tbuckley/cabot-search huggingface dataset:
Birch pollen allergy in Europe
Authors: T. Biedermann, L. Winther, S. J. Till, P. Panzner, A. Knulst, E. Valovirta
Journal: Allergy (2019)

Abstract Birch and other related trees of the families Betulaceae and Fagaceae (alder, hazel, oak, hornbeam, chestnut, and beech) constitute the birch homologous group. This grouping is primarily based on the extensive IgE cross‐reactivity of allergen homologs to the major birch allergen Bet v 1. Birch pollen is the most dominant tree pollen in Northern and Central Europe and is a major cause of allergic rhinitis and, possibly, asthma symptoms. Over the last few decades, levels of birch pollen have risen and the period of exposure has increased due to climate changes. Subsequently, the prevalence of birch pollen sensitization has also increased. The cross‐reactivity and sequential pollen seasons within the birch homologous group create a prolonged symptomatic allergy period beyond birch pollen alone. Furthermore, many plant food allergens contain homologs to Bet v 1, meaning that the majority of patients with birch pollen allergy suffer from secondary pollen food syndrome ( PFS ). As a result, the negative impact on health‐related quality of life ( HRQ oL) in patients allergic to birch pollen is significant. The purpose of this manuscript was to narratively review topics of interest such as taxonomy, cross‐reactivity, prevalence, clinical relevance, PFS , and HRQ oL with regard to birch pollen allergy from a European perspective.
Abstract P116: The Impact of Diet Low in Fruits and Vegetables on Cardiovascular Disease Burden Across 195 Countries in 2015
Authors: Patrick J Sur, Ashkan Afshin
Journal: Circulation (2017)

Introduction: While cardio-protective effects of fruits and vegetables are well-established, the impact of their suboptimal intake on the CVD burden across nations and levels of development has not been evaluated. Objective: To systematically quantify the burden of CVD attributable to low intake of fruits and low intake of vegetables in 195 countries by age, sex, country, and development status in 2015. Methods: We obtained data on consumption of fruits and vegetables from nationally or subnationally representative nutrition surveys and data on their national availability from the UN FAO. Etiologic effect sizes of fruits and vegetables on CVD endpoints were obtained from meta- analyses of prospective cohort studies. The optimal level of intakes for each was determined based on the levels associated with lowest risk of mortality in prospective observational studies. A comparative risk assessment analysis was conducted to quantify the proportion of disability- adjusted life years (DALYs) attributable to low intake of each. The variation of this burden was further evaluated across different levels of our newly developed socio-demographic index (SDI). Results: In 2015, low intake of fruits accounted for 57.3 (95% UI: 37.1- 78.4) million DALYs due to CVD globally (41.5% from IHD and 58.5% from stroke). Low intake of vegetable caused 44.6 (23.6- 68.8) million CVD DALYs (67.3% IHD and 32.7% stroke). The highest burden of CVD attributable to low intake of fruits and vegetables was seen in the middle and low-middle SDI quintiles (17.2 and 14.3% of total DALYs), while the lowest burden for each was seen in high and high-middle SDI quintiles (12.7 and 11.2%). At the country level, the attributable CVD burden ranged from 5.1% of total DALYs (Rwanda) to 23.2% (Bangladesh) for low intake of fruit and from 5.9% (North Korea) to 19.4% (Mongolia) for low intake of vegetable. Conclusion: Our findings suggest that population inventions to increase consumption of fruits and vegetables at population level could save millions of life years globally. Figure. Age-standardized proportion of disability-adjusted life years attributable to low intake of fruits (A) and vegetables (B) from cardiovascular disease among adults (&gt; 25y) in 2015.
