tbuckley/cabot-search huggingface dataset:
The Chronic Lymphocytic Leukemia Comorbidity Index (CLL-CI): A Novel Comorbidity Score Derived from a Large Multicenter Retrospective Cohort Study of Patients Treated with Ibrutinib and/or Chemo-Immunotherapy (CIT)
Authors: Max J. Gordon, Andy Kaempf, Andrea Sitlinger, Tareq Salous, Hamood Alqahtani, Michael C. Churnetski, Paul Wisniewski, Xavier Issac Rivera, Krish Patel, Daniel O. Persky, Jonathon B. Cohen, Michael Y. Choi, Brian T. Hill, Mazyar Shadman, Deborah M. Stephens, Danielle M. Brander, Byung Park, Alexey Danilov
Journal: Blood (2019)
RARE-34. TUMOR IMMUNITY AND EXTRACRANIAL METASTASES, AND MECHANISM OF PD-L1 EXPRESSION IN INTRACRANIAL SOLITARY FIBROUS TUMOR/HEMANGIOPERICYTOMA
Authors: Dai Kamamoto, Kentaro Ohara, Yohei Kitamura, Kazunari Yoshida, Hikaru Sasaki
Journal: Neuro-Oncology (2019)

Abstract Intracranial solitary fibrous tumor (SFT) /hemangiopericytoma (HPC) are rare, however, these tumors are often associated with aggressive clinical course with recurrence and/or extracranial metastasis. PD-1, PD-L1 play important roles as immune-checkpoint mediators within tumor microenvironment, and the antibodies to these molecules are now approved for the treatment of various kinds of cancers. Some mechanisms of activation of PD-L1 are reported, including cytokines or chemokines from immune cells in tumor microenvironment, and genetic mutations such as translocation, or amplification. We have investigated the expression of PD-1, PD-L1, and tumor infiltrating lymphocytes (TIL) in 16 cases of SFT/HPC by immunohistochemistry. Kaplan-Meier method and log-rank/Wilcoxon tests were used to analyze the relationship between their expression with overall survival (OS), progression free survival (PFS), metastasis free survival (MFS), and time to treatment failure (TTF; metastasis or death). Additionally, we have analyzed amplification of PD-L1 gene by FISH, translocation between promotor region of CIITA and PD-L1 by PCR, and mutation in 3’-UTR by immunohistochemistry with antibody recognizes C-terminus (clone; SP-142) of PD-L1. PD-L1 was expressed in most of tumor cells. The intensity of PD-L1 expression was negatively associated with MFS (p=0.04), and diffuse pattern of PD-L1 expression showed trends towards shorter TTF compared with partial expression (p=0.08). Notably, with the combination analysis of PD-L1 and CD8(+) TIL, the diffuse PD-L1 expression with less CD8(+) was significantly associated with shorter TTF (p=0.005). However, there was no significant relevance between the expression of those immune-checkpoint molecules and OS or PFS. Although neither amplification of PD-L1 gene, 9p24.1, nor translocