tbuckley/cabot-search huggingface dataset:
皮肤附属器肿瘤和 SCC 风险
Authors: V. De Giorgi, L. Salvati, A. Barchielli, A. Caldarella, A. Gori, F. Scarfì, I. Savarese, N. Pimpinelli, C. Urso, D. Massi
Journal: British Journal of Dermatology (2019)

整体而言,皮肤癌是一种最常见的癌症形式。有若干类型,最常见的是非黑色素瘤皮肤癌,包括基底细胞癌(BCC)和鳞状细胞癌(SCC)。在英国,每年诊断超过 10 万例新发非黑色素瘤皮肤癌病例。皮肤附属器肿瘤 (CAC) 是罕见肿瘤,通常难以诊断。这项来自意大利的研究旨在评估人群中的 CAC 数量随时间推移如何变化,和确定存在 CAC 和 SCC 发生风险之间的关系。分析了来自 Tuscany 癌症注册 (TCR) 1985 至 2010 年间 25 年中的数据。从这一时间段中鉴定出了 242 名患者,CAC 患者的数量从 1985 ‐ 1987 年的 2.5 例/百万人增长至 2009 ‐2010 年的 19 例/百万人。在 1997 到 2010 年,人群中的 CAC 患病率增高了 159%。还发现,CAC 患者在晚年发生 SCC 的可能性比无 CAC 的患者高 34 倍,提示这是一个显著的风险因素。此研究的作者预测,由于正在衰老的人群,CAC 患者的数量可能继续增多。这一点加上 CAC 和 SCC 之间的联系强调了需要在未来改进 CAC 的诊断。
PREVALENCE OF NON-ISCHEMIC VALVULAR DISEASES: AN EPIDEMIOLOGICAL STUDY OF A BLACK INNER-CITY POPULATION
Authors: Phyllis Supino, Jason Lazar, Miriam Vincent, Antony Innasimuthu, Sanjay Kumar, Sriya Avadhani, Ofek Hai, Ridita Nizam, Jeffrey Borer
Journal: Journal of the American College of Cardiology (2019)
CONTEMPORARY OUTCOMES OF CHRONIC TOTAL OCCLUSION PERCUTANEOUS CORONARY INTERVENTIONS: UPDATE FROM THE PROGRESS CTO (PROSPECTIVE GLOBAL REGISTRY FOR THE STUDY OF CHRONIC TOTAL OCCLUSION INTERVENTION) REGISTRY
Authors: Iosif Xenogiannis, Dimitrios Karmpaliotis, Khaldoon Alaswad, Oleg Krestyaninov, Dmitrii Khelimskii, James Choi, Farouc Jaffer, Mitul Patel, Ehtisham Mahmud, David Kandzari, Anthony Doing, Michalis Koutouzis, M. Nicholas Burke, Jaikirshan Khatri, Catalin Toma, Robert Yeh, R. Michael Wyman, Wissam Jaber, Taral Patel, Srinivasa Potluri, Peter Tajti, Allison B. Hall, Bavana Rangan, Subhash Banerjee, Emmanouil S. Brilakis
Journal: Journal of the American College of Cardiology (2019)
Abstract 306: Identifying Downstream Effectors of the Extracellular Signal-related Kinase 1/2-controlled Directional Growth Response in Cardiomyocytes
Authors: Kelly M Grimes, Marjorie Maillet, Jeffery D Molkentin
Journal: Circulation Research (2018)

