tbuckley/cabot-search huggingface dataset:
AB0189 Bone turn-over and the influence of low dose glucocorticosteroids on bone mass in rheumatoid arthritis patients
Authors: JK Lacki, P Leszczynski, I Korczowska, P Hrycaj
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> <h3>Objectives</h3> The present study has been undertaken to evaluate bone turn-over in rheumatoid arthritis (RA) patients as well as the influence of low dose glucocorticosteroids (GCS) on bone mass loss. <h3>Methods</h3> Ninety patients with establish RA has been investigated. The patients have been divided into two groups: 44 patients treated with GCS (age 52,5 ± 12,4 years, disease duration 122 ± 102 months, total dose of GCS, equivalent to prednisone -7,4 ± 8,3 g) and 46 patients who were not treated with GCS (Age 54,3 ± 9,7 years, disease duration 134 ± 120 month). Fifty patients have been assessed twice (after 12 month). Bone mineral content and bone mineral density have been determined in all patients in distal forearm. Additionally, some biochemical markers of osteoporosis: osteocalcin, alkaline phosphatase-bone formation, carboxyterminal telopeptides of type I collagen (CTx), procollagen type I carboxyterminal propeptide (PICP), deoxypyridynoline and some proinflammatory cytokine: IL-1a, IL-6, TNF-alpha, GM-CSF has been determined. No difference in bone metabolism between RA patients receiving GCS treatment and those treated without GCS was shown. <h3>Results</h3> <h3>Conclusion</h3> It is concluded that anti-inflammatory effect of GCS may balance the direct effect of GCS on bone mass in RA patients, particularly those with short term treatment.
TCT CONNECT-251 Outcomes of Percutaneous Coronary Intervention of Native Artery Versus Bypass Graft in Patients With Prior Coronary Artery Bypass Graft Surgery: A Systematic Review and Meta-Analysis
Authors: Ying Gue, Emmanouil Brilakis, Mohaned Egred, Mohamed Farag
Journal: Journal of the American College of Cardiology (2020)
TCT CONNECT-337 Comparative Outcomes of Mitral Valve in Valve Implantation vs. Redo Mitral Valve Replacement for Degenerated Bioprostheses
Authors: Mohammed Osman, Mohammed Al-Hijji, Akram Kawsara, Brijesh Patel, Mohamad Alkhouli
Journal: Journal of the American College of Cardiology (2020)
TCT CONNECT-313 OCT-Guided Left Main Stem Percutaneous Coronary Interventions: Results of the Multicenter LEMON (Left Main OCT-Guided Interventions) Cohort Study
Authors: Nicolas Amabile, Gregoire Rangé, Geraud Souteyrand, Matthieu Godin, Nicolas Meneveau, Guillaume Cayla, Frederic Casassus, Thierry Lefevre, Imane Bagdadi, Christophe Caussin
Journal: Journal of the American College of Cardiology (2020)
Decoding of facial strains via conformable piezoelectric interfaces
Authors: Tao Sun, Farita Tasnim, Rachel T. McIntosh, Nikta Amiri, Dana Solav, Mostafa Tavakkoli Anbarani, David Sadat, Lin Zhang, Yuandong Gu, M. Amin Karami, Canan Dagdeviren
Journal: Nature Biomedical Engineering (2020)
CDK9 Inhibition with LDC526 Is an Effective Treatment for T-Cell Prolymphocytic Leukemia (T-PLL) in Vitro
Authors: Patricia Johansson, Peter Habenberger, Ludger Klein-Hitpass, Ulrich Duehrsen, Ralf Küppers, Carsten Schultz-Fademrecht, Axel Choidas, Jan Dürig
Journal: Blood (2017)
An Ex Vivo Analysis of Thrombin Generation and Thromboelastometry in Patients Undergoing Treatment with Rivaroxaban Demonstrates Sustained Anticoagulant Effect and High Inter-Individual Variability
Authors: Stella Salta, Patrick Van Dreden, Loula Papageorgiou, Jawed Fareed, Ismail Elalamy, Grigorios T. Gerotziafas
Journal: Blood (2017)
Race, Ethnicity, and Age Trends in Persons Who Died from COVID-19 — United States, May–August 2020
Authors: Jeremy A.W. Gold, Lauren M. Rossen, Farida B. Ahmad, Paul Sutton, Zeyu Li, Phillip P. Salvatore, Jayme P. Coyle, Jennifer DeCuir, Brittney N. Baack, Tonji M. Durant, Kenneth L. Dominguez, S. Jane Henley, Francis B. Annor, Jennifer Fuld, Deborah L. Dee, Achuyt Bhattarai, Brendan R. Jackson
Journal: MMWR Morbidity and Mortality Weekly Report (2020)

