tbuckley/cabot-search huggingface dataset:
Abstract 109: Site-specific Acetylation of Cardiac Troponin I Regulates Myofilament Relaxation and Calcium Sensitivity
Authors: Kathleen C Woulfe, Ying H Lin, William Schmidt, Anthony Cammarato, D B Foster, Brandon J Biesiadecki, Timothy A McKinsey
Journal: Circulation Research (2019)

Objective: Cardiac troponin I (cTnI) is an essential regulator of cardiac contractility and relaxation. Mutations within key regions of this regulator lead to cardiomyopathies. Further, post-translational modification of cTnI through phosphorylation impacts myofibril relaxation and calcium sensitivity. Recent studies have also demonstrated that myofibril proteins are acetylated leading to faster relaxation. These studies highlight the potential significance of myofilament acetylation; however, it is not known if site-specific acetylation of cTnI can lead to mechanical changes in the myofibril. The objective of this study was to determine if acetylation at a single site of cTnI (lysine-132; K132) is sufficient to alter myofibril protein mechanics. Methods: Adult rat ventricular cardiomyocytes infected with adenoviral constructs expressing either cTnI K132 replaced with glutamine (K132Q; to mimic acetylation) or K132 replaced with arginine (K132R; to prevent acetylation) were subjected to cell contractility and isolated myofibril mechanic measurements. Additionally, skinned myofibrils were exchanged with troponin containing wildtype (WT) or K132Q cTnI and mechanics assessed. Finally, dynamics of reconstituted thin filaments containing WT or K132Q cTnI were assessed by in vitro motility assay. Results: Cardiomyocytes expressing cTnI K132Q relaxed faster and had decreased calcium sensitivity compared to WT cTnI at the whole cell and myofibril level. Relaxation or calcium sensitivity did not differ between cardiomyocytes infected with WT cTnI and cTnI K132R. Myofibrils with cTnI K132Q exchanged ex vivo demonstrate faster relaxation and decreased calcium sensitivity as well as decreased motility. Conclusions: Our results indicate for the first time that acetylation at a specific cTnI lysine can alter myofibril relaxation and calcium sensitivity. This work underscores the importance of understanding how acetylation affects specific sarcomeric proteins in the context of cardiac disease, and suggests that modulation of myofilament lysine acetylation may represent a novel therapeutic target to alter cardiac relaxation.
Abstract 361: Deacetylation of Lc3 Drives Autophagy and Proteome Remodeling in Skeletal Muscle During Oncometabolic Stress
Authors: Anja Karlstaedt, Heidi Vitrac, Benjamin D Gould, Rebecca Salazar, David Taylor, Weston Spivia, Daniel Soetkamp, An Dinh, Koen Raedschelders, Helen Burks, Walter Schiffer, Daniel McNavish, Blake Hanson, Roberta A Gottlieb, Jennifer VanEyk, Heinrich Taegtmeyer
Journal: Circulation Research (2019)

Metabolic rewiring is a hallmark of cancer and muscle cells. In isocitrate dehydrogenase 1 and 2 mutant tumors, increased plasma levels of the oncometabolite D-2-hydroxyglutarate (D2-HG) are associated with systemic effects, including myopathy. Our recent in vivo work showed that increased D2-HG supply by IDH-mutant cells causes heart and skeletal muscle atrophy, and decreases cellular ATP and NADH. Although heart failure and cachexia in cancer are commonly associated with chemotherapy, cancer survivors have a 5-fold increased risk of heart failure independent of any cytostatic treatment. The connection between metabolic and proteomic remodeling in this context remain poorly understood. We hypothesize that D2-HG-mediated alpha-ketoglutarate dehydrogenase (AKGDH) inhibition in myocytes results in metabolomic perturbations, increases autophagy and proteomic remodeling. Here, we report that LC3, a key regulator of autophagy, is activated in the nucleus of myocytes in presence of D2-HG through deacetylation by the nuclear deacetylase Sirt1. Activation of Sirt1 is driven by increased NAD + levels through D2-HG-mediated AKGDH inhibition. We used LC3 mutants with arginine and glutamine replacements at lysine residues to show that deacetylation of LC3 at K49 and K51 by Sirt1 shifts LC3 distribution from the nucleus into the cytosol, where it is able to undergo lipidation at pre-autophagic membranes. Live cell imaging with GFP-tagged LC3 in L6 myocytes indicated that the cycle of acetylation-deacetylation allows LC3 to redistribute from the nucleus to the cytosol within less than 24 h. Co-immunoprecipitation of LC3 followed by proteomics analysis revealed that LC3 binds to dynein in presence of D2-HG. Furthermore, D2-HG promoted skeletal muscle atrophy and reduced grip strength in wild-type C57BL/J6 mice in vivo. Using LC-MS/MS-based proteomics and metabolomics combined with RNA-sequencing, we assessed the effect of D2-HG on a systems level in skeletal muscle. Pathway-enrichment analysis revealed that D2-HG induces upregulation of key metabolic enzymes involved in glycolysis and the pentose phosphate pathway. In short, autophagy activation supports proteome remodeling in muscle cells during IDH-mutant leukemia.
