tbuckley/cabot-search huggingface dataset:
Abstract 136: The Role of Glucose as a Promoter for Cardiac Regeneration
Authors: Viviana Fajardo, Haruko Nakano, Ellen Lien, Rong Tian, Bao Chen, Peter Clark, Austin Nakano
Journal: Circulation Research (2019)

Heart failure is the leading cause of death worldwide. Our focus is on non-genetic mechanisms by which cardiac regeneration can be lengthened or enhanced. Specifically, we are interested in the cyto-protective effects of glucose in cardiomyocyte growth, differentiation and proliferation and how this knowledge can be applied to regeneration therapies. Our preliminary data showed that glucose induces cardiomyocyte proliferation and inhibits cardiomyocyte maturation in human embryonic stem cells derived cardiomyocytes (hESC-CM) via the Pentose Phosphate Pathway in a dose dependent manner. Whether this pathway can be a therapeutic target for heart regeneration is unknown. Our hypothesis is that glucose promotes neonatal heart regeneration in a murine model. Non-Transmural cryoinjury was performed to the apex of the left ventricle in wild-type pups and cardiac specific overexpression of Glucose Transporter 1 Transgenic pups. In the acute phase (P1-P7), the level of cardiomyocyte cell proliferation was measured via flow cytometry analysis and immunostaining with PH3 and cTnnt. Glucose uptake by cardiomyocytes was measured by 18F-FDG assay and Glut1 immunostaining. In the chronic phase (P14, P21, P40), we quantified the level of fibrosis by histology (H&amp;E and Picrosirius Red) and neovascularization by immunostaining with PECAM. Increased cardiomyocyte proliferation was observed in the Transgenic Glut1 pups. Myocardial glucose uptake declines from the muscular layer towards the trabecular layer, corresponding with maturation of the heart. We observed that Glut1 cardiomyocyte-specific overexpression resulted in improved cardiac repair compared to wild type (WT) mice at 21 days postnatally. Compared to wild-type, Glut1 hearts showed increased angiogenesis around the site of injury secondary to an increase in cardiomyocyte proliferation. This study is the first to demonstrate the potential role of glucose as a promoter for cardiac regeneration and reveal a potential mechanism for congenital cardiomyopathy associated with diabetic pregnancy.
Impact of Inotersen on Functioning and Activities of Daily Living for Patients with Hereditary TTR Amyloidosis: Results from a Double-Blind Placebo-Controlled Trial
Authors: Aaron Yarlas, Giampaolo Merlini, Michelle K White, Asia Sikora Kessler, Andrew Lovley, Spencer D Guthrie, Michael Pollock, Morie A. Gertz
Journal: Blood (2018)
Abstract 884: Expression of Anti-mir-33a-5p in Cultured Endothelial Cells Increases Macrophage and Smooth Muscle Cell Cholesterol Efflux by Exosome-mediated Transfer of Anti-mir-33a-5p
Authors: Alexis Stamatikos, Lucia Vojtech, Ethan Knight, Lianxiang Bi, Bradley Wacker, Chongren Tang, David Dichek
Journal: Circulation Research (2019)

Background: The microRNA miR-33a-5p impairs apoAI-mediated cholesterol efflux by silencing ABCA1 expression. Systemic injection of antagomirs to miR-33a-5p reduces atherosclerosis but can cause hepatic steatosis and hypertriglyceridemia. In contrast, local delivery of miR-33a-5p antagomirs to lipid-laden intimal cells [smooth muscle cells (SMC) and macrophages (Mϕ)] could potentially treat atherosclerosis without causing metabolic abnormalities. Helper-dependent adenoviral vectors (HDAd) provide durable transgene expression in endothelial cells (EC) in vivo; however, HDAd does not cross an intact large vessel EC layer and therefore cannot deliver antagomirs directly to SMC and Mϕ. We hypothesized that transducing EC with an HDAd expressing anti-miR-33a-5p (HDAdAnti) could result in packaging of anti-miR-33a-5p into EC-derived exosomes that, in turn, deliver anti-miR-33a-5p to neighboring SMC and Mϕ. Inhibition of miR-33a-5p in SMC and Mϕ would upregulate ABCA1, and enhance apoAI-mediated cholesterol efflux. Methods: We transduced cultured EC with either HDAdAnti or a control HDAd expressing a “scrambled” shRNA (HDAdScr), harvested conditioned medium (CM) from the EC, and treated SMC and Mϕ (some of which were cholesterol-loaded) with the CM. We measured levels of anti-miR-33a-5p and miR-33a-5p, ABCA1 protein, and apoAI-mediated cholesterol efflux in the treated SMC and Mϕ. Results: Exosomes containing anti-miR-33a-5p were present only in CM from HDAdAnti-transduced EC. Compared to Mϕ incubated with CM from EC transduced with HDAdScr, Mϕ incubated with CM from HDAdAnti-transduced EC had 80% lower levels of miR-33a-5p, a 2.2-fold increase in ABCA1 protein, and a 1.6-fold increase in apoAI-mediated cholesterol efflux (all P&lt;0.001). Similar results were obtained with SMC: 65% lower levels of miR-33a-5p expression, 1.6-fold increase in ABCA1 protein, and 1.4-fold increase in apoAI-mediated cholesterol efflux (all P≤0.01). Conclusions: EC transduced with HDAdAnti release exosomes containing anti-miR-33a-5p. These exosomes transfer anti-miR-33a-5p to SMC and Mϕ, increasing cholesterol efflux. Application of this approach in vivo may accelerate vessel wall cholesterol efflux, preventing and reversing atherosclerosis.
