tbuckley/cabot-search huggingface dataset:
LOW IRON IS STRONGLY ASSOCIATED WITH ADVERSE OUTCOMES IN ACUTE DECOMPENSATED HEART FAILURE (ADHF) PATIENTS: FROM NARA-HF STUDY
Authors: Tomoya Ueda, Satomi Ishihara, Yasuki Nakada, Makoto Watanabe, Rika Kawakami, Hiroyuki Okura, Yoshihiko Saito
Journal: Journal of the American College of Cardiology (2019)
THE PROBABILITY OF FINDING CORONARY ARTERY DISEASE BY CORONARY CT ANGIOGRAPHY IN PATIENTS WITH SYSTOLIC HYPERTENSION BELOW AGE 60 IN A LARGE, MULTI-PHYSICIAN OUTPATIENT CARDIOLOGY PRIVATE PRACTICE
Authors: Ronak Agarwal, Yesh Dhruva, Rajiv Agarwal
Journal: Journal of the American College of Cardiology (2019)
TRANSCATHETER AORTIC VALVE REPLACEMENT VERSUS SURGICAL AORTIC VALVE REPLACEMENT IN PATIENTS WITH RHEUMATOID ARTHRITIS (INSIGHTS FROM THE NATIONWIDE INPATIENT DATABASE)
Authors: Ayman Elbadawi, Kirolos Barssoum, Ahmed H. Mohamed, Gbolahan Ogunbayo, Islam Elgendy, Hamdy Ahmed
Journal: Journal of the American College of Cardiology (2019)
High throughput somatic profiling of the Ras-Raf-MAP and PI3K-PTEN-Akt pathways in advanced colorectal cancer and correlations with response to cetuximab
Authors: Christopher Smith, Bart Claes, D Fisher, R Adams, R Kaplan, A Meade, Diether Lambrechts, T Maughan, J Cheadle
Journal: Annals of Oncology (2010)
CHARACTERISTICS AND LONG TERM OUTCOMES OF PATIENTS WITH PRIOR CORONARY ARTERY BYPASS GRAFTING UNDERGOING PRIMARY PERCUTANEOUS CORONARY INTERVENTION FOR ST-ELEVATION MYOCARDIAL INFARCTION
Authors: S. Michael Gharacholou, Freddy Del-Carpio Munoz, Mandeep Singh, Gurpreet Sandhu, Rajiv Gulati, Bradley Lewis, Matthew Johnson, Arashk Motiei, Gary Lane, Peter Pollak, Dilip Pillai, Charanjit Rihal, Patricia Pellikka, Si Pham, Sina Rahimpour, Gregory Barsness
Journal: Journal of the American College of Cardiology (2019)
L-Type Cav 1.2 Calcium Channel-α-1C Regulates Response to Rituximab in Diffuse Large B-Cell Lymphoma
Authors: Jiu-Yang Zhang, Pei-Pei Zhang, Wen-Ping Zhou, Jia-Yu Yu, Zhi-Hua Yao, Jun-Feng Chu, Shu-Na Yao, Cheng Wang, Waseem Lone, Qing-Xin Xia, Jie Ma, Shu-Jun Yang, Kang-Dong Liu, Zi-Gang Dong, Yong-Jun Guo, Lynette M. Smith, Timothy W. McKeithan, Wing C. Chan, Javeed Iqbal, Yan-Yan Liu
Journal: Clinical Cancer Research (2019)

One third of patients with diffuse large B-cell lymphoma (DLBCL) succumb to the disease partly due to rituximab resistance. Rituximab-induced calcium flux is an important inducer of apoptotic cell death, and we investigated the potential role of calcium channels in rituximab resistance.The distinctive expression of calcium channel members was compared between patients sensitive and resistant to rituximab, cyclophosphamide, vincristine, doxorubicin, prednisone (RCHOP) regimen. The observation was further validated through mechanistic in vitro and in vivo studies using cell lines and patient-derived xenograft mouse models.A significant inverse correlation was observed between CACNA1C expression and RCHOP resistance in two independent DLBCL cohorts, and CACNA1C expression was an independent prognostic factor for RCHOP resistance after adjusting for International Prognostic Index, cell-of-origin classification, and MYC/BCL2 double expression. Loss of CACNA1C expression reduced rituximab-induced apoptosis and tumor shrinkage. We further demonstrated direct interaction of CACNA1C with CD20 and its role in CD20 stabilization. Functional modulators of L-type calcium channel showed expected alteration in rituximab-induced apoptosis and tumor suppression. Furthermore, we demonstrated that CACNA1C expression was directly regulated by miR-363 whose high expression is associated with worse prognosis in DLBCL.We identified the role of CACNA1C in rituximab resistance, and modulating its expression or activity may alter rituximab sensitivity in DLBCL.