A better understating of the mechanisms by which cardiomyocytes grow in different directions could open up new therapeutic avenues for hypertrophic and dilated cardiomyopathies, diseases that include the lengthening and widening of cardiomyocytes, respectively. To-date the only known proteins found to control this directional growth of cardiomyocytes are MEK1, mitogen-activated protein kinase kinase 1, and ERK1/2, extracellular signal-related kinase 1/2. The only known role of MEK1 is to phosphorylate ERK1/2 after MEK1 itself becomes phosphorylated through RAS/RAF signaling. Upon phospho-activation, ERK1/2 can interact with targets in the cytoplasm or translocate to the nucleus to induce cell growth and proliferation pathways. We previously found that cardiac overexpression of activated MEK1 causes cardiac hypertrophy and cardiomyocyte widening, while genetic ablation of ERK1/2 proteins in the heart causes dilation and cardiomyocyte lengthening. To determine how these proteins may control this directional growth response, we conducted a phosphoproteomic screen using neonatal rat ventricular myocytes (NRVMs) treated with activated MEK1 adenovirus, U0126 (a MEK1 inhibitor), or GFP adenovirus (control). For proteins with the greatest change in phosphorylation upon MEK1 activation or inhibition, we have verified the screen results using Phos-tag gels and western blots. Many of these hits have cytoskeletal or actin regulatory functions, and a few have also been implicated in stress-sensing in previous literature in other cells types. Furthermore, many hits showed increased protein levels in addition to augmented phosphorylation in NRVMs treated with activated MEK1 adenovirus. Given our nearly 20 interesting candidate proteins, we are currently conducting an in vivo screen in which each gene is individually expressed in mice using AAV9. After injection of virus into the thoracic cavities of P5 wild type mice, we are assessing if cardiac hypertrophy/dilation or cardiomyocyte dimensional growth are present at 4 months of age. Any novel candidates identified in this manner will be presented.
Silencing Long Non-Coding RNA ST3GAL6-AS1 Inhibits Adhesion and Migration of Myeloma Cells in Vitro
Authors: Ying Shen, Yuandong Feng, Hongli Chen, Yachun Jia, Yue Peng, Ru Zhang, Yun Yang, Jian-Li Wang, Ju Bai, Fang-Xia Wang, Yan Xu, Jinsong Hu, Aili He
Journal: Blood (2018)
Alternative oxidase inhibitors: Mitochondrion‐targeting as a strategy for new drugs against pathogenic parasites and fungi
Authors: Godwin U. Ebiloma, Emmanuel O. Balogun, Eduardo J. Cueto‐Díaz, Harry P. de Koning, Christophe Dardonville
Journal: Medicinal Research Reviews (2019)

Abstract The alternative oxidase (AOX) is a ubiquitous terminal oxidase of plants and many fungi, catalyzing the four‐electron reduction of oxygen to water alongside the cytochrome‐based electron transfer chain. Unlike the classical electron transfer chain, however, the activity of AOX does not generate adenosine triphosphate but has functions such as thermogenesis and stress response. As it lacks a mammalian counterpart, it has been investigated intensely in pathogenic fungi. However, it is in African trypanosomes, which lack cytochrome‐based respiration in their infective stages, that trypanosome alternative oxidase (TAO) plays the central and essential role in their energy metabolism. TAO was validated as a drug target decades ago and among the first inhibitors to be identified was salicylhydroxamic acid (SHAM), which produced the expected trypanocidal effects, especially when potentiated by coadministration with glycerol to inhibit anaerobic energy metabolism as well. However, the efficacy of this combination was too low to be of practical clinical use. The antibiotic ascofuranone (AF) proved a much stronger TAO inhibitor and was able to cure Trypanosoma vivax infections in mice without glycerol and at much lower doses, providing an important proof of concept milestone. Systematic efforts to improve the SHAM and AF scaffolds, aided with the elucidation of the TAO crystal structure, provided detailed structure‐activity relationship information and reinvigorated the drug discovery effort. Recently, the coupling of mitochondrion‐targeting lipophilic cations to TAO inhibitors has dramatically improved drug targeting and trypanocidal activity while retaining target protein potency. These developments appear to have finally signposted the way to preclinical development of TAO inhibitors.
POLYPHARMACY INCREASES IN PREVALENCE AND SEVERITY FOLLOWING A HEART FAILURE HOSPITALIZATION
Authors: Ozan Unlu, Tina Dharamdasani, Alexi Archambault, Ivan Diaz, Ligong Chen, Emily Levitan, Joseph Hanlon, Mathew Maurer, Mark S. Lachs, Monika Safford, Parag Goyal
Journal: Journal of the American College of Cardiology (2019)
SACUBITRIL-VALSARTAN VERSUS ANGIOTENSIN CONVERTING ENZYME INHIBITORS OR ANGIOTENSIN RECEPTOR BLOCKERS IN SYSTOLIC HEART FAILURE: COMPARATIVE OUTCOMES IN CLINICAL PRACTICE
Authors: Nicholas Tan, Lindsey Sangaralingham, Jeson Sangaralingham, Xiaoxi Yao, Nilay Shah, Shannon Dunlay
Journal: Journal of the American College of Cardiology (2019)
FRAILTY, DIASTOLIC DYSFUNCTION, AND LATENT HEART FAILURE IN THE COMMUNITY-LIVING ELDERLY IN HONG KONG: CROSS-SECTIONAL FINDINGS FROM THE UFO STUDY
Authors: Erik Yee Mun George Fung, Xiaobo Yang, Leong Ting Lui, Qi Li, King Fai Cheng, Daljit Sahota, Yiting Fan, Jenny S.W. Lee, Alex P.W. Lee, Elsie Hui, Jean Woo
Journal: Journal of the American College of Cardiology (2019)
Abstract 550: Exosomes Released by Human Induced Pluripotent Stem Cell-Cardiomyocytes Induce In-Vitro Angiogenesis: A New Strategy for Cell-Free Therapeutics
Authors: Julie A Dougherty, Naresh Kumar, Mohammad Noor, Mark G Angelos, Chun-An Chen, Mahmood Khan
Journal: Circulation Research (2018)