Post-Progression Treatment Eligibility of Unresectable Hepatocellular Carcinoma Patients Treated with Lenvatinib
Authors: Atsushi Hiraoka, Takashi Kumada, Shinya Fukunishi, Masanori Atsukawa, Masashi Hirooka, Kunihiko Tsuji, Toru Ishikawa, Koichi Takaguchi, Kazuya Kariyama, Ei Itobayashi, Kazuto Tajiri, Noritomo Shimada, Hiroshi Shibata, Hironori Ochi, Toshifumi Tada, Hidenori Toyoda, Keisuke Yokohama, Kazuhiro Nouso, Akemi Tsutsui, Takuya Nagano, Norio Itokawa, Korenobu Hayama, Taeang Arai, Michitaka Imai, Kouji Joko, Yohei Koizumi, Yoichi Hiasa, Kojiro Michitaka, Masatoshi Kudo
Journal: Liver Cancer (2019)

&lt;b&gt;&lt;i&gt;Background/Aim:&lt;/i&gt;&lt;/b&gt; Post-progression treatment following tyrosine-kinase inhibitor (TKI) failure in patients with unresectable hepatocellular carcinoma (u-HCC) is important to prolong post-progression survival (PPS), which has a good correlation with overall survival (OS). This study aimed to elucidate the clinical features of progressive disease (PD) in patients treated with lenvatinib (LEN). &lt;b&gt;&lt;i&gt;Materials/Methods:&lt;/i&gt;&lt;/b&gt; From March 2018 to June 2019, 156 u-HCC patients with Child-Pugh A were enrolled (median age: 71 years, Child-Pugh score 5:6 = 105:51, BCLC A:B:C = 8:56:92, modified albumin-bilirubin grade (mALBI) 1:2a:2b = 59:42:55, past history of sorafenib:regorafenib = 57:17). Clinical features were retrospectively evaluated. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; The median observation period was 8.5 months. Median OS was not obtained, while median time to decline to Child-Pugh B (CPB) was 11.4 months, median time to progression (TTP) was 8.4 months, and the period of LEN administration was 7.3 months. When we compared predictive values for time to decline to CPB based on Child-Pugh score and mALBI, values for Akaike information criterion (AIC) score and c-index of mALBI were superior as compared to Child-Pugh score (AIC: 592.3 vs. 599.7) (c-index: 0.655 vs. 0.597). Of the 73 patients with PD, 32 (43.8%) showed no decline to CPB or death. After excluding 3 without alpha-fetoprotein data at PD determination, only 14 (20.0%) of 70 showed REACH-2 eligibility. Non-mALBI 1/2a at the start of LEN was a significant risk factor for decline to CPB during LEN treatment (HR 2.552, 95% CI: 1.577–4.129; &lt;i&gt;p&lt;/i&gt; &amp;#x3c; 0.001). &lt;b&gt;&lt;i&gt;Conclusion:&lt;/i&gt;&lt;/b&gt; Introduction of TKI therapy including LEN for u-HCC patients with better hepatic function (mALBI 1/2a: ALBI score ≤–2.27), when possible, increases the chance of undergoing post-progression treatment, which can improve PPS.