Abstract 263: Cytosolic RBFox1 in Cardiac Pathological Remodeling
Authors: Chen Gao, Yun-Hua (Esther) Hsiao, Menglong Wang, Zhaojun Xiong, Shuxun Ren, Christoph D Rau, Katelyn Li, Xinshu(Grace) Xiao, Yibin Wang, Yi Xing
Journal: Circulation Research (2018)

Background: RBFox1 is known to be an RNA splicing regulator with enriched expression in cardiac muscle. Loss of RBFox1 expression is a molecular hallmark associated with heart failure in mouse and human. Genetic manipulation of RBFox1 reveals a major function of RBFox1 in the pathogenesis of cardiac hypertrophy, fibrosis and dysfunction under pathological stresses. However, much of our current knowledge about RBFox1 focuses on the nuclear RBFox1 with a major impact on global alternative splicing changes. Yet, RBFox1 gene also generates a cytosolic isoform-RBFox1c through alternative splicing, and the specific function of RBFox1c has not been characterized. Goal and Methods: This study investigated the functional impact and the underlying mechanism of the RBFox1c in cardiac pathological remodeling and targeted gene regulation. Results: RBFox1c expression is significantly repressed in stressed cardiomyocytes in vivo and in vitro. RNA-Seq combined with IPA analyses from cardiomyocytes revealed RBFox1c but not the nucleus RBFox1 specifically suppressed pro-inflammatory genes. In the cardiac specific RBFox1 knockout mice, enhanced cardiac fibrosis is observed following I/R injury associated with elevated expression of pro-inflammatory genes. In contrast, cardiac specific expression of RBFox1c reduced cardiac fibrosis and inflammatory gene expression following pressure-overload and myocardial infarct injury associated with improved ejection fraction. Motif enrichment analysis identified significant enrichment of the RBFox1 binding motif in the 3’UTR of the RBFox1c regulated genes. We performed CLIP analysis followed by RT-PCR and observed RBFox1c interacted with inflammatory gene 3’UTR. Lastly, we explored the interactome of RBFox1c and found RBFox1c specifically interacted with a component of RNA decay machinery-Upf1. Indeed, while expression of RBFox1c repressed inflammatory gene expression, inactivation of Upf1 abolished this effect in cardiomyocytes. Conclusion: RBFox1 regulates cardiac transcriptome reprogramming at two post-transcriptional steps. The RBFox1 nuclei isoform regulates RNA splicing reprogramming, and the RBFox1c represses proinflammatory genes via recruitment of Upf1 mediated RNA degradation.