Rafoxanide, an Organohalogen Drug, Triggers Apoptosis and Cell Cycle Arrest in Multiple Myeloma By Enhancing DNA Damage Responses and Suppressing the p38 MAPK Pathway
Authors: Jumei Shi, Wenqin Xiao, Zhijian Xu, Shuaikang Chang, Lu Gao, Yi Tao, Yingcong Wang, Xiaosong Wu, Weiliang Zhu
Journal: Blood (2018)
Ferritin-H and a Phytotherapeutic, Alone or Combined, Reprogram RBC Precursor Cells From SCD Patients to Produce Levels of Fetal Hemoglobin That Constitute a Phenotypic Cure for Sickle Cell As Well As Providing Resistance to Malaria and a Probable Treatment for Beta-Thalassemia
Authors: Robert H. Broyles, Visar Belegu, Austin C. Roth, Emily J. Curry, Robert A. Floyd, Sonia Levi, Paolo Arosio, Paolo Santambrogio, Marie Trudel, Sunil K. Joshi
Journal: Blood (2011)
Eph-A4 Plays a Important Role in Metastasis and Invasive Activity of Myeloid Leukemia Cells
Authors: Liu Xiaoli, Xuan Zhou, Yuan Zuo, Lulu Xu, Jinfang Zhang, Na Xu, Bintao Huang, Xiaozhen Xiao, Yuanlu Huang, Qingfeng Du
Journal: Blood (2012)
CSF1R and BTK Inhibitions As Novel Strategies to Disrupt the Dialogue between Mantle Cell Lymphoma and Macrophages
Authors: Antonin Papin, Benoit Tessoulin, Céline Bellanger, Anne Moreau, Yannick LE Bris, Herve Maisonneuve, Philippe Moreau, Cyrille Touzeau, Martine Amiot, Catherine Pellat-Deceunynck, Steven Le Gouill, David Chiron
Journal: Blood (2018)
A quality improvement initiative for reducing morning hypoglycemia in children undergoing treatment for acute lymphoblastic leukemia.
Authors: Ashraf Mahmoud Mohamed, Christine Marie Bolen, Jennifer Morgan, Patricia Rice, Meredith Speas, Carolyn Russo
Journal: Journal of Clinical Oncology (2019)

240 Background: Hypoglycemia has been observed in children receiving Acute Lymphoblastic Leukemia (ALL) therapy. It affects patients’ outcome. The current quality initiative was piloted at two of the St Jude affiliate clinics. Each month about 10% of children with ALL develop hypoglycemia in those two clinics. Methods: Data was collected for the eight months prior to intervention. Root Cause Analysis (RCA) using fish bone diagram, and Pareto chart to find out the most likely causes of hypoglycemia. Prolonged hours of fasting for procedures, giving 6MP at night on empty stomach, seem to further prolong hours of fasting, and lack of awareness of the new 6MP administration guidelines were the top likely causes. Interventions based on RCA: Developed Hypoglycemia educational brochure addressing causes and prevention of hypoglycemia for care givers followed by knowledge assessment tool, in addition two educational sessions for staff. Plan, Do, Study, Act (PDSA) was used to guide implementation. 4 PDSA cycles were done. Results: Combined monthly average number of ALL patients seen in both centers was 43 (range 38-51) patients with monthly average of 94 (range 71-141) blood glucose samples drawn from them. Process Measure 1: % care givers received hypoglycemia education after 1 st cycle was 16.3% which increased to 88% after PDSA cycle # 4. Process Measure 2: % of caregivers scored above 75% in the knowledge of morning hypoglycemia after education were 78%. Outcome Measure: At the end of intervention the average monthly patients with hypoglycemia decreased from 9.4% to 7.8% representing 17% reduction. Hypoglycemic episodes dropped from 6% to 4.2%, showing 30% reduction in hypoglycemic episodes. More reduction in hypoglycemic episodes was observed in clinic 1 (68%) compared to 22% reduction in clinic 2. Conclusions: Using quality improvement methodology in implementing hypoglycemia education led to drop in hypoglycemia episodes among children on ALL therapy. Despite using similar approach, yet one of the two clinics showed higher improvement compared to the other. This may reflect the possible impact of local institutional factors on implementation.