Abstract 765: Sex Difference in Cardiomyocyte Functional Etiology in Heart Failure With Preserved Ejection Fraction
Authors: Claire L Curl, Antonia J Raaijmakers, James R Bell, Tristan W Harding, Stephen B Harrap, Lea M Delbridge
Journal: Circulation Research (2019)

Heart failure with preserved ejection fraction (HFpEF) accounts for &gt;50% of heart failure patients and is particularly prevalent in women. A mechanistic understanding of the intrinsic cardiomyocyte pathology in HFpEF is limited with no selective treatments identified. Gender-specific aspects of HFpEF etiology have not been well characterized. The aim of this study was to experimentally evaluate sex difference in cardiac and cardiomyocyte performance in HFpEF, using a novel recently developed rodent model of HFpEF - the ‘Hypertrophic Heart Rat’. Echocardiography was performed in 50 week male and female HHR/NHR (Normal Heart Rat) using a GE Vivid 9. Fibrosis measurements employed picrosirius red staining. Single myocyte force, shortening and intracellular Ca 2+ measurements were obtained (Myostretcher, Ionoptix). Male and female HHR hearts were hypertrophic (M: 4.9±0.3 vs 3.7±0.1; F: 6.6±0.5 vs 4.4±0.1mg/g CWI) with significant diastolic dysfunction (M:27.8±1.4 vs 18.0±1.7; F: 28.9±1.2 vs 18.9±1.0 E/E’) and preserved systolic function (M:78.4±1.9 vs 74.5±1.3; F: 80.9±1.3 vs 78.1±0.8 EF). Female HHR, but not males, exhibited diffuse interstitial fibrosis (M: 3.33±0.1 vs 3.51±0.1; F: 11.45±0.4 vs 8.44±0.2%). In male, but not female, cardiomyocytes, hypercontractility and high cytosolic operational Ca 2+ levels were observed (64% and 116% increase respectively). The force-length gradient produced by serial stretches of isolated cardiomyocytes was increased in male and female HHR (M:6.8±0.4 vs 4.3±0.8; F: 7.4±0.5 vs 3.0±0.4 nN/%SL stretch) indicating stiffer cardiomyocytes in the HFpEF hearts. The increase in stiffness was significantly accentuated in females. This study indicates that in HFpEF the cardiomyocyte functional etiology is different in males and females. Whilst in males the relationship between cardiomyocyte hypercontractility is the most prominent characteristic of HFpEF, in females the remodelling of the extracellular matrix exacerbates instrinsic myocyte stiffness. Further investigation of the molecular pathways involved in these processes is required for identification of potential therapeutic targets.
Prognostic Value of Minimal Residual Disease before Allogeneic Hematopoietic Stem Cell Transplantation in Patients with Acute Myeloid Leukemia
Authors: Olga Pérez-López, Teresa Caballero-Velázquez, Enrique Colado, Sara Alonso, José González-Campos, Concepción Prats-Martín, Nancy Rodríguez-Torres, Virginia Escamilla Gomez, Ildefonso Espigado, Jose Antonio Pérez-Simón
Journal: Blood (2018)
Hematopoietic Stem Cell Transplantation in Acute Lymphocytic Leukemia Patients: Umbilical Cord Blood Versus Bone Marrow Transplant.
Authors: Zimin Sun, Huilan Liu, Liangquan Geng, Xin Liu, Huizhi Yang, Weibo Zhu, Kaiyang Ding, Wen Yao, Xiao Yuan
Journal: Blood (2007)
Low agreement between mMRC rated by patients and clinicians: implications for practice
Authors: Magnus Ekström, Sungwon Chang, Miriam J. Johnson, Belinda Fazekas, Slavica Kochovska, Chao Huang, David C. Currow
Journal: European Respiratory Journal (2019)

<b>Chronic activity-related breathlessness often assessed on the mMRC scale has low agreement between clinicians and patients. Self-ratings are important when available and improved objective assessment methods are emerging and should be used.</b>http://bit.ly/314wkVS
Comparison of attitudes and beliefs about cancer clinical trial enrollment between physicians, research staff, and cancer patients.
