tbuckley/cabot-search huggingface dataset:
Abstract 14057: IL-19 Preserves the Metabolic Activity of Adipocytes in Obesity
Authors: Tatsuo Kawai, Rebecca Petre-Sullivan, Michael Autieri, Rosario G Scalia
Journal: Circulation (2021)

Lack of compensatory vascularization causes hypoxia with adipose tissue dysfunction in obesity. Dysfunctional adipocytes instigate systemic low-grade inflammation which is associated with increased morbidity and mortality of metabolic disorders and related cardiovascular disease. A remaining challenge in the field is how to preserve adipocyte metabolic function by suppressing the negative aspect of inflammation, without blocking its angiogenic function. We investigated the role of IL-19, a uniquely immuno-modulatory, pro-angiogenic interleukin expressed also in adipose tissue. We hypothesize that IL-19 acts as a novel adipokine whose expression in expanding adipose depots is essential for maintaining glucose homeostasis. We report that IL-19 is expressed in adipose tissue at both the transcript and protein level and its expression is increased in inflamed visceral adipose tissue but not subcutaneous adipose tissue (p&lt;0.05). Utilizing Il19 -/- knockout mice, we found the loss of IL-19 leads to a metabolic phenotype characterized by reduced glucose and insulin tolerance, increased adipose tissue hypoxia and fibrosis, decreased adipose tissue vessel density and increased adipocyte hypertrophy both in response to standard chow diet and chronic high fat diet (p&lt;0.05). Acute treatment with IL-19 reduced glucose and insulin intolerance in obese wild-type mice (p&lt;0.05). In primary murine epididymal adipocytes the addition of IL-19 leads to increased glucose uptake (p&lt;0.05). These metabolic actions of IL-19 were linked to upregulation of the insulin type-2 receptor and subsequent increased expression/phosphorylation of the protein kinase B (Akt) in adipocytes. Overall, these data propose that IL-19 has novel therapeutic potential in that it can effectively allow adipose tissue expansion without concomitant inflammation and insulin insensitivity.
Bacterial membrane vesicles and phages in blood after consumption of<i>Lacticaseibacillus rhamnosus</i>JB-1
Authors: Kevin Champagne-Jorgensen, Tamina A. Jose, Andrew M. Stanisz, M. Firoz Mian, Alexander P. Hynes, John Bienenstock
Journal: Gut Microbes (2021)

Gut microbiota have myriad roles in host physiology, development, and immunity. Though confined to the intestinal lumen by the epithelia, microbes influence distal systems via poorly characterized mechanisms. Recent work has considered the role of extracellular vesicles in interspecies communication, but whether they are involved in systemic microbe-host interaction is unclear. Here, we show that distinctive nanoparticles can be isolated from mouse blood within 2.5 h of consuming Lacticaseibacillus rhamnosus JB-1. In contrast to blood nanoparticles from saline-fed mice, they reproduced lipoteichoic acid-mediated immune functions of the original bacteria, including activation of TLR2 and increased IL-10 expression by dendritic cells. Like the fed bacteria, they also reduced IL-8 induced by TNF in an intestinal epithelial cell line. Though enriched for host neuronal proteins, these isolated nanoparticles also contained proteins and viral (phage) DNA of fed bacterial origin. Our data strongly suggest that oral consumption of live bacteria rapidly leads to circulation of their membrane vesicles and phages and demonstrate a nanoparticulate pathway whereby beneficial bacteria and probiotics may systemically affect their hosts.
POLARGO: Randomized Phase III Study of Polatuzumab Vedotin Plus Rituximab, Gemcitabine, and Oxaliplatin in Relapsed/Refractory Diffuse Large B-Cell Lymphoma
Authors: Matthew J. Matasar, Corinne Haioun, Juan-Manuel Sancho, Andreas Viardot, Jamie Hirata, Thomas Perretti, Lisa Musick, Andrew K McMillan
Journal: Blood (2021)
Impact of Age, Body Surface Area, and Body Mass Index on Pegaspargase Toxicity and Pharmacokinetics: A Report from the DFCI ALL Consortium
Authors: Jonathan D. Paolino, Yael Flamand, Kristen E. Stevenson, Victoria Koch, Uma H. Athale, Peter D. Cole, Lisa M. Gennarini, Justine M. Kahn, Kara M. Kelly, Caroline Laverdiere, Jean-Marie Leclerc, Bruno Michon, Andrew E. Place, Jeffrey G. Supko, Thai Hoa Tran, Jennifer J.G. Welch, Donna S. Neuberg, Stephen E. Sallan, Lewis B. Silverman, Lynda M. Vrooman
Journal: Blood (2021)
<i>Mds1 CreERT2</i>-Based Lineage-Tracing Reveals Increasing Contributions of HSCs to Fetal Hematopoiesis and to Adult Tissue-Resident Macrophages in the Marrow
Authors: Kathleen E. McGrath, Yi Zhang, Edward Ayoub, Paul D. Kingsley, Hongbo Yu, Katherine H Fegan, Kelly A McGlynn, Sarah Rudzinskas, Archibald S. Perkins, James Palis
Journal: Blood (2021)
An <i>E</i> <i>x Vivo</i> Model of Oxidatively Stressed Red Blood Cells Demonstrates a Role for Exogenous Amino Acids in Enhancing Red Blood Cell Function and Morphology
Authors: Heather N. Colvin, Elmira Alipour, Jordan Buzzett, Glen Marrs, Daniel B. Kim-Shapiro, Regina Joice Cordy
Journal: Blood (2021)
Matching Adjusted Indirect Comparison (MAIC) of Oral Azacitidine (Oral-AZA) Versus Injectable AZA in Patients (pts) with Acute Myeloid Leukemia (AML) in First Remission after Intensive Induction Chemotherapy
Authors: Clara Chen, Gerwin A. Huls, Heather Cameron, Beatrice Suero, Alberto Vasconcelos, Lona Gaugler, C.L. Beach
Journal: Blood (2021)
Durability of Hemoglobin Response and Reduction in Transfusion Burden Is Maintained over Time in Patients with Pyruvate Kinase Deficiency Treated with Mitapivat in a Long-Term Extension Study
Authors: Rachael F. Grace, Andreas Glenthoej, Wilma Barcellini, Madeleine Verhovsek, Jennifer A. Rothman, Marta Morado, D. Mark Layton, Oliver Andres, Frédéric Galactéros, Eduard J. Van Beers, Koichi Onodera, Vip Viprakasit, Satheesh Chonat, John B. Porter, Malia P. Judge, Penelope A. Kosinski, Peter Hawkins, Sarah Gheuens, Emily Xu, Bryan McGee, Vanessa Beynon, Hanny Al-Samkari
Journal: Blood (2021)
Abstract 10312: Intermittent Fasting and Increased Galectin-3 Reveal a Potential Protective Mechanism Against Risk of Heart Failure and Type 2 Diabetes
Authors: Benjamin D Horne, Jeffrey L Anderson, Heidi T May, Viet T Le, Oxana Galenko, Stavros G Drakos, Tami L Bair, Kirk U Knowlton, Joseph B Muhlestein
Journal: Circulation (2021)

Introduction: Intermittent fasting decreases cardiometabolic risk factors, heart failure (HF) risk, and type 2 diabetes risk. Sodium-glucose transport 2 (SGLT-2) inhibitors reduce diabetes and HF risk and a study of canagliflozin reported that it raised galectin-3 levels (Januzzi 2017). Previously in the WONDERFUL trial (NCT02770313), intermittent fasting caused declines in the Metabolic Syndrome Score (MSS) and homeostatic model assessment of insulin resistance (HOMA-IR). This study evaluated intermittent fasting’s effects on galectin-3 in a post hoc analysis of the WONDERFUL Trial. Methods: People aged 21-70 years were enrolled who had ≥1 metabolic syndrome feature or type 2 diabetes, were free of anti-diabetic and statin medications, and had elevated LDL-C. Subjects had 26-week galectin-3 data (N=67; n=36 intermittent fasting, n=31 controls). Subjects were randomized to a 24-hour water-only fasting intervention (fasting twice per week for 4 weeks, then once each week for 22 weeks) or a parallel control arm ( ad libitum eating). This study evaluated the 26-week galectin-3 change score and other changes in HF biomarkers. Results: At 26 weeks, the galectin-3 change score was increased in intermittent fasting (0.575±2.63 ng/mL) vs control (-0.624±2.79 ng/mL; p=0.021). Changes in galectin-3 were inversely correlated with HOMA-IR change score (r= -0.288, p=0.018) and MSS change score (r= -0.238, p=0.052). Changes in galectin-3 at 4 weeks (intermittent fasting: 0.345±2.68 ng/mL; control: -0.465±3.18 ng/mL; p=0.27) and 13 weeks (fasting: 0.917±4.96; control: -0.097±2.83 ng/mL; 0.15) were not significantly different. B-type natriuretic peptide went down in intermittent fasting (-0.328±12.29 pg/mL) but this was not significant compared to controls (15.50±75.34 pg/mL, p=0.23). Other HF biomarkers were unchanged. Conclusions: Water-only 24-hour intermittent fasting increased galectin-3. This rise in galectin-3 was correlated with declining HOMA-IR and MSS and may be similar to reported effects of SGLT-2 inhibitors. Increased galectin-3 may be an adaptive response that could prevent chronic disease by decreasing inflammation, ameliorating insulin resistance, or modifying related mechanisms.
Tyrosyl DNA phosphodiesterase 1 (Tdp1) is a fidelity factor for non-homologous end-joining reactions.
Authors: Karim Bahmed, Karin Nitiss, Aman Seth, John Nitiss
Journal: Cancer Research (2008)

5780  DNA strand break repair is critical for maintaining cell survival following exposure to agents such as ionizing radiation or cytotoxic anti-cancer drugs. Two major pathways involved in repairing DNA double strand breaks are homologous recombination, a highly accurate repair pathway, and non-homologous end-joining (NHEJ), a pathway that can generate translocations that may lead to oncogenesis. We are studying tyrosyl-DNA phosphodiesterase 1 (Tdp1), a protein that can remove phosphotyrosyl-linked peptides from the ends of DNA. The Tdp1p reaction is important for repairing damage arising from agents that block the reaction cycle of topoisomerases at a point where the enzymes are covalently bound to DNA. We found that yeast Tdp1 has an unexpected role in NHEJ. We used a plasmid recircularization assay to assess the efficiency of end-joining and the accuracy of the repair reaction. When plasmids were linearized with HindIII or EcoRI (generating a 5′ overhang) there was no change in the efficiency of the end-joining reaction in Δtdp1 cells. However, loss of TDP1 led to a large increase in junctions with sequence alterations. The altered junctions in Δtdp1 cells were mainly 2-4 nucleotide insertions, a type of joining error seldom seen in wild type cells. The sequence of the insertions was consistent with filling-in of the cohesive ends by a DNA polymerase prior to ligation. The errors depend on an intact NHEJ pathway, since the errors were not seen in cells lacking both TDP1 and NHEJ components such as Ku80 (YKU80) or DNA ligase IV (DNL4). The addition reactions occur in Δtdp1 Δrad52 cells showing that homologous recombination is not required for nucleotide additions. Also, the addition reactions were not seen in plasmids cut with Pst1 (generating a 3′ overhang), supporting the hypothesis that the additions arise from polymerase filling in. Since yeast Pol4 has been implicated in some NHEJ reactions, we tested whether Δtdp1 Δpol4 cells generated additions. We showed that the addition reactions were dependent on a functional POL4 gene, strongly suggesting that Pol4 carries out the addition reactions. We also find that Δtdp1 influences the efficiency of endjoining with DNA substrates with blunts ends. Δtdp1 strains exhibit more efficient repair of DNA with blunt ends than do wild type cells. Our results indicate that ′′simple ligations′′ of DNA with cohesive ends frequently require end-processing enzymes to ensure their fidelity. We hypothesize that the critical activity of Tdp1p in NHEJ is a previously characterized 3′ nucleosidase activity. Since removal of a nucleoside results in a 3′ phosphate, DNA molecules following Tdp1 reactions are blocked, preventing additions by DNA polymerases, and perhaps blocking nucleolytic digestion by 3′-5′ exonucleases. A biochemical role for Tdp1 in joining of blunt end substrates is less clear, but may also be related to controlling the ability of different enzymes to process DNA ends.
