and shortages of CASCAs specifically result in increased medication errors, delayed administration of life-saving therapy, inferior outcomes, and patient deaths. One way to mitigate drug shortages is to adopt an essential medicines list and ensure that these medications remain in adequate supply at all times. We argue for creation of a CASCA-specific essential medicines list for childhood cancer and provide ethical and policy-based reasoning for this approach. We recognize that such a call has implications beyond pediatric cancer, in that children with other serious disease should have an equal claim to access to guaranteed evidence-based medicines. We provide these arguments as an example of what should be claimed for medical indications that are deemed essential to preserve life and function.
Rapid, biphasic CRF neuronal responses encode positive and negative valence
Authors: Jineun Kim, Seongju Lee, Yi-Ya Fang, Anna Shin, Seahyung Park, Koichi Hashikawa, Shreelatha Bhat, Daesoo Kim, Jong-Woo Sohn, Dayu Lin, Greg S. B. Suh
Journal: Nature Neuroscience (2019)
SAFETY AND EFFICACY OF MITRACLIP IN FUNCTIONAL VERSUS DEGENERATIVE MITRAL REGURGITATION: A META-ANALYSIS OF OBSERVATIONAL STUDIES
Authors: Vikramaditya Samala Venkata, Varunsiri Atti, Bhavi Pandya, Varun Kumar, Sushruth Edla, Surya Kiran Aedma, Nileshkumar Patel, Calvin Lui, Nikhil Nalluri, Chad Kliger
Journal: Journal of the American College of Cardiology (2019)
T-WAVE AXIS DEVIATION PREDICTS INCIDENT HEART FAILURE AND FATAL OUTCOMES IN HIGH RISK SUBJECTS UNDERGOING CORONARY ANGIOGRAPHY
Authors: Zakaria Almuwaqqat, Ayman Alkhoder, Ayman Samman Tahhan, Matt Amin, Belal Kaseer, Muaaz Choudhary, Ghazzal Bahjat, Devinder Dhindsa, Murtuza Jafri, Wesley O'Neal, Sidra Siddiqui, Rami Abdulbaki, Saqib Qadir, Arianna Sidoti, Afnan Khan, Muhammad Dhanani, Elsayed Soliman, Viola Vaccarino, Arshed Quyyumi, Amit Shah
Journal: Journal of the American College of Cardiology (2019)
Abstract 304: Protein Phosphatase 1 Contributes to Atrial Stunning in Atrial Fibrillation
Authors: Srikanth Perike, Katherina M Alsina, Arvind Sridhar, Xander H Wehrens, Dawood Darbar, Mark D McCauley
Journal: Circulation Research (2018)

Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia. AF increases stroke risk 5-fold, and is partially mediated by reduced atrial contractility (stunning). However, it’s mechanism is relatively unknown. Recent data from our lab indicate protein phosphatase 1 (PP1) dephosphorylation of myosin light chain 2a (MLC2a) as contributor to Atrial stunning in AF Aim: To determine role of PP1 regulatory subunit (PPP1R12C) and catalytic subunit (PP1c) in modifying atrial sarcomere phosphorylation in AF Methods: We analyzed protein binding and phosphorylation of PPP1R12C, PP1c, and MLC2a in transfected HL1 and HEK cells, and AF prone Pitx2 null+/– mice. We also characterized the MRCK site on PPP1R12C that regulates PP1c and MLC2a phosphorylation using BDP5290 (PPP1R12C phosphorylation inhibitor), phosphomimetic (T560D) and phospho-ablated (T560A) versions of PPP1R12C Results: In Pitx2 null +/– mice, PPP1R12C increased by 2-fold ( P &lt;0.01) and had a 40% reduction in S-19-MLC2a phosphorylation ( P &lt;0.058). BDP5290 