tbuckley/cabot-search huggingface dataset:
Abstract 9724: The Use of the Model for End-Stage Liver Disease Score Predicts 90-Day Mortality in Patients Undergoing HeartMate II Implantation
Authors: Evan Kransdorf, Jaime Moriguchi, Michelle Kittleson, Carmelita Runyan, Charito Olay, Rhodora Jocson, Lawrence Czer, Alfredo Trento, Fardad Esmailian, Jon Kobashigawa
Journal: Circulation (2012)

Purpose: Careful patient selection for left ventricular assist device (LVAD) therapy is essential to ensure optimal outcomes after device implantation. Although several risk assessment scores are available, there is no consensus on the most accurate score to use in patients undergoing HeartMate II (HMII) implantation. The Lietz-Miller Destination Therapy Risk Score (DTRS) was derived from analysis of patients undergoing HeartMate XVE implantation for destination therapy (Lietz et al. Circulation 2007). The Model for End-Stage Liver Disease (MELD) was shown to predict outcome in patients undergoing primarily HeartMate I implantation (Matthews et al. Circulation 2010). We evaluated the utility of these scores in predicting outcomes following HMII implantation. Methods: Retrospective analysis was performed on 48 patients undergoing HMII implantation at our institution between 2009 and 2011. The DTRS and MELD scores were calculated from clinical data on day of device implantation and outcomes assessed. Results: Device implantation was for bridge to transplant (69%) or destination therapy (31%). 14 patients (29%) underwent heart transplant and 17 patients died (35%), with a mean LVAD support time of 301 days and 85 days, respectively. At end of the study period 17 patients were alive (mean LVAD support time 389 days). The majority of deaths (71%) occurred within 90 days of device implantation. Mortality at 90 days was higher in patients with INTERMACS class 1 (class 1 29.4% vs. class 2 to 4 22.6%), high-risk DTRS values (high 33.3% vs. low-medium 22.2%), and high MELD values (MELD 20 50% vs. MELD &lt; 20 16.6%). Only a MELD score 20 was statistically associated with outcome at 90 days with a hazard ratio of 3.5 (p=0.03) using a Cox proportional hazards model. Conclusions: A MELD score 20 predicts mortality at 90 days in patients undergoing HMII implantation. Further validation of the MELD score in a larger population is needed. Elaboration of the score using cardiac-specific factors may further improve its predictive ability.
An intravenous clarithromycin lipid emulsion with a high drug loading, H-bonding and a hydrogen-bonded ion pair complex exhibiting excellent antibacterial activity
Authors: Haoyu Gong, Sicong Geng, Qi Zheng, Puxiu Wang, Lifeng Luo, Xiuzhi Wang, Yan Zhang, Yu Zhang, Haibing He, Xing Tang
Journal: Asian Journal of Pharmaceutical Sciences (2016)

The aim of this study was to develop an intravenous clarithromycin lipid emulsion (CLE) with good stability and excellent antibacterial activity. The CLE was prepared by the thin-film dispersed homogenization method. The interaction between clarithromycin (CLA) and cholesteryl hemisuccinate (CHEMS) was confirmed by DSC, FT-IR and 1H NMR analysis. The interfacial drug loading, thermal sterilization, freeze–thaw stability, and in vitro and in vivo antibacterial activity were investigated systematically. DSC, FT-IR and 1H NMR spectra showed that CHEMS (CLA: CHEMS, M ratio 1:2) could interact with CLA through H-bonding and a hydrogen-bonded ion pair. The CHEMS was found necessary to maintain the stability of CLE. Ultracentrifugation showed that almost 88% CLA could be loaded into the interfacial layer. The optimized CLE formulation could withstand autoclaving at 121 °C for 10 min and remain stable after three freeze–thaw cycles. The in vitro susceptibility test revealed that the CLA–CHEMS ion-pair and CLE have similar activity to the parent drug against many different bacterial strains. The in vivo antibacterial activity showed that the ED50 of intravenous CLE was markedly lower than that of CLA solution administrated orally. CLE exhibited pronounced antibacterial activity and might be a candidate for a new nanocarrier for CLA with potential advantages over the current commercial formulation.
A true Brunner’s gland adenoma
Authors: K. Suda, S. Hamada, M. Takahashi, Y. Kumashiro, T. Yao, K. Sugimachi, D. Korenaga, K. Takenaka
Journal: Endoscopy (2007)

