tbuckley/cabot-search huggingface dataset:
Abstract 494: Mitral to Meninges: Aspergillus Endocarditis With Septic Emboli
Authors: Christopher T Smith, Dantwan Smith, Waqaar Arshad
Journal: Circulation Research (2020)

Introduction: Fungal endocarditis comprises less than 2% of infective endocarditis, with Aspergillus causing less than 28% of fungal endocarditis. Fungal endocarditis should be suspected in immunocompromised patients with persistent fevers, negative blood cultures, and vegetation on echocardiography. Invasive Aspergillus can affect any organ, but typically begins in the respiratory tract. Mortality rates climb to 90% with signs of hematogenous spread, such as cerebral abscesses. Case Presentation: Patient is a 53-year-old female with a past medical history of Sweet syndrome and chronic pancreatitis. Patient was admitted for persistent fevers and confusion. Patient was tachycardic but normotensive with a temperature of 102.5 F. Labs included significantly elevated serum LDH and Beta-D-Glucan. Blood cultures remained negative. Lumbar puncture cultures were negative; CSF cytology revealed pleocytosis with positive Aspergillus galactomannan serum antigen. Head MRI revealed multiple peripherally enhancing supratentorial lesions and intracranial abscesses (largest 8.4 mm) with ventriculitis of lateral ventricles, right greater than left. Transesophageal Echocardiogram (TEE) revealed mitral valve vegetation at A2 segment, no surrounding perivalvular abscess, minimal mitral regurgitation (MR). Management: Antibiotics were discontinued and patient was counseled on avoiding glucocorticoids. Patient was transferred to large tertiary center for Neurosurgery evaluation but was not candidate for biopsy/aspiration of the ring-enhancing lesions per Neurosurgery. Cardiothoracic Surgery was also consulted and patient was not a candidate for mitral valve replacement due to small size of vegetation without abscess and only mild MR. Voriconazole was continued and patient ultimately demonstrated a slow improvement in her strength and mental status over the next 6 months. Discussion: Mitral endocarditis from Aspergillus is rare but has a very high mortality rate. This case illustrates the importance of early recognition of systemic fungal infections in the setting of immunosuppression. Glucocorticoids and broad-spectrum antibiotics placed this patient at elevated risk for invasive Aspergillosis, which led to mitral endocarditis and subsequent cerebral abscesses from septic emboli.
Development and Exploitation of a Fully Human and Modular Organotypic Bone Marrow Niche Model to Study the Role of Stroma-Produced Factors in Human MDS
Authors: Alexander Schaeffer, Ewelina Czlonka, Irene Tirado-González, Thomas Böse, Jennifer Beauvarlet, Ivan Kur, Aline Bözec, Halvard Bönig, Christian H. Brandts, Uwe Platzbecker, Katharina S. Götze, Hind Medyouf
Journal: Blood (2020)
Conventional and Genetic Evidence on the Association between Adiposity and CKD
Authors: Pengfei Zhu, William G. Herrington, Richard Haynes, Jonathan Emberson, Martin J. Landray, Cathie L.M. Sudlow, Mark Woodward, Colin Baigent, Sarah Lewington, Natalie Staplin
Journal: Journal of the American Society of Nephrology (2020)

The size of any causal contribution of central and general adiposity to CKD risk and the underlying mechanism of mediation are unknown.Data from 281,228 UK Biobank participants were used to estimate the relevance of waist-to-hip ratio and body mass index (BMI) to CKD prevalence. Conventional approaches used logistic regression. Genetic analyses used Mendelian randomization (MR) and data from 394 waist-to-hip ratio and 773 BMI-associated loci. Models assessed the role of known mediators (diabetes mellitus and BP) by adjusting for measured values (conventional analyses) or genetic associations of the selected loci (multivariable MR).Evidence of CKD was found in 18,034 (6.4%) participants. Each 0.06 higher measured waist-to-hip ratio and each 5-kg/m2 increase in BMI were associated with 69% (odds ratio, 1.69; 95% CI, 1.64 to 1.74) and 58% (1.58; 1.55 to 1.62) higher odds of CKD, respectively. In analogous MR analyses, each 0.06-genetically-predicted higher waist-to-hip ratio was associated with a 29% (1.29; 1.20 to 1.38) increased odds of CKD, and each 5-kg/m2 genetically-predicted higher BMI was associated with a 49% (1.49; 1.39 to 1.59) increased odds. After adjusting for diabetes and measured BP, chi-squared values for associations for waist-to-hip ratio and BMI fell by 56%. In contrast, mediator adjustment using multivariable MR found 83% and 69% reductions in chi-squared values for genetically-predicted waist-to-hip ratio and BMI models, respectively.Genetic analyses suggest that conventional associations between central and general adiposity with CKD are largely causal. However, conventional approaches underestimate mediating roles of diabetes, BP, and their correlates. Genetic approaches suggest these mediators explain most of adiposity-CKD-associated risk.
Phased diploid genome assemblies and pan-genomes provide insights into the genetic history of apple domestication
Authors: Xuepeng Sun, Chen Jiao, Heidi Schwaninger, C. Thomas Chao, Yumin Ma, Naibin Duan, Awais Khan, Seunghyun Ban, Kenong Xu, Lailiang Cheng, Gan-Yuan Zhong, Zhangjun Fei
Journal: Nature Genetics (2020)