READMISSION RISK FOR ACUTE MYOCARDIAL INFARCTION AFTER ACUTE MYOCARDIAL INFARCTION STRATIFIED BY INITIAL PRESENTATION OF STEMI VERSUS NSTEMI
Authors: Grant Henderson, Mouin Abdallah, Michael Johnson, Moses Anabila, Kathleen Kravitz, Jeevanantham Rajeswaran, Venu Menon, Stephen Ellis, A. Lincoff, Eugene Blackstone, Samir Kapadia, Umesh Khot
Journal: Journal of the American College of Cardiology (2019)
Abstract 100: PRDM16 is a Novel Regulator of Cardiac Hypertrophy, Remodeling and Mitochondrial Dynamics
Authors: Karla Maria Pires, Sihem Boudina
Journal: Circulation Research (2018)

Elucidation of the mechanisms that cause cardiac hypertrophy is essential for developing novel therapeutic strategies to prevent or reverse these prevalent conditions. Prdm16/Mel1 (PRDM16) belongs to the Prdm family of transcription factors involved in cell fate determination and development. PRDM16 deletion, found in humans with 1p36 deletion syndrome, has been associated with two main cardiomyopathies: left ventricle non-compaction (LVNC) and dilated cardiomyopathy. Nonetheless, its role in the heart and the underlying mechanisms by which these mutations contribute to the development of cardiomyopathy are unknown. We sought to directly assess the role of Prdm16 in the developing and adult heart by generating both a germline (cPRDM16) and a tamoxifen-inducible (ciPRDM16) cardiomyocyte-specific Prdm16 knockout mice. cPRDM16KO mice died shortly after birth, showing grossly abnormal ventricles that were reduced in size and often exhibiting a cleft at their apex, consistent with LVCN. Both heterozygous mice (cPRDM16KOhet) and ciPRDM16KO are viable and displayed markedly increased heart size, cardiomyocyte cross sectional area, collagen deposition and expression of genes involved in cardiac hypertrophy and ECM production. We observed an increased in TGF-β receptors mRNA expression as well as activation of Smad signaling in the hearts of cPRDM16KO neonates, cPRDM16 heterozygous, and ciPRDM16 KO mice. Interestingly, we observed a systematic reduction in Drp1 phosphorylation on Ser616 (activation) in the hearts of cPRDM16KO and cPRDM16het mice. The reduction in Drp1 phosphorylation was associated with more tubular mitochondria in cPRDM16KO mice. Interestingly, by 25 weeks, cPRDM16het mice accumulated more mitochondrial proteins, despite exhibiting no change in PGC1α. Together, these data reveal previously unknown roles for Prdm16 in protection against cardiac hypertrophy and fibrosis through the suppression of TGF-β/Smad signaling in the heart. They also reveal roles for PRDM16 in the modulation of mitochondrial dynamics and clearance in the heart, a process that likely involves the fission protein Drp1.
Abstract 501: Anemia of Inflammation in an Exonuclease Deficient Lupus Mouse
Authors: Stephen L Rego, Scott Harvey, Sean R Simpson, Wayne O Hemphill, Jason M Grayson, Fred W Perrino
Journal: Circulation Research (2018)

Background: Patients with chronic inflammatory conditions, such as autoimmune diseases, infections, and cancer, often display anemia of inflammation (AI). 50% of patients with systemic lupus erythematosus display clinical signs of anemia. Mutations at aspartate residue 18 of the three prime repair exonuclease 1 ( TREX1 ) gene, which codes for the primary mammalian exonuclease, cause a monogenic form of cutaneous lupus erythematosus in humans and the genetically precise TREX1 D18N mice recapitulate a lupus-like disease. Objective: The link between failed DNA degradation during erythropoiesis and anemia prompted our studies to investigate whether TREX1 dysfunction might contribute to AI. Methods: AI in TREX1 D18N mice was determined through analysis of hematocrit, hemoglobin, gene expression analysis, immunohistochemistry (IHC) and flow cytometry. Response to phenylhydrazine (PHZ) induced anemia and activation of DNA sensing pathways were determined through IHC and interferon stimulatory gene (ISG) expression analysis of the liver, spleen and erythroblastic islands. Results: The TREX1 D18N mice exhibit altered erythropoiesis including reduced hematocrit, increased erythropoietic and hematotoxic gene expression levels in the spleen (~10-20 fold) and phenotypic signs of normocytic normochromic anemia. Anemia in TREX1 lupus mice is accompanied by increased erythropoietin (Epo) and extramedullary hematopoiesis. Furthermore, the TREX1 D18N mice display an inappropriate response to anemic challenge. Enhanced ISG expression is apparent and results from failed processing and sensing of undegraded erythroblast DNA. Conclusion: These results support a critical role for TREX1 in the degradation of erythroblast DNA and identify a distinct AI phenotype in TREX1 D18N mice.