increased binding of PPP1R12C-PP1c and MLC2a &gt;3-fold in HL1 and HEK cells ( P &lt;0.01). Also, the constitutively activated T560A site on PPP1R12C significantly increased binding of PPP1R12C-MLC2a and PP1c Conclusion: In Pitx2 null+/- mice, increased expression of PPP1R12C is associated with PP1 holoenzyme targeting to sarcomeric MLC2a, and is associated with reduced S19-MLC2a phosphorylation. Additionally, BDP5290 and PPP1R12C (T560A) enhanced PPP1R12C-PP1c interaction and decreased MLC2a phosphorylation, thereby modelling PP1 activity in AF. Future studies will examine effects of altered Ppp1r12c expression on atrial contractility in vivo
Heterozygous CTC1 Variants in Acquired Bone Marrow Failure
Authors: Wenyi Shen, Cassandra M. Hirsch, Bartlomiej P. Przychodzen, Reda Z. Mahfouz, Tomas Radivoyevitch, Louis Williams, Mohammad Fahad B. Asad, Jaroslaw P. Maciejewski
Journal: Blood (2018)
Abstract 503: Modeling Premature Cardiac Aging by Induced Pluripotent Stem Cell From a Patient With Hutchinson-Gilford Progeria Syndrome
Authors: Gustavo Monnerat, Tais Brunswick, Karina Asensi, Danubia Santos, Raiana Andrade, Fernanda Mesquita, João Paulo Albuquerque, Raphaela Ferreira, João Simões, Mariana Muniz, Camila Wendit, Erika Velasquez, Gilberto Dumont, Fabio Nogueira, Antonio C Campos de Carvalho
Journal: Circulation Research (2018)

Background: Hutchinson-Gilford Progeria Syndrome (HGPS) is an extremely rare genetic disorder characterized by accelerated aging and high incidence of cardiovascular complications and metabolic alterations. However, the underlying mechanisms of this syndrome are not fully understood. Methods and Results: This study modelled HGPS using cardiomyocytes generated from induced pluripotent stem cells (iPSc) derived from a patient affected by the syndrome, characterizing the molecular and biophysical alterations found in cardiomyocytes obtained from three distinct differentiation protocols run in parallel with a control iPSc. Electrophysiology recordings were performed with intracellular microelectrodes and the Progeria cardiomyocytes fired action potentials similar to those from control iPSc-derived cardiomyocytes. High resolution respirometry performed on Oroboros system in isolated cardiomyocytes showed that Progeria cardiomyocytes have a tendency to decrease the oxygen consumption under basal condition and after FCCP, when compared to control cardiomyocytes (P=0.06). Furthermore, HGPS cardiomyocytes produced less ROS under basal and after 100uM Hydrogen peroxide treatment. However, mitotracker analysis shows no difference on mitochondrial content. Electron tomography and 3D reconstruction analysis suggest structural abnormalities in the mitochondria of Progeria cardiomyocytes. Proteomics analysis, performed with Liquid Chromatography tandem mass spectrometry (LC-MS/MS) in a high-resolution system (Q-Exactive Plus, Thermo Fischer), shows differential protein expression between Progeria (183 unique proteins) and Control (225 unique proteins) IPSc - derived cardiomyocytes. Conclusions: Our work demonstrate that iPSc- derived cardiomyocytes from Progeria patients have significant alterations in cellular respiration and protein expression.