Abstract Domestication of the apple was mainly driven by interspecific hybridization. In the present study, we report the haplotype-resolved genomes of the cultivated apple ( Malus domestica cv. Gala) and its two major wild progenitors, M. sieversii and M. sylvestris . Substantial variations are identified between the two haplotypes of each genome. Inference of genome ancestry identifies ~23% of the Gala genome as of hybrid origin. Deep sequencing of 91 accessions identifies selective sweeps in cultivated apples that originated from either of the two progenitors and are associated with important domestication traits. Construction and analyses of apple pan-genomes uncover thousands of new genes, with hundreds of them being selected from one of the progenitors and largely fixed in cultivated apples, revealing that introgression of new genes/alleles is a hallmark of apple domestication through hybridization. Finally, transcriptome profiles of Gala fruits at 13 developmental stages unravel ~19% of genes displaying allele-specific expression, including many associated with fruit quality.
Abstract 474: ERK4-deficiency Potentiates the TAC-induced Increase in Collagen1-α <sub>1</sub> Messenger RNA in Mice
Authors: Joelle Trepanier, Dharmendra D Dingar, Marc-Antoine Gillis, Pramod Sahadevan, Yan Fen Shi, Martin G Sirois, Sylvain Meloche, Jean-claude Tardif, Bruce G Allen
Journal: Circulation Research (2020)

Cardiac hypertrophy, a common consequence of cardiopathologies such as hypertension and myocardial infarcts, involves formation of excessive interstitial fibrosis, which may impair cardiac function. Fibroblasts are the primary source of extracellular matrix protein. Extracellular-regulated kinase 4 (ERK4) is an atypical mitogen-activated protein kinase (MAPK). The regulation and role of ERK4 in the heart are currently unidentified and its only known target is MAP kinase-activated protein kinase 5 (MK5), a kinase involved in regulating fibroblast function. Following constriction of the transverse aorta (TAC), MK5 haplodeficient mice showed an attenuation of the TAC-induced increase in collagen 1-α 1 mRNA at 2-wk post-TAC and reduced hypertrophy 8-wk post-TAC. Further studies revealed MK5 immunoreactivity in cardiac fibroblasts but not myocytes. MK5 immunoprecipitates from whole heart contain ERK3 immunoreactivity, but not that of ERK4 or p38 MAPK. This study was to examine the role of ERK4 in myocardial structure, function, and remodeling 3-wk post-TAC. At 12 wk of age, echocardiographic imaging revealed systolic and diastolic function in male ERK4 -/- mice were similar to wild-type littermates (ERK4 +/+ ). Three weeks post-TAC, hypertrophy was similar in ERK4 +/+ and ERK4 -/- mice. Transcripts for BNP and βMHC increased to similar extent in TAC- ERK4 +/+ and TAC- ERK4 -/- mice. Two-way ANOVA indicated that ERK4 deficiency altered the effect of TAC on TGFβ 1 and collagen 1-α 1 transcript levels with each being higher in TAC-ERK4 -/- mice. Furthermore, MK5 immunoprecipitates from cardiac fibroblast lysates did not contain ERK4 immunoreactivity. Additional experiments revealed the presence of ERK4 immunoreactivity in myocytes but not fibroblasts. These results suggest 1) ERK4 may be involved in myocyte - fibroblast communication during myocardial remodeling and 2) in cardiac myocytes, ERK4 is part of a novel signaling cascade that does not involve MK5.
Dose Reductions and Discontinuations with Chronic Lymphocytic Leukemia (CLL) Patients Receiving Ibrutinib in Community and Academic Settings
Authors: Jing-Zhou Hou, Kellie Ryan, Senxi Du, Bruno S. Fang, Stanley M. Marks, Ray Page, Eileen Peng, Keith Szymanski, Sharon Winters, Hannah Le
Journal: Blood (2020)
Interleukin‐6: A novel biomarker for monoclonal antibody and chemotherapy‐associated hypersensitivity confirms a cytokine release syndrome phenotype‐endotype association
Authors: Baruch D. Jakubovic, Soledad Sanchez‐Sanchez, Sahar Hamadi, Donna‐Marie Lynch, Mariana Castells
Journal: Allergy (2020)