Brunner’s gland adenoma is an extremely rare neoplasm, which may be confused with Brunner’s gland hyperplasia or hamartoma. The present report describes a case of “true” Brunner’s gland adenoma resected by surgery.
Primary Central Nervous System Lymphoma: Time to Ask the Question
Authors: Howard A. Fine
Journal: Journal of Clinical Oncology (2002)

Article Tools EDITORIALS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2002.20.24.4615 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 12488403 Primary Central Nervous System Lymphoma: Time to Ask the Question Howard A. FinexHoward A. FineSearch for articles by this author Show More Neuro-Oncology Branch, National Cancer Institute, National Institutes of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD https://doi.org/10.1200/JCO.2002.20.24.4615 First Page Full Text PDF Figures and Tables © 2002 by American Society of Clinical Oncology
The Association of Pre-Transplant Sarcopenia and Cirrhotic Cardiomyopathy with Postoperative Complications after Liver Transplant
Authors: Tripti Gupta, Ryan M. Durel, Qingyang Luo, Daniel Devun, John Seal, Emily Ahmed, David S. Bruce, Trevor W. Reichman, Shobha Joshi, Natalie H. Bzowej, Nigel Girgrah, Humberto E. Bohorquez, Ari J. Cohen, Ian C. Carmody, George E. Loss, George Therapondos
Journal: Hepatology (2015)
Oral Hydroxyurea Before Intensive Chemotherapy For Hyperleucocytic Acute Myeloid Leukemia Patients
Authors: Anne-claire Mamez, Emmanuel Raffoux, Sylvie Chevret, Virginie Lemiale, Nicolas Boissel, Emmanuel Canet, Benoît Schlemmer, Herve Dombret, Elie Azoulay, Etienne Lengliné
Journal: Blood (2013)
Initiating sacubitril/valsartan (LCZ696) in heart failure: results of TITRATION, a double‐blind, randomized comparison of two uptitration regimens
Authors: Michele Senni, John J.V. McMurray, Rolf Wachter, Hugh F. McIntyre, Antonio Reyes, Ivan Majercak, Peter Andreka, Nina Shehova‐Yankova, Inder Anand, Mehmet B. Yilmaz, Harinder Gogia, Manuel Martinez‐Selles, Steffen Fischer, Zsolt Zilahi, Franco Cosmi, Valeri Gelev, Enrique Galve, Juanjo J. Gómez‐Doblas, Jan Nociar, Maria Radomska, Beata Sokolova, Maurizio Volterrani, Arnab Sarkar, Bernard Reimund, Fabian Chen, Alan Charney
Journal: European Journal of Heart Failure (2016)

Abstract Aims To assess the tolerability of initiating/uptitrating sacubitril/valsartan (LCZ696) from 50 to 200 mg twice daily (target dose) over 3 and 6 weeks in heart failure (HF) patients (ejection fraction ≤35%). Methods and results A 5‐day open‐label run‐in (sacubitril/valsartan 50 mg twice daily) preceded an 11‐week, double‐blind, randomization period [100 mg twice daily for 2 weeks followed by 200 mg twice daily (‘condensed’ regimen) vs. 50 mg twice daily for 2 weeks, 100 mg twice daily for 3 weeks, followed by 200 mg twice daily (‘conservative’ regimen)]. Patients were stratified by pre‐study dose of angiotensin‐converting enzyme inhibitor/angiotensin‐receptor blocker (ACEI/ARB; low‐dose stratum included ACEI/ARB‐naïve patients). Of 540 patients entering run‐in, 498 (92%) were randomized and 429 (86.1% of randomized) completed the study. Pre‐defined tolerability criteria were hypotension, renal dysfunction and hyperkalaemia; and adjudicated angioedema, which occurred in (‘condensed’ vs. ‘conservative’) 9.7% vs. 8.4% ( P = 0.570), 7.3% vs. 7.6% ( P = 0.990), 7.7% vs. 4.4% ( P = 0.114), and 0.0% vs. 0.8% of patients, respectively. Corresponding proportions for pre‐defined systolic blood pressure &lt;95 mmHg, serum potassium &gt;5.5 mmol/L, and serum creatinine &gt;3.0 mg/dL were 8.9% vs. 5.2% ( P = 0.102), 7.3% vs. 4.0% ( P = 0.097), and 0.4% vs. 0%, respectively. In total, 378 (76%) patients achieved and maintained sacubitril/valsartan 200 mg twice daily without dose interruption/down‐titration over 12 weeks (77.8% vs. 84.3% for ‘condensed’ vs. ‘conservative’; P = 0.078). Rates by ACEI/ARB pre‐study dose stratification were 82.6% vs. 83.8% ( P = 0.783) for high‐dose/‘condensed’ vs. high‐dose/‘conservative’ and 84.9% vs. 73.6% ( P = 0.030) for low‐dose/‘conservative’ vs. low‐dose/‘condensed’. Conclusions Initiation/uptitration of sacubitril/valsartan from 50 to 200 mg twice daily over 3 or 6 weeks had a tolerability profile in line with other HF treatments. More gradual initiation/uptitration maximized attainment of target dose in the low‐dose ACEI/ARB group.
Hematopoietic Progenitor Cell Mobilization In Response To G-CSF Is More Robust In Healthy African American Compared To Caucasian Donors
Authors: Sandhya R. Panch, Yu Ying Yau, Courtney Fitzhugh, Matthew M. Hsieh, John F. Tisdale, Charles D. Bolan, Susan F. Leitman
Journal: Blood (2013)
A Phase Ii Trial of Gefitinib in Combination with Bevacizumab As First-Line Therapy for Advanced Non-Small-Cell Lung Cancer with Activating Egfr Gene Mutations: Olcsg 1001
Authors: N. Nogami, E. Ichihara, T. Kozuki, T. Kubo, D. Kishino, S. Kuyama, A. Bessho, M. Fujii, N. Takigawa, K. Chikamori, K. Aoe, T. Nagata, N. Fujimoto, S. Hosokawa, S. Harita, H. Kamei, H. Ueoka, K. Hotta, M. Tanimoto, K. Kiura
Journal: Annals of Oncology (2014)
Exogenous Overexpression Of DLEU1 Significantly Induces Programmed Cell Death and Inhibits Cell Proliferation In Burkitt Lymphoma (BL) and Sensitizes Rituximab (RTX) Resistant BL Cells To RTX Induced Apoptosis
Authors: Sanghoon Lee, Changhong Yin, Janet Ayello, Timmy O'Connell, Carmella van de Ven, Miguel Muniz, Matthew J. Barth, Mitchell S. Cairo
Journal: Blood (2013)
Glomerular epithelial cells in secondary focal segmental glomerulosclerosis
Authors: Alexander J. Howie
Journal: Kidney International (2016)