2019 (COVID-19) pandemic resulted in approximately 7,900,000 aggregated reported cases and approximately 216,000 deaths in the United States.*Among COVID-19-associated deaths reported to national case surveillance during February 12-May 18, persons aged ≥65 years and members of racial and ethnic minority groups were disproportionately represented (1).This report describes demographic and geographic trends in COVID-19-associated deaths reported to the National Vital Statistics System † (NVSS) during May 1-August 31, 2020, by 50 states and the District of Columbia.During this period, 114,411 COVID-19-associated deaths were reported.Overall, 78.2% of decedents were aged ≥65 years, and 53.3% were male; 51.3% were non-Hispanic White (White), 24.2% were Hispanic or Latino (Hispanic), and 18.7% were non-Hispanic Black (Black).The number of COVID-19-associated deaths decreased from 37,940 in May to 17,718 in June; subsequently, counts increased to 30,401 in July and declined to 28,352 in August.From May to August, the percentage distribution of COVID-19-associated deaths by U.S. Census region increased from 23.4% to 62.7% in the South and from 10.6% to 21.4% in the West.Over the same period, the
A Novel Endocrine Role for the BAT-Released Lipokine 12,13-diHOME to Mediate Cardiac Function
Authors: Kelsey M. Pinckard, Vikram K. Shettigar, Katherine R. Wright, Eaman Abay, Lisa A. Baer, Pablo Vidal, Revati S. Dewal, Devleena Das, Silvia Duarte-Sanmiguel, Diego Hernández-Saavedra, Peter J. Arts, Adam C. Lehnig, Valerie Bussberg, Niven R. Narain, Michael A. Kiebish, Fanchao Yi, Lauren M. Sparks, Bret H. Goodpaster, Steven R. Smith, Richard E. Pratley, E. Douglas Lewandowski, Subha V. Raman, Loren E. Wold, Daniel Gallego-Perez, Paul M. Coen, Mark T. Ziolo, Kristin I. Stanford
Journal: Circulation (2020)

Background: Brown adipose tissue (BAT) is an important tissue for thermogenesis, making it a potential target to decrease the risks of obesity, type 2 diabetes, and cardiovascular disease, and recent studies have also identified BAT as an endocrine organ. Although BAT has been implicated to be protective in cardiovascular disease, to this point there are no studies that identify a direct role for BAT to mediate cardiac function. Methods: To determine the role of BAT on cardiac function, we utilized a model of BAT transplantation. We then performed lipidomics and identified an increase in the lipokine 12,13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME). We utilized a mouse model with sustained overexpression of 12,13-diHOME and investigated the role of 12,13-diHOME in a nitric oxide synthase type 1 deficient (NOS1 -/- ) mouse and in isolated cardiomyocytes to determine effects on function and respiration. We also investigated 12,13-diHOME in a cohort of human patients with heart disease. Results: Here, we determined that transplantation of BAT (+BAT) improves cardiac function via the release of the lipokine 12,13-diHOME. Sustained overexpression of 12,13-diHOME using tissue nanotransfection negated the deleterious effects of a high-fat diet on cardiac function and remodeling, and acute injection of 12,13-diHOME increased cardiac hemodynamics via direct effects on the cardiomyocyte. Furthermore, incubation of cardiomyocytes with 12,13-diHOME increased mitochondrial respiration. The effects of 12,13-diHOME were absent in NOS1 −/− mice and cardiomyocytes. We also provide the first evidence that 12,13-diHOME is decreased in human patients with heart disease. Conclusions: Our results identify an endocrine role for BAT to enhance cardiac function that is mediated by regulation of calcium cycling via 12,13-diHOME and NOS1.
Differential Treatment Strategy in Polycythemia Vera Patients with Stable Suboptimal Response to Hydroxyurea: Clinical Correlations and Impact on Survival
Authors: Francesca Palandri, Daniela Bartoletti, Giulia Benevolo, Massimo Breccia, Elena M Elli, Francesco Cavazzini, Gianni Binotto, Alessia Tieghi, Mario Tiribelli, Florian H. Heidel, Massimiliano Bonifacio, Novella Pugliese, Giovanni Caocci, Monica Crugnola, Francesco Mendicino, Enrica A Martino, Alessandra D'Addio, Simona Tomassetti, Bruno Martino, Giuseppe Auteri, Lucia Catani, Rossella Stella, Fabio D'Amore, Luigi Scaffidi, Nicola Polverelli, Fabrizio Pane, Antonio Cuneo, Mauro Krampera, Gianpietro Semenzato, Roberto M. Lemoli, Nicola Vianelli, Michele Cavo, Giuseppe A. Palumbo, Roberto Latagliata
Journal: Blood (2020)
cGMP Mass Production of FT538, a First-of-Kind, Off-the-Shelf, Multiplexed Engineered Natural Killer Cell Cancer Immunotherapy Derived from a Clonal Master Induced Pluripotent Stem Cell Line
Authors: Betsy Rezner, Luis Solchaga, Luane Reyes, Alice Lin, Ramzey Abujarour, Tom Lee, Bahram Valamehr, Wen Bo Wang
Journal: Blood (2020)
Abstract 446: Exploring the Myosin-dependence of Mechanical Control of Relaxation
Authors: Melissa J Bukowski, Alexandra R Matus, Dlugas Hunter, Madison P Wang, Lindsay A Pittman, Teresa L Czeiszperger, Charles S Chung
Journal: Circulation Research (2020)

Impaired relaxation is a prevalent form of diastolic dysfunction, present in nearly all cases of heart failure and in many asymptomatic adults. To date, there are no accepted treatments for impaired relaxation, despite its biochemical control by calcium reuptake, thin filament deactivation, and crossbridge kinetics. Mechanical modification of relaxation was previously theorized to occur through afterload; we, however, have recently shown that relaxation was actually modified by the strain rate of myocardial lengthening. We termed this Mechanical Control of Relaxation, or the sensitivity of the relaxation rate to the strain rate. The mechanisms underlying Mechanical Control of Relaxation are unknown, but computational models and our preliminary data suggest a dependence on myosin detachment. The objective of this study was to evaluate whether myosin was a modifying factor of Mechanical Control of Relaxation. Intact cardiac trabeculae and cardiomyocytes were obtained from rats (Sprague Dawley both treated and untreated with propylthiouracil, Spontaneously Hypertensive, and Wistar Kyoto strains) and underwent load-clamp studies. Mechanical Control of Relaxation could be improved by reducing preload (length) 5%, increasing the sensitivity of the relaxation rate to strain rate by 28±16%. Treatment with 400μM Omecamtiv Mecarbil, a myosin-ATPase specific drug, induced similar increases. Myosin isoform differences were also studied. Collagenase treatment of intact trabeculae increased Mechanical Control by 21±3%; intact myocyte studies show no collagen-dependence. These data provide evidence that the properties of myosin’s response to strain rate are major factors that modify Mechanical Control of myocardial Relaxation.
Metabolically healthy obesity, transition to unhealthy metabolic status, and vascular disease in Chinese adults: A cohort study
Authors: Meng Gao, Jun Lv, Canqing Yu, Yu Guo, Zheng Bian, Ruotong Yang, Huaidong Du, Ling Yang, Yiping Chen, Zhongxiao Li, Xi Zhang, Junshi Chen, Lu Qi, Zhengming Chen, Tao Huang, Liming Li
Journal: PLoS Medicine (2020)

Metabolically healthy obesity (MHO) and its transition to unhealthy metabolic status have been associated with risk of cardiovascular disease (CVD) in Western populations. However, it is unclear to what extent metabolic health changes over time and whether such transition affects risks of subtypes of CVD in Chinese adults. We aimed to examine the association of metabolic health status and its transition with risks of subtypes of vascular disease across body mass index (BMI) categories.
First Description of Upfront Target Therapy Treating AML and Bcll Presented Simultaneously As First Line
Authors: Juliana Santos Carvalho, Anna Flávia Silva Alves Silva, Maysa Coité Silva, Itala Gomes Santos, Laryssa Pinto Aragão, Larissa Ferreira Lucas, Herbert Henrique de Melo Santos, Mônica Botura, Alex Nano Magalhães Rêgo, Maria da Gloria B. Arruda, Edvan De Queiroz Crusoe, Alessandro de M. Almeida, Renata Alves, Marianna Batista Vieira Lima, Victor Oliveira Sousa Guimarães, Marco Aurelio Salvino
Journal: Blood (2020)
Psilocybin-Assisted Supportive Psychotherapy in the Treatment of Major Depression—Quo Vadis?
Authors: Charles F. Reynolds
Journal: JAMA Psychiatry (2020)

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Abstract 430: Immature Cardiac Fibroblasts With Upregulated P53 Contributed to Fibrosis in Ikke Deficient Mouse Myocardial Infarction Model
Authors: Yong Sook Kim, Hyang Hee Cho, Ju Hee Jun, Dong Im Cho, Meeyoung Cho, Youngkeun Ahn
Journal: Circulation Research (2020)

Background: Inhibitor of NF-κB kinase (IKK), an upstream of nuclear factor-kappa B (NF-κB), is a critical modulator for pathophysiological inflammation. IKKε is a non-classical IKK and has been studied in infectious diseases and cancers. However, the role of IKKε in a myocardial infarction (MI) has not been addressed. Methods and Results: In this study, we used IKKε knockout (KO) mice to induce MI by coronary artery ligation. The IKKε KO group showed poor early survival rate, large cardiac fibrosis (14.7±4.8% in KO vs. 31.1±10.2% in WT, p &lt;0.05), and low fractional shortening (13.47±1.21% in KO vs. 16.36±4.46% in WT, p &lt;0.05) compared with WT group. Next, we investigated the inflammatory responses and found that inflammatory markers such as inducible nitric oxide synthase (iNOS) and CD80 were much higher in both cardiac macrophages and bone marrow-derived macrophages (BMDM) in the IKKε KO group than in the wild type (WT) group. To explore the responsible mediator, we performed phosphorylated protein array and found phosphorylated p38 was significantly downregulated in the IKKε knockout BMDM. Conversely, both knockdown of p38 by siRNA and inhibition of p38 by SB203580 treatment in RAW264.7 cells upregulated iNOS. More interestingly, IKKε deficient cardiac fibroblasts showed highly accumulated nuclear p53 and exhibited immature differentiation. The levels of myofibroblast markers containing α-smooth muscle actin, periostin, and transforming growth factor-β1 were lower, and functional contractility was substantially impaired in the cardiac fibroblasts isolated from IKKε KO mice. Conclusion: Our data showed excessive inflammation was associated with p38 inactivation in macrophages and pathological fibrosis was resulted from immature myofibroblast phenotype with p53 upregulation. Collectively, IKKε is involved in the control of inflammation resolution and wound healing process in the infarcted myocardium.
T Cell Immunoprofiling of Patients with Relapsed and/or Refractory Myeloma Who Receive Daratumumab Monotherapy: Longitudinal Analysis during 7 Cycle Follow-up of the Rebuild Phase 2 Study
Authors: Elisavet Vlachonikola, Efstathios Kastritis, Evdoxia Hatjiharissi, Eirini Katodritou, Alexandra Siorenta, Electra Sofou, Marina Gerousi, Konstantia Kotta, Maria Karipidou, Maria Gavriatopoulou, Sosana Delimpasi, Argiris Symeonidis, Kostas Stamatopoulos, Meletios A Dimopoulos, Evangelos Terpos, Anastasia Chatzidimitriou
Journal: Blood (2020)
COPD assessment test for the evaluation of COVID-19 symptoms
Authors: Enya Daynes, Charlotte Gerlis, Samuel Briggs-Price, Paul Jones, Sally J Singh
Journal: Thorax (2020)