The authors declare that they have no conflicts of interest. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Endothelial p300 Promotes Portal Hypertension and Hepatic Fibrosis Through C‐C Motif Chemokine Ligand 2–Mediated Angiocrine Signaling
Authors: Jinhang Gao, Bo Wei, Mengfei Liu, Petra Hirsova, Tejasav S. Sehrawat, Sheng Cao, Xiao Hu, Fei Xue, Usman Yaqoob, Ningling Kang, Huarui Cui, William C.K. Pomerantz, Enis Kostallari, Vijay H. Shah
Journal: Hepatology (2020)

During liver fibrosis, liver sinusoidal endothelial cells (LSECs) release angiocrine signals to recruit inflammatory cells into the liver. p300, a master regulator of gene transcription, is associated with pathological inflammatory response. Therefore, we examined how endothelial p300 regulates angiocrine signaling and inflammation related to portal hypertension and fibrogenesis.CCl4 or partial inferior vena cava ligation (pIVCL) was used to induce liver injury. Mice with LSEC-specific p300 deletion (p300LSECΔ/Δ ) or C-C motif chemokine ligand 2 (Ccl2) deficiency, nuclear factor kappa B (NFκB)-p50 knockout mice, and bromodomain containing 4 (BRD4) inhibitors in wild-type mice were used to investigate mechanisms of inflammation regulation. Leukocytes were analyzed by mass cytometry by time-of-flight. Epigenetic histone marks were modified by CRISPR endonuclease-deficient CRISPR-associated 9-fused with the Krüppel associated box domain (CRISPR-dCas9-KRAB)-mediated epigenome editing. Portal pressure and liver fibrosis were reduced in p300LSECΔ/Δ mice compared to p300fl/fl mice following liver injury. Accumulation of macrophages was also reduced in p300LSECΔ/Δ mouse livers. Ccl2 was the most up-regulated chemokine in injured LSECs, but its increase was abrogated in p300LSECΔ/Δ mice. While the macrophage accumulation was increased in NFκB-p50 knockout mice with enhanced NFκB activity, it was reduced in mice with LSEC-specific Ccl2 deficiency and mice treated with specific BRD4 inhibitors. In vitro, epigenome editing of CCL2 enhancer and promoter regions by CRISPR-dCas9-KRAB technology repressed TNFα-induced CCL2 transcription through H3K9 trimethylation. In contrast, TNFα activated CCL2 transcription by promoting p300 interaction with NFκB and BRD4, leading to histone H3 lysine 27 acetylation at CCL2 enhancer and promoter regions.In summary, endothelial p300 interaction with NFκB and BRD4 increases CCL2 expression, leading to macrophage accumulation, portal hypertension, and liver fibrosis. Inhibition of p300 and its binding partners might serve as therapy in the treatment of liver diseases.
Abstract 337: Cardiac Inflammation Contributes to Heart Failure With Preserved Ejection Fraction (HFpEF) in Diabetic Mice With Low Aldehyde Dehydrogenase 2 (aldh2) Activity
Authors: Guodong Pan, Suresh S Palaniyandi
Journal: Circulation Research (2020)