EFFECTIVENESS AND SAFETY OF NON-VITAMIN K ANTAGONIST ORAL ANTICOAGULANTS COMPARED TO WARFARIN AMONG FRAIL NONVALVULAR ATRIAL FIBRILLATION PATIENTS
Authors: Gregory Y.H. Lip, Allison Keshishian, Amiee Kang, Amol Dhamane, Xuemei Luo, Xiaoyan Li, Neeraja Balachander, Lisa Rosenblatt, Jack Mardekian, Xianying Pan, Manuela Di Fusco, Alessandra Bassalobre Garcia, Huseyin Yuce, Steven Deitelzweig
Journal: Journal of the American College of Cardiology (2019)
INCIDENCE, PREDICTORS, AND IMPACT OF READMISSIONS TO NON-INDEX HOSPITALS AFTER TRANSCATHETER AORTIC VALVE REPLACEMENT ON IN-HOSPITAL OUTCOMES: FROM THE NATIONWIDE READMISSION DATABASE
Authors: Tomo Ando, Oluwole Adegbala, Pedro Villablanca, Emmanuel Akintoye, Said Ashraf, Mohamed Shokr, Fayez Siddiqui, Alexandros Briasoulis, Hisato Takagi, Cindy Grines, Luis Afonso
Journal: Journal of the American College of Cardiology (2019)
AORTIC ROOT INFECTION WITH AORTOCAVITARY FISTULA: A RARE PRESENTATION OF NATIVE VALVE GEMELLA MORBILLORUM ENDOCARDITIS
Authors: Abdur Rehman, Umbreen Hussain, Balaji Shanmugam, Mohammed Abdulrazzaq, Theresa Ratajczak, Muhanad Al-Zubaidi
Journal: Journal of the American College of Cardiology (2019)
T-cell mitochondrial dysfunction and lymphopenia in DOCK2-deficient patients
Authors: Mohammed F. Alosaimi, Hiba Shendi, Abdallah Beano, Kelsey Stafstrom, Rabab El Hawary, Safa Meshaal, Nermeen Galal, Sung-Yun Pai, Aisha El-Marsafy, Raif S. Geha, Janet Chou
Journal: Journal of Allergy and Clinical Immunology (2019)
REPORTING THE PRESENCE OF CORONARY ARTERY CALCIUM IN THE FINAL IMPRESSION OF NON-GATED CT CHEST SCANS INCREASES APPROPRIATE UTILIZATION OF STATINS
Authors: Raymond Fisher, Anthony Vandehei, Charles Haller, Brian Shipley, Christopher Kaatz, Satoshi R. Shin, Jaclyn Harris, Jessica Rouse, Joshua Boster, Sarah Davis, Lisa Townsend, Dustin Thomas
Journal: Journal of the American College of Cardiology (2019)
PROPHYLACTIC IMPLANTABLE CARDIOVERTER DEFIBRILLATORS IN PATIENTS WITH CONTINUOUS FLOW LEFT VENTRICULAR ASSIST DEVICES: ARE THEY COST-EFFECTIVE?
Authors: Safia Chatur, Derek Chew, Nakul Sharma, Mathew Church, Satish R. Raj, Braden Manns, Stephen Wilton
Journal: Journal of the American College of Cardiology (2019)
MITRAL ANNULAR EXCURSION IN HEART FAILURE WITH PRESERVED EJECTION FRACTION DURING EXERCISE: THE IMPACT OF A FAULTY CARDIAC PISTON
Authors: James MacNamara, Michinari Hieda, William Cornwell, Sheryl Livingston, Mitchel Samels, Braden Everding, Benjamin Levine, Satyam Sarma
Journal: Journal of the American College of Cardiology (2019)
MYOCARDIAL WORK: A NOVEL INDEX OF LEFT VENTRICULAR SYSTOLIC FUNCTION IN SOUTH ASIAN HALF-MARATHON RUNNERS CORRELATED WITH ECHOCARDIOGRAPHIC AND CLINICAL VARIABLES
Authors: Renuka Jain, Shantanu Sengupta, Susan Olet, Nitin Burkule, Bijoy Khandheria
Journal: Journal of the American College of Cardiology (2019)
PREDICTING PERMANENT PACEMAKER NEED AFTER TRANSCATHETER AORTIC VALVE REPLACEMENT BY ASSESSING POST-DEPLOYMENT ATRIAL PACING RESPONSE: A MULTI-CENTER STUDY