DJ4 Targets Rho-associated Protein Kinase Pathway and Attenuates Disease Progression in Pre-clinical Murine Models of Acute Myeloid Leukemia
Authors: Melanie Ehudin, Upendarrao Golla, Charyguly Annageldiyev, Zheng Zeng, Diwakar Bastihalli Tukaramrao, Anna Tarren, Dhimant Desai, David F. Claxton, Sinisa Dovat, Arati Sharma
Journal: Blood (2021)
<i>A Randomized Placebo-Controlled Trial of Primary Prophylaxis with Weekly Alendronate</i> <i>Against Glucocorticoid-Induced Osteoporosis in Lymphoma Patients Treated with Steroid-Containing Chemotherapy.</i>
Authors: Paw Jensen, Lasse H. Jakobsen, Martin Bøgsted, Joachim Baech, Simon Lykkeboe, Marianne Tang Severinsen, Peter Vestergaard, Tarec Christoffer El-Galaly
Journal: Blood (2021)
Smad3 deficiency improves islet-based therapy for diabetes and diabetic kidney injury by promoting β cell proliferation <i>via</i> the E2F3-dependent mechanism
Authors: Hong-Lian Wang, Biao Wei, Hui-Jun He, Xiao-Ru Huang, Jing-Yi Sheng, Xiao-Cui Chen, Li Wang, Rui-Zhi Tan, Jian-Chun Li, Jian Liu, Si-Jin Yang, Ronald CW Ma, Hui-Yao Lan
Journal: Theranostics (2021)

Rationale: Poor β cell proliferation is one of the detrimental factors hindering islet cell replacement therapy for patients with diabetes. Smad3 is an important transcriptional factor of TGF-β signaling and has been shown to promote diabetes by inhibiting β cell proliferation. Therefore, we hypothesize that Smad3-deficient islets may be a novel cell replacement therapy for diabetes. Methods: We examined this hypothesis in streptozocin-induced type-1 diabetic mice and type-2 diabetic db/db mice by transplanting Smad3 knockout (KO) and wild type (WT) islets under the renal capsule, respectively. The effects of Smad3KO versus WT islet replacement therapy on diabetes and diabetic kidney injury were examined. In addition, RNA-seq was applied to identify the downstream target gene underlying Smad3-regulated β cell proliferation in Smad3KO-db/db versus Smad3WT-db/db mouse islets. Results: Compared to Smad3WT islet therapy, treatment with Smad3KO islets produced a much better therapeutic effect on both type-1 and type-2 diabetes by significantly lowering serum levels of blood glucose and HbA1c and protected against diabetic kidney injuries by preventing an increase in serum creatinine and the development of proteinuria, mesangial matrix expansion, and fibrosis. These were associated with a significant increase in grafted β cell proliferation and blood insulin levels, resulting in improved glucose intolerance. Mechanistically, RNA-seq revealed that compared with Smad3WT-db/db mouse islets, deletion of Smad3 from db/db mouse islets markedly upregulated E2F3, a pivotal regulator of cell cycle G1/S entry. Further studies found that Smad3 could bind to the promoter of E2F3, and thus inhibit β cell proliferation via an E2F3-dependent mechanism as silencing E2F3 abrogated the proliferative effect on Smad3KO β cells. Conclusion: Smad3-deficient islet replacement therapy can significantly improve both type-1 and type-2 diabetes and protect against diabetic kidney injury, which is mediated by a novel mechanism of E2F3-dependent β cell proliferation.
Drepadom - Establishment of Home Care Services and Hospitalizations for Sickle Cell Disease Patients As Standard Care Since the Covid-19 Pandemic
Authors: Yanís Pelinski, Cindy Mescam, Christian Kassasseya, Gonzalo De Luna, Henri Guillet, Clara Noizat, Sylvain Lejeune, Suella Martino, Dora Bachir, Françoise Driss, Amna Jebali, Anne-Laure Pham Hung D'Alexandry D'Orengiani, Nicolas Lemonier, France Pirenne, Anoosha Habibi, Pablo Bartolucci
Journal: Blood (2021)
Acute Myeloid Leukemia (AML) Hospitalizations: Racial Disparity in Outcomes of Patients with Comorbidities
Authors: Sara Taveras Alam, Deepa Dongarwar, Elyse Lopez, Sarvari Venkata Yellapragada, Gustavo Rivero, Courtney Nicole Miller-Chism, Martha P. Mims, Quillan Huang, Hamisu Salihu
