tbuckley/cabot-search huggingface dataset:
SAT0016 Ultrasound densitometry and dxa in patients with ankylosing spondylitis – how do they correlate?
Authors: H Franck, T Meurer
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Patients with ankylosing spondylitis are well-known to have an increased incidence of osteoporosis/osteopenia. Consequently, control measurements of bone densitometry should be done more frequently than in the normal population. Ultrasound densitometry has the advantage to be free of radiation and having been used widely. However, DXA is still a "gold standard". <h3>Objectives</h3> The aim of our study was to look at the relationship of the ultrasound densitometry and DXA-measurements in patients with ankylosing spondylitis. <h3>Methods</h3> We have examined 184 patients with ankylosing spondylitis. All patients fulfilled the modified New York criteria. We measured the bone mineral density of the right hip and lumbar spine with DXA (QDR 4500) and of the calcaneus with ultrasound (UBIS 5000). <h3>Results</h3> The best correlation was found between DXA of the right hip and ultrasound of the calcaneus. The correlation of BMD hip total with ultrasound BUA was r = 0.235(p &lt; 0.001, with ultrasound T-Score r = 0,205 (P &lt; 0,005) and with ultrasound Z-Score r = 0.203 (p &lt; 0,006). The corresponding correlations of BMD of the lumbar spine with ultrasound BUA (r = 0,135 P = 0,067) were not significant. <h3>Conclusion</h3> The hip total measured by DXA present with significant (p &gt; 0,005) correlations with ultrasound measurements of the calcaneus. In contrast, BMD of the lumbar spine did not show significant correlations with the ultrasound measurements. As measurements of BMD of the lumbar spine in patients with ankylosing spondylitis have limitations due to disease specific changes of the lumbar vertebra, ultrasound of the calcaneus measurement should be considered as an alternative, too.
Abstract 278: Metabolic Reprogramming is Essential for Cell Cycle Progression in Cardiomyocytes
Authors: Riham Abouleisa, Lindsey McNally, Qinghui Ou, Krishna Choudhary, Reuben Thomas, Bradford G Hill, Tamer m Mohamed
Journal: Circulation Research (2020)

Myocardial infarction causes irreversible loss of cardiomyocytes (CMs) and often leads to heart failure. To replace the lost cells, we identified a combination of cell-cycle regulators that induces stable cytokinesis in adult post-mitotic cells. Specifically, adenoviral overexpression of cyclin-dependent kinase 1 (CDK1), CDK4, cyclin B1, and cyclin D1 (collectively known as ‘four factors’, or simply 4F) induced cell division in ~15% of post-mitotic mouse, rat, and human CMs. Identifying the major roadblocks during the process of CM proliferation is a key for advancing this field. This was not possible before due to the lack of efficient methods to induce CM proliferation. The goal of the current study is to understand why a subpopulation of CMs divide while most CMs, despite expressing 4F, resist cell cycle reentry. To investigate transcriptional changes during cell cycle progression at the single cell level, we conducted temporal single cell RNAseq on 60-day-old matured hiPS-CMs infected with either LacZ (control) or 4F for 24, 48 and 72 h. We found a unique cell population that appears 48 h after infection with the 4F; this population was identified as the proliferating population and expressed high levels of cytokinesis genes (Ki67, Aurora Kinase A and B, E2F1, CDC20, ANLN, TK1, CCNA2, PLK1 and PCNA). Consistent with our published data, this population represents ~15% of the total CMs population expressing 4F. Compared with the quiescent population from the same sample, this unique population of proliferating CMs shows significant upregulation of the cell cycle program and major downregulation of mitochondrial electron transport chain genes. In line with these transcriptomic changes, hiPS-CMs had 50% lower rates of oxidative phosphorylation 48 h after 4F infection. Furthermore, in 4F-overexpressing iPS-CMs, stable isotope tracing demonstrated significantly higher enrichment of glucose-derived 13 C in NAD and UDP-HexNAc, suggesting activation of NAD synthesis and the hexosamine biosynthetic pathway. We conclude that proliferating CMs diminish catabolic pathway activity and augment biosynthetic pathway activity. The capacity of CM subpopulation to reprogram their metabolism is likely to facilitate their ability to complete cell division.