Authors: Amar Krishnaswamy, Yasser Sammour, Amer Kadri, Antonette Karrthik, Kinjal Banerjee, Najdat Bazarbashi, Manpreet Kaur, Megan Lyden, Stephanie Mick, Lars Svensson, Grant Reed, Antonio Mangieri, Samir Kapadia, Azeem Latib
Journal: Journal of the American College of Cardiology (2019)
ANTIPLATELET THERAPY PRESCRIPTION PATTERNS AND ASSOCIATIONS WITH CLINICAL OUTCOMES IN MEDICARE BENEFICIARIES WITH ATRIAL FIBRILLATION PRESCRIBED NO ORAL ANTICOAGULATION AFTER ACUTE ISCHEMIC STROKE
Authors: Kay-Won Chang, Ying Xian, Xin Zhao, Roland Matsouaka, Lee Schwamm, Gregg Fonarow, Deepak L. Bhatt, Shreyansh Shah, Barbara Lytle, Eric Smith, Jonathan Hsu
Journal: Journal of the American College of Cardiology (2019)
Abstract 247: Mitochondrial Damage Associated Molecular Patterns Promotes Endothelial Dysfunction in the Microcirculation
Authors: Karima Ait-Aissa, Andrew O Kadlec, Dawid S Chabowski, Joseph C Hockenberry, Jasmine M Linn, David D Gutterman, Andreas M Beyer
Journal: Circulation Research (2018)

Vascular endothelial dysfunction is an early event in the development of atherosclerosis. Flow-mediated dilation (FMD) can be used to identify such endothelial dysfunction which is characterized by a decrease of nitric oxide (NO). Indeed, in subjects with coronary artery disease (CAD), microvascular FMD switches from a NO-mediated to a H 2 O 2 -mediated mechanism with corresponding elevations in mitochondrial reactive oxygen species (ROS). Recent evidence has shown an increase circulating mitochondrial DNA Damage-Associated Molecular Patterns ( mt DAMPs) in Coronary Heart Disease subjects and has been linked to vascular dysfunction. mt DAMPs signaling can activate the inflammatory response directly through activation of Toll Like Receptors 9 (TLR9). The effect of mt DAMPs on the endothelial function in the human microcirculation and the potential role for TLR9- mtDNA signaling axis to affect microvascular FMD, is unknown. In this study, we hypothesized that increased levels of mt DAMPs result in changes in microvascular redox environment that promote a loss of NO mediated dilation and elevation in mitochondrial derived ROS The incubation of cultured endothelial cells (ECs) with mt DAMPs decreased the ratio peNOS:teNOS in a time-dependent manner supporting the idea that mt DAMPs reduce NO bioavailability. This effect was eliminated when the ECs were pre-incubated with TLR9-targeted si-RNA. Prolonged (15-20H) ex vivo exposure to low dose of mt DAMPs (1ug/mL) changed the mechanism of FMD from NO to compensatory increase in H 2 O 2 to preserve overall dilator capacity in non-CAD human adipose micro-arterioles (% Max Diameter: Control 84.7±8.2; + L-NAME: 89.4±5.5; + Peg-Cat 35.4±10.8*; N=5, *p&lt;0.05). With higher dose of mt DAMPs (2.5ug/mL), the magnitude of the FMD was however significantly altered (% Max Diameter: high dose: 42.8 ±9.1* vs. low dose of mt DAMPs 84.7±8.2; N=4; p&lt;0.05). Our data suggest a potential pathogenic role of mt DAMPs in microvascular function through TLR9 to reduce NO bioavailability and induce endothelial dysfunction.