Journal: Blood (2021)
Abstract 11443: Where NO <sub>2</sub> Meets Omega-3 Polyunsaturated Fatty Acids: Health Impact of Short-Term Ambient Air Pollution Exposure in Healthy Adults
Authors: Haiyan Tong, Hao Chen, Siqi Zhang, Wan Shen, Claudia Salazar, Alexandra Schneider, Lauren Wyatt, Ana Rappold, David Diaz-Sanchez, Robert Devlin, James Samet
Journal: Circulation (2021)

Introduction: Exposure to ambient nitrogen dioxide (NO 2 ) is associated with adverse respiratory and cardiovascular outcomes. Supplementation of omega-3 polyunsaturated fatty acids (PUFA) has shown health benefits against exposure to air pollution. Hypothesis: Dietary omega-3 PUFA intake offers cardiovascular and respiratory benefits against short-term exposure to ambient NO 2 in healthy adults. Methods: Sixty-two healthy participants were enrolled into low or high omega-3 groups based on their habitual dietary omega-3 PUFA intake. Each participant was repeatedly assessed for blood lipids, markers of coagulation and fibrinolysis, vascular function, heart rate variability (HRV), and lung function up to five times separated by at least 7 days between October 2016 and September 2019. Daily ambient NO 2 concentrations were obtained from nearby air quality monitoring stations. The associations between NO 2 concentrations and the measured biomarkers were evaluated using the linear mixed-effects models stratified by the omega-3 intake levels. Results: In the high omega-3 group, an IQR increase in NO 2 concentrations was associated with reductions in total cholesterol at lag2 [-2.6% (-4.4, -0.9)], LDL at lag2 [-3.1% (-5.5, -0.7)], and HDL at lag1 [-2.4% (-4.4, -0.3)] and lag2 [-2.0% (-3.8, -0.1)]; increases in flow-mediated dilatation of brachial artery at lag1[5.7% (0.1, 11.2)] and lag2 [5.7% (0.8, 10.6)]; decreases in plasma levels of endothelin-1at lag3 [-25.6% (-50.0, -1.2)] and lag4 [-22.9% (-45.9, -0.01)]; decreased high frequency (HFn) of HRV [-7.2% (-13.6, -0.8)] and increased LF/HF ratio [13.4% (0.2, 28.3)] at lag3; as well as increased lung function. In the low omega-3 group, blood lipids, vascular function biomarkers and lung function were not significantly associated with NO 2 exposure. However, NO 2 exposure was associated with elevations in coagulation markers (von Willebrand Factor and D-dimer) and a decrease in very-low frequency of HRV at lag0 in the low omega-3 group. Conclusions: The results imply that high dietary omega-3 PUFA intake may offer benefits to cardiovascular and respiratory health in response to exposure to low-level ambient NO 2 in healthy adults. THIS ABSTRACT OF A PROPOSED PRESENTATION DOES NOT NECESSARILY REFLECT EPA POLICY.
Antibody Response to 2-Dose Sars-Cov-2 mRNA Vaccine in Allogeneic Hematopoietic Cell Transplant Recipients
Authors: Alexis Maillard, Rabah Redjoul, Marion Klemencie, Hélène Labussière, Amandine Le Bourgeois, Maud d'Aveni, Anna Berceanu, Sylvain Chantepie, Carmen Botella, Michael Loschi, Magalie Joris, Cristina Castilla-Llorente, Sylvie Francois, Mathieu Leclerc, Patrice Chevallier, Stephanie Nguyen Quoc
Journal: Blood (2021)
A Novel Methodology for Building Longitudinal, Patient-Centric Real World Datasets in Hemophilia A
Authors: Mark W Skinner, Gillian Hanson, Tao Xu, Richard Ofori-Asenso, Richard H. Ko, Emily Cibelli, Francis Nissen, Michelle Witkop, Fabian Sanabria, Amy D. Shapiro
Journal: Blood (2021)
A Novel and Successful Patient or Donor-Derived CD7-Targeted CAR T-Cell Therapy for Relapsed or Refractory T-Cell Lymphoblastic Lymphoma (R/R T-LBL)
Authors: Junfang Yang, Xiao Yang, Ying Liu, Qinglong Wang, Hui Wang, Jianqiang Li, Peihua Lu
Journal: Blood (2021)
Midostaurin Plus Intensive Chemotherapy for Younger and Older Patients with Acute Myeloid Leukemia and FLT3 Internal Tandem Duplications