Authors: Grace Hillyer, Melissa Beauchemin, Dawn L. Hershman, Moshe A. Kelsen, Frances L Brogan, Rossy Sandoval, Karen M. Schmitt, Andria Reyes, Mary Beth Terry, Andrew B. Lassman, Gary K. Schwartz
Journal: Journal of Clinical Oncology (2019)

170 Background: Essential to bringing innovative cancer treatments to patients is voluntary participation in clinical trials but fewer than 10% of cancer patients are enrolled onto a trial. We used a domain-oriented framework to assess barriers to cancer clinical trial enrollment (CTE). Methods: Physicians and research staff completed an online survey in 2017; adult cancer patients not currently enrolled in a trial were interviewed in 2018. Perceived structural, provider- and patient-level barriers to CTE were assessed. Differences in perceptions, attitudes and beliefs toward CTE between physicians and staff, patients by ethnicity, and physicians/staff and patients were examined. Results: In total, 120 physician/staff (64.4% response rate) and 150 cancer patient completed surveys. Interacting with the patients’ family was seen as a CTE barrier by nearly one-third of physicians/staff overall, however, staff much more often stated this barrier than did physicians (44.0% vs. 18.2%, p= 0.007). Hispanic patients more often stated they would join a trial, even if standard therapy was an option compared to non-Hispanic patients ( p= 0.004). Overall, patients, more often than physicians/staff, believed that clinical trials are only offered to people whose disease is hopeless (27.3% vs. 8.7%, p &lt; 0.001) and that CTE does not help patients personally (32.9% vs. 1.8%, p &lt; 0.001). More often physicians/staff believed that patients decline CTE due to language or cultural barriers (57.5% vs. 27.3%, p &lt; 0.001), lack of understanding about clinical trials (63.3% vs. 9.1%, p = 0.001), and mistrust of the medical system (69.2% vs. 36.4%, p= 0.043) than was reported by patients. Patients less often reported declining CTE because of concerns about invasive procedures (9.1% vs. 41.7%, p = 0.02), toxicity (18.2% vs. 60.0%, p= 0.006) or reluctance to be randomized/receive a placebo (27.3% vs. 70.8%, p= 0.005). Conclusions: Our findings indicate a wide gap between provider and patient attitudes and beliefs about CTE. Reconciling these differences will require tailored education to dispel misperceptions and strategies to improve the quality of patient-provider communication.
Expression and Function of the P-Glycoprotein (P-gp) In Myelodysplastic Syndromes (MDS) Treated with Azacytidine (AZA)
Authors: Marie Sebert, Elodie Lainey, PAscale Lepelley, Sylvain Thepot, Maximilien Tailler, Claude Gardin, Guido Kroemer, Simone Boehrer, Lionel Ades, Pierre Fenaux
Journal: Blood (2011)
Complete Hematological, Molecular and Histological Remissions without Cytoreductive Treatment Lasting After Pegylated-Interferon α-2a (peg-IFNα-2a) Therapy in Polycythemia Vera (PV): Long Term Results of a Phase 2 Trial
Authors: Pascal Turlure, Nathalie Cambier, Murielle Roussel, Sylvia Bellucci, Jean-Marc Zini, Jean-Didier Rain, Philippe Rousselot, William Vainchenker, Lina Abdelkader, Kamel Ghomari, Jean-Luc Dutel, Yasmine Chait, Sylvie Chevret, Christine Chomienne, Bruno Cassinat, Jean-Jacques Kiladjian
Journal: Blood (2011)
Development and validation of a risk-prediction model for in-hospital major adverse cardiovascular events in patients admitted to hospital with acute myocardial infarction: results from China PEACE retrospective and prospective studies
Authors: Chaoqun Wu, Xiqian Huo, Jiamin Liu, Lihua Zhang, Jiapeng Lu, Xueke Bai, Shuang Hu, Xi Li, Xin Zheng, Haibo Zhang, Jing Li
Journal: The Lancet (2019)
Cytokine Induced Killer Cells Are Feasible and Safe for Both Autologous and Allogeneic Applications in Patients with Haematological Malignancies
Authors: Yeh Ching Linn, Tsyr jong Lim, Madelaine Niam, Garnet Suck, Yeow Tee Goh, William Hwang, Yvonne Loh, Lee Hui Ng, Hao Xiang Yong, Mickey Boon Chai Koh
Journal: Blood (2008)
Abstract 290: Lpp3 Deficiency Impairs Mitochondrial Function And Enhances Myocardial Lpa Mediated Signaling
Authors: Sumitra Miriyala, Manikandan Panchatcharam, Md.Shenuarin Bhuiyan,, Diana Escalante Alcalde, Kevin McCarthy, Christopher Kevil
Journal: Circulation Research (2019)