Abstract 431: KLF15 Regulates the Circadian Susceptibility to Ischemia Reperfusion Injury in the Heart
Authors: Le Li, Hui Li, Chih-Liang Tien, Rongli Zhang, Xudong Liao, Mukesh K. Jain, Lilei Zhang
Journal: Circulation Research (2018)

The onset and the injury of heart attacks both show a circadian rhythmicity with a peak during the sleep to active transition. Studies using cell type specific clock mutant demonstrated the intrinsic varying susceptibility of the cardiomyocytes to the ischemia reperfusion (I/R) injury in a time-of-the-day dependent fashion, however, the molecular mechanisms remain unclear. Transcription factor KLF15 expresses in a circadian fashion and is significantly reduced in ischemia cardiomyopathy in human and in mice, but its role in the cardiac I/R injury is unknown. Recently, we show that KLF15 coordinates the diurnal expression of catabolic genes in the heart during the active phase, suggesting it may also be involved in regulating the cardiac reactive oxygen species (ROS), which is not only a byproduct of catabolism but also the main injury during reperfusion. Here we show that cardiomyocyte specific KLF15 deficient mice have exaggerated I/R injury in vivo during the sleep to active transition when KLF15 expression is at peak, but not during the active to sleep transition, demonstrating its critical role in governing the circadian rhythmicity of myocardial injury. We found acute KLF15 deficiency in the primary cardiomyocytes is associated with increased ROS and exaggerated susceptibility to oxidative stress, which can be rescued by a MnSOD mimetic Tempol, but not by several other anti-oxidants. We further demonstrate that KLF15 deficiency in the cardiomyocytes in vitro and in vivo are both associated with increased mitochondrial acetylation, including MnSOD acetylation at Lysine 122, which leads to reduced MnSOD activity. There is no change in mitochondrial sirtuin SIRT3 level, the main deacetylase for mitochondrial acetylated proteins including MnSOD K122 , however its co-enzyme NAD + level and NAD + /NADH ratio are drastically reduced with KLF15 deficiency. Furthermore, NAD + precursor NMN rescues the increased susceptibility to ROS in KLF15 deficient cardiomyocytes and I/R injury in vivo. Finally, we show that KLF15 directly regulates nicotinamide phosphoribosyltransferase (NAMPT), the rate limiting enzyme of NAD + salvage pathway and the main NAD + determinant in the heart. Collectively, our results demonstrate that KLF15 coordinates cardiac metabolism and ROS clearance in a circadian fashion through mitochondrial NAD + ; loss of KLF15 expression in ischemic cardiomyopathy likely contributes to an enhanced susceptibility to additional I/R insult in a time-of-the-day dependent fashion.
Suv39h1 Represses the Progression of MLL-Rearranged Myeloid Leukemia Via Hoxb13
Authors: Yajing Chu, Yangpeng Chen, Huidong Guo, Mengke Li, Jun Shi, Tao Cheng, Feng-Chun Yang, Mingjiang Xu, Weiping Yuan
Journal: Blood (2018)
von Willebrand Factor and Management of Heart Valve Disease
Authors: Eric Van Belle, Flavien Vincent, Antoine Rauch, Caterina Casari, Emmanuelle Jeanpierre, Valentin Loobuyck, Mickael Rosa, Cedric Delhaye, Hughes Spillemaeker, Camille Paris, Nicolas Debry, Basile Verdier, André Vincentelli, Annabelle Dupont, Peter J. Lenting, Sophie Susen
Journal: Journal of the American College of Cardiology (2019)
LNCRNA SNHG1 ELICITS HEART REGENERATION THROUGH PTEN/AKT/MYC POSITIVE FEEDBACK LOOP
Authors: Yanmei Chen, Mengsha Li, Bing Li, Yijin Chen, Guojun Chen, Xiaofei Feng, Hao Zheng, Jianping Bin
Journal: Journal of the American College of Cardiology (2019)
Abstract P3-03-33: Withdrawn
Authors: VI Blackhall, M Bugelli, NA Abbott, R Mullen
Journal: Cancer Research (2019)

Abstract This abstract was withdrawn by the authors. Citation Format: Blackhall VI, Bugelli M, Abbott NA, Mullen R. Withdrawn [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P3-03-33.