Preliminary Results of a Phase 2 Study of Camidanlumab Tesirine (Cami), a Novel Pyrrolobenzodiazepine-Based Antibody-Drug Conjugate, in Patients with Relapsed or Refractory Hodgkin Lymphoma
Authors: Alex F. Herrera, Carmelo Carlo-Stella, Graham P. Collins, Kami J. Maddocks, Nancy L. Bartlett, Kerry J. Savage, Paolo F Caimi, Brian T. Hess, Pier Luigi Zinzani, Hans G Cruz, Luqiang Wang, Jay Feingold, Jens Wuerthner, Stephen M. Ansell
Journal: Blood (2020)
The Combination of AXL Inhibitor Bemcentinib and Low Dose Cytarabine Is Well Tolerated and Efficacious in Elderly Relapsed AML Patients: Update from the Ongoing BGBC003 Phase II Trial (NCT02488408)
Authors: Sonja Loges, Michael Heuser, Jörg Chromik, Carlos Enrique Vigil, Peter Paschka, Francesca Re, Nicola Di Renzo, Roberto M. Lemoli, Daniele Giovanni Mattei, Isabel Ben-Batalla, Monica Hellesoy, Katherine Lorens, Joseph Birkett, Stuart McPherson, Jaya Nautiyal, David Micklem, Hani Gabra, James B. Lorens, Walter Fiedler, Yesid Alvarado, Bjorn T. Gjertsen
Journal: Blood (2020)
Science Denial and COVID Conspiracy Theories
Authors: Bruce L. Miller
Journal: JAMA (2020)

The US public health response to coronavirus disease 2019 (COVID-19) has been dismal, characterized by antimask behavior, antivaccine beliefs, conspiracy theories about the origins of COVID-19, and vocal support by elected officials for unproven therapies.Less than half of the people in the US heed health recommendations to wear a mask when out in public. 1Antiscience rhetoric has consequences.While only 4% of the world's population resides in the US, the US has accounted for 20% of the world's deaths related to COVID-19 and has performed less well than several other wealthy nations. 2 Low science literacy contributes to denial of science.The relationship between antiscience viewpoints and low science literacy underscores new findings regarding the brain mechanisms that form and maintain false beliefs. Science Literacy Is EssentialCOVID-19 science is complex, and the public is presented with a dizzying array of graphs, statistics, and proposed therapies.Also, communications by scientists changed as they learned about the infectivity and virulence of COVID-19, exacerbating mistrust of scientists by some.In 2015, in a survey of 11 000 12th-grade students
Initial Clinical Activity of FT596, a First-in-Class, Multi-Antigen Targeted, Off-the-Shelf, iPSC-Derived CD19 CAR NK Cell Therapy in Relapsed/Refractory B-Cell Lymphoma
Authors: Veronika Bachanova, Zuzan Cayci, Dixie Lewis, Joseph E. Maakaron, Murali Janakiram, Andersen Bartz, Steven Payne, Carol Wong, Sarah Cooley, Bahram Valamehr, Yu-Waye Chu, Jeffrey S. Miller
Journal: Blood (2020)
Tnfα Promotes an Immunosuppressive Microenvironment in Cutaneous T Cell Lymphoma and Regulates PD-L1 Expression
Authors: Emine Gulsen Gunes, Sung Hee Kil, Xiwei Wu, Chingyu Su, Zhen Han, Hanjun Qin, Ting-Fang He, Jing Chen, Yukiko Yamaguchi, Jasmine M. Zain, Farah Abdulla, Saul Priceman, Mingye Feng, Peter P. Lee, Steven T. Rosen, Christiane Querfeld
Journal: Blood (2020)
COVID-19 Mitigation Behaviors by Age Group — United States, April–June 2020
Authors: Helena J. Hutchins, Brent Wolff, Rebecca Leeb, Jean Y. Ko, Erika Odom, Joe Willey, Allison Friedman, Rebecca H. Bitsko
Journal: MMWR Morbidity and Mortality Weekly Report (2020)

No. of mitigation behaviors ≥60 yrs 45-59 yrs 30-44 yrs 18-29 yrs Abbreviation: COVID-19 = coronavirus disease 2019.* Wore a face mask; washed or sanitized hands; kept 6 feet of distance; avoided public or crowded places; canceled or postponed pleasure, social, or recreational activities; and avoided some or all restaurants.† Weighted to be representative of noninstitutionalized U.S. adults; values <5% not shown.§ Trend for overall change in behavior over time, p-value <0.001.¶ Chi-squared p-value <0.001 for differences in cumulative number of mitigation behaviors reported across age groups, within all survey waves.** Chi-squared p-value <0.05 for differences in cumulative number of mitigation behaviors reported across age groups, within April and June waves only † † Not inclusive of the survey item "wore a face mask." § § Trend for overall change in behavior over time p-value <0.05 (among those who reported wearing a mask: p-value = 0.003).