Authors: Hartmut Döhner, Daniela Weber, Julia Krzykalla, Walter Fiedler, Gerald Wulf, Helmut R. Salih, Michael Lübbert, Michael W.M. Kühn, Thomas Schroeder, Hans Salwender, Katharina S. Götze, Jörg Westermann, Lars Fransecky, Karin Mayer, Bernd Hertenstein, Mark Ringhoffer, Hans-Joachim Tischler, Sigrid Machherndl-Spandl, Anika Schrade, Peter Paschka, Verena I Gaidzik, Frauke Theis, Felicitas R Thol, Michael Heuser, Richard F. Schlenk, Lars Bullinger, Maral Saadati, Axel Benner, Konstanze Döhner, Arnold Ganser
Journal: Blood (2021)
Cytokine-Induced Memory-like NK Cells Have a Distinct Single Cell Transcriptional Profile and Persist for Months in Adult and Pediatric Leukemia Patients after Adoptive Transfer
Authors: Jennifer A. Foltz, Melissa M. Berrien-Elliott, David A. Russler-Germain, Carly C. Neal, Jennifer Tran, Margery Gang, Pamela Wong, Matthew Mosior, Jeffrey J. Bednarski, Clare Zimmerman, Celia C. Cubitt, Nancy D. Marin, Alice Y. Zhou, Miriam T. Jacobs, Mark Foster, Timothy Schappe, Ethan McClain, Sweta Desai, Patrick Pence, Michelle Becker-Hapak, Lynne Marsala, Obi L. Griffith, Malachi Griffith, Saad M. Khan, Bryan Fisk, Amanda F. Cashen, Allegra A. Petti, Todd A. Fehniger
Journal: Blood (2021)
Retrospective Analysis of Response Rates to Anti-CD38 Monoclonal Antibody Containing Regimens Among Multiple Myeloma Patients with Prior Exposure to Daratumumab or Isatuximab
Authors: David Yashar, Bernard Sean S. Regidor, Scott Kristian Jew, Sean Bujarski, Marissa-Skye Goldwater, Regina Swift, Gary Edward Schwartz, Shahrooz Eshaghian, Robert Vescio, James R. Berenson
Journal: Blood (2021)
Palliative Care Utilization, Transfusion Burden and Symptoms for Patients with Multiple Myeloma at the End of Life
Authors: Geoffrey McInturf, Kimberly Younger, Courtney Sanchez, Charles Walde, Al-Ola Abdallah, Leyla Shune, Nausheen Ahmed, Douglas W. Sborov, Amandeep Godara, Brian McClune, Christian Sinclair, Ghulam Rehman Mohyuddin
Journal: Blood (2021)
Autologous Stem Cell Transplantation in AL-Amyloidosis Following Yttrium-90 Labelled Anti-CD66 Monoclonal Antibody As Sole Conditioning Is Associated with Low Toxicity and Demonstrable Disease Responses
Authors: Kim H. Orchard, Jon Langford, Paul Lloyd-Evans, Denise Phillips, Matthew Guy, Sofia Michopoulou, Gemma Lewis, Julian Williams, Clint Zvavamwe, Claire Hutchison, Jane Nunnick, Amanda Blackwell, Pei-San Chan, Caspar Wickham, Ann-Marie Quigley, Mark Cook, Graham Jackson, Philip N Hawkins, Ashutosh D. Wechalekar
Journal: Blood (2021)
Mesenchymal stem/stromal cells in cancer therapy
Authors: Tianxia Lan, Min Luo, Xiawei Wei
Journal: Journal of Hematology & Oncology (2021)

Abstract The multipotent mesenchymal stem/stromal cells (MSCs), initially discovered from bone marrow in 1976, have been identified in nearly all tissues of human body now. The multipotency of MSCs allows them to give rise to osteocytes, chondrocytes, adipocytes, and other lineages. Moreover, armed with the immunomodulation capacity and tumor-homing property, MSCs are of special relevance for cell-based therapies in the treatment of cancer. However, hampered by lack of knowledge about the controversial roles that MSC plays in the crosstalk with tumors, limited progress has been made with regard to translational medicine. Therefore, in this review, we discuss the prospects of MSC-associated anticancer strategies in light of therapeutic mechanisms and signal transduction pathways. In addition, the clinical trials designed to appraise the efficacy and safety of MSC-based anticancer therapies will be assessed according to published data.
Effectiveness of Monthly Low-Dose Emicizumab Prophylaxis without 4-Week Loading Doses Among Patients with Hemophilia a with and without Inhibitor: A Case Series Report
Authors: Ampaiwan Chuansumrit, Nongnuch Sirachainan, Suphaneewan Jaovisidha, Tachit Jiravichitchai, Praguywan Kadegasem, Ketsuda Kempka, Monratta Panuwannakorn, Wannaphorn Rotchanapanya, Thunyakorn Nuntiyakul
Journal: Blood (2021)