Kuppe et al.1Kuppe C. Gröne H.-J. Ostendorf T. et al.Common histological patterns in glomerular epithelial cells in secondary focal segmental glomerulosclerosis.Kidney Int. 2015; 88: 990-998Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar showed that in a variety of glomerular disorders, cellular adhesions between the glomerular tuft and Bowman’s capsule contain podocyte markers or parietal epithelial cell markers or both, and that areas of segmental sclerosis in these conditions contain parietal epithelial cell markers. The site of the adhesions and sclerosed areas within the tuft is not reported. There is known to be a range of pathogenetic mechanisms of segmental sclerosing lesions, and these can largely be differentiated by the site and appearance of the lesions within the tuft.2Howie A.J. Problems with ‘focal segmental glomerulosclerosis’.Pediatr Nephrol. 2011; 26: 1197-1205Crossref PubMed Scopus (11) Google Scholar Overload-type changes typically begin at the glomerular hilum. Changes at the tubular origin, or tip changes, follow prolapse of the tuft into the tubular opening. Sclerotic changes resulting from vasculitic lesions may be at any site. Doxorubicin (adriamycin) in experimental animals, which is mentioned by Kuppe et al.,1Kuppe C. Gröne H.-J. Ostendorf T. et al.Common histological patterns in glomerular epithelial cells in secondary focal segmental glomerulosclerosis.Kidney Int. 2015; 88: 990-998Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar produces lesions randomly scattered in the tuft, as an example of toxic damage to the glomerulus. The position of lesions within glomeruli is neglected in many experimental and clinical studies of focal segmental glomerulosclerosis, but these overlook a large body of evidence about the significance of the position and its help in understanding the pathogenesis.2Howie A.J. Problems with ‘focal segmental glomerulosclerosis’.Pediatr Nephrol. 2011; 26: 1197-1205Crossref PubMed Scopus (11) Google Scholar The Columbia classification of segmental sclerosing disorders recognizes that determination of the site of lesions is of clinical significance.3D'Agati V.D. Fogo A.B. Bruijn J.A. Jennette J.C. Pathologic classification of focal segmental glomerulosclerosis: a working proposal.Am J Kidney Dis. 2004; 43: 368-382Abstract Full Text Full Text PDF PubMed Scopus (535) Google Scholar The Authors ReplyKidney InternationalVol. 89Issue 6PreviewOur study1 describes common histological patterns in secondary focal and segmental glomerulosclerosis lesions. The major finding was that parietal epithelial cells can be detected in virtually all sclerotic lesions (91%) independent of the primary glomerular disease that triggered secondary focal and segmental glomerulosclerosis (Figure 1). Thus, we proposed that activation of parietal epithelial cells is a common pathomechanism in focal and segmental glomerulosclerosis and a potential pharmacologic target. Full-Text PDF Open Archive
Early, Incomplete, or Preclinical Autoimmune Systemic Rheumatic Diseases and Pregnancy Outcome
Authors: Arsenio Spinillo, Fausta Beneventi, Elena Locatelli, Vèronique Ramoni, Roberto Caporali, Claudia Alpini, Giulia Albonico, Chiara Cavagnoli, Carlomaurizio Montecucco
Journal: Arthritis & Rheumatology (2016)

Objective To evaluate the impact of preclinical systemic autoimmune rheumatic disorders on pregnancy outcome. Methods In this longitudinal cohort study, patients were enrolled during the first trimester of pregnancy if they reported having had connective tissue disorder symptoms, were found to be positive for circulating autoantibodies, and on clinical evaluation were judged to have a preclinical or incomplete rheumatic disorder. The incidence of fetal growth restriction (FGR), preeclampsia, and adverse pregnancy outcomes in patients with preclinical rheumatic disorders was compared with that in selected controls, after adjustment for confounders by penalized logistic regression. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Results Of 5,232 women screened, 150 (2.9%) were initially diagnosed as having a suspected rheumatic disorder. After a mean ± SD postpartum follow‐up of 16.7 ± 5.5 months, 64 of these women (42.7%) had no clinically apparent rheumatic disease and 86 (57.3%) had persistent symptoms and positive autoantibody results, including 10 (6.7%) who developed a definitive rheumatic disease. The incidences of preeclampsia/FGR and of small for gestational age (SGA) infants were 5.1% (23 of 450) and 9.3% (42 of 450), respectively, among controls, 12.5% (8 of 640) (OR 2.7 [95% CI 1.1–6.4]) and 18.8% (12 of 64) (OR 2.2 [95% CI 1.1–4.5]), respectively, among women with no clinically apparent disease, and 16.3% (14 of 86) (OR 3.8 [95% CI 1.9–7.7]) and 18.6% (16 of 86) (OR 2.3 [95% CI 1.2–4.3]), respectively, among those with persisting symptoms at follow‐up. Mean ± SD umbilical artery Doppler pulsatility indices were higher among women with no clinically apparent disease (0.95 ± 0.2) and those with persisting symptoms (0.96 ± 0.21) than in controls (0.89 ± 0.12) ( P = 0.01 and P &lt; 0.001, respectively). Conclusion In our study population, preclinical rheumatic disorders were associated with an increased risk of FGR/preeclampsia and SGA. The impact of these findings and their utility in screening for FGR/preeclampsia need to be confirmed in population studies.
Effect of Macitentan on the Development of New Ischemic Digital Ulcers in Patients With Systemic Sclerosis
Authors: Dinesh Khanna, Christopher P. Denton, Peter A. Merkel, Thomas Krieg, Franck-Olivier Le Brun, Angelina Marr, Kelly Papadakis, Janet Pope, Marco Matucci-Cerinic, Daniel E. Furst
Journal: JAMA (2016)

