tbuckley/cabot-search huggingface dataset:
A TRAGIC END OR AN EXPECTED DESTINY: A RARE CASE OF A FLASH PULMONARY EDEMA DUE TO SEWING RING DEHISCENCE OF BIO PROSTHETIC MITRAL VALVE
Authors: Bader Abu Ghalyoun, Dhaval Shah, Dema Shamoon, Rahul Vasudev, Hamdi Battah, Fayez Shamoon
Journal: Journal of the American College of Cardiology (2019)
Abstract 580: A β-arrestin-Biased β2-Adrenergic Receptor-Specific Pepducin Confers Cardioprotection
Authors: Laurel A Grisanti, Toby P Thomas, Claudio de Lucia, Rhonda L Carter, Erhe Gao, Walter J Koch, Jeffrey L Benovic, Douglas G Tilley
Journal: Circulation Research (2018)

Reperfusion as a therapeutic intervention for acute myocardial infarction-induced cardiac injury itself induces further cardiomyocyte death. We recently demonstrated that the pepducin ICL1-9, a small lipidated peptide fragment designed from the first intracellular loop of β2AR, allosterically engaged pro-survival signaling cascades and enhanced cardiomyocyte contractile function in a βarr-dependent manner in vitro. Thus, in this study we tested whether ICL1-9 relays cardioprotection against ischemia/reperfusion (I/R)-induced injury in vivo. Wild-type (WT) C57BL/6 mice received intracardiac injections of either ICL1-9 or a scrambled control pepducin (Scr) at the time of ischemia (30 min) followed by reperfusion for either 24 hours, to assess infarct size and cardiomyocyte death, or 4 weeks, to monitor the impact of ICL1-9 on long-term cardiac structure and function. Intramyocardial injection of ICL1-9 at the time of I/R reduced infarct size, cardiomyocyte death and improved cardiac function in a β2AR- and βarr-dependent manner, which led to less cardiac fibrosis and improved cardiac function over time. Neonatal rat ventricular myocytes (NRVM) were used in conjunction with serum deprivation or hypoxia/reoxygenation (H/R) models to assess the mechanism by which ICL1-9 promotes cardiomyocyte survival. Notably, ICL1-9 attenuated mitochondrial superoxide production and promoted cardiomyocyte survival in a RhoA-dependent manner. ICL1-9 did not alter β2AR density in NRVM or whole heart even up to 24 hr post-treatment, at which timepoint both ICL1-9 localization in cardiomyocytes and RhoA activation were detected, indicating long-lasting presence and effects of ICL1-9 on βarr-dependent β2AR signaling. Thus, βarr-biased β2AR-selective allosteric modulation represents a novel therapeutic approach to reduce reperfusion-induced cardiac injury and relay long-term structural and functional benefits.
Synergy of Dual Pathway Inhibition in Chronic Cardiovascular Disease
Authors: Michiel Coppens, Jeffrey I. Weitz, John W.A. Eikelboom
Journal: Circulation Research (2019)

Although acetylsalicylic acid is of proven benefit for secondary prevention in patients with cardiovascular disease, the risk of recurrent ischemic events remains high. Intensification of antithrombotic therapy with more potent antiplatelet drugs, dual antiplatelet therapy, or vitamin K antagonists further reduces the risk of major adverse cardiovascular events compared with acetylsalicylic acid alone but increases the risk of bleeding without reducing mortality. In patients with prior coronary artery disease or peripheral arterial disease the COMPASS (Cardiovascular Outcomes for People Using Anticoagulation Strategies) trial revealed that compared with acetylsalicylic acid alone, dual pathway inhibition with low-dose rivaroxaban (2.5 mg twice-daily), an oral factor Xa inhibitor, plus acetylsalicylic acid reduced major adverse cardiovascular event by 24%, major adverse limb events by 47%, and mortality by 18%. Major bleeding was increased by 70%, but there was no increase in fatal or intracranial bleeding. This article (1) reviews the results of the COMPASS trial, (2) explains why dual pathway inhibition is superior to antiplatelet or anticoagulant therapy alone, (3) compares the results with rivaroxaban plus aspirin with those with other antithrombotic regimens, and (4) provides insight into how best to apply the COMPASS results into practice.
AN UNEXPECTED AND RARE FINDING ON CORONARY ANGIOGRAM: MULTIVESSEL CORONARY ARTERY ECTASIA IN A YOUNG WOMAN WITH CHEST PAIN
Authors: Akshar Jaglan, Tarek Ajam, Mohsin Khan, John Crouch, Ramagopal Tumuluri, Port Steven, C. Tanvir Bajwa, A. Jamil Tajik
Journal: Journal of the American College of Cardiology (2019)
SUSCEPTIBLE POPULATION FOR FLUOROQUINOLONE-ASSOCIATED AORTIC DISSECTION AND AORTIC ANEURYSM: A POPULATION-BASED ANALYSIS
Authors: Ronan Hsieh, Meng-Tse Gabriel Lee, Lorenzo Porta, Wan-Chien Lee, Sie-Huei Lee, Shy-Shin Chang, Shyr-Chyr Chen, Chien-Chang Lee
Journal: Journal of the American College of Cardiology (2019)
Glioblastoma-Derived IL6 Induces Immunosuppressive Peripheral Myeloid Cell PD-L1 and Promotes Tumor Growth
Authors: Jonathan B. Lamano, Jason Balquidera Lamano, Yuping D. Li, Joseph D. DiDomenico, Winward Choy, Dorina Veliceasa, Daniel E. Oyon, Shayan Fakurnejad, Leonel Ampie, Kartik Kesavabhotla, Rajwant Kaur, Gurvinder Kaur, Dauren Biyashev, Dusten J. Unruh, Craig M. Horbinski, C. David James, Andrew T. Parsa, Orin Bloch
Journal: Clinical Cancer Research (2019)

Upregulation of programmed death-ligand 1 (PD-L1) on circulating and tumor-infiltrating myeloid cells is a critical component of GBM-mediated immunosuppression that has been associated with diminished response to vaccine immunotherapy and poor survival. Although GBM-derived soluble factors have been implicated in myeloid PD-L1 expression, the identity of such factors has remained unknown. This study aimed to identify factors responsible for myeloid PD-L1 upregulation as potential targets for immune modulation.Conditioned media from patient-derived GBM explant cell cultures was assessed for cytokine expression and utilized to stimulate naïve myeloid cells. Myeloid PD-L1 induction was quantified by flow cytometry. Candidate cytokines correlated with PD-L1 induction were evaluated in tumor sections and plasma for relationships with survival and myeloid PD-L1 expression. The role of identified cytokines on immunosuppression and survival was investigated in vivo utilizing immunocompetent C57BL/6 mice bearing syngeneic GL261 and CT-2A tumors.GBM-derived IL6 was identified as a cytokine that is necessary and sufficient for myeloid PD-L1 induction in GBM through a STAT3-dependent mechanism. Inhibition of IL6 signaling in orthotopic murine glioma models was associated with reduced myeloid PD-L1 expression, diminished tumor growth, and increased survival. The therapeutic benefit of anti-IL6 therapy proved to be CD8+ T-cell dependent, and the antitumor activity was additive with that provided by programmed death-1 (PD-1)-targeted immunotherapy.Our findings suggest that disruption of IL6 signaling in GBM reduces local and systemic myeloid-driven immunosuppression and enhances immune-mediated antitumor responses against GBM.
Letter to the Editor: Hypotheses and Assumptions in Mendelian Randomization: Proceed With Caution
Authors: Christopher J. Danford, Ghideon Ezaz
Journal: Hepatology (2019)

Potential conflict of interest: Nothing to report. To the Editor: We read with interest the article by Wang et al.1 regarding gallstone disease (GSD) and type 2 diabetes (DM2) risk. Below, we discuss three issues regarding the study’s design. First, when conducting a Mendelian randomization (MR) study, a strong hypothesis regarding a causal mechanism is needed to test the underlying assumption that a genetic risk score is associated with a given outcome only through its relationship with the exposure. We are unaware of any mechanisms by which gallstones would cause DM2, without which it is difficult to select appropriate genes that meet the assumptions underlying MR study design. For example, CYP8B1 was included under the assumption that it mediates the effect on DM2 risk through GSD; however, CYP8B1 is also related to glucose hemostasis through GLP‐1,2 potentially violating the exclusion restriction assumption. Second, the study’s genetic risk score is primarily composed of single‐nucleotide polymorphisms (SNPs) derived from studies conducted in European populations. The same genome‐wide association study (GWAS) meta‐analysis from which these SNPs were selected showed that, although four SNPs were positively correlated with GSD in a European population, only two SNPs were positively correlated and one was negatively correlated in African Americans.3 According to Wang et al.,1 four of the eight chosen SNPs were not present at a high frequency or did not have a significant effect on GSD in the Chinese population. Moreover, the authors do not describe the method by which these low‐frequency SNPs were replaced with other polymorphisms in the same gene. If they were simply replaced by SNPs with a higher minor allele frequency that were associated with GSD in the same data set, then there is a potential risk of overfitting data. Third, the study is underpowered to detect a causal relationship between GSD and DM2. The genetic risk score explains 1.1% of the total variation in GSD risk. With DM2 prevalence of 31.9% in the study population, a sample size of 77,000 would be needed to adequately test the observed odds ratio of 1.22 of GSD on DM2 at a power of 0.8 and alpha of 0.05.4 Therefore, it may not be plausible to suggest that GSD does not cause DM2.