Heart failure with preserved ejection fraction (HFpEF) is the prevalent form of cardiac complication in type 2 diabetes, which is associated with higher mortality. Inflammation plays a central role in the development of HFpEF, although the mechanism is unclear. Aldehyde dehydrogenase 2 (ALDH2), a mitochondrial enzyme, detoxifies oxidative-stress mediated 4-hydroxy-2-nonenal (4HNE) and thereby confers cardioprotective in diabetes. ALDH2*2 is the most common genetic mutation which causes a low ALDH2 activity. We hypothesize that low ALDH2 activity increases cardiac inflammation and consequentially aggravates HFpEF in diabetic mice. We bred a diabetic mouse model which carries mutant leptin receptor (same as db/db mice) and mutant ALDH2*2 (AL mice). The mice with double mutations are termed as ALDH2*2-fat (AF) mice. The ejection fraction (EF) is preserved in db/db (65.9±2.2%) and AF (67.2±3.9%) diabetic mice compared to db/m (68.5±4.6%, p&gt;0.05 vs db/db) and AL (68.6±4.8%, p&gt;0.05 vs AF) non-diabetic mice at 20 weeks. The running stress by treadmill decreased EF in AF mice (56.3±5.0%) compared to db/db (65.0±3.3%; p&lt;0.05), db/m (70.5±2.8%; p&lt;0.01) and AL (66.4±4.1%; p&lt;0.05). The maximum running distance was significantly decreased in AF (128.7±28.8m) mice compared to db/db (193.2±14.2m; p&lt;0.05), AL (305.2±21.5m; p&lt;0.01) and db/m (371.3±16.6m; p&lt;0.01) mice. In heart sections, the CD64+ macrophages in AF mice (88.64±22.12 /mm 2 ) were significantly increased, compared to db/db (53.24±12.55 /mm 2 , p&lt;0.05), db/m (12.57±2.56 /mm 2 , p&lt;0.01) and AL mice (47.89±13.97/mm 2 , p&lt;0.05). In conclusion, the low ALDH2 activity contributes to cardiac inflammation and thus HFpEF in diabetic mice.
Depression in individuals who subsequently develop inflammatory bowel disease: a population-based nested case–control study
Authors: Jonathan Blackwell, Sonia Saxena, Irene Petersen, Matthew Hotopf, Hanna Creese, Alex Bottle, Christopher Alexakis, Richard C Pollok
Journal: Gut (2020)

Objective Depression is a potential risk factor for developing IBD. This association may be related to GI symptoms occurring before diagnosis. We aimed to determine whether depression, adjusted for pre-existing GI symptoms, is associated with subsequent IBD. Design We conducted a nested case–control study using the Clinical Practice Research Datalink identifying incident cases of UC and Crohn’s disease (CD) from 1998 to 2016. Controls without IBD were matched for age and sex. We measured exposure to prevalent depression 4.5–5.5 years before IBD diagnosis. We created two sub-groups with prevalent depression based on whether individuals had reported GI symptoms before the onset of depression. We used conditional logistic regression to derive ORs for the risk of IBD depending on depression status. Results We identified 10 829 UC cases, 4531 CD cases and 15 360 controls. There was an excess of prevalent depression 5 years before IBD diagnosis relative to controls (UC: 3.7% vs 2.7%, CD 3.7% vs 2.9%). Individuals with GI symptoms prior to the diagnosis of depression had increased adjusted risks of developing UC and CD compared with those without depression (UC: OR 1.47, 95% CI 1.21 to 1.79; CD: OR 1.41, 95% CI 1.04 to 1.92). Individuals with depression alone had similar risks of UC and CD to those without depression (UC: OR 1.13, 95% CI 0.99 to 1.29; CD: OR 1.12, 95% CI 0.91 to 1.38). Conclusions Depression, in the absence of prior GI symptoms, is not associated with subsequent development of IBD. However, depression with GI symptoms should prompt investigation for IBD.
US voters decriminalize hard drugs and marijuana but restrict abortion in state elections
Authors: Janice Hopkins Tanne
Journal: BMJ (2020)

Voters in several US states made local changes easing access to hard drugs and marijuana, but possibly restricting abortion, in state elections held on 3 November, many as part of ballots during the presidential election.

The west coast state of Oregon decriminalized the possession of heroin, methamphetamine, LSD, oxycodone, and other hard drugs. Oregon was the first state to decriminalize possession of marijuana in 1973 and passed a “dignity in dying” act in 1997, which allows Oregon residents with a terminal illness to use a dose of prescribed lethal medication.