<h3>Importance</h3> Digital ulcers in patients with systemic sclerosis are associated with pain and poor quality of life. Endothelin-1 promotes vasculopathy in systemic sclerosis after macitentan, an endothelin-1 blocker. <h3>Objective</h3> To evaluate the efficacy of macitentan in reducing the number of new digital ulcers in patients with systemic sclerosis. <h3>Design, Setting, and Participants</h3> Two international, randomized, double-blind, placebo-controlled trials (DUAL-1, DUAL-2) were conducted between January 2012 and February 2014. Participants were patients with systemic sclerosis and active digital ulcers at baseline. Target enrollment for each study was 285 patients. <h3>Interventions</h3> Patients were randomized (1:1:1) to receive oral doses of 3 mg of macitentan, 10 mg of macitentan, or placebo once daily and stratified according to number of digital ulcers at baseline (≤3 or &gt;3). <h3>Main Outcomes and Measures</h3> The primary outcome for each trial was the cumulative number of new digital ulcers from baseline to week 16. Treatment effect was expressed as the ratio between treatment groups. <h3>Results</h3> In DUAL-1, among 289 randomized patients (mean age 51.2 years; 85.8% women), 226 completed the study. The adjusted mean number of new digital ulcers per patient over 16 weeks was 0.94 in the 3-mg macitentan group (n = 95) and 1.08 in the 10-mg macitentan group (n = 97) compared with 0.85 in the placebo group (n = 97) (absolute difference, 0.09 [95% CI, −0.37 to 0.54] for 3 mg of macitentan vs placebo and 0.23 [−0.27 to 0.72] for 10 mg of macitentan vs placebo). Among 265 patients randomized in DUAL-2 (mean age 49.6 years; 81.9% women), 216 completed the study. In DUAL-2, the adjusted mean number of new digital ulcers was 1.44 in the 3-mg macitentan group (n = 88) and 1.46 in the 10-mg macitentan group (n = 88) compared with 1.21 in the placebo group (n = 89) (absolute difference, 0.23 [95% CI, −0.35 to 0.82] for 3 mg of macitentan vs placebo and 0.25 [95% CI, −0.34 to 0.84] for 10 mg of macitentan vs placebo). Adverse events more frequently associated with macitentan than with placebo were headache, peripheral edema, skin ulcer, anemia, upper respiratory tract infection, diarrhea, and nasopharyngitis. <h3>Conclusions and Relevance</h3> Among patients with systemic sclerosis and active ischemic digital ulcers, treatment with macitentan did not reduce new digital ulcers over 16 weeks. These results do not support the use of macitentan for the treatment of digital ulcers in this patient population. <h3>Trial Registration</h3> clinicaltrials.gov Identifiers:NCT01474109,NCT01474122
Adenocarcinoma of the Glandular Stomach Following 3-Methylcholanthrene, N-Nitrosodiethylamine, or N-Nitrosodimethylamine Feeding in Carcinogen-Susceptible Inbred Syrian Hamsters2
Authors: F. Homburger, A. H. Handler, E. Soto, S.-S. Hsueh, C. G. Van Dongen, A. B. Russfield
Journal: JNCI Journal of the National Cancer Institute (1976)

Invasive adenocarcinoma of the glandular stomach was induced in 3 BIO® 87.20 inbred Syrian hamsters by the administration of 1 ppm N-nitrosodiethylamine or N-nitrosodimethylamine in the drinking water, and in 2 BIO® 15.16 and 5 BIO® 72.29 inbred Syrian hamsters by gavage of 3-methylcholanthrene. In contrast, many other similarly treated inbred Syrian hamster lines did not develop carcinoma of the glandular stomach. The glandular stomachs of rats and mice are resistant to polycyclic hydrocarbon carcinogenesis; however, the glandular stomachs of certain inbred Syrian hamsters develop adenocarcinoma after polycyclic hydrocarbon gavage. This work demonstrated the importance of genetic factors.
Safety and efficacy of a genetic vaccine targeting Telomerase plus chemotherapy for the therapy of canine B-cell lymphoma
Authors: Alessandra Gavazza, George Lubas, Arthur Fridman, Daniela Peruzzi, Joseph A Impellizeri, Laura Luberto, Emanuele Marra, Giuseppe Roscilli, Gennaro Ciliberto, Luigi Aurisicchio
Journal: Journal for ImmunoTherapy of Cancer (2013)