An Increasing Trend of Incidence, Prevalence and Mortality, and Occurrence of Second Primary Malignancies Among Patients with B-Cell Non-Hodgkin Lymphoma: A 10-Year Longitudinal Population-Based Retrospective Cohort Study in South Korea
Authors: Jin Seok Kim, Yanfang Liu, Kyoung Hwa Ha, Hong Qiu, Lee Anne Rothwell, Yu Ri Kim, Hyeon Chang Kim
Journal: Blood (2018)
NON-INVASIVE ELECTROANATOMICAL MAPPING FOR PREDICTING SITE OF ORIGIN OF OUTFLOW TRACT VENTRICULAR TACHCYARDIAS
Authors: Aditi Vaishnav, Stavros Mountantonakis, Jeremy Jacobson, Neil Bernstein, Kabir Bhasin, Laurence Epstein, Nicholas Skipitaris
Journal: Journal of the American College of Cardiology (2019)
Mosaicism in women with focal dermal hypoplasia
Authors: L. Heinz, E. Bourrat, P. Vabres, J. Thevenon, A. Hotz, S. Hörer, J. Küsel, A.D. Zimmer, S. Alter, R. Happle, J. Fischer
Journal: British Journal of Dermatology (2019)

This report from Germany and France describes four women with focal dermal hypoplasia (FDH), a genetic condition affecting the skin, skeleton, teeth and eyes. FDH is caused by a mutant (abnormal) gene called PORCN, found on the X chromosome. Male embryos with the mutant gene do not usually survive. Females are more complicated. Firstly, they have two X chromosomes, but for FDH to show up it only needs the mutant gene to be present on one of them. Secondly, soon after conception one of the two X chromosomes in each cell of the embryo is randomly deactivated. Cell lines (daughter cells) from cells where the normal X chromosome remains active develop normally; cell lines where the abnormal X chromosome remains active develop abnormally owing to the mutant gene. This phenomenon, where cell lines in an individual represent different genetic populations, is called mosaicism (and, incidentally, explains why tortoiseshell cats are always female). The FDH mutation also frequently happens spontaneously after fertilisation, in the earliest stages of development, but before X chromosome deactivation. The main message from this report is that one cannot exclude FDH simply by using standard genetic tests on blood alone. In affected women, in whom the clinical signs may be subtle and a blood test negative, because of mosaicism the abnormal gene may still be found in those skin cells where the X chromosome carrying it remains active. Importantly, the ovaries may also contain such cells, in which case the condition could be passed on to children.
AN IPAD-BASED MEASURE OF PROCESSING SPEED IN OLDER ADULTS HOSPITALIZED FOR HEART FAILURE
Authors: Eiran Z. Gorodeski, Anson B. Rosenfeldt, Karen Fang, Cynthia Kubu, Stephen M. Rao, Amy E. Jansen, Tanujit Dey, Jay L. Alberts
Journal: Journal of the American College of Cardiology (2019)
β-hydroxybutyrate attenuates renal ischemia-reperfusion injury through its anti-pyroptotic effects
Authors: Takaya Tajima, Ayumi Yoshifuji, Ayumi Matsui, Tomoaki Itoh, Kiyotaka Uchiyama, Takeshi Kanda, Hirobumi Tokuyama, Shu Wakino, Hiroshi Itoh
Journal: Kidney International (2019)

Ketone bodies including β-hydroxybutyrate (β-OHB) have been shown to protect against ischemic tissue injury when present at low concentrations. We evaluated the impact of β-OHB on renal ischemia/reperfusion injury (IRI). Mice were treated with a continuous infusion of β-OHB using an osmotic mini-pump before and after IRI. We also tested the effects of increasing endogenous serum β-OHB levels by fasting. Renal IRI was attenuated by β-OHB treatment compared to saline control, with similar results in the fasting condition. β-OHB treatment reduced the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells and increased expression of forkhead transcription factor O3 (FOXO3), an upstream regulator of pyroptosis. Although β-OHB treatment did not impact markers of apoptosis, it decreased the expression of caspase-1 and proinflammatory cytokines, indicating that β-OHB blocked pyroptosis. In a human proximal tubular cell line exposed to hypoxia and reoxygenation, β-OHB reduced cell death in a FOXO3-dependent fashion. Histone acetylation was decreased in kidneys exposed to IRI and in proximal tubular cells exposed to hypoxia and reoxygenation, and this effect was ameliorated by β-OHB through the inactivation of histone deacetylases. In vitro, β-OHB treatment restored histone acetylation at the FOXO3 promoter. Consistent with epigenetic molecular effects, the renoprotective effects of β-OHB were still observed when the continuous infusion was stopped at the time of IRI. Thus, β-OHB attenuates renal IRI through anti-pyroptotic effects, likely mediated by an epigenetic effect on FOXO3 expression.