COMPUTED TOMOGRAPHIC 3: DIMENSIONAL VIRTUAL DISSECTION AIDING SURGICAL PLANNING IN A RARE PEDIATRIC CASE OF BICUSPID AORTIC VALVE WITH ASCENDING AORTIC PSEUDOANEURYSM
Authors: Jeremy Steele, Stephanie Tseng, Tarek Alsaied, Eric Crotty, Justin Tretter
Journal: Journal of the American College of Cardiology (2019)
Harnessing the Power of Global Health Studies for Sickle Cell Disease: Validation of a Rapid, Open-Source, Paper-Based Screening Assay in a Cohort of 1103 Tanzanian Children
Authors: Julien Delobel, Kristina Keitel, Katia Balmas-Bourloud, Tarsis Mlaganile, Valerie D'Acremont, Raffaele Renella
Journal: Blood (2018)
MACHINE LEARNING USING SIMILARITY ANALYSIS IMPROVES RISK STRATIFICATION BEYOND SURGICAL RISK SCORES IN PATIENTS UNDERGOING TRANSCATHETER AORTIC VALVE REPLACEMENT
Authors: Yasir Abdul Ghaffar, Faizan Shaukat, Anand Desai, Muhammad Khalil, Mohamad Alkhouli, Bryan Raybuck, Vinay Badhwar, Partho Sengupta
Journal: Journal of the American College of Cardiology (2019)
CHARACTERISTIC AND PROGNOSIS OF VASOSPASTIC ANGINA PATIENTS WITH IMPLANTABLE CARDIOVERTER DEFIBRILLATOR FOR SECONDARY PREVENTION: COMPARISON WITH ORGANIC CORONARY STENOSIS
Authors: Yutaka Ogino, Kazuo Kimura, Kiyoshi Hibi, Yasushi Matsuzawa, Noriaki Iwahashi, Nobuhiko Maejima, Masami Kosuge, Toshiaki Ebina, Masaaki Konishi
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF AORTIC VALVE CALCIFICATION IN PATIENTS UNDERGOING TRANSCATHETER AORTIC VALVE IMPLANTATION
Authors: Konstantinos Stathogiannis, Konstantinos Toutouzas, Maria Drakopoulou, George Latsios, Andreas Synetos, Maria Xanthopoulou, Vasiliki Penesopoulou, George Oikonomou, Stergios Soulaidopoulos, George Trantalis, Dimitris Tousoulis
Journal: Journal of the American College of Cardiology (2019)
30-DAY READMISSIONS FOLLOWING SPONTANEOUS CORONARY ARTERY DISSECTION: INSIGHTS FROM THE NATIONWIDE READMISSIONS DATABASE 2010-2014
Authors: Tara Shah, Ming Zhong, Dmitriy Feldman, Robert Minutello, Harsimran Singh, Geoffrey Bergman, Shing-Chiu Wong, Jim Cheung, Luke Kim
Journal: Journal of the American College of Cardiology (2019)
P068 Rheumatoid arthritis peripheral CD14+ monocytes are hyper-inflammatory, hyper-glycolytic and retain a memory bias toward m1 macrophages
Authors: T Mcgarry, M Hanlon, U Fearon, DJ Veale
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Career situation of first and presenting author</h3> Post-doctoral fellow. <h3>Introduction</h3> Myeloid cells with a monocyte/macrophages phenotype are present in large numbers in the rheumatoid arthritis (RA) joint, significantly contributing to disease. <h3>Objectives</h3> This study aimed to assess whether peripheral monocytes in RA are pre-programmed to become M1 pro-inflammatory macrophages. <h3>Methods</h3> Blood was collected from healthy donors, at-risk individuals (Those with arthralgia, ACPA+/RF+, normal CRP and no evidence of synovitis) and established RA patients. CD14+ monocytes were isolated from peripheral blood mononuclear cells using a CD14 magnetic bead separation kit. Cells were stimulated with LPS (100 ng/ml) for 3–24 hours and to assess the effects of STAT3 inhibition, cells were pre-treated with STATTIC (10 µM) for 30mins. A Human Cytokine and Chemokine PCR array was carried out and those genes most differentially expression were further validated in a larger cohort of patients using RT-PCR. The metabolic profile of cells was analysed using Seahorse XFE Technology, which concomitantly analysis glycolysis and mitochondrial respiration