TCT-270 Comparison of Cardiac Computerized Tomography Angiography and Transesophageal Echocardiography For Device Surveillance After Endovascular Left Atrial Appendage Closure
Authors: Sadia Qamar, Jacqueline Saw, Savvas Nicolaou, Sabeena Jalal, Michael Tsang
Journal: Journal of the American College of Cardiology (2017)
Determinants of Prophylaxis Regimen Choice for Patients with Hemophilia Α Switching to Bay 81-8973: Real World Findings from the Taurus Non-Interventional Study
Authors: Beng Fuh, Cristina Santoro, Philip Maes, Maria Eva Mingot-Castellano, Rubén Berrueco, Phu-Quoc Le, Stephan Rauchensteiner, Michael Wang
Journal: Blood (2018)
Gain-of-Function NOTCH1 Mutations Occur Frequently in Human T Cell Acute Lymphoblastic Leukemia.
Authors: Andrew P. Weng, Adolfo A. Ferrando, Woojoong Lee, John P. Morris, Lewis B. Silverman, C Sanchez-Irizarry, Stephen C. Blacklow, Thomas Look, Jon C. Aster
Journal: Blood (2004)
Epitope Mapping of a Monoclonal Antibody to Factor VIII That Inhibits Factor IXa:Factor VIIIa Interaction and Thrombin Activation of Factor VIII
Authors: Amanda S. Messer, Barbara Ulmasov, Yogesh Kumar, Kanagasabai Vadivel, Degang Zhong, Philip Fay, S. Paul Bajaj
Journal: Blood (2011)
Abstract 311: Signal Transducer and Activator of Transcription 3 Inhibits the Opening of Mitochondrial Calcium Uniporter Against Cardiac Ischemia/reperfusion in Hydrogen Peroxide Postconditioning
Authors: Lan Wu, Ji-liang Tan, Zhong-yan Chen, Gang Huang
Journal: Circulation Research (2019)

Reactive oxygen species (ROS) generated during early reperfusion activated signal transducer and activator of transcription 3 (STAT3) contribute to intermittent hypobaric hypoxia (IHH)-afforded cardioprotection against ischemia/reperfusion (I/R)-induced mitochondrial calcium overload, but its mechanisms are not fully understood. This study investigated whether ROS signaling activated STAT3 is involved in moderate hydrogen peroxide postconditioning (H 2 O 2 PoC) mimicked IHH against cardiac I/R injury and the possible downstream target of STAT3 in mitochondria that mediates H 2 O 2 PoC-afforded cardioprotection. Moderate H 2 O 2 PoC not only improved the post-ischemic recovery of myocardial contractile performance and reduce the infarct size in isolated rat I/R hearts, but also alleviated cytosolic Ca 2+ and mitochondrial Ca 2+ overload and improved Ca 2+ transients and cell contraction in rat I/R cardiomyocytes. However, the cardioprotective effects of moderate H 2 O 2 PoC was abrogated by janus kinase 2 (JAK2)/STAT3 inhibitor AG490 in rat hearts as well as adenovirus-delivered shRNAs specific for STAT3 and the opener of mitochondrial calcium uniporter (MCU) spermine, respectively, in rat adult cardiomyoctes with simulated I/R. Besides, the moderate H 2 O 2 PoC-afforded cardioprotection abrogated by spermine could be rescued by STAT3 overexpression in rat cardiomyoctes with simulated I/R. Moreover, H 2 O 2 PoC enhanced the expression of serine 727 phosphorylation of STAT3 and STAT3 in mitochondria of rat cardiomyoctes with simulated I/R. Furthermore, immunofluorescence and co-immunoprecipitation assay revealed a co-localization/interaction of STAT3 and MCU in rat cardiomyoctes with moderate H 2 O 2 PoC at reperfusion 5 min and reperfusion 30 min but not in I/R cells. Co-immunoprecipitation further confirmed that STAT3 interacted with the N-terminal domain (NTD) of MCU in rat cardiomyoctes with moderate H 2 O 2 PoC. These findings indicate that STAT3 mediates the cardioprotection of moderate H 2 O 2 PoC against I/R injury by alleviating mitochondrial calcium overload through inhibiting MCU opening via the interaction with the NTD of MCU. Our finds provide new insight into the mechanisms of STAT3 in the cardioprotection.