Repeated Phenotypic Evolution by Different Genetic Routes in Pseudomonas fluorescens SBW25
Authors: Jenna Gallie, Frederic Bertels, Philippe Remigi, Gayle C Ferguson, Sylke Nestmann, Paul B Rainey
Journal: Molecular Biology and Evolution (2019)

Repeated evolution of functionally similar phenotypes is observed throughout the tree of life. The extent to which the underlying genetics are conserved remains an area of considerable interest. Previously, we reported the evolution of colony switching in two independent lineages of Pseudomonas fluorescens SBW25. The phenotypic and genotypic bases of colony switching in the first lineage (Line 1) have been described elsewhere. Here, we deconstruct the evolution of colony switching in the second lineage (Line 6). We show that, as for Line 1, Line 6 colony switching results from an increase in the expression of a colanic acid-like polymer (CAP). At the genetic level, nine mutations occur in Line 6. Only one of these-a nonsynonymous point mutation in the housekeeping sigma factor rpoD-is required for colony switching. In contrast, the genetic basis of colony switching in Line 1 is a mutation in the metabolic gene carB. A molecular model has recently been proposed whereby the carB mutation increases capsulation by redressing the intracellular balance of positive (ribosomes) and negative (RsmAE/CsrA) regulators of a positive feedback loop in capsule expression. We show that Line 6 colony switching is consistent with this model; the rpoD mutation generates an increase in ribosomal gene expression, and ultimately an increase in CAP expression.
PREDICTORS OF TARGET LESION REVASCULARIZATION AFTER DRUG-COATED BALLOON ANGIOPLASTY FOR IN-STENT RESTENOSIS
Authors: Shinsuke Mori, Yoshiaki Ito, Toshihiko Kishida, Tomoya Fukagawa, Shigemitsu Shirai, Kenji Makino, Yohsuke Honda, Masakazu Tsutsumi, Yasunari Sakamoto, Norihiro Kobayashi, Motoharu Araki, Masahiro Yamawaki, Keisuke Hirano
Journal: Journal of the American College of Cardiology (2019)
CONCOMITANT TRICUSPID VALVE ANNULOPLASTY AT THE TIME OF MITRAL VALVE SURGERY COMPARED TO ISOLATED MITRAL VALVE SURGERY
Authors: Mohanad Hamandi, Robert Smith, William Ryan, Paul Grayburn, Alexander Crawford, Anupama Vasudevan, Jordan Wooley, Laith Batarseh, Timothy George, Anita Krueger, Kelly Hutcheson, Katherine Harrington, William Brinkman, Molly Szerlip, David Moore, J. Michael DiMaio, Michael Mack
Journal: Journal of the American College of Cardiology (2019)
Child health unravelling in UK
Authors: David C Taylor-Robinson, Eric T Lai, Margaret Whitehead, Ben Barr
Journal: BMJ (2019)

White-nose syndrome (WNS) is an emerging disease of hibernating bats associated with cutaneous infection by the fungus Geomyces destructans (Gd), and responsible for devastating declines of bat populations in eastern North America. Affected bats appear emaciated and one hypothesis is that they spend too much time out of torpor during hibernation, depleting vital fat reserves required to survive the winter. The fungus has also been found at low levels on bats throughout Europe but without mass mortality. This finding suggests that Gd is either native to both continents but has been rendered more pathogenic in North America by mutation or environmental change, or that it recently arrived in North America as an invader from Europe. Thus, a causal link between Gd and mortality has not been established and the reason for its high pathogenicity in North America is unknown. Here we show that experimental inoculation with either North American or European isolates of Gd causes WNS and mortality in the North American bat, Myotis lucifugus. In contrast to control bats, individuals inoculated with either isolate of Gd developed cutaneous infections diagnostic of WNS, exhibited a progressive increase in the frequency of arousals from torpor during hibernation, and were emaciated after 3–4 mo. Our results demonstrate that altered torpor-arousal cycles underlie mortality from WNS and provide direct evidence that Gd is a novel pathogen to North America from Europe.