Meeting abstracts Client-owned pet dogs represent exceptional translational models for advancement of Cancer Research, as they reflects the complex heterogeneity observed in human cancer. We have recently shown that a genetic vaccine targeting dog telomerase (dTERT) and based on Ad/DNA-EGT
Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit
Authors: Stephane Gaudry, David Hajage, Frederique Schortgen, Laurent Martin-Lefevre, Bertrand Pons, Eric Boulet, Alexandre Boyer, Guillaume Chevrel, Nicolas Lerolle, Dorothee Carpentier, Nicolas De Prost, Alexandre Lautrette, Anne Bretagnol, Julien Mayaux, Saad Nseir, Bruno Megarbane, Marina Thirion, Jean-Marie Forel, Julien Maizel, Hodane Yonis, Philippe Markowicz, Guillaume Thiery, Florence Tubach, Jean-Damien Ricard, Didier Dreyfuss, Michel Slama
Journal: New England Journal of Medicine (2016)

The timing of renal-replacement therapy in critically ill patients who have acute kidney injury but no potentially life-threatening complication directly related to renal failure is a subject of debate.
Abstract 1055: The 70 kDa Heat Shock Cognate Protein Plays A Novel Role In Myocardial Chemokine Expression And Cardiac Dysfunction Following Ischemia And Reperfusion Injury
Authors: Ning Zou, Lihua Ao, Xiaoping Yang, Xin Su, David A Fullerton, Xianzhong Meng
Journal: Circulation (2007)

Myocardial ischemia and reperfusion (I/R) causes the release of cellular proteins including heat shock proteins (HSPs). The inducible HSP70 induces cytokine production in monocytes and dendritic cells through Toll-like receptor 4 (TLR4) signaling. In evaluation of the role of HSPs in myocardial inflammatory response in a mouse heart global I/R model, we found that the 70 kDa heat shock cognate protein (HSC70), but not HSP70, was released into the extracellular space and the coronary effluent during I/R. These observations prompted us to hypothesize that HSC70 plays a novel role in postischemic myocardial inflammatory response and cardiac dysfunction. Methods: We subjected mouse hearts to global I/R (20 min/60 min) or perfusion using the Langendorff method. We examined: the effect of HSC70 antibody on myocardial chemokine expression and cardiac functional recovery following I/R, the effect of recombinant HSC70 on myocardial chemokine expression and cardiac function and the role of TLR4 and the HSC70 substrate-binding domain in the effect of HSC70 on the heart. Results: In comparison with non-immune IgG, anti-HSC70 reduced myocardial expression of KC and MCP-1 mRNAs and proteins following I/R. Moreover, treatment with anti-HSC70 improved postischemic cardiac functional recovery (66±5.4% of baseline vs. 28±5.1% of baseline in hearts treated with non-immune IgG, p&lt;0.01). Recombinant HSC70 induced myocardial expression of KC and MCP-1 mRNAs and proteins and caused cardiac dysfunction (72±2.6% of baseline vs. 98±3.9% of baseline in perfusion controls, p&lt;0.001) in hearts with competent TLR4 (C3H/HeN). Interestingly, these effects of HSC70 were abrogated in hearts with defective TLR4 (C3H/HeJ). The potency of HSC70 was completely lost in the absence of its substrate-binding domain. Conclusions: Taken together, our studies demonstrate, for the first time, that HSC70 plays an important role in the induction of myocardial chemokines and cardiac dysfunction during I/R. The effect of HSC70 is dependent on TLR4 and requires the presence of the substrate-binding domain. The results suggest that the release of HSC70 into the extracellular space elicits an inflammatory response and causes mechanic dysfunction in the heart.
Increased Tumorigenesis In Ribosomal Proteins L5 and S24 Heterozygous Mice
Authors: Shideh Kazerounian, Pedro Ciarlini, Roxanne Ghazvinian, Meritxell Alberich-Jorda, Daniel Yuan, Mugdha Joshi, Hong Zhang, Alan Beggs, Hanna T. Gazda
Journal: Blood (2013)