Including the Family in Perioperative Care of Older Adults—A Call for HELP
Authors: Victoria Tang, Emily Finlayson, Ken Covinsky
Journal: JAMA Internal Medicine (2019)

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Abstract 501: Selective i <i>n vivo</i> Modulation of Vagal-Muscarinic Signaling Prevents Sudden Cardiac Death in a Pressure Overload Model of Heart Failure
Authors: Jeffrey S Crocker, Daiana C Vieira, Kenneth G Parks, Brian O'Rourke, Swati Dey, Deeptankar DeMazumder
Journal: Circulation Research (2019)

Introduction: Sudden cardiac death (SCD) from ventricular tachyarrhythmias (VT/VF) claims a quarter millions lives/year in USA. Patients with heart failure (HF) have high SCD risk. We previously demonstrated that differential remodeling of cardiac muscarinic receptors plays a critical role in pathogenesis and for effective therapy of HF and SCD risk [PMID: 25733594]. Ongoing clinical trials of chronic vagus nerve stimulation (cVNS) aimed at improving left ventricular (LV) function in HF patients have had mixed preliminary results. However, the effect of cVNS on SCD risk is unexplored. While acute VNS terminates VT/VF, cVNS likely alters the arrhythmogenic substrate. A better understanding of the underlying mechanisms is necessary for the design of new, more effective therapies. Hypothesis: cVNS prevents SCD by reducing calcium, autonomic and redox derangements in LV myocytes and improving repolarization reserve in pressure overloaded hearts. Methods: Guinea pigs are randomized to Sham or aortic constriction (AC) with daily brief (30-min) low-dose β-adrenergic stress (Shami; ACi), with and without in vivo cVNS therapy via an implanted device, with and without in vivo end-organ muscarinic receptor blockade (MRB) using glycopyrrolate. Echocardiography and continuous 24-hour ECG analyses are performed. Animals are sacrificed at 4 weeks for biochemical, excised perfused heart (pressure-volume, electrophysiology, optical mapping) and isolated LV myocyte studies at 37°C. PRELIMINARY RESULTS: Compared to Sham, the M2 subtype of muscarinic receptors are upregulated in AC and ACi, along with reduced calcium cycling, sarcomere shortening and β-adrenergic responsiveness. Whereas ACi+MRB markedly increased SCD incidence, ACi+cVNS prevented SCD. Interestingly, cVNS prolonged but also stabilized the ECG QT interval by reducing dispersion of repolarization in ACi model. Echocardiographic fractional shortening was also higher in ACi+cVNS (52±1%; 4 weeks) compared to ACi (27±2%; 4 weeks) and ACi+MRB (23±5%; 2 weeks). Conclusions: Chronic in vivo perturbation of cholinergic signaling may be an effective strategy for SCD therapy. Ongoing experiments are aimed at dissecting underlying mechanisms and identifying potential targets for SCD therapy.