LIPID-LOWERING THERAPY IN DIFFERENT REGIONS OF THE UNITED STATES: INSIGHTS FROM GETTING TO AN IMPROVED UNDERSTANDING OF LOW-DENSITY LIPOPROTEIN CHOLESTEROL AND DYSLIPIDEMIA MANAGEMENT (GOULD): A REGISTRY OF HIGH CARDIOVASCULAR RISK PATIENTS IN THE UNITED STATES
Authors: Christie M. Ballantyne, Christopher Cannon, James de Lemos, Robert Rosenson, Kiran Philip, Katherine Mues, Shusama Alam, Yuyin Liu, Deepak L. Bhatt, Mikhail Kosiborod
Journal: Journal of the American College of Cardiology (2019)
D-DIMER AS A NOVEL MARKER OF INFLAMMATION IN PERICARDITIS
Authors: Chandra Kanth Ala, Kinjal Banerjee, Johnny Chahine, Beni Verma, Arnav Kumar, Muhammad Furqan, Kimi Sato, Rory Hachamovitch, Christine Jellis, Stanley L. Hazen, Luis Afonso, Allan Klein
Journal: Journal of the American College of Cardiology (2019)
PREDICTORS OF RESTENOSIS AFTER NON-STENTING CORONARY INTERVENTION WITH DRUG-COATED BALLOON ASSESSED BY OPTICAL COHERENCE TOMOGRAPHY
Authors: Shun Nakagama, Taishi Yonetsu, Takayuki Niida, Yuuji Matsuda, Taichi Nakamura, Yu Hatano, Taro Sasaoka, Tomoyuki Umemoto, Tetsumin Lee, Kenzo Hirao
Journal: Journal of the American College of Cardiology (2019)
Abstract 260: Adverse Transverse-Tubule Remodeling in a Rat Model of Heart Failure is Attenuated by Triiodothyronine (T3) Treatment
Authors: Shimin An, Jes Kuruvilla, Adam Muncan, Nimra Gilani, Yuan Huang, Youhua Zhang, Anthony M Gerdes, Kaie Ojamaa
Journal: Circulation Research (2018)

Pre-clinical animal studies have shown that triiodothyronine (T3) replacement therapy improves cardiac contractile function after myocardial infarction (MI). We hypothesized that T3 treatment could prevent adverse post-MI cardiomyocyte remodeling by maintaining T-tubule (TT) organization, thus improving contractility. Methods: Coronary artery ligation (MI) or sham surgeries were performed on female Sprague-Dawley rats (aged 12 wks), followed by treatment with T3 (5ug/kg/d) or vehicle in drinking water for 16 wks (10/gp). After echocardiographic/hemodynamic analyses, ventricular myocytes were isolated by collagenase digestion and plated on laminin-coated glass coverslips for TT analysis or analyzed for contractility using IonOptix’s edge-detection method. Live cell staining with wheat germ agglutinin (WGA)-488 or di-8-ANNEPS labeled sarcolemma and TT, and multiple z-stack images were captured by scanning confocal microscopy and TT organization measured using TTorg program. Ventricular RNA was analyzed by qPCR. Results: Echocardiography and in vivo hemodynamic measurements showed significantly improved systolic and diastolic function in T3- vs vehicle-treated MI rats. IonOpix analysis of isolated ventricular myocytes showed significant dysfunction in measures of relaxation in MI myocytes compared to sham, and improvements with T3: max relaxation velocity (Vmax), 2.98±1.41 vs 1.59±0.33, p&lt;0.05; time to Vmax (sec), 0.23±0.04 vs 0.31±0.02, p&lt;0.001, MI+T3 vs MI). Similarly, time to peak contraction was shortened by T3 treatment (0.16±0.02 vs 0.20±0.01 sec., MI+T3 vs MI; p&lt;0.01. TT power measured by TTorg analysis of WGA-488 or di-8-ANNEPS labeled myocytes showed significant disorganization of the TT system in MI myocytes that was normalized by T3-treatment (TTpower = 82±7 sham, 74±8 MI and 79±6 MI+T3; sham vs MI p&lt;0.0001; MI vs MI+T3, p&lt;0.0001). qPCR results indicated that reduced expression of Bin1, Jph2, RyR2 and LTCC in the MI myocardium was normalized by T3. In conclusion, T3 treatment prevented TT disorganization in the post-MI cardiomyocyte, normalized contractile and relaxation parameters and improved cardiac output, thus supporting the therapeutic potential of T3 in heart failure.