TRENDS IN ORAL ANTICOAGULANT USE FOR THE TREATMENT OF VENOUS THROMBOEMBOLISM IN THE UNITED STATES, 2010-2016
Authors: Ashwin Nathan, Zhi Geng, Swathi Raman, Elias Dayoub, Srinath Adusumalli, Bram Geller, Taisei Kobayashi, Jay Giri, Peter Groeneveld
Journal: Journal of the American College of Cardiology (2019)
RENAL RECOVERY AFTER DECONGESTION AMONG PATIENTS WITH ACUTE HEART FAILURE: DOES TIMING MATTER?
Authors: Chanattha Thimphitthaya, Pajaree Sriparn, Pakin Lalitnithi, Moongmun Anuntasainont, Sirinda Kittiprachakul, Angkawipa Trongtorsak, Aekarach Ariyachaipanich
Journal: Journal of the American College of Cardiology (2019)
AN UNUSUAL CASE OF SERIAL LEFT VENTRICULAR OUTFLOW OBSTRUCTION: COINCIDENT HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY AND SUBAORTIC MEMBRANE MANAGED OPERATIVELY
Authors: Andy Lee, Aaron Mercado-Reza, Clay Barbin, Zachary Rosol, Nishi Patel, Ari Cedars, William Roberts, Robert Hebeler, Amarinder Bindra
Journal: Journal of the American College of Cardiology (2019)
Abstract 20675: Prevalence and Rate of Spontaneous Closure of Ventricular Septal Defects Identified by Echocardiographic Screening of 10.000 Newborns
Authors: Christian A Pihl, Anna Axelsson, Anne-Sophie Sillesen, Niels Vejlstrup, Kasper Iversen, Henning Bundgaard
Journal: Circulation (2017)

Background: Ventricular septal defect (VSD) is one of the most common congenital heart disease and has previously been estimated to affect approximately 0.5% of all newborns. The Copenhagen Baby He...
IMPACT OF BODY WEIGHT AT AGE 20 AND WEIGHT GAIN DURING ADULTHOOD ON MIDLIFE CORONARY ARTERY CALCIUM IN 15,000 MEN AND WOMEN: AN INTERIM ANALYSIS OF THE SWEDISH CARDIOPULMONARY BIOIMAGE STUDY
Authors: Emil Hagstrom, Göran Bergström, Annika Rosengren, Elin B. Brolin, John Brandberg, Kerstin Cederlund, Gunnar Engström, Jan Engvall, Maria J. Eriksson, Isabel Gonçalves, Stefan James, Tomas Jernberg, Mikael Lilja, Martin Magnusson, Anders Persson, Margaretha Persson, Anette Sandström, Caroline Schmidt, Linn Skoglund Larsson, Johan Sundstrom, Eva Swahn, Stefan Söderberg, Kjell Torén, Carl Johan Östgren, Lars Lind
Journal: Journal of the American College of Cardiology (2019)
ASSESSMENT OF THE HIGH RISK AND UNMET NEED IN PATIENTS WITH CAD AND TYPE 2 DIABETES (ATHENA): US BURDEN OF ILLNESS IN THE DIABETES COLLABORATIVE REGISTRY
Authors: Eric Wittbrodt, Narinder Bhalla, Karolina Andersson Sundell, Qi Gao, Liyan Dong, Matthew Cavender, Phillip Hunt, Nathan Wong
Journal: Journal of the American College of Cardiology (2019)
CHANGES IN CARDIOVASCULAR BIOMARKERS WITH BREAST CANCER THERAPY AND ASSOCIATIONS WITH CARDIAC DYSFUNCTION
Authors: Biniyam Demissei, Rebecca A. Hubbard, Liyong Zhang, Amanda M. Smith, Karyn Sheline, Caitlin McDonald, Vivek Narayan, Susan M. Domchek, Angela DeMichele, Payal Shah, Amy S. Clark, Kevin Fox, Jennifer Matro, Angela R. Bradbury, Hayley Knollman, Wai Hong Tang, Peter Liu, Bonnie Ky
Journal: Journal of the American College of Cardiology (2019)
MYOCARDIAL INFLAMMATION/FIBROSIS DETECTION BY PULSE-CANCELLATION ECHOCARDIOGRAPHY IN PATIENTS WITH CARDIAC SARCOIDOSIS-CORRELATION WITH FDG-PET
Authors: Lane Zhang, Steven Fein, Ping Lu, Fantauzzi John, David Steckman, Ashar Ata, Yao Yao, Marc Judson, Radmila Lyubarova
Journal: Journal of the American College of Cardiology (2019)
Abstract 15115: Including Intra- and Post-operative Factors in Delirium Predictive Rule After Coronary Artery Bypass Graft Could Increase Its Accuracy
Authors: Shu Ding, Xinwei Feng, Xiangjun Tao, Sai Lu, Pixiong Su, Yuzhi Shen, Haibo Zhao, Ying Wu
Journal: Circulation (2015)

Objectives: Postoperative Delirium (POD) frequently occurs after coronary artery bypass graft (CABG). Patients screened with an appropriate POD predictive rule (PR) may benefit from targeted preventive treatment. The accuracy of current available PRs, however, remained modest with the C statistic below 0.75, partially because none of which include intra- and post-operative (IPOP) as well as preoperative (preop) risk factors at the same time. Since POD is a postoperative (postop) phenomenon, IPOP factors might play important roles. This study aimed to develop and validate a PR based on perioperative (periop) factors to predict POD after CABG. Methods: This prospective study included two cohorts (derivation [n = 132] and validation [n = 53]) of patients who underwent first isolated CABG. POD was assessed using the Confusion Assessment Method for Intensive Care Unit twice daily until 5 days after operation. Logistic regression and a bootstrap resampling procedure were used for model development and internal validation. Rule performance was measured with the C statistic. Points were assigned to each variable and a simplified rule was derivated to identify subjects at low, moderate, and high risk of POD based on their total risk score. The proportion of subjects with POD in each risk group was calculated. Results: The PR included 5 periop factors: age (≥68y), female, intraoperative intra-aortic balloon pump use, postop atrial fibrillation and serum IL-6 ≥ 478 pg/ml at 18th hour. The relative risk of POD in moderate (2~5 points) and high risk group (6~8 points) were 6.7 and 10.9 folds higher compared with low risk group (0~1 point), respectively (Fig A). The model C statistic was 0.861 (Fig B) in the derivation cohort, 0.829 in internal validation, and 0.754 in validation cohort. Conclusion: We developed a POD PR for patients undergoing CABG, which includes IPOP risk factors as well as preop risk factors. The new developed rule demonstrated more powerful in predicting POD after CABG.