Timed Sequential Busulfan and Post-Transplantation Cyclophosphamide in Matched and Haploidentical Transplantation: Results of a Phase II Study
Authors: Uday Popat, Rohtesh S. Mehta, Roland L. Bassett, Amanda L. Olson, Julianne Chen, Sairah Ahmed, Amin M. Alousi, Paolo Anderlini, Gheath Alatrash, Qaiser Bashir, Stefan O. Ciurea, Chitra Hosing, Jin S Im, Partow Kebriaei, Issa F. Khouri, David Marin, Yago Nieto, Betul Oran, Katy Rezvani, Muzaffar H. Qazilbash, Elizabeth J. Shpall, Richard E Champlin, Borje S Andersson
Journal: Blood (2018)
B3a2 Transcript Is an Independent Factor for the Achievement of a Deep Molecular Response in Chronic Phase - Chronic Myeloid Leukemia Patients Treated with Imatinib in First-Line
Authors: Matheus Sebastian Da Silva, Eliana C Miranda, Marcia Torresan Delamain, Gislaine Oliveira Duarte, Bruna R Vergilio, Ana Beatriz Pascoal Lopes, Jessica CN Vianna, Carmino Antonio De Souza, Erich Vinicius De Paula, Katia B Pagnano
Journal: Blood (2018)
FISH Abnormalities (including R-ISS defining and IgH mutations) Are Similar across Race and Ethnicity Among Patients with Multiple Myeloma (except higher rates of t(4:14) in Minorities and 1q Amplifications in Asian/Indians)
Authors: Noa Biran, Camille Johnson, Andrew D Norden, Roger Kumar, David H. Vesole, Seth H. Berk, Denis B. Fitzgerald, David S Siegel, Stuart L. Goldberg
Journal: Blood (2018)
ALK-Negative Anaplastic Large Cell Lymphomas with 6p25.3 Translocations Show a Histone-Modifying Gene Expression Signature
Authors: Andrew L. Feldman, Gaofeng Huang, Julie C Porcher, Sertac Kip, Stephen M Ansell, Ahmet Dogan, Wee-Joo Chng
Journal: Blood (2011)
Abstract 541: Uncovering the Physiological Role of Mitochondrial Respiratory Supercomplexes in the Heart
Authors: Xavier R Chapa-Dubocq, Keishla M Rodriguez-Graciani, Roberto A Guzman-Hernandez, Sehwan Jang, Sabzali Javadov
Journal: Circulation Research (2019)

The assembly of mitochondrial electron transport chain (ETC) supercomplexes (SCs), particularly the respirasome containing complexes I, III, and IV have been shown to participate in facilitating electron transport, reducing ROS production and maintaining the structural integrity of individual ETC complexes. However, the physiological role of SCs in high energy demanding tissues such as the heart remains unknown. Here, we elucidated whether disassembly of SCs affects the cardiac function. Hearts isolated from adult male Sprague Dawley rats were perfused using a Langendorff-mode perfusion with Krebs-Henseleit solution (KHS) for the first 20 min (equilibration period) followed by perfusion in the following groups: (i) 40-min perfusion with KHS (n=4), (ii, iii) 20-min perfusion with rotenone (an inducer of SC dissociation) or vehicle (ethanol, n=8 for both), and (iv, v) 20-min perfusion with rotenone or vehicle followed by a 20-min perfusion with KHS without rotenone or vehicle (n=6 for both). Cardiac function was monitored throughout the entire perfusion period. At the end of each protocol, the mitochondria were isolated for analysis of SCs, permeability transition, respiration rates, and ROS production. We found that cardiac function between rats perfused with KHS (i) and ethanol (i, iii) had no significant difference, though rotenone perfused rats (ii and iv) had a significant reduction (&lt;40%) in cardiac function associated with reduced oxygen consumption rates in these groups. Furthermore, a significant increase in ROS production (ii) and permeability transition pore opening (iv) was observed when the hearts were perfused with rotenone with and without subsequent washout, respectively. Analysis of SCs by blue native PAGE displayed a significant reduction in SC levels in both ethanol (iii and v) and rotenone (ii and iv) perfused rats. Surprisingly, there were no differences in SC levels between the ethanol (iii and v) and rotenone (ii and iv) perfused groups. In addition, incubation of isolated intact mitochondria with ethanol and acetaldehyde did not demonstrate any direct effects of these compounds on ETC SC assembly. In conclusion, our data demonstrate a lack of an associative link between mitochondrial ETC SCs and cardiac function in rats.