Abstract 213: Sarcolemma Genes Related to the Transverse Tubule Structure Are Mostly Not Expressed in Differentiating Human iPSC-derived Cardiomyocytes
Authors: Eliseo T Vazquez, David Torres Barba, Janhavi S Sharma, Elizabeth Cortez-Toledo, Xiaodong Zhang, Omar De la Cruz Cabrera, Javier E Lopez
Journal: Circulation Research (2018)

Background: Transverse tubules (TT) are tunnel-like extensions of sarcolemma studded with ion channels coupling excitation, through the cytoplasm, to contraction in the sarcomere of matured cardiomyocytes (CMs). Expression timing of sub-cellular TT-related genes (TT-rgs) in individual human iPSC-derived CMs (hiPSC-CMs) has not yet been reported. Objective: Map out the gene program of TT-rgs by sub-cellular locations during hiPSC-CM differentiation using single-cell transcriptomics (scRNA Seq.). Methods: hiPSC-CMs were differentiated from 2 commercially available lines using sequential GSK3 and Wnt signaling inhibition. The %CMs were assayed by flow cytometry for sarcomeric myosin heavy chain protein, a CM biomarker. Baseline cells (iPSCs, n=24) and day 14 (n=45), 30 (n=64), and 60 (n=5) post differentiation cells were sampled for scRNA Seq. using the Fluidigm C1 platform. We categorized 73 TT-rgs by cellular location of the coded protein (i.e. sarcomere, cytoplasm or sarcolemma). The expression pattern for each location was categorized as induced, repressed, or neither based on the median transcript per million for each individual cell normalized to iPSCs. Results: CMs increased from &lt;1% in iPSCs to 21%, 37% and 59% at D14, D30 and D60 post differentiation (adj. p &lt;0.03 by ANOVA), respectively. 33 genes (45%) had no detectable RNA while 21 (29%) were induced to D60. See table. Conclusion: Single-cell transcriptomes in differentiating hiPSC-CMs revealed a discordance between sarcolemma (mostly not expressed) and sarcomeric genes being induced. Defining timing and within cell variability of TT sub-cellular genes will be critical to understand human CM maturation.