USE OF EVIDENCE-BASED PREVENTIVE MEDICAL THERAPIES 1-3 YEARS POST-MYOCARDIAL INFARCTION IN THE PROSPECTIVE GLOBAL TIGRIS REGISTRY
Authors: Dirk Westermann, David Brieger, Timothy Collier, Stuart J. Pocock, Mauricio G. Cohen, Shaun G. Goodman, Christopher B. Granger, Richard Grieve, Jose C. Nicolau, Tabassome Simon, Satoshi Yasuda, Gunnar Brandrup-Wognsen, Kirsten L. Rennie, Karolina Andersson Sundell, Ji Yan Chen
Journal: Journal of the American College of Cardiology (2019)
Abstract 439: Elevating 2-deoxy Adenosine Triphosphate Improves Contraction in a Mouse Model of Genetic Dilated Cardiomyopathy
Authors: Farid Moussavi-Harami, Maria V Razumova, Jordan M Klaiman, Yuanhua Cheng, Jil C Tardiff, Michael Regnier
Journal: Circulation Research (2018)

Several studies have identified reduced tension and Ca 2+ sensitivity as key regulators that precipitate dilated cardiomyopathy (DCM). We are developing a novel therapy to increase tension using adeno-associated viral (AAV) vectors that increase intracellular 2 deoxy-ATP (dATP) via overexpression of the enzyme ribonucleotide reductase (RNR). We have reported that dATP substitution for ATP increases the magnitude and rate of contraction and that RNR overexpression increases intracellular dATP and enhances cardiac function. Here we use a multiscale approach to test the effect of dATP in a genetic model of dilated cardiomyopathy (DCM) with a missense mutation (D230N) in alpha-tropomyosin (Tm). Using recombinant proteins in the in vitro motility assay, we found that filament velocity was lower with D230N compared to WT Tm (2.03±0.04 vs. 2.44±0.04 μm/s). This deficit was corrected when dATP was substituted for ATP (2.90±0.04 μm/s). Next, we used transgenic D230N mice that show progressive ventricular dilation and systolic dysfunction. Intact and demembranated trabeculae from these mice have decreased tension and calcium sensitivity of force, and loss of length-dependent activation (LDA) compared to WT mice. Substitution of dATP for ATP, increased Ca 2+ sensitivity in D230N Tm myocardium (pCa 50 =5.48±0.02 vs. 5.57±0.02) and restored LDA. Complete replacement of ATP with dATP resulted in an ~70% increase in force at submaximal [Ca 2+ ] and force at submaximal Ca 2+ was significantly increased by replacement of only 5% of the nucleotide pool with dATP. For isolated myofibrils from D230N Tm and WT mice, tension at submaximal Ca 2+ (pCa=5.6) was lower in D230N mice compared to WT mice (51±4 vs. 75±8 mN/mm 2 ) and this deficit was improved with dATP (68±5 mN/mm 2 ). Similarly, the rate of activation in D230N myofibrils was slower than in WT mice (2.1±0.2 vs.3.3±0.2 s -1 ) and partially corrected with dATP (2.7±0.2 s -1 ). These results demonstrate that enhanced cross bridge binding, via increasing dATP, can recover lost contractile function in a thin filament mutation model of DCM. In ongoing studies, we are testing the ability of elevated dATP, via AAV- RNR, to protect against reduced systolic function and progressive ventricular dilation in 2-3 week old D230N mice .
HYPERCONTRACTILITY IN WOMEN WITH HIGH RESTING CORONARY VELOCITY AND LOW CORONARY FLOW RESERVE: RESULTS FROM THE WOMEN'S ISCHEMIA SYNDROME EVALUATION-CORONARY VASCULAR DYSFUNCTION (WISE-CVD) PROJECT
Authors: Nissi Sharon Suppogu, Janet Wei, Michael D. Nelson, Galen Cook-Wiens, Chrisandra Shufelt, Louise Thomson, Balaji Tamarapoo, Daniel Berman, Bruce Samuels, Babak Azarbal, David R. Anderson, John W. Peterson, Carl J. Pepine, C. Noel Bairey Merz
Journal: Journal of the American College of Cardiology (2019)
Abstract 471: Development of a Cardiomyocyte Targeting Delivery System Utilizing Cardiosphere-Derived Cell Exosomes
Authors: Kyle I Mentkowski, Jennifer K Lang
Journal: Circulation Research (2018)

Research has shown that treating the heart with stem cell populations, including cardiosphere-derived cells (CDCs), post myocardial infarction stimulates regeneration, angiogenesis, and functional improvement. While this treatment has shown promise in early stage clinical trials, there remains a gap in the ability to efficiently deliver tissue-specific agents directly to the heart while avoiding nonspecific delivery to other organs. Our aim was to develop an efficient delivery system that can target cardiomyocytes and transport drugs, siRNA, and/or miRNA to aid in the treatment of cardiovascular diseases. Methods: Lamp-2b was cloned with cDNA from C2C12 cells and ligated downstream of the CMV promoter in a lentiviral transfer plasmid. Primers designed to encode a cardiomyocyte targeting peptide were used to introduce the targeting ligand between XhoI and BspEI at the N terminus of Lamp-2b forming the final vector (LV-CMP). We subsequently generated CMP lentivirus by triple transfection of LV-CMP with helper plasmids pLP/VSVG and psPAX2 into 293T cells. CDCs were transduced at 1 MOI in the presence of polybrene. Exosomes were isolated from infected and non-infected CDCs and labelled with a nucleic acid dye. Cultured mouse cardiomyocytes were incubated with 1 ug of fluorescent labeled CDC-exosomes or CMP CDC-exosomes for 24 hours then imaged. Results: To achieve exosomal cardiomyocyte targeting, we engineered CDCs to express Lamp-2b, an exosomal membrane protein, fused to a cardiomyocyte specific peptide. Primary cardiomyocytes showed a 3.8-fold increase in uptake of targeted CMP CDC-exosomes in vitro when compared with their non-engineered CDC control, establishing the efficacy of our system and laying the groundwork for further experiments to assess the efficiency of cardiac localization and cardiomyocyte uptake in vivo. Conclusions: Cardiomyocytes show enhanced in vitro uptake of CDC-derived exosomes engineered to express a cardiomyocyte targeting peptide fused with Lamp-2b. Improving exosomal uptake by cardiomyocytes following myocardial infarction would allow for improved delivery of beneficial drug and gene therapies and may result in an increase in viable myocardium and improved functional capacity of the heart.