Due to the poor regenerative properties of cardiac tissue, acute ischemic events can lead to progressive terminal heart failure unless cardiac regeneration can be stimulated. Recent evidence using stem cell therapy in the heart demonstrates a greater role of their paracrine signaling potential, as cell survival post-transplantation is very low. The main objective of this study was to characterize exosomes secreted by human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and evaluate their in vitro angiogenic potential. HiPSC-CMs were cultured under normal conditions with exosome-free serum. Isolated exosomes were characterized by TEM, NTA, and immunoblotting. Angiogenic potential was assessed by wound-healing, proliferation, and tube formation assays using bovine aortic endothelial cells (BAECs). TEM imaging showed secretion of exosomes for hiPSC-CMs, as confirmed by the size and shape of the isolated particles. The size of exosomes was determined to be 71.4 nm (mode), within the characteristic exosomal range. Immunoblot analysis of exosome lysate demonstrated enrichment of known exosome-specific protein markers (CD63 and Hsp70). Most importantly, BAECs treated with exosomes showed significant (p &lt; 0.05) increases in migration, proliferation, and tube formation, as compared to the no exosome control. Overall, our results demonstrate that treating BAECs with exosomes isolated from hiPSC-CMs enhances angiogenesis. Overall, this study demonstrates the angiogenic potential of human iPSC-CM- derived exosomes. The cell-free therapeutics using exosomes constitutes a novel innovative approach for future clinical therapy to induce angiogenesis in the post-ischemic heart.
ASSESSMENT OF THE HIGH RISK AND UNMET NEED IN PATIENTS WITH CAD AND TYPE 2 DIABETES (ATHENA): US BURDEN OF ILLNESS IN A COMMERCIALLY-INSURED POPULATION
Authors: Eric Wittbrodt, Narinder Bhalla, Karolina Andersson Sundell, Phillip Hunt, Janek Rudnik, Nathan Wong
Journal: Journal of the American College of Cardiology (2019)
EFFICACY OF SURGICAL AND MEDICAL INTERVENTION FOR TREATMENT OF LEFT-SIDED INFECTIVE ENDOCARDITIS
Authors: Stergios Gatzoflias, Matthew Beier, Marcia Gailes, Karina Guaman, Michal Segall, Anisha Vasireddi, Catherine Wang, Hiroo Takayama, Vinayak Nilkanth Bapat, Yoshifumi Naka, Michael Argenziano, Craig Smith, Paul Kurlansky, Isaac George
Journal: Journal of the American College of Cardiology (2019)
REVERSE CARDIAC REMODELING IN HEART FAILURE AFTER CARDIAC RESYNCHRONIZATION THERAPY IS ASSOCIATED TO REDUCTION OF RHO KINASE ACTIVATION IN PERIPHERAL MONONUCLEAR BLOOD CELLS
Authors: Jorge E. Jalil, Rodrigo Altamirano, Ana de León, Jackeline Moya, Cristián Mancilla, Luigi Gabrielli, Paul MacNab, Samuel Córdova, Alejandro Paredes, Ismael Vergara, Alex Bittner, Ivonne Padilla, Karime Sabat, Karla Pastorini, María Paz Ocaranza
Journal: Journal of the American College of Cardiology (2019)
Programming of macrophages by UV-irradiated apoptotic cancer cells inhibits cancer progression and lung metastasis
Authors: Yong-Bae Kim, Young-Ho Ahn, Ji-Hae Jung, Ye-Ji Lee, Jin-Hwa Lee, Jihee Lee Kang
Journal: Cellular and Molecular Immunology (2019)

Apoptotic cell clearance by phagocytes is essential in tissue homeostasis. We demonstrated that conditioned medium (CM) from macrophages exposed to apoptotic cancer cells inhibits the TGFβ1-induced epithelial–mesenchymal transition (EMT), migration, and invasion of cancer cells. Apoptotic 344SQ (ApoSQ) cell-induced PPARγ activity in macrophages increased the levels of PTEN, which was secreted in exosomes. Exosomal PTEN was taken up by recipient lung cancer cells. ApoSQ-exposed CM from PTEN knockdown cells failed to enhance PTEN in 344SQ cells, restore cellular polarity, or exert anti-EMT and anti-invasive effects. The CM that was deficient in PPARγ ligands, including 15-HETE, lipoxin A4, and 15d-PGJ2, could not reverse the suppression of PPARγ activity or the PTEN increase in 344SQ cells and consequently failed to prevent the EMT process. Moreover, a single injection of ApoSQ cells inhibited lung metastasis in syngeneic immunocompetent mice with enhanced PPARγ/PTEN signaling both in tumor-associated macrophages and in tumor cells. PPARγ antagonist GW9662 reversed the signaling by PPARγ/PTEN; the reduction in EMT-activating transcription factors, such as Snai1 and Zeb1; and the antimetastatic effect of the ApoSQ injection. Thus, the injection of apoptotic lung cancer cells may offer a new strategy for the prevention of lung metastasis.
SILENT THREAT: SUCCESSFUL SURGICAL TREATMENT OF GIANT AORTIC ANEURYSM IN A PATIENT WITH MARFAN'S SYNDROME
Authors: America Gwendolyne Urbina Vazquez, Nilda Espinola-Zavaleta, Andrés Herrera, Humberto Martínez-Hernández, Susana Ortega Silva, Grecia Iveth Maryelis Raymundo Martinez, Alexandra Arias-Mendoza
Journal: Journal of the American College of Cardiology (2019)
TWENTY-EIGHT YEAR TRENDS IN ACUTE MYOCARDIAL INFARCTION WITH INPATIENT-ONSET: THE ATHEROSCLEROSIS RISK IN COMMUNITIES SURVEILLANCE STUDY, 1987-2014
Authors: Sameer Arora, Matthew Cavender, Arman Qamar, Muthiah Vaduganathan, Ambarish Pandey, Kunihiro Matsushita, John Vavalle, Joseph Rossi, George Stouffer, Melissa Caughey
Journal: Journal of the American College of Cardiology (2019)
Abstract 347: Mechanistic Basis of Neonatal Heart Regeneration Revealed by Transcriptome and Histone Modification Profiling
Authors: Zhaoning Wang, Miao Cui, Wenduo Ye, Wei Tan, Giovanni Botten, John McAnally, John M Shelton, Min S Kim, Venkat Malladi, Beibei Chen, Rhonda Bassel-Duby, Ning Liu, Eric N Olson
Journal: Circulation Research (2018)

The adult mammalian heart has very limited capacity to regenerate upon injury. Following myocardial infarction, cardiomyocytes are extensively lost and fibroblasts are activated to form a scar, resulting in compromised cardiac function. In contrast, the heart of a neonatal mouse has full capacity to regenerate after myocardial infarction, although such regenerative ability is lost by postnatal (P) day 7. The molecular properties of neonatal hearts that enable regeneration remain unknown. To uncover the mechanisms of neonatal heart regeneration, we induced myocardial infarction (MI) in P1 and P8 hearts, and profiled transcriptomic and epigenomic dynamics by RNA-Seq, H3K27ac ChIP-Seq and H3K27me3 ChIP-Seq at various time points following the surgery. Analysis of differentially expressed genes and groups of enhancers that acquire active status post-MI revealed distinct post-infarction responses between P1 and P8 hearts. Dramatic differences in immune response and developmental gene programs were identified in regenerative P1 versus non-regenerative P8 hearts. Furthermore, we analyzed transcription factors involved in the injury response post MI and constructed gene regulatory networks during neonatal cardiac injury. This work provides insights into the molecular basis of neonatal heart regeneration, and identifies potential genes and cis-regulatory elements that can be modulated to facilitate heart regeneration.
Abstract 538: Reduced Protein and mRNA Levels of Velosin Containing Protein in Left Ventricular Myocardium of Dogs With Advanced Heart Failure Are Restored Following Chronic Therapy With Elamipretide
Authors: Ramesh C Gupta, Vinita S Gupta, Hani Sabbah
Journal: Circulation Research (2018)

Introduction: The failing heart manifests abnormalities of mitochondrial function characterized by reduced respiration, reduced membrane potential and opening of permeability transition pore (mPTP). Recent studies have shown that velosin containing protein (VCP), an ATPase associate protein, preserves mitochondrial respiration and prevents opening of the mPTP. Long-term therapy with elamipretide (ELAM), a novel mitochondria-targeting tetra-peptide, was previously shown improve mitochondrial respiration, membrane potential and prevent opening of the mPTP in dogs with intracoronary microembolization-induced heart failure (HF). Hypothesis: This study tested the hypothesis that mRNA and protein levels of VCP are decreased in left ventricular (LV) myocardium of dogs with HF and that chronic therapy with ELAM reverses this dysregulation. Methods: Studies were performed using LV tissue from 14 HF dogs randomized to 3 months monotherapy with subcutaneous injections of ELAM (HF+ELAM, 0.5 mg/kg once daily, n=7) or no therapy at all (control, HF-CON, n=7). LV tissue from 6 normal (NL) dogs was used for comparisons. Protein levels of VCP and GAPDH, an internal loading control, were determined in LV SDS-extracts using Western blotting coupled with chemiluminescence detection and band intensity was expressed in densitometric units (du). Using isolated RNA and specific primers, mRNA expression of VCP normalized to GAPDH. Results: mRNA and protein levels of GAPDH in LV tissue remained unchanged among the 3 study groups. Compared to NL, mRNA expression of VCP was reduced by 3.67 fold in HF-CON. Compared to NL, protein level of VCP was significantly reduced compared to HF-CON (0.30 ± 0.04 vs. 1.77 ± 0.31 du, p&lt;0.05). In HF+ELAM treated dogs, mRNA expression of VCP was reduced by only 1.07 fold compared to HF-CON (p&lt;0.05). Similarly, in HF+ELAM, protein levels of VCP were significantly higher than in HF-CON (1.03 ± 0.16 du, p&lt;0.05). Conclusions: VCP mRNA and protein levels are significantly reduced in LV myocardium of dogs with chronic HF. Long-term therapy with ELAM reverses this dysregulation. The findings support the observations of improved mitochondrial respiration and reduced mPTP opening in dogs with advanced HF following chronic therapy with ELAM.
Abstract 530: The Ufm1 Specific Ligase 1 Regulates Endoplasmic Reticulum Homeostasis and Protects Against Heart Failure
Authors: Jie Li, Guihua Yue, Wenxia Ma, Aizhen Zhang, Jianqiu Zou, Jun Wang, Honglin Li, Huabo Su
Journal: Circulation Research (2018)

Protein modifications by ubiquitin and ubiquitin-like proteins are emerging as an important regulatory mechanism of protein function and involved in various cellular processes. Ufm1 (ubiquitin-fold modifier 1) is a novel ubiquitin-like protein that modifies protein targets in a UBA5 (E1) - Ufc1 (E2) - Ufl1 (E3) dependent manner. While defects in ubiquitin- and SUMO-modification have been shown to provoke cardiac remodeling and dysfunction, the importance of Ufm1 modification has not been explored in the normal and stressed heart. Western blotting revealed that Ufm1 specific ligase 1 (Ufl1), an enzyme essential for Ufm1 modification, was increased in hypertrophic mouse hearts but reduced in the failing hearts of patients with dilated cardiomyopathy. To determine the functional role of Ufl1 in the heart, we generated a cardiac-specific knockout mouse and showed that Ufl1-deficient mice developed age-dependent cardiomyopathy and heart failure, as indicated by elevated cardiac fetal gene expression, increased fibrosis and impaired cardiac contractility. When challenged with pressure overload, Ufl1-deficient hearts exhibited remarkably greater hypertrophy, exacerbated fibrosis and worsened cardiac contractility compared with control counterparts. Transcriptome analysis identified that genes associated with the endoplasmic reticulum (ER) function were dysregulated in Ufl1-deficient hearts. Biochemical analysis revealed that excessive ER stress preceded and deteriorated along with the development of cardiomyopathy in Ufl1-deficient hearts. Mechanistically, Ufl1 depletion impaired PERK signaling and aggravated cardiomyocyte cell death following ER stress. Administration of the chemical ER chaperone tauroursodeoxycholic acid to Ufl1-deficient mice alleviated ER stress and attenuated pressure overload-induced cardiac dysfunction. Our results advance a novel concept that the Ufm1 system is essential for cardiac homeostasis through regulation of ER function and that upregulation of myocardial Ufl1 could be protective against heart failure.
Sport and exercise medicine as a vehicle for advocacy? The Canadian perspective
Authors: Jane S Thornton, Margaret Burghardt
Journal: British Journal of Sports Medicine (2019)

As sport and exercise medicine practitioners we have a unique opportunity to advocate for our athletes, our patients and our society. In this Canadian Academy of Sport and Exercise Medicine (CASEM)-led issue, we highlight several articles that serve as calls to action.