ASSESSING OUTCOMES IN THE DUAL ANTIPLATELET (DAPT) CLINICAL TRIAL USING MEDICARE CLAIMS: INSIGHTS FROM THE EXTEND-DAPT STUDY
Authors: Kamil Faridi, Hector Tamez Aguilar, Eric Secemsky, Yang Song, Laura Mauri, Jeptha Curtis, Changyu Shen, Robert Yeh
Journal: Journal of the American College of Cardiology (2019)
IMPROVED DIAGNOSIS OF VESSEL-SPECIFIC ISCHEMIA BY STEPWISE CONSIDERATION OF STENOSIS SEVERITY, NON-CALCIFIED PLAQUE VOLUME, AND CORONARY LUMEN VOLUME: RESULTS FROM THE PROSPECTIVE, MULTICENTER, INTERNATIONAL CREDENCE TRIAL
Authors: Alexander van Rosendael, Inge van den Hoogen, Jung Hyun Choi, So Yeon Choi, Joon-Hyung Doh, Ae-Young Her, Bon-Kwon Koo, Chang-Wook Nam, Sangshoon Shin, Jason Cole, Alessia Gimelli, Muhammad Khan, Faisal Nabi, Ryo Nakazato, U. Joseph Schoepf, Hyuk-Jae Chang, Philippe Genereux, Paul Knaapen, Gianluca Pontone, Wijnand Stuijfzand, Fay Lin, Leslee J. Shaw, James Min
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF HOSPITAL TYPE ON IN-HOSPITAL MORTALITY IN PATIENTS UNDERGOING PERCUTANEOUS MITRAL VALVE REPAIR
Authors: Antonette Kanishka Karrthik, Mohamed Gad, Keerat Rai Ahuja, Najdat Bazarbashi, Amer Kadri, Manpreet Kaur, Kamalpreet Dhaliwal, Samir Kapadia
Journal: Journal of the American College of Cardiology (2019)
OUTCOMES OF NON-SURGICAL PATIENTS WITH SEVERE TRICUSPID REGURGITATION AND CONGESTIVE HEART FAILURE
Authors: Amer N. Kadri, Vivek Menon, Yasser Sammour, Rama Dilip Gajulapalli, Chandramohan Meenakshisundaram, Leen Nusairat, Divyanshu Mohananey, Adrian Hernandez, Jose Navia, Amar Krishnaswamy, Brian Griffin, L. Leonardo Rodriguez, Serge Harb, Samir Kapadia
Journal: Journal of the American College of Cardiology (2019)
Brentuximab Vedotin Plus Bendamustine Is an Effective Salvage Regimen for Pediatric Patients with Relapsed Hodgkin Lymphoma
Authors: Nitya Gulati, Farid Boulad, Maria I. Cancio, Kevin J. Curran, Carolyn Jackson, Nancy Kernan, Andrew L. Kung, Richard O'Reilly, Susan Prockop, Kavitha Ramaswamy, Andromachi Scaradavou, Barbara Spitzer, Neerav Shukla, Peter G. Steinherz, Christopher Forlenza
Journal: Blood (2017)
RELATIONSHIP BETWEEN SOLUBLE F11 RECEPTOR, TOTAL NITRIC OXIDE LEVELS, AND VASCULAR FUNCTION IN AFRICAN AMERICANS WITH TYPE II DIABETES
Authors: Ajibola Monsur Adedayo, Ayobami Eluwole, Fasika Tedla, Arye Kremer, Nicole Mastrogiovanni, Muhammad Afzal Khan, Carl Rosenberg, Paul Dreizen, John LaRosa, Louis Salciccioli, Mohamed Boutdjir, Mary Ann Banerji, Clinton Brown, Moro Salifu, Jason Lazar, Ahmed Bakillah
Journal: Journal of the American College of Cardiology (2019)
TIMING OF HOLTER DETECTED RECURRENCES DURING FOLLOW-UP AFTER CRYOBALLOON ABLATION FOR PAROXYSMAL ATRIAL FIBRILLATION: IN SEARCH OF THE OPTIMAL FOLLOW-UP TIMEPOINT
Authors: Stijn Van Vugt, Sjoerd Westra, Rick Volleberg, Jeroen Jaspers Focks, Reinder Evertz, Martin Hemels, Rypko Beukema, Carlo de Asmundis, Marc Brouwer, Jean Baptiste Chierchia
Journal: Journal of the American College of Cardiology (2019)
All-Trans Retinoic Acid (ATRA) up-Regulates Cell Surface CD38 Expression Which Promotes Pro-Tumoral Mitochondrial Trafficking from Stromal Cells to Multiple Myeloma
Authors: Christopher Richard Marlein, Rebecca H Horton, Rachel E Piddock, Jayna J Mistry, Charlotte Hellmich, Cesar A. Gomez, Kristian Bowles, Stuart Rushworth
Journal: Blood (2018)