Although possession of hard drugs was …
Transgenic CD8αβ co-receptor rescues endogenous TCR function in TCR-transgenic virus-specific T cells
Authors: Gagan Bajwa, Inès Lanz, Mara Cardenas, Malcolm K Brenner, Caroline Arber
Journal: Journal for ImmunoTherapy of Cancer (2020)

Background Genetically engineered virus-specific T cells (VSTs) are a platform for adoptive cell therapy after allogeneic hematopoietic stem cell transplantation. However, redirection to a tumor-associated antigen by the introduction of a transgenic T-cell receptor (TCR) reduces anti-viral activity, thereby impeding the possibility of preventing or treating two distinct complications—malignant relapse and viral infection—with a single cell therapy product. Availability of CD8αβ co-receptor molecules can significantly impact class I restricted T-cell activation, and thus, we interrogated whether transgenic CD8αβ improves anti-viral activity mediated by native VSTs with or without a co-expressed transgenic TCR (TCR8). Methods Our existing clinical VST manufacturing platform was adapted and validated to engineer TCR+ or TCR8+ VSTs targeting cytomegalovirus and Epstein-Barr virus. Simultaneous anti-viral and anti-tumor function of engineered VSTs was assessed in vitro and in vivo. We used pentamer staining, interferon (IFN)-γ enzyme-linked immunospot (ELISpot), intracellular cytokine staining (ICS), cytotoxicity assays, co-cultures, and cytokine secretion assays for the in vitro characterization. The in vivo anti-tumor function was assessed in a leukemia xenograft mouse model. Results Both transgenic CD8αβ alone and TCR8 had significant impact on the anti-viral function of engineered VSTs, and TCR8+ VSTs had comparable anti-viral activity as non-engineered VSTs as determined by IFN-γ ELISpot, ICS and cytotoxicity assays. TCR8-engineered VSTs had improved anti-tumor function and greater effector cytokine production in vitro, as well as enhanced anti-tumor function against leukemia xenografts in mice. Conclusion Incorporation of transgenic CD8αβ into vectors for TCR-targetable antigens preserves anti-viral activity of TCR transgenic VSTs while simultaneously supporting tumor-directed activity mediated by a transgenic TCR. Our approach may provide clinical benefit in preventing and treating viral infections and malignant relapse post-transplant.
Bone Marrow Multiparametric Magnetic Resonance Imaging with Texture Analysis for Follow-up of Advanced Stage Myelofibrosis after Transplantation
Authors: Massimiliano Gambella, Federico Zaottini, Stefania Bregante, Riccardo Picasso, Emanuele Barabino, Carlo Martinoli, Emanuele Angelucci
Journal: Blood (2020)
Chromosomal Aberrations in Pre-HCT Blood Samples and Outcomes after Transplantation in Patients with Myelofibrosis
Authors: Youjin Wang, Derek W Brown, Weiyin Zhou, Tao Wang, Meredith Yeager, Andrew St. Martin, Stephen R. Spellman, Stephanie J. Lee, Stephen J. Chanock, Wael Saber, Mitchell Machiela, Shahinaz Gadalla
Journal: Blood (2020)
A Phase I Pharmacokinetic (PK) and Safety Study of Trph-222 in Patients with Relapsed/Refractory B-Cell Non-Hodgkin Lymphoma (R/R NHL): Dose-Escalation Results
Authors: Francisco J. Hernandez-Ilizaliturri, Ian W. Flinn, John Kuruvilla, Sarit E Assouline, Matthew L. Ulrickson, Beth A. Christian, Daniel J. Landsburg, Monic Stuart, Henry Lowman, Nancy Levin
Journal: Blood (2020)
Effect of Prior Treatment with Proteasome Inhibitors on the Efficacy and Safety of Once-Weekly Selinexor, Bortezomib, and Dexamethasone in Comparison with Twice-Weekly Bortezomib and Dexamethasone in Relapsed or Refractory Multiple Myeloma: Subgroup Analysis from the Boston Study
Authors: Maria Mateos, Maria Gavriatopoulou, Thierry Facon, Holger W Auner, Xavier Leleu, Roman Hajek, Meletios A Dimopoulos, Sosana Delimpasi, Maryana Simonova, Ivan Spicka, Ludek Pour, Irina Kryachok, Halyna Pylypenko, Vadim A Doronin, Ganna Usenko, Reuben Benjamin, Tuphan Kanti Dolai, Dinesh Kumar Sinha, Christopher P. Venner, Mamta Garg, Don A. Stevens, Hang Quach, Sundar Jagannath, Philippe Moreau, Moshe Levy, Ashraf Z. Badros, Larry D. Anderson, Nizar J. Bahlis, Michele Cavo, Yi Chai, Melina Arazy, Jatin Shah, Sharon Shacham, Michael G Kauffman, Paul G. Richardson, Sebastian Grosicki
Journal: Blood (2020)
Association of Baseline and Postinfusion Biomarkers with Safety and Efficacy Endpoints in Patients Treated with Orvacabtagene Autoleucel (orva-cel; JCARH125) in the Phase 1/2 Evolve Study (NCT03430011)
Authors: Julia Piasecki, Todd Devries, Aditya Radhakrishnan, Yan Li, Mark Heipel, Brian A. Fox, Valeria Beckett, Mariana Cota Stirner, Kristin Conte, Thomas Doerr, Sham Mailankody, Sandy W. Wong, Philip L. McCarthy
Journal: Blood (2020)
Multicenter, Randomized, Phase III Trial of Neoadjuvant Chemoradiation With Capecitabine and Irinotecan Guided by <i>UGT1A1</i> Status in Patients With Locally Advanced Rectal Cancer
Authors: Ji Zhu, Anwen Liu, Xinchen Sun, Luying Liu, Yaqun Zhu, Tao Zhang, Jianhui Jia, Shisheng Tan, Junxin Wu, Xin Wang, Juying Zhou, Jialin Yang, Chen Zhang, Hongyan Zhang, Yuanyuan Zhao, Gang Cai, Wei Zhang, Fan Xia, Juefeng Wan, Hui Zhang, Lijun Shen, SanJun Cai, Zhen Zhang
Journal: Journal of Clinical Oncology (2020)