in real-time. Gene and protein expression of key inflammatory and glycolytic markers was also carried out by RT-PCR, western blotting and ELISA. <h3>Results</h3> CD14+ RA monocytes are hyper-inflammatory upon stimulation, with significantly higher expression of IL-1β, TNFα, IL-6, IL-27, CXCL10 and CXCL11 compared to healthy controls, which is indicative of a M1-like pro-inflammatory phenotype. These hyper-inflammatory cells are highly glycolytic, with increased expression of HIF1α, HK and PFKFB3, key glycolytic enzymes. Both baseline glycolysis and baseline oxidative phosphorylation are increased in RA CD14+ monocytes, paralleled by increased ATP synthesis and maximal respiratory capacity, suggesting a hyper-energetic phenotype. This hyper-inflammatory, hyper-glycolytic phenotype is mediated by STAT3, as selective STAT3 inhibition can significantly decrease M1-like cytokines and PFKFB3 and HK2 expression. In addition, STAT3 inhibition significantly decreases both oxidative phosphorylation and glycolysis pathways. Finally, this pro-inflammatory phenotype in evident in CD14+ monocytes from arthralgia ACPA+/RF+ people at risk of developing disease, demonstrating that these processes may precede clinical manifestations in RA. <h3>Conclusions</h3> This study demonstrates the unique inflammatory and metabolic phenotype of RA monocytes, suggesting that peripheral CD14+ monocytes may be pre-programmed to become M1-like pro-inflammatory macrophages. In addition, the observation of this phenotype in at-risk individuals indicates that these features may precede clinical manifestations of RA and therefore could be useful as a biomarker for early diagnosis. <h3>Disclosure of Interest</h3> None declared.
IL1R1 is required for celastrol’s leptin-sensitization and antiobesity effects
Authors: Xudong Feng, Dongxian Guan, Thomas Auen, Jae Won Choi, Mario Andrés Salazar Hernández, Jaemin Lee, Hyonho Chun, Farhana Faruk, Esther Kaplun, Zachary Herbert, Kyle D. Copps, Umut Ozcan
Journal: Nature Medicine (2019)
EFFECTS OF CANAGLIFLOZIN ON HEART FAILURE OUTCOMES WITH AND WITHOUT PRESERVED EJECTION FRACTION IN TYPE 2 DIABETES: RESULTS FROM THE CANVAS PROGRAM
Authors: Gemma Figtree, Karin Rådholm, Terrance D. Barrett, Vlado Perkovic, Kenneth W. Mahaffey, Dick de Zeeuw, Greg Fulcher, David R. Matthews, Wayne Shaw, Bruce Neal
Journal: Journal of the American College of Cardiology (2019)
VITAMIN C INTRAVENOUS TREATMENT IN THE SETTING OF ATRIAL FIBRILLATION ABLATION: RESULTS FROM THE RANDOMIZED, DOUBLE-BLINDED, PLACEBO-CONTROLLED CITRIS-AF STUDY
Authors: Cory Trankle, Laura Puckett, Theresa Swift-Scanlan, Christine DeWilde, Robin Sculthorpe, Kenneth Ellenbogen, Alpha Fowler, Jayanthi Koneru
Journal: Journal of the American College of Cardiology (2019)
Validation of the CALGB and EORTC Prognostic Models for Mesothelioma based on multiple CALGB Trials (Alliance)
Authors: Hmh Pang, Lydia Hodgson, RobertA Kratzke, Jeffrey Crawford, Hedy Kindler, EverettE Vokes, Xiaofei Wang
Journal: Journal of Thoracic Oncology (2013)
QUANTIFICATION OF AORTIC REGURGITATION SEVERITY AND RESULTANT IMPACT ON LEFT VENTRICULAR REMODELING: A COMPARATIVE STUDY OF ECHOCARDIOGRAPHY AND CARDIAC MAGNETIC RESONANCE IMAGING
Authors: Albree Tower-Rader, Yash Kumar, Nancy Obuchowski, Eoin Donnellan, Louis Williams, Zoran Popovic, Michael Bolen, Dermot Phelan, Scott Flamm, Brian Griffin, Leslie Cho, Lars Svensson, Gosta Pettersson, Deborah Kwon
Journal: Journal of the American College of Cardiology (2019)