Optimising the impact of direct-acting antiviral treatment in Hepatitis C: Lessons from a universal access, real-world cohort
Authors: Phoebe A. Thwaites, Alicia Braund, Amy Legg, Karen Beckman, Joanne C. Mina, Deborah McIntyre, Olivia Cullen, Mary Fenech, Mark Redden, Anzel Jansen van Rensburg, Xinyi Tom Zhou, Andrew Hallam, Tony Rahman, Marnie Wood, Barbara Leggett, Richard Skoien
Journal: Hepatology (2017)
VALUE OF NT PROBNP IN THE PREDICTION OF CANCER IN PATIENTS WITH STABLE CORONARY ARTERY DISEASE
Authors: Alvaro Aceña, Sergio Ramos-Cillan, Marta Lopez Castillo, Ana Maria Pello, Carmen Cristobal, Nieves Tarín, Ana Huelmos, Oscar Lorenzo, Juan Martinez Milla, Jesus Fuentes Antras, Carlos Gutierrez-Landaluce, Oscar González Lorenzo, Maria Martin Mariscal, Ignacio Hernandez Gonzalez, Jose Tuñon
Journal: Journal of the American College of Cardiology (2019)
Gly101Val BCL2 Mutation: One Step Closer to Understanding Venetoclax Resistance in CLL
Authors: Shanmugapriya Thangavadivel, John C. Byrd
Journal: Cancer Discovery (2019)

In this issue, Blombery and colleagues show that the chronic lymphocytic leukemia (CLL) cells bearing Gly101Val mutation confer resistance to venetoclax by reducing the affinity of BCL2 for venetoclax by 180-fold in cell lines and in patient cells. Detection of this mutation provides a potential biomarker for impending disease progression and an opportunity for targeted and combinational therapy to treat CLL.See related article by Blombery et al., p. 342.
NATURAL UNBIASED STRATIFICATION OF RISK IN HEART FAILURE WITH PRESERVED EJECTION FRACTION USING UNSUPERVISED CLUSTERING OF CLINICAL AND ECHOCARDIOGRAPHIC VARIABLES
Authors: Alaa M. Omar, Sukrit Narula, Alla Yugay, Jairo Tejada, William Sanchez, Arsalan Rehmani, Ahmed Elwan, Edgar Argulian, Jonathan N. Bella
Journal: Journal of the American College of Cardiology (2019)
Immunologic mechanisms of a short-course of Lolium perenne peptide immunotherapy: A randomized, double-blind, placebo-controlled trial
Authors: Hanisah Sharif, Iesha Singh, Lubna Kouser, Ralph Mösges, Marie-Alix Bonny, Angeliki Karamani, Rebecca V. Parkin, Nicolas Bovy, Uday Kishore, Abigail Robb, Michael Katotomichelakis, Gabriële Holtappels, Lara Derycke, Francis Corazza, Rémy von Frenckell, Nathalie Wathelet, Jean Duchateau, Thierry Legon, Sabine Pirotton, Stephen R. Durham, Claus Bachert, Mohamed H. Shamji
Journal: Journal of Allergy and Clinical Immunology (2019)