Differentiating the irinotecan dose on the basis of the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) genotype improves the pathologic complete response (pCR) rate. In this study, we further investigated preoperative irinotecan combined with capecitabine-based chemoradiotherapy for locally advanced rectal cancer.We conducted this randomized, open-label, multicenter, phase III trial in China. Eligible patients with clinical T3-4 and/or N+ rectal adenocarcinoma, UGT1A1 genotype *1*1 or *1*28 were randomly allocated to the control group: pelvic radiation of 50 Gy/25 fractions with concurrent capecitabine, followed by oxaliplatin and capecitabine; or the experimental group: radiation with capecitabine combined with weekly irinotecan 80 mg/m2 for patients with UGT1A1*1*1 or 65 mg/m2 for patients with UGT1A1*1*28, followed by irinotecan and capecitabine. The primary end point was pCR. This trial was registered with ClinicalTrials.gov (ClinicalTrials.gov identifier: NCT02605265).Of the 360 patients initially enrolled, 356 were evaluated as the modified intention-to-treat population (n = 178 in both groups). Surgery was performed in 87% and 88% of patients in the control and experimental groups, respectively. The pCR rates were 15% (n = 27 of 178) and 30% (n = 53 of 178) in the control and experimental groups (risk ratio, 1.96; 95% CI, 1.30 to 2.97; P = .001). Four and 6 patients achieved complete clinical response in the control and experimental groups, respectively. Grade 3-4 toxicities were recorded in 11 (6%) and 68 (38%) patients in the control and experimental groups, respectively (P < .001). The commonest grade 3-4 toxicities were leukopenia, neutropenia, and diarrhea. The overall surgical complication rate was not significantly different between the two groups (11% v 15%; P < .001).Adding irinotecan guided by UGT1A1 genotype to capecitabine-based neoadjuvant chemoradiotherapy significantly increased complete tumor response in Chinese patients.
Outcomes of Adult and Pediatric Patients with Hematologic Malignancies and COVID-19: A Systematic Review and Meta-Analysis of 1847 Patients
Authors: Abi Vijenthira, Inna Gong, Thomas A Fox, Stephen Booth, Gordon Cook, Bruno Fattizzo, Fernando Martín Moro, Jerome Razanamahery, John Riches, Jeffrey I. Zwicker, Rushad Patell, Marie Christiane Vekemans, Lydia Scarfo, Thomas Chatzikonstantinou, Halil Yildiz, Raphael Lattenist, Ioannis Mantzaris, William Wood, Lisa K. Hicks
Journal: Blood (2020)