Abstract 526: Unraveling the Molecular Signature of Pregnancy Induced Hypertrophy
Authors: Helen E Collins, Kyle Fulghum, Lindsey A McNally, Mallory L Foster, Kenneth Brittian, Shizuka Uchida, Matthew A Nystoriak, Steven P Jones, Bradford G Hill
Journal: Circulation Research (2020)

Cardiovascular disease is the leading cause of death in pregnant and postpartum women. During pregnancy, the maternal heart rapidly adapts to the increasing physiological and metabolic demands of the growing fetus. This adaptation often takes the form of a physiological hypertrophy in which the maternal heart grows to increase cardiac output; however, the molecular processes underlying pregnancy-induced hypertrophy (PIH) are poorly understood. The goal of this study was to examine the transcriptomic and metabolic signatures associated with the structural and functional adaptations of the heart to pregnancy. Therefore, we performed timed pregnancy studies in 12-week-old female FVB/NJ mice, which were distributed into the following groups: non-pregnant control (NP; n = 14), mid-pregnancy (MP, 6d pregnant; n = 11), late-pregnancy (LP, 16d pregnant; n = 13), and 1-wk post birth (PB; n = 8). Heart weight to tibia length were higher in MP (7.77±1.02 mg/mm; p &lt;0.05), LP (7.84±0.87 mg/mm; p &lt;0.05), and PB mice (9.86±1.14 mg/mm; p &lt;0.05) compared with NP mice (6.54±0.74 mg/mm). The sustained increase in PB heart weight was associated with increased myocyte cross sectional area, consistent with cardiomyocyte hypertrophy. Compared with NP hearts, echocardiographic measurements suggest significant increases in both end diastolic (36.0±5.1 vs 61.2±5.9 μl; p &lt;0.05) and systolic LV volume (9.4±3.8 vs 21.0±1.4 μl; p &lt;0.05) in PB hearts. These changes in PB hearts were associated with a significant increase in LV mass and a decline in ejection fraction. In LP and PB hearts, we also found higher expression of markers of hypertrophy ( Nppa, Nppb, Myh7 ). Subsequent RNA-seq analyses revealed enrichment in genes involved in cell proliferation, cytokinesis, and transcription in MP hearts; in metabolism genes in LP hearts; and in fibrotic and extracellular matrix genes in PB hearts. Together, these findings reveal the key molecular signature underlying the structural and functional adaptation of the heart during pregnancy and parturition, and may shed light on the molecular processes underlying PIH.
Abstract 450: The Role of CD38 as a Therapeutic Target for Protection Against Doxorubicin-induced Cardiotoxicity Through Nad+ Boosting
Authors: Thais R Peclat, Guillermo Agorrody, Lilian S Gomez, Eduardo N Chini
Journal: Circulation Research (2020)

Background: Doxorubicin is a chemotherapy medication used to treat several types of cancer. Its major adverse effect is cardiotoxicity, which may limit its use. Doxorubicin-induced cardiotoxicity (DIC), once developed, carries a poor prognosis. Therefore strategies to prevent or treat DIC are of paramount importance but have not yet been fully developed. Being NAD + a critical nucleotide which is involved in oxy-reduction reactions and CD38 the main NAD + -consuming enzyme responsible for NAD levels regulation and homeostasis, we aim to investigate the link of CD38 and NAD + metabolism in DIC and its potential role as a therapeutic target. Methods: We compared Wild-type (WT) control mice with WT mice treated with a single dose injection of 15 mg/kg of doxorubicin who received vehicle or an antibody that blocksCD38 ecto-enzymatic activity. We also compared genetically CD38 catalytic inactive (CI) mice treated or not with the same single dose injection. Results: Doxorubicin caused a decrease in Ejection Fraction (EF) in WT mice. We also observed that CD38 CI mice treated with doxorubicin did not have changes in EF compared to their control. When compared to WT receiving just doxorubicin, WT mice treated also with the antibody had a trend to improve EF. As for exercise performance, our results show a decrease in exercise capacity induced by doxorubicin that was reversed in the antibody group and did not happen in the CD38 CI mice treated with doxorubicin. Doxorubicin caused a decrease in heart rate variability (HRV) which was improved in the antibody treated group. Moreover, our results show a survival rate that is similar to what has been previously shown, with 50% mortality associated with doxorubicin. Blockage of CD38 activity with antibody reduced mortality in this model to approximately 20%. Mechanistically, we did not observe decreases in NAD+ levels induced by Doxorubicin. However, boost of NAD induced by blocking CD38 was related to protection against DIC. Conclusion: Our results indicate that the damage mechanism of DIC may not be related directly with NAD decrease, but NAD boosting induced by CD38 blockage seems to have a positive effect in protection against cardiac dysfunction related to this chemotherapeutic treatment.