What are the long-term effects of concussion? What are risk factors for a poor outcome from concussion? From Newcastle under Lyme’s Keele University, psychology Professor Andrew Rutherford and colleagues explore the contentious debate over heading in football and risk of dementia in later life. Any rule changes made as a result of these concerns, they argue, would be based on opinion, not evidence; and reinforce the call for appropriately designed studies ( see page 321 ). In a submission for BJSM’s novel initiative, the PhD Academy Award, University of Michigan’s Dr Kathryn O’Connor elaborates on factors that increase concussion risk and prolong recovery, and the role of mental health, from studying 800 concussions in 10 604 military cadets ( see page 368 ). The take home message? Female cadets and cadets with greater somatic symptoms at baseline are at higher risk of concussion and may need specific interventions or monitoring; injury and environmental factors are what dictate prolonged recovery.

To make real progress in managing …
THE RELATIONSHIP BETWEEN OBESITY AND ECHOCARDIOGRAPHIC IMAGE QUALITY: A CASE FOR CONTRAST
Authors: Katherine Ellenberger, Joanne Kitley, Prajith Jeyaprakash, Avitasha Darshni, Sukhmandeep Sangha, Shanthosh Sivapathan, Faraz Pathan
Journal: Journal of the American College of Cardiology (2019)
THE OUTCOMES AND BASELINE CHARACTERISTICS OF HEART FAILURE WITH MID-RANGE EJECTION FRACTION COMPARED TO HEART FAILURE WITH REDUCED EJECTION FRACTION
Authors: Hassan Alkhawam, Timothy Vittorio, James Ampadu, Preetham Reddy Muskula, Joseph Lieber, Tarek Helmy, Deana Mikhalkova
Journal: Journal of the American College of Cardiology (2019)
NON-TRANSFEMORAL TRANSCATHETER AORTIC VALVE REPLACEMENT APPROACH IS ASSOCIATED WITH A HIGHER RISK OF NEW-ONSET ATRIAL FIBRILLATION: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: Natthapon Angsubhakorn, Veraprapas Kittipibul, Narut Prasitlumkum, Jakrin Kewcharoen, Patompong Ungprasert
Journal: Journal of the American College of Cardiology (2019)
EVALUATION OF CARDIAC BIOMARKERS OF FIBROSIS DIFFERENTIATES BETWEEN HEART FAILURE PATIENTS WITH PRESERVED OR REDUCED EJECTION FRACTION
Authors: Evangelos Oikonomou, Gerasimos Siasos, Vasiliki Tsigkou, Konstantinos Mourouzis, Efstathios Dimitropoulos, Savvas Mazaris, Evanthia Bletsa, Maria-Paraskevi Panoilia, Panagiota Stampouloglou, Angeliki Papastavrou, Eleni Kokkou, Sotirios Tsalamandris, Georgia Vogiatzi, Marina Zaromytidou, Manolis Vavuranakis, Dimitris Tousoulis
Journal: Journal of the American College of Cardiology (2019)
A CASE OF TRANS-SEPTAL LEFT ATRIAL THROMBECTOMY UTILIZING ANGIOVAC EXTRACORPOREAL VENOUS-VENOUS CARDIOPULMONARY BYPASS FILTER CIRCUIT IN A PATIENT WITH OBSTRUCTIVE SHOCK FROM LARGE LA AND PROSTHETIC VALVE THROMBOSIS POST TMVR
Authors: Moses Ashukem, Lucas Seibolt, Divya Ratan Verma, Akil Loli, Timothy Byrne
Journal: Journal of the American College of Cardiology (2019)
TRS2P PREDICTS MORTALITY AFTER MI IN YOUNG ADULTS: FROM THE PARTNERS YOUNG-MI REGISTRY
Authors: Avinainder Singh, Arman Qamar, Erin Bohula, Ersilia M. DeFilippis, Sanjay Divakaran, Marc Sabatine, David Morrow, Eugene Braunwald, Deepak L. Bhatt, Ron Blankstein
Journal: Journal of the American College of Cardiology (2019)