Pomalidomide and Dexamethasone Grant Rapid Hematologic Responses in Patients with Relapsed and Refractory AL Amyloidois: A European Retrospective Series of 150 Patients
Authors: Paolo Milani, Faye Sharpley, Stefan Schönland, Marco Basset, Shameem Mahmood, Christoph Kimmich, Andrea Foli, Sajitha Sachchithanantham, Giampaolo Merlini, Ashutosh D. Wechalekar, Giovanni Palladini, Ute Hegenbart
Journal: Blood (2018)
Abstract 252: Activated Fibroblast-specific Deletion of RhoA Reduces Cardiac Fibrosis Through Regulation of the Non-canonical p38-MAPK Signaling Pathway
Authors: Leena A Kaikkonen, Valerie Sätzler, Ashbeel Roy, Mauricio Contreras, Bing Xu, Stefanie Stroll, Jason McCarthy, Jeffery D Molkentin, Saumya Das, Maria Kontaridis
Journal: Circulation Research (2019)

Objective: Heart failure is a progressive disease characterized by cardiomyocyte (CM) loss, interstitial fibrosis, loss of ventricular compliance and chamber remodeling. Role of cardiac fibroblasts is implicated in the process, but specific molecular mechanisms regulating their function remain unclear. Previously, we showed that in mice, in response to stress, CM-specific deletion of RhoA, a Ras-related small G protein, accelerated cardiac dilation, with significant loss of contractile function, but it also significantly reduced cardiac fibrosis. Therefore, here, we focused on understanding the role of RhoA specifically in myofibroblast transformation and the fibrotic response. Results: We generated mice with activated fibroblast-specific deletion of RhoA using a tamoxifen (TMX) inducible periostin-cre promoter (RhoAfl/fl::PSTN Cre/+). 10-wk-old male RhoAfl/fl::PSTN Cre/+ or control mice were treated with angiotensin-phenylephrine (AngPE) or saline for 4 wk using osmotic minipumps and fed either with TMX or regular diet. Following TMX-AngPE treatment, the RhoAfl/fl::PSTN Cre/+ mice showed significantly decreased cardiac fibrosis, as compared to controls (0.9% vs. 3.2%, respectively). Moreover, while overall cardiac function following AngPE treatment was similar at 4 wk in all groups, hearts from the TMX-RhoAfl/fl::PSTN Cre/+ mice had significantly reduced septal thickness, as compared to controls. Expression of fetal genes, ANF, BNP, and β-MHC, as well as markers of fibrosis, including α-SMA and CTGF, were similarly induced in control and TMX-RhoAfl/fl::PSTN Cre/+ mice. However, TMX-RhoAfl/fl::PSTN Cre/+ mice had reduced expression of TGF-β1, thrombospondin-5 and Col1a2. Finally, RhoA deletion in activated fibroblasts did not affect the canonical TGFβ signaling pathway, as expected; instead, we found TMX-RhoAfl/fl::PSTN Cre/+ hearts had reduced non-canonical p38-MAPK signaling, suggestive of cellular-specific effects of RhoA regulation in the onset of cardiac disease and fibrosis. Conclusions: These data confirm the primacy of the RhoA pathway in the fibrotic response in vivo and identify potential novel downstream targets and possible therapeutic strategies for treatment of cardiac fibrosis and heart failure.
The role of bacterial and viral infection in exacerbation of bronchiectasis: a prospective study
Authors: Chun-Lan Chen, Yan Huang, Jing-Jing Yuan, Hui-Min Li, Xiao-Rong Han, Miguel Angel Martinez-Garcia, Rong-Chang Chen, Wei-Jie Guan, Nan-Shan Zhong
Journal: The Lancet (2019)
Discrimination Indices as Screening Tests for Beta-Thalassemic Trait.
Authors: George Ntaios, Anastasia Chatzinikolaou, Zoi Saouli, Fotios Girtovitis, Georgia Kaiafa, Zisis Kontoninas, Dimitrios Agapakis, Christos Savopoulos, Athanasios Papadopoulos
Journal: Blood (2007)