DECLINE IN DEVICE DERIVED ACTIVITY: THE HARBINGER OF DEATH
Authors: Sina Jame, Thomas Cascino, Raymond Yeow, Teetouch Ananwattanasuk, Michael Ghannam, John Coatney, Ghanshyam Shantha, Eugene H. Chung, Mohammed Saeed, Ryan Cunnane, Rakesh Latchamsetty, Hamid Ghanbari, Aman Chugh, Frank Pelosi, Frank Bogun, Hakan Oral, Krit Jongnarangsin
Journal: Journal of the American College of Cardiology (2019)
Translating Developmental Neuroscience to Understand Risk for Psychiatric Disorders
Authors: Heidi C. Meyer, Francis S. Lee
Journal: American Journal of Psychiatry (2019)

The transition from childhood to adulthood represents the developmental time frame in which the majority of psychiatric disorders emerge. Recent efforts to identify risk factors mediating the susceptibility to psychopathology have led to a heightened focus on both typical and atypical trajectories of neural circuit maturation. Mounting evidence has highlighted the immense neural plasticity apparent in the developing brain. Although in many cases adaptive, the capacity for neural circuit alteration also induces a state of vulnerability to environmental perturbations, such that early-life experiences have long-lasting implications for cognitive and emotional functioning in adulthood. The authors outline preclinical and neuroimaging studies of normative human brain circuit development, as well as parallel efforts covered in this issue of the Journal, to identify brain circuit alterations in psychiatric disorders that frequently emerge in developing populations. Continued translational research into the interactive effects of neurobiological development and external factors will be crucial for identifying early-life risk factors that may contribute to the emergence of psychiatric illness and provide the key to optimizing treatments.
High synovial fluid interleukin-1 receptor antagonist (IL-1 RA)/interleukin-1 beta (IL-1beta) ratio naturally occurs in human knee osteoarthritis
Authors: P. Richette, M. Francois, T. Bardin, C. Bazille, C. Fitting, J. Cavaillon, M. Corvol, F. Rannou
Journal: Annals of the Rheumatic Diseases (2006)
ATRIAL FIBRILLATION INCIDENCE, PREVALENCE, AND RISK FACTORS IN THE PRECISION TRIAL: A COHORT STUDY
Authors: Eoin Donnellan, Kathy Wolski, Venu Menon, Mohamed Kanj, Oussama Wazni, Steven Nissen, Khaldoun Tarakji
Journal: Journal of the American College of Cardiology (2019)
Hepatitis B Virus Induces Autophagy to Promote its Replication by the Axis of miR‐192‐3p‐XIAP Through NF kappa B Signaling
Authors: Jingwen Wang, Jianwen Chen, Yang Liu, Xianhuang Zeng, Mingcong Wei, Shaoshuai Wu, Qiushuang Xiong, Feifei Song, Xu Yuan, Yu Xiao, Yun Cao, Changyong Li, Lang Chen, Mingxiong Guo, Yun‐Bo Shi, Guihong Sun, Deyin Guo
Journal: Hepatology (2018)

Hepatitis B virus (HBV) is a major risk factor for the development and progression of hepatocellular carcinoma. It has been reported that viral infection can interfere with cellular microRNA (miRNA) expression and participate in the pathogenesis of oncogenicity. Here, we report that decreasing levels of the expression of the miRNA miR-192-3p is associated with rising levels of HBV DNA in the serum of HBV patients. We revealed that HBV infection repressed the expression of miR-192-3p through hepatitis B x protein interaction with c-myc. We further showed that miR-192-3p was repressed by HBV transfection in vitro and in a mouse model, leading to cellular autophagy. Using an miRNA target prediction database miRBase, we identified X-linked inhibitor of apoptosis protein (XIAP) as a target gene of miR-192-3p and demonstrated that miR-192-3p directly targeted the XIAP 3'-untranslated region of XIAP messenger RNA. Importantly, we discovered that HBV promoted autophagy through miR-192-3p-XIAP axis and that this process was important for HBV replication in vitro and in vivo. We demonstrated that miR-192-3p functioned through the nuclear factor kappa B signaling pathway to inhibit autophagy, thereby reducing HBV replication. Conclusions: Our findings indicate that miR-192-3p is a regulator of HBV infection and may play a potential role in hepatocellular carcinoma. It may also serve as a biomarker or therapeutic target for HBV patients.
DECREASED GLOBAL LONGITUDINAL STRAIN WITH MYOCARDITIS FROM IMMUNE CHECKPOINT INHIBITORS AND OCCURRENCE OF MAJOR ADVERSE CARDIAC EVENTS
Authors: Magid Awadalla, Syed Mahmood, John Groarke, Shiying Liu, Malek Z.O. Hassan, Sean P.T. Murphy, Maeve Jones-O'Connor, Anju Nohria, Lucie M. Heinzerling, Ryan J. Sullivan, Carol Chen, Dipti Gupta, Sarju Ganatra, Muhammad A. Rizvi, Paaladinesh Thavendiranathan, Gagan Sahni, Alexander R. Lyon, Carlo G. Tocchetti, Judy Hung, Michael Picard, Franck Thuny, Stephane Ederhy, Michael Fradley, Tomas G. Neilan
Journal: Journal of the American College of Cardiology (2019)