There is evidence to demonstrate the ongoing symptoms of COVID-19; however, there are currently no agreed outcomes to assess these symptoms. This study examined the use of the chronic obstructive pulmonary disease (COPD) assessment test (CAT) for patients recovering from COVID-19. 131 patients who were admitted with COVID-19 were followed up over the phone to assess symptoms. The median (IQR) CAT score was 10 (5–16). Cough, phlegm and chest tightness domains were within range for healthy people, but there was evidence of significant breathlessness, loss of energy, and activity and sleep disturbance. The CAT is a useful tool to assess symptoms of COVID-19 recovery.
Correspondence on ‘Prevalence and clinical outcomes of COVID-19 in patients with autoimmune diseases: a systematic review and meta-analysis’
Authors: Elisa Gremese, Giovanni Brondani, Luca Apollonio, Gianfranco Ferraccioli
Journal: Annals of the Rheumatic Diseases (2020)

We read with great interest the meta-analysis by Akiyama et al showing that out of 62 studies with over 300 000 patients with autoimmune diseases, glucocorticosteroids (GC) therapy was significantly associated with an increased risk of COVID-19.1

These data raise interest on the use of GC in the therapeutic approach to inflammatory pneumonia associated with SARS-CoV-2 infection. A recent editorial entitled ‘Curing COVID-19’ in the October issue of the Lancet Infectious Disease discussed in fact the role of steroids to treat COVID-19 pneumonia. Dexamethasone is suggested by the WHO as part of the therapeutic approach.2 The evidence is that data on steroids are partly positive (RECOVERY and REMAP-CAP doi:10.1001/jama0.2020.17022) and partly negative (CAPE-COD-doi:10.1001/jama. 2020.16761), yet the meta-analysis of the randomised trials shows a statistical effect on mortality in very severe cases, with differences among the different steroids.3 The differences between steroids and standard of care treatment are significant, yet far away from solving the puzzle of the best therapy. Certainly, the inflammation occurring in SARS-CoV-2 pneumonia, certified by increased C-reactive protein (CRP), interleukin (IL)-6 and sometimes by ferritin, strongly suggests that GC might help to control the course of the disease. Yet recent data by Carsana et al 4 and Grasselli et al 5 suggest that pneumonitis may have at least two pathophysiology backgrounds and that ‘subsetting’ might …
Idecabtagene Vicleucel (ide-cel, bb2121) in Relapsed and Refractory Multiple Myeloma: Analyses of High-Risk Subgroups in the KarMMa Study
Authors: Noopur S. Raje, David S. Siegel, Sundar Jagannath, Sagar Lonial, Nikhil C. Munshi, Philippe Moreau, Hartmut Goldschmidt, Michele Cavo, Anna Truppel-Hartmann, Everton Rowe, Liping Huang, Amit Agarwal, Julie Wang, Timothy B. Campbell, Jesus F. San-Miguel, Donna E. Reece
Journal: Blood (2020)
Abstract 254: Profiling Transcriptional Changes and Identifying Novel Molecular Markers During the Dedifferentiation of Cardiomyocyte
Authors: Yike Zhu, Wilson Tan Lek Wen, Do Dang Vinh, Matthew A Ackers-Johnson, Roger Foo
Journal: Circulation Research (2020)

The loss of cardiomyocytes (CMs) during heart failure (HF) cannot be replaced by new CMs due to their limited proliferative capacity. Regenerating the failing heart by promoting CM cell-cycle re-entry has thus become a possible solution rigorously pursued. Some genes have been proven to promote endogenous CM proliferation, nearly always preceded by CM dedifferentiation, wherein terminally-differentiated CMs are reversed back initially to a less-matured status, preceding cell division. However, very little else is known about CM dedifferentiation, including the lack of robust molecular markers, the mechanisms driving it, whether it necessarily leads to CM proliferation, and the effect of CM dedifferentiation alone on cardiac function. Therefore, investigating CM dedifferentiation is of great significance. Here, we profiled genome-wide transcriptional changes and identified novel molecular markers during CM dedifferentiation. We used the established in vitro model where adult mouse CMs dedifferentiated and re-differentiated (DR) upon 2-week long culture, without detectable cell division. DR was evident by breakdown and rebuilding of sarcomeres, and differential regulation of cardiac fetal genes. Tracking the transcriptome change pointed to gene pathways involved in this process and potential markers of CM dedifferentiation. Another assumption is that transient induction of Yamanaka factors ( Oct4, Sox2, Klf4, Myc, OSKM ) induces CM dedifferentiation of CMs in vivo , since the four factors are themselves sufficient to induce pluripotency of human and mouse somatic cells. Our preliminary results show that CM-specific overexpression of OSKM using adeno-associated virus serotype 9 (AAV9) induced fetal-like hallmarks, down-regulation of sarcomeric genes, re-activation of cell cycle, reduced fatty acid utilization, and associated loss of cardiac function . Putative markers identified in the in vitro model was also validated to be upregulated in OSKM -overexpressed CMs. In conclusion, through 2 models of CM dedifferentiation, we have screened out potential novel markers and regulators of CM dedifferentiation which now requires further validation.
Impact of test-and-treat and risk reduction strategies on HCV transmission among MSM living with HIV in France: a modelling approach
Authors: Mathieu Castry, Anthony Cousien, Virginie Supervie, Annie Velter, Jade Ghosn, A David Paltiel, Yazdan Yazdanpanah, Sylvie Deuffic-Burban
Journal: Gut (2020)

Since the early 2000s, there has been an epidemic of HCV occurring among men who have sex with men (MSM) living with HIV, mainly associated with high-risk sexual and drug-related behaviours. Early HCV diagnosis and treatment, and behavioural risk-reduction, may be effective to eliminate HCV among MSM living with HIV.We developed a deterministic dynamic compartmental model to simulate the impact of test-and-treat and risk-reduction strategies on HCV epidemic (particularly on incidence and prevalence) among MSM living with HIV in France. We accounted for HIV and HCV cascades of care, HCV natural history and heterogeneity in HCV risk behaviours. The model was calibrated to primary HCV incidence observed between 2014 and 2017 among MSM living with HIV in care (ANRS CO4-French hospital database on HIV (FHDH)).With current French practices (annual HCV screening and immediate treatment), total HCV incidence would fall by 70%, from 0.82/100 person-years in 2015 to 0.24/100 person-years in 2030. It would decrease to 0.19/100 person-years in 2030 with more frequent screening and to 0.19 (0.12)/100 person-years in 2030 with a 20% (50%) risk-reduction. When combining screening every 3 months with a 50% risk-reduction, HCV incidence would be 0.11/100 person-years in 2030, allowing to get close to the WHO target (90% reduction from 2015 to 2030). Similarly, HCV prevalence would decrease from 2.79% in 2015 to 0.48% in 2030 (vs 0.71% with current practices).Combining test-and-treat and risk-reduction strategies could have a marked impact on the HCV epidemic, paving the way to HCV elimination among MSM living with HIV.