tbuckley/cabot-search huggingface dataset:
Canonical Notch signaling functions as a commitment switch for intestinal epithelial cells.
Authors: Sandra Guilmeau, Marta Flandez, Helena Jm Smartt, Keejung Yoon, Nicholas Gaiano, Leonard H Augenlicht
Journal: Cancer Research (2007)

1011  Development of colon cancer is driven by alterations in intestinal cell maturation, and therefore understanding mechanisms that regulate the balance among different cell lineages is critical to understanding intestinal tumorigenesis. Here, through isolation of intestinal epithelial cells as a function of their position along the crypt-villus axis (CVA), we report that active canonical Notch/Hes1 signaling in vivo marks the uncommitted, proliferative cells in the small intestine of the mouse, with Math1 showing complementary up-regulation as cells migrate along the CVA towards the intestinal lumen. Consistent with this pattern of in vivo expression, HES1 was down-regulated in both Caco-2 and HT29 Cl16E human colon carcinoma cell lines in culture during their spontaneous differentiation along the enterocyte and goblet cell lineages, respectively. In HT29 Cl16E cells, impaired activation of Notch receptors by treatment with 10 μM gamma-secretase led to cell cycle arrest at G1 and p21 promoter activation, and concomitant induction of expression of the MUC2 and TFF3 goblet cell markers. Conversely, the co-culture of HT29 Cl16E cells with mouse L fibroblasts engineered to express the Delta1 ligand, as well as infection with an adenovirus that expressed a constitutively active Notch1 receptor, repressed the expression of HATH1, MUC2 and TFF3 at the mRNA and protein levels. This effect was mediated by HATH1 since its targeted knock-down by specific siRNAs also inhibited MUC2 and TFF3 expression. Surprisingly, in Caco2 cells, the Notch/Hes1 signaling pathway also repressed enterocyte differentiation, as indicated by inhibition of alkaline phosphatase, sucrase isomaltase and liver fatty acid binding protein expression, all enterocyte specific markers. Of interest, HATH1 expression level was higher in HT29 Cl16E goblet-like cells than in Caco-2 absorptive cells and its transcripts were repressed upon sodium butyrate treatment, a physiological inducer of cell cycle arrest and absorptive cell differentiation. Our results suggest that Notch signaling is required to maintain both intestinal cell progenitors and colon cancer cells in a highly proliferative state, and provide novel insight into the molecular mechanisms involved in intestinal cell fate specification induced by Notch signaling, both key to the maintenance of mucosal homeostasis.
Towards Molecularly Informed Acute Myeloid Leukemia Subtyping Reflective of Pathogenesis
Authors: Hassan Awada, Arda Durmaz, Yasunobu Nagata, Teodora Kuzmanovic, Ashwin Kishtagari, Jibran Durrani, Cassandra M Kerr, Anjali S. Advani, Hetty E. Carraway, Tomas Radivoyevitch, Manja Meggendorfer, Aziz Nazha, Valeria Visconte, Mikkael A. Sekeres, Torsten Haferlach, Jaroslaw P. Maciejewski
Journal: Blood (2019)
The Nephrotic Syndrome
Authors: Stanley E. Bradley, Cornelius J. Tyson
Journal: New England Journal of Medicine (1948)

THE "nephrotic syndrome" is one of the most striking phenomena of renal disease. The combination of gross edema, hypoproteinemia, hypercholesterolemia, lipidemia and heavy proteinuria, in the absence of congestive heart failure, is unique and easily recognized. It frequently appears during the course of chronic diffuse glomerulonephritis (the nephrotic phase).1 Other causes are renal amyloidosis, syphilis, intercapillary glomerulosclerosis and renal-vein thrombosis. In children and young adults the syndrome occasionally develops in the absence of renal disease as so-called "pure," "genuine" or lipoid nephrosis. A prolonged debate has centered about this entity. It is claimed on the one hand that the disorder . . .
Identification of DHODH as a therapeutic target in small cell lung cancer
Authors: Leanne Li, Sheng Rong Ng, Caterina I. Colón, Benjamin J. Drapkin, Peggy P. Hsu, Zhaoqi Li, Christopher S. Nabel, Caroline A. Lewis, Rodrigo Romero, Kim L. Mercer, Arjun Bhutkar, Sarah Phat, David T. Myers, Mandar Deepak Muzumdar, Peter M. K. Westcott, Mary Clare Beytagh, Anna F. Farago, Matthew G. Vander Heiden, Nicholas J. Dyson, Tyler Jacks
Journal: Science Translational Medicine (2019)

Small cell lung cancer (SCLC) is an aggressive lung cancer subtype with extremely poor prognosis. No targetable genetic driver events have been identified, and the treatment landscape for this disease has remained nearly unchanged for over 30 years. Here, we have taken a CRISPR-based screening approach to identify genetic vulnerabilities in SCLC that may serve as potential therapeutic targets. We used a single-guide RNA (sgRNA) library targeting ~5000 genes deemed to encode "druggable" proteins to perform loss-of-function genetic screens in a panel of cell lines derived from autochthonous genetically engineered mouse models (GEMMs) of SCLC, lung adenocarcinoma (LUAD), and pancreatic ductal adenocarcinoma (PDAC). Cross-cancer analyses allowed us to identify SCLC-selective vulnerabilities. In particular, we observed enhanced sensitivity of SCLC cells toward disruption of the pyrimidine biosynthesis pathway. Pharmacological inhibition of dihydroorotate dehydrogenase (DHODH), a key enzyme in this pathway, reduced the viability of SCLC cells in vitro and strongly suppressed SCLC tumor growth in human patient-derived xenograft (PDX) models and in an autochthonous mouse model. These results indicate that DHODH inhibition may be an approach to treat SCLC.
Expanded Meta-Analyses Confirms the Association between MRD and Long-Term Survival Outcomes in Multiple Myeloma (MM)
Authors: Nikhil C. Munshi, Herve Avet-Loiseau, Kenneth C. Anderson, Paola Neri, Bruno Paiva, Mehmet Samur, Meletios A. Dimopoulos, Margarita Kulakova, Bart Heeg, Mahmoud Hashim, Jon Ukropec, Kevin Liu, Maria Krevvata, Annette Lam, Sarah Cote, Nizar Bahlis
Journal: Blood (2019)
A commentary on “Effect of Parkinson's disease on primary total joint arthroplasty outcomes: A meta-analysis of matched control studies” (Int J Surg 2019; Sep 26;71:124–131. doi: 10.1016/j.ijsu.2019.09.013)
Authors: Qifeng Tao, Jie Ming, Yuping Lan
Journal: International Journal of Surgery (2019)
Identification of T-Cell Receptors Specific to Antigens Presented By HLA-B4002 and B5401 in Acquired Aplastic Anemia
Authors: Kohei Hosokawa, Eiji Kobayashi, Yoshiki Akatsuka, Luis Espinoza, Noriharu Nakagawa, Tanabe Mikoto, Noriaki Tsuji, Takeshi Yoroidaka, Hiroki Mizumaki, Thi Mai Anh Nguyen, Takamasa Katagiri, Kiyomi Shitaoka, Hiroshi Hamana, Hiroyuki Kishi, Shinji Nakao
Journal: Blood (2019)
US to probe Google deal to manage healthcare data
Authors: Owen Dyer
Journal: BMJ (2019)

The Office for Civil Rights of the US Department of Health and Human Services has opened an inquiry into a partnership between Google and one of the country’s largest non-profit Catholic health systems, in which the corporate giant is handling patients’ medical data without their knowledge or consent.

The government stepped in after media reports questioned whether a company that collects data to target advertising should be handling personal medical records, as Google employees do under the terms of Project Nightingale, a collaboration with Ascension, which operates 151 hospitals and more than 2000 clinics in 21 states. The Office for …
Clinical significance of <i>BRAF/NRAS</i> concurrent mutations in a clinic‐based metastatic melanoma cohort
Authors: L. Regno, B. Louveau, M. Battistella, A. Sadoux, B. Baroudjian, J. Delyon, K. Serror, C. Allayous, C. Lebbe, S. Mourah, F. Jouenne
Journal: British Journal of Dermatology (2019)
An Innovative Telemedicine Platform to Provide Expert Access to Patients with Chronic Lymphocytic Leukemia (CLL)
Authors: DR. Brian Koffman, John M. Pagel, Andy Kaempf, Byung Park, Liza Avruch, Christopher Lee, Babak Movassaghi, John C. Byrd, Alan Skarbnik, Matthew S. Davids, Alexey Danilov
Journal: Blood (2019)
IMMU-28. TARGETING IMMUNOSUPPRESSIVE MYELOID DERIVED SUPPRESSOR CELLS VIA MIF/CD74 SIGNALING AXIS TO ATTENUATE GBM GROWTH
Authors: Tyler Alban, Defne Bayik, Balint Otvos, Matthew Grabowski, Manmeet Ahluwalia, Richard Bucala, Michael Vogelbaum, Justin Lathia
Journal: Neuro-Oncology (2019)

Abstract The immunosuppressive microenvironment in glioblastoma (GBM) enables persistent tumor growth and evasion from tumoricidal immune cell recognition. Despite a large accumulation of immune cells in the GBM microenvironment, tumor growth continues, and evidence for potent immunosuppression via myeloid derived suppressor cells (MDSCs) is now emerging. In agreement with these observations, we have recently established that increased MDSCs over time correlates with poor prognosis in GBM, making these cells of interest for therapeutic targeting. In seeking to reduce MDSCs in GBM, we previously identified the cytokine macrophage migration inhibitory factor (MIF) as a possible activator of MDSC function in GBM. Here, using a novel in vitro co-culture system to reproducibly and rapidly create GBM-educated MDSCs, we observed that MIF was essential in the generation of MDSCs and that MDSCs generated via this approach express a repertoire of MIF receptors. CD74 was the primary MIF receptor in monocytic MDSCs (M-MDSC), which penetrate the tumor microenvironment in preclinical models and patient samples. A screen of MIF/CD74 interaction inhibitors revealed that MN-166, a clinically relevant blood brain barrier penetrant drug, which is currently fast tracked for FDA approval, reduced MDSC generation and function in vitro. This effect was specific to M-MDSC subsets expressing CD74, and appeared as reduced downstream pERK signaling and MCP-1 secretion. In vivo, MN-166 was able reduce tumor-infiltrating MDSCs, while conferring a significant increase in survival in the syngeneic glioma model GL261. These data provide proof of concept that M-MDSCs can be targeted in the tumor microenvironment via MN-166 to reduce tumor growth and provide a rationale for future clinical assessment of MN-166 to reduce M-MDSCs in the tumor microenvironment. Ongoing studies are assessing the effects of MDSC inhibition in combination with immune activating approaches, in order to inhibit immune suppression while simultaneously activating the immune system.
Orally disintegrating rimegepant increased freedom from pain and from most bothersome symptom at 2 h in acute migraine
Authors: Lucas McCarthy
Journal: Annals of Internal Medicine (2019)

Source Citation Croop R, Goadsby PJ, Stock DA, et al. Efficacy, safety, and tolerability of rimegepant orally disintegrating tablet for the acute treatment of migraine: a randomised, phase 3, double-blind, placebo-controlled trial. Lancet. 2019;394:737-45. 31311674
The U1 Spliceosomal RNA: A Novel Non-Coding Hotspot Driver Mutation Independently Associated with Clinical Outcome in Chronic Lymphocytic Leukemia
Authors: Ferran Nadeu, Shimin Shuai, Ander Diaz-Navarro, Irene López, Silvia Martín, Hiromichi Suzuki, Romina Royo, Guillem Clot, Julio Delgado, Tycho Baumann, Junyan Lu, Alba Navarro, Marta Kulis, Sachin A Kumar, Ana Gutierrez-Fernandez, Miguel Alcoceba, Marcos González, Enrique Colado, Angel Ramirez Payer, Cristina Capdevila, Miguel Osuna, Marta Aymerich, Rosó Mares, Monica Lopez-Guerra, Laura Magnano, Pablo Mozas, Alfredo Rivas-Delgado, Maria Jose Terol, Anna Enjuanes, Wolfgang Huber, Armando Lopez-Guillermo, Sílvia Beà, José I. Martin-Subero, Thorsten Zenz, Michael D Taylor, Dolors Colomer, Xose S Puente, Lincoln D Stein, Elias Campo
Journal: Blood (2019)
US rule would strip science from environmental policies and increase premature deaths, warn scientists
Authors: Owen Dyer
Journal: BMJ (2019)

Decades of landmark public health studies on matters such as air pollution and water quality could be eliminated from consideration in future decision from the US Environmental Protection Agency (EPA), health experts have warned.

Scientists told the House Committee on Science, Space, and Technology that the Trump administration is demanding access to the underlying data behind health studies used in decision making, including confidential patient information. They appeared before a Congressional hearing on a rule change—which has been billed as a means of improving transparency—proposed by the Trump appointed EPA administrator, Andrew Wheeler.

Since allowing access to such data would breach confidentiality agreements between researchers and study participants, many studies would be excluded from consideration when drawing up new rules on problems like lead contamination or vehicle emissions, said the scientists. Included among these would be many landmark studies underpinning knowledge of the harms these pollutants …
HOUT-25. PROGNOSTIC FACTORS FOR PROLONGED LENGTH OF STAY AND READMISSION FOLLOWING CRANIOTOMY FOR PRIMARY BRAIN TUMORS
Authors: Nam Tran, Aboubakr Amer, Mohammah Alhazaimeh, Quan Tran, Ashleigh Schroering, Corin Agoris, Anthony Clark, Muhammad Imam, Gautam Rao, Sydney Weisman, Mudit Dutta, Anu Dhanashekar, Arnold Etame, Solmaz Sahebjam
Journal: Neuro-Oncology (2019)

Abstract BACKGROUND Escalating costs of healthcare has brought on a paradigm shift that links reimbursement to quality care. Important quality metric measures include hospital length of stay, 30-day readmission and re-operation rates. Identifying modifiable factors can provide information essential for reducing medical costs and improving the quality of medical care patients receive. METHODS The authors performed a retrospective chart review of all patients who underwent craniotomies for resection of primary brain tumors at the Moffitt Cancer Center from 2004–2014. Patient demographics (age, gender), clinical characteristics (comorbidities, steroid dose, seizure status, neurologic deficit, KPS), tumor characteristics (tumor type, location), surgical factors (primary or redo, length of surgery, blood loss), 30-day complications (infection, DVT/PE, seizure), 30-day readmission, and length of stay were assessed. Multivariate analysis was performed to determine risk factors associated with prolonged length of stay and 30-day readmission. RESULTS 806 consecutive patients underwent craniotomies for primary brain tumors. High BMI (p&lt; 0.001), CAD (p&lt; 0.001), hyperglycemia (p&lt; 0.04), peri-operative seizures (p&lt; 0.03), low Karnofsky Performance Status score (p&lt; 0.001), prolonged operative times (p&lt; 0.001), and surgical blood loss (p&lt; 0.001) contributed to prolonged length of hospital stay; whereas, preoperative hyperglycemia and perioperative seizures were associated with 30-day readmission. CONCLUSIONS This study identifies modifiable risk factors that contribute to poorer outcome following craniotomies for primary brain tumors and lays the groundwork for risk stratifying patients undergoing surgery.
Peri-Transplant Steroids Enhance GVL and Attenuate GVHD By Redistributing Alloreactive Donor T Cells from the Gut into the Bone Marrow
Authors: Takayuki Inouye, Motoko Koyama, Ensbey Kathleen, Nicholas Greene, Luke Samson, Hiroyasu Ogawa, Geoffrey R. Hill
Journal: Blood (2019)
Dysregulation of Glutamate Transport Enhances Treg Function That Promotes VEGF Blockade Resistance in Glioblastoma
Authors: Yu Long, Haipeng Tao, Aida Karachi, Adam J. Grippin, Linchun Jin, Yifan (Emily) Chang, Wang Zhang, Kyle A. Dyson, Alicia Y. Hou, Meng Na, Loic P. Deleyrolle, Elias J. Sayour, Maryam Rahman, Duane A. Mitchell, Zhiguo Lin, Jianping Huang
Journal: Cancer Research (2019)

Anti-VEGF therapy prolongs recurrence-free survival in patients with glioblastoma but does not improve overall survival. To address this discrepancy, we investigated immunologic resistance mechanisms to anti-VEGF therapy in glioma models. A screening of immune-associated alterations in tumors after anti-VEGF treatment revealed a dose-dependent upregulation of regulatory T-cell (Treg) signature genes. Enhanced numbers of Tregs were observed in spleens of tumor-bearing mice and later in tumors after anti-VEGF treatment. Elimination of Tregs with CD25 blockade before anti-VEGF treatment restored IFNγ production from CD8+ T cells and improved antitumor response from anti-VEGF therapy. The treated tumors overexpressed the glutamate/cystine antiporter SLC7A11/xCT that led to elevated extracellular glutamate in these tumors. Glutamate promoted Treg proliferation, activation, suppressive function, and metabotropic glutamate receptor 1 (mGlutR1) expression. We propose that VEGF blockade coupled with glioma-derived glutamate induces systemic and intratumoral immunosuppression by promoting Treg overrepresentation and function, which can be pre-emptively overcome through Treg depletion for enhanced antitumor effects. SIGNIFICANCE: Resistance to VEGF therapy in glioblastoma is driven by upregulation of Tregs, combined blockade of VEGF, and Tregs may provide an additive antitumor effect for treating glioblastoma.
iPSC-Derived NK Cells Synergize with T Cells and Anti-PD-1 Antibody to Mediate Durable Anti-Tumor Responses In Vivo
Authors: Jeffrey S. Miller, Ryan Bjordahl, Svetlana Gaidarova, Sajid Mahmood, Paul Rogers, Ge Moyar, Bruce R. Blazar, Dan S Kaufman, Bahram Valamehr, Frank Cichocki
Journal: Blood (2019)
Copanlisib, a PI3K Inhibitor, Demonstrates a Favorable Long-Term Safety Profile in a Pooled Analysis of Patients with Hematologic Malignancies
Authors: Pier Luigi Zinzani, Armando Santoro, Luigina Mollica, Sirpa Leppä, George A Follows, Georg Lenz, Won Seog Kim, Arnon Nagler, Panayiotis Panayiotidis, Judit Demeter, Franck Morschhauser, Javier Munoz, Ashok Miriyala, Alice Benson, Jose Garcia-Vargas, Barrett H Childs, Martin Dreyling
Journal: Blood (2019)
Transcutaneous Electrical Nerve Stimulation Reduces Movement‐Evoked Pain and Fatigue: A Randomized, Controlled Trial
Authors: Dana L. Dailey, Carol G. T. Vance, Barbara A. Rakel, M. Bridget Zimmerman, Jennie Embree, Ericka N. Merriwether, Katharine M. Geasland, Ruth Chimenti, Jon M. Williams, Meenakshi Golchha, Leslie J. Crofford, Kathleen A. Sluka
Journal: Arthritis & Rheumatology (2019)

Objective Fibromyalgia ( FM ) is characterized by pain and fatigue, particularly during physical activity. Transcutaneous electrical nerve stimulation ( TENS ) activates endogenous pain inhibitory mechanisms. This study was undertaken to investigate if using TENS during activity would improve movement‐evoked pain and other patient‐reported outcomes in women with FM . Methods Participants were randomly assigned to receive active TENS (n = 103), placebo TENS (n = 99), or no TENS (n = 99) and instructed to use it at home during activity 2 hours each day for 4 weeks. TENS was applied to the lumbar and cervicothoracic regions using a modulated frequency (2–125 Hz) at the highest tolerable intensity. Participants rated movement‐evoked pain (primary outcome measure) and fatigue on an 11‐point scale before and during application of TENS . The primary outcome measure and secondary patient‐reported outcomes were assessed at baseline (time of randomization) and at 4 weeks. Results After 4 weeks, a greater reduction in movement‐evoked pain was reported in the active TENS group versus the placebo TENS group (group mean difference –1.0 [95% confidence interval –1.8, –0.2]; P = 0.008) and versus the no TENS group (group mean difference –1.8 [95% confidence interval –2.6, –1.0]; P &lt; 0.0001). A reduction in movement‐evoked fatigue was also reported in the active TENS group versus the placebo TENS group (group mean difference –1.4 [95% confidence interval –2.4, –0.4]; P = 0.001) and versus the no TENS group (group mean difference –1.9 [95% confidence interval –2.9, –0.9]; P = &lt;0.0001). A greater percentage of the patients in the active TENS group reported improvement on the global impression of change compared to the placebo TENS group (70% versus 31%; P &lt; 0.0001) and the no TENS group (9%; P &lt; 0.0001). There were no TENS ‐related serious adverse events, and &lt;5% of participants experienced minor adverse events from TENS . Conclusion Among women who had FM and were on a stable medication regimen, 4 weeks of active TENS use compared to placebo TENS or no TENS resulted in a significant improvement in movement‐evoked pain and other clinical outcomes. Further research is needed to examine effectiveness in a real‐world setting to establish the clinical importance of these findings.
Meds433, a New Dihydroorotate Dehydrogenase Inhibitor, Induces Apoptosis and Differentiation in Acute Myeloid Leukemia
Authors: Valentina Gaidano, Paola Circosta, Alessandro Cignetti, Mohammad Houshmand, Nicoletta Vitale, Stefano Sainas, Agnese Pippione, Manuela Marraudino, Brigitta Bonaldo, Marta Giorgis, Donatella Boschi, Marco Lucio Lolli, Giuseppe Saglio
Journal: Blood (2019)
RTHP-29. HYPOFRACTIONNATED RADIOTHERAPY FOR REFRACTORY SKULL BASE CHORDOMA
Authors: Linbo Cai, Shaoqun Li, Mingyao Lai, Changguo Shan, Juan Li, Junjie Zhen, Weiping Hong
Journal: Neuro-Oncology (2019)

Abstract OBJECTIVE Skull base chordoma is difficult to be totally excised by surgery because of the complex anatomical structures of skull base. Postoperative radiotherapy is one of the most important treatment options for skull base chordoma. However, the response of chordoma to conventional fractionation radiotherapy is poor. Therefore, it is of great value to explore the therapeutic effects of hypofractionnated radiotherapy for refractory skull base chordoma. METHODS A retrospective analysis was performed on the clinical data of patients with refractory skull base chordomas who were admitted to Guangdong Sanjiu Brain Hospital from 2007 to April 2019. The characteristics of the selected cases and prognosis-related factors were analyzed with Kaplan-Meier method. RESULTS A total of 21 patients were enrolled in this study, including 11 male (52.4%) and 10 female (47.6%). Twenty patients received surgery, including gross total resection in 5 cases (25%), subtotal resection in 14 cases (70%) and biopsy in 1 case (5%). Among 18 patients who received radiotherapy, 17 (94.4%) received radiotherapy after the first diagnosis; 1 (5.6%) were treated with radiotherapy after tumor recurrence; and 3 (16.7%) received the secondary radiotherapy after tumor recurrence. The median overall survival of 11 patients receiving hypofractionnated radiotherapy (45-60Gy/8-20F) and 7 patients receiving conventional fractionation radiotherapy (40-60Gy/20-30F) reached 33 months (7–130) and 68 months (27–105), respectively. The results of Kaplan-Meier analysis revealed that the overall survival of patients who were treated with hypofractionnated radiotherapy was significantly longer than that of those receiving conventional fractionation radiotherapy. No one suffered from radiation-induced acute brain injury (≥grade 3), and only 1 patient who received hypofractionnated radiotherapy developed radiation-induced brain necrosis at 3 years after hypofractionnated radiotherapy. CONCLUSION Hypofractionnated radiotherapy for refractory skull base chordoma can not only achieve a therapeutic effect, but also reduce the risk of radiation-induced necrosis.
Liposomal Daunorubicin/Cytarabine As a Bridge to Donor Lymphocyte Infusion or Allogeneic Stem Cell Transplantation for High-Risk Acute Myelogenous Leukemia
Authors: Daulath Singh, Patrick Hagen, Nasheed Hossain, Scott E. Smith, Patrick J. Stiff, Stephanie B. Tsai
Journal: Blood (2019)
Evaluation of the International Prognostic Index for Chronic Lymphocytic Leukemia (CLL-IPI) and Validation of a Proposed Novel Risk Model (BALL Score) in Real-World Relapsed/Refractory (R/R) CLL Patients Receiving Idelalisib and Rituximab
Authors: Massimo Gentile, Gianluigi Reda, Francesca Romana Mauro, Paolo Sportoletti, Luca Laurenti, Marta Coscia, Anna G Recchia, Marzia Varettoni, Roberta Murru, Annalisa Chiarenza, Adalgisa Condoluci, Riccardo Moia, Daniela Pietrasanta, Giacomo Loseto, Ugo Consoli, Ilaria Scortechini, Ernesto Vigna, Cirino Botta, Vincenzo Ludovico Fraticelli, Alessio Di Prima, Giovanni Tripepi, Davide Rossi, Gianluca Gaidano, Valter Gattei, Fortunato Morabito
Journal: Blood (2019)