Selinexor Efficacy and Safety Are Independent of Renal Function in Patients with Relapsed/Refractory Diffuse Large B-Cell Lymphoma (DLBCL): A Post-Hoc Analysis from the Pivotal Phase 2b Sadal Study
Authors: Michael W. Schuster, Miguel A Canales, Jason Westin, Josée M Zijlstra, George A Follows, Reem Karmali, Nagesh Kalakonda, Andre H. Goy, Rene-Olivier Casasnovas, Joost Vermaat, Eric Van Den Neste, Sylvain Choquet, Catherine Thieblemont, Federica Cavallo, Maria de Fatima De La Cruz, Brian T. Hill, Herve Tilly, Shireen Kassam, Reda Bouabdallah, Ulrich Jaeger, Ronit Gurion, Paolo Caimi, Peter Martin, Andrew Davies, Sonali M. Smith, Graham P. Collins, Fritz C. Offner, Gilles Salles, Xiwen Ma, Kelly Corona, Jean-Richard Saint-Martin, Anita A. Joshi, Kamal Chamoun, Hongwei Wang, Jatin J. Shah, Sharon Shacham, Michael G Kauffman, Marie Maerevoet
Journal: Blood (2020)
Correction of the Energetic Defects in Pyruvate Kinase Deficiency through Genome Editing in Hematopoietic Stem and Progenitor Cells
Authors: Sara Fañanas-Baquero, Oscar Quintana Bustamante, Daniel P. Dever, Omaira Alberquilla, Rebeca Sanchez-Dominguez, Joab Camarena, Rolf Turk, José Luis López Lorenzo, Paola Bianchi, Mark Behlke, Juan A Bueren, Matt Porteus, José C Segovia
Journal: Blood (2020)
Abstract 262: Regional Transcriptomics of Left Atrial Cardiac Tissue in a Patient With Atrial Fibrillation
Authors: Samuel J Harwood, John Barnard, Han Sun, Kenneth R McCurry, Toshihiro Okamoto, Jonathan D SMITH, David R Van Wagoner, Mina K Chung
Journal: Circulation Research (2020)

Background: Common genetic variants and inflammatory factors are associated with atrial fibrillation (AF) risk. Although the top AF risk locus is near PITX2 (associated with pulmonary vein (PV) development), regional differential expression (DE) of AF risk genes in the left atrium (LA) and PVs is not well studied. While LAA and PV gene expression have been compared, transcriptome mapping of the entire LA has not been done. We tested the hypothesis that there is significant regional DE in LA structures. Methods: RNAseq was performed in 25 regions within the PVs (n=12), LA body (LAB) (n=10), and LA appendage (LAA) (n=3) from a 75 year old male with hypertension and AF who died of a stroke. DE analysis of regional clusters (R 3.6 Limma package) and gene set enrichment analysis (GSEA) (Broad Institute) were performed. Results: In full transcriptome (n=20664) sequencing, 118 genes were significantly (q &lt; 0.05) upregulated in the LAA, including FOSB (fold change [FC] 67.0), IL6 (FC 15.4), TNF (FC 2.4) and NLRP3 (FC 2.4), and 56 downregulated, including developmental genes such as SHOX2 (FC -12.9) and HOXA4 (FC -4.1). LAA GSEA showed enrichment (FDR &lt; 0.05) of inflammatory response genes and TNF-α, IL-2, IL-6, and IgG signaling pathways. 2454 genes were significantly upregulated and 3737 downregulated in the PVs while 4021 genes were upregulated and 2998 were downregulated in the LAB. In an AF implicated gene set (n=190), 28 genes were upregulated in the PVs, including SIRT1 (FC 1.7), and 31 downregulated, including PMNT (FC -2.1) and CGA (FC -3.2). NEURL1 was significantly upregulated in the inferior PV (n=4) compared to the superior PV (n=8) (FC 3.6). In the LAB, 33 genes were upregulated, including MYH7 (FC 2.2) and PMNT (FC 2.1) , and 38 downregulated including SIRT1 (FC -1.9). PITX2 did not show any significant DE in any gene set. Conclusions: This data shows that genes involved in AF pathogenesis can have substantial regional expression difference, particularly when comparing the LA body, PVs, and LAA. Inflammatory activation in the LAA may contribute to increased stroke risk.
Blocking IL1 Beta Promotes Tumor Regression and Remodeling of the Myeloid Compartment in a Renal Cell Carcinoma Model: Multidimensional Analyses
Authors: David H. Aggen, Casey R. Ager, Aleksandar Z. Obradovic, Nivedita Chowdhury, Ali Ghasemzadeh, Wendy Mao, Matthew G. Chaimowitz, Zoila A. Lopez-Bujanda, Catherine S. Spina, Jessica E. Hawley, Matthew C. Dallos, Cheng Zhang, Vinson Wang, Hu Li, Xinzheng V. Guo, Charles G. Drake
Journal: Clinical Cancer Research (2020)

Abstract Purpose: Intratumoral immunosuppression mediated by myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM) represents a potential mechanism of immune checkpoint inhibitor (ICI) resistance in solid tumors. By promoting TAM and MDSC infiltration, IL1β may drive adaptive and innate immune resistance in renal cell carcinoma (RCC) and in other tumor types. Experimental Design: Using the RENCA model of RCC, we evaluated clinically relevant combinations of anti-IL1β plus either anti-PD-1 or the multitargeted tyrosine kinase inhibitor (TKI), cabozantinib. We performed comprehensive immune profiling of established RENCA tumors via multiparameter flow cytometry, tumor cytokine profiling, and single-cell RNA sequencing (RNA-seq). Similar analyses were extended to the MC38 tumor model. Results: Analyses via multiparameter flow cytometry, tumor cytokine profiling, and single-cell RNA-seq showed that anti-IL1β reduces infiltration of polymorphonuclear MDSCs and TAMs. Combination treatment with anti-IL1β plus anti-PD-1 or cabozantinib showed increased antitumor activity that was associated with decreases in immunosuppressive MDSCs and increases in M1-like TAMs. Conclusions: Single-cell RNA-seq analyses show that IL1β blockade and ICI or TKI remodel the myeloid compartment through nonredundant, relatively T-cell–independent mechanisms. IL1β is an upstream mediator of adaptive myeloid resistance and represents a potential target for kidney cancer immunotherapy.
Pure Red Cell Aplasia in Systemic Lupus Erythematosus, a Nationwide Retrospective Cohort and Review of the Literature
Authors: Herv xC Lobbes, Matthieu Mahevas, Sophie Alviset, Lionel Galicier, Nathalie Costedoat-Chalumeau, Zahir Amoura, Laurent Alric, Arnaud Hot, St xC phane Durupt, Marc Michel, Bertrand Godeau
Journal: Blood (2020)
The T117S Variant of Cytochrome b5 Reductase 3 Increases the Risk for Ischemic Stroke with Enhanced Anemia in Mice with Sickle Cell Disease
Authors: Katherine C Wood, Heidi M Schmidt, Scott Hahn, Subramaniam Sanker, Samit Ghosh, Solomon Fiifi Ofori-Acquah, Seyed Mehdi Nouraie, Mark T Gladwin, Adam C Straub
Journal: Blood (2020)
Safety and Efficacy of Ruxolitinib in Steroid-Resistant Graft Versus Host Disease: A Systematic Review and Meta-Analysis
Authors: Rimsha Ali, Muhammad Ashar Ali, Taaha Muddassir Mirza, Aqsa Mumtaz, Farwah N. Fatima, Nayab Mirza, Sana Khan, Wajeeha Aiman, Anum Javaid, Muhammad Yasir Anwar, Faiz Anwer
Journal: Blood (2020)
Abstract MP105: Python Post-prandial Cardiac Adaptation is Supported by Enhanced Metabolism, Reduced Sarcomere Passive Tension, and Epigenetic Remodeling
Authors: Claudia Crocini, Kc Woulfe, Cierra J Walker, Christopher D Ozeroff, leslie A leinwand
Journal: Circulation Research (2020)

Pythons are infrequent feeders that can ingest meals equal to their own body mass. The extreme metabolic response required to digest such large meals is associated with a dramatic increase in the mass of most organs, including the heart. Recently, we have been able to assess functional effects of feeding using isolated python cardiomyocytes and myofibrils, advancing our understanding of extreme cardiac adaptation in python ( Python regius ). Twenty-four hours after feeding, python cardiomyocytes showed prolonged Ca 2+ transients, increased maximal tension and Ca 2+ sensitivity of myofibrils as compared to fasted pythons. Post-prandial positive inotropy was accompanied by enhanced metabolic output via increased mitochondrial ATP production rate and by AMP-dependent kinase (AMPK) activation and phosphofructokinase-2 reduction, suggesting a key role for fatty acid, but not glucose, metabolism after feeding. In addition, 24h post-fed hearts had significantly reduced tissue stiffness and myofibril passive tension. Finally, chromatin condensation was reduced about 30% after feeding in python cardiomyocytes and confirmed by increased histone acetylation, indicating a predominant role for epigenetics in post-prandial adaptation. These results suggest that feeding promotes positive cardiac inotropy in python via a number of coordinated mechanisms to enhance energy production, increase myofibril and tissue compliance, and increase chromatin accessibility. As heart failure is commonly characterized by depressed contractility, compromised energetics, and increased tissue stiffness, assessing post-prandial adaptation in python hearts provides us with powerful insights that could inform the development of therapeutics for human heart diseases.
Infection Risk in Lymphoproliferative Diseases (LPD) Treated with Targeted Drugs. Geltamo Real-Life Experience
Authors: Maria Stefania Infante, Ana Fernandez-Cruz, Lucia Nuñez, Cecilia Carpio, Ana Jimenez-Ubieto, Javier Lopez Jimenez, Lourdes Vázquez, Raquel Del Campo, Samuel Romero, Carmen Alonso Prieto, Daniel Murillo, Margarita Prat, Jose Luis Plana Cuenca, Paola Villaverde Gutiérrez, Gabriela Bastidas, Ana Bocanegra, Ángel Serna, Rodrigo de Nicolas, Juan Marquet Palomanes, Julio Garcia-Suarez, Maria Carmen Mas Ochoa, Alessandra Comai, Xabier Martin, Cristina Seri, Belen Navarro Matilla, Jose Angel Hernandez-Rivas, Armando Lopez-Guillermo, Isabel Ruiz-Campos, Carlos Grande
Journal: Blood (2020)
Outcomes in Patients with AL (Light-Chain) Cardiac Amyloidosis
Authors: Jeremy L. Ramdial, Mahmoud R. Gaballa, Taha Al-Juhaishi, Qaiser Bashir, Samer A. Srour, Neeraj Saini, Yago Nieto, Chitra Hosing, Uday R. Popat, Regan Murphy, Hans C. Lee, Krina K. Patel, Elisabet E. Manasanch, Sheeba K. Thomas, Donna M. Weber, Gregory P. Kaufman, Robert Z. Orlowski, Richard E. Champlin, Muzaffar H. Qazilbash
Journal: Blood (2020)
Abstract 11170: Change in Atrial Fibrillation Burden Over Time
Authors: Philipp Krisai, Stefanie Aeschbacher, Matthias Bossard, Steffen Blum, Pascal Meyre, Michael Kühne, Stefan Osswald, Beat A Kaufmann, David Conen
Journal: Circulation (2018)

Introduction: The natural course of atrial fibrillation (AF) is unkown. Hypothesis: We aimed to investigate the change in AF-burden over time using yearly 7-day Holter-ECG recordings and its associ...
Real World Evaluation of Deviation Outcomes in an Immune Effector Cell Quality Program
Authors: Geoffrey Shouse, Sylvia O Dulan, Jamie Wagner, Michelle Mott, Alex Ly, Donna Ujiiye, Mary C. Clark, Kathie Viers, Stephen J. Forman, Eileen P. Smith, David S Snyder, Lihua E Budde
Journal: Blood (2020)