The bioactive lysophosphatidic acid (LPA) plays a well-known role in atherosclerotic disease, whereas, its role in myocardial function remains virtually unexplored. Following acute myocardial infarction, serum LPA concentration rises by six-fold over control human subjects, suggesting LPA may contribute to the pathogenesis of myocardial infarction. LPA production involves hydrolysis of lysophosphatidylcholine by the secreted enzyme autotaxin, whereas lipid phosphate phosphatase-3 (LPP3) catalyzes LPA dephosphorylation to generate lipid products that are not receptor active. We present the first evidence that cardiac ischemia/reperfusion (I/R) injury enhances myocardial autotaxin levels and decreases myocardial LPP3 expression, and this is associated with increased serum LPA levels. Upon reperfusion, reactive oxygen species production arises as a burst of superoxide from mitochondria following I/R injury. The redox-sensitive transcription factor NFAT has been shown to bind to the autotaxin promoter and induce its expression. Therefore, we looked at the autotaxin and LPP3 regulation in mice following I/R injury in the myocardium. After 1h ligation followed by 3h reperfusion in the myocardium, we observed a 3-fold increase in the autotaxin protein levels, whereas LPP3 protein levels were significantly downregulated as observed through Western blot analysis in these myocardial ischemic tissues. Autotaxin and miR-92a mRNA expression levels were significantly upregulated, whereas KLF2 and LPP3 mRNA expressions were significantly downregulated following I/R injury at 24 hours. Western blot analysis showed a 3-fold increase autotaxin protein levels and immunohistochemistry of human infarct tissues at 24 hours showed disruption of the sarcomere with decreased LPP3 staining. We found that I/R injury transactivates miR-92a, and inhibit KLF2, an upstream activator of LPP3. Taken together, us in vivo data, from the myocardial I/R injury and human infarct tissues, suggest that regulation of autotaxin and LPP3 activity might cause the rise in serum LPA levels as reported with acute myocardial infarct patients
Abstract 225: Evaluating Pro-Inflammatory and Pro-Resolving Lipid Modulations in an Oral 15-HETE Model of Pulmonary Hypertension
Authors: Ellen I Oconnor, Gregoire Ruffenach, Victor Grijalva, David Meriwether, Jeremy Papesh, Nasrin Dorreh, Anna Dorfman, Mansoureh Eghbali, Srinivasa Reddy
Journal: Circulation Research (2019)

Pulmonary arterial hypertension (PH) is a chronic lung disease with a mortality rate of 50% at 5 years after diagnosis. PH is characterized by progressive increase in pulmonary arterial pressure leading to right ventricular (RV) increase in afterload, hypertrophy, and failure. Despite the availability of multiple animal models of PH, finding relief or cure for PH patients has been elusive to date. Recent studies in our laboratory have shown that levels of hydroxyeicosatetraenoic acids (HETEs) and hydroxyoctadecadienoic acids (HODEs) are elevated in the lungs and plasma of patients with PH as well as in animal models of PH. In testing for causality, we showed that administration of 5 μg of 15-HETE/day to wild type male mice for 3 weeks was sufficient to cause increase in pulmonary pressure, vascular resistance, plasma levels of HETEs and HODEs, right ventricle hypertrophy, and right ventricle systolic pressure (RVSP), consistent with PH. We set out to utilize this new mouse model of PH to understand the mechanisms in PH pathology by first examining the role of lipid mediators of inflammation in the development of PH. Our lab has developed a mass spectrometry method for measuring the levels of 39 inflammatory pathway lipid mediators from the cyclooxygenase (COX) and lipoxygenase (LOX) pathways that has been validated for use in tissue, plasma, and cell supernatant. Utilizing this panel with samples from mice fed 15-HETE and supernatant from an intestinal epithelial cell line; IEC-6 cells treated with 15-HETE, we have observed significant changes in multiple lipid mediators of inflammation. In addition to seeing increases in HETEs and HODEs with 15-HETE treatment, we observed significant increases in leukotriene C4 (LTC4) and 14(S)-hydroxy docosahexaenoic acid (14S-HDHA) and trending increases in thromboxane B2 (TXB2), and leukotriene E4 (LTE4) in the plasma, significant increases in 20 different lipids in lung tissue, including LTC4, TXB2, and LTE4, and significant increases in LTC4 and 5-oxo-eicosatetraenoic acid (5-oxoETE) in the supernatant of IEC-6 cells incubated with 15-HETE for 12 hours. These results indicate that novel inflammatory lipids and pathways may play an important in the development of hypertension and help identify new targets for therapies.
HSP90 Inhibition Has Potent Activity Against T-Cell Acute Lymphoblastic Leukemia (T-ALL) Through Degradation Of TYK2 Kinase
Authors: Koshi Akahane, Takaomi Sanda, Marc R. Mansour, Julia Etchin, Ng Cherry, David M. Weinstock, Anthony Letai, Daniel J. DeAngelo, A. Thomas Look
Journal: Blood (2013)
Implementation and efficacy of a large-scale radiation oncology case-based peer-review quality program across a multinational cancer network.
Authors: Ethan B. Ludmir, Karen E. Hoffman, Anuja Jhingran, Mee-Chung Puscilla Ip, Seth D. Frey, Matthew S. Ning, Bruce D. Minsky, Mary Frances McAleer, Gregory Chronowski, Isidora Arzu, Valerie Klairisa Reed, Amit K. Garg, Terence Roberts, Patel Ashish, Michael R. Olson, Ugur Selek, Molly Gabel, Albert Koong, Joseph M. Herman, Deborah A. Kuban
Journal: Journal of Clinical Oncology (2019)

1 Background: With rapid community expansion of academic cancer centers, ensuring high-quality delivery of care across all affiliated network sites is critical. Here we report the results of a radiation oncology peer-review system implemented across a large multinational cancer network. Methods: Weekly radiation oncology peer-review conferences were held between network centers and the main campus of a major cancer system; results of standardized peer-review for each case were recorded. Peer-review resulted in each case being scored as concordant or nonconcordant on initial review; nonconcordance was based on institutional guidelines, national standards, and/or expert opinion. Results: Between 2014 and 2018, 28,730 patient radiation treatment plans underwent peer-review at 10 network centers. The peer-review case volume increased over this study period, from 1,420 cases in 2014 to 9,112 in 2018, concomitant with network expansion. Examining cases reviewed in 2018 (N = 9,112), the most-commonly reviewed cases by disease site were breast (28.9%), head and neck (HN; 13.9%), and lung (12.6%). Of all cases in 2018, 452 (5.0%) were deemed nonconcordant. Higher nonconcordance rates were noted for HN cases (14.0%), and lower rates for lung cases (2.3%; p &lt; 0.001). Of nonconcordant HN cases, the majority (69.5%) were deemed nonconcordant based on target volume delineation. Of nonconcordant breast cases, most (67.1%) were nonconcordant based on radiation field design. For centers added to the network during the study period, we observed a significant decrease in the nonconcordance rate over time after joining the network (average annual decrease of 5.4% in nonconcordant cases; p &lt; 0.001). Conclusions: These data demonstrate the feasibility and efficacy of a large-scale multinational cancer network radiation oncology weekly peer-review program. Nonconcordance rates were highest for HN cases, primarily due to target volume delineation. With improved nonconcordance rates for newly-added network centers, these results offer the promise of improving the quality of radiotherapy delivery across an extensive cancer network with a major academic center as the nucleus.
Rapid Engraftment and Immune Recovery in Treatment Refractory Severe Aplastic Anemia Patients Undergoing Ex Vivo Nicotinamide-Expanded (NAM-Expanded) Unrelated Cord Blood Transplantation
Authors: Richard W. Childs, Phuong T. Vo, Georg Aue, Jennifer Wilder, Brian Wells, Joseph Clara, Reem Shalabi, Patricia Prince, David F. Stroncek, Robert Reger, Willy A. Flegel, Sharon Adams, Kristen Gunn, Tatyana Worthy, Lisa Cook, Xin Tian
Journal: Blood (2018)
The Role of Prothrombinase Complex Assembly and in Situ Fibrin Deposition on the Surface of Acute Promyelocytic Leukemia Cells in Hemorrhage
Authors: Tao Li, Xiaoyan Yang, Yan Zhang, Baorong LI, Yinmiao Liu, Cong Zhang, Yan Kou, Lili Zou, Hui Liang, Li Hou, Chunxu Wang, Muxin Yu, Jingwen Du, Haijiao Jing, Yueyue Li, Jin Zhou, Jialan Shi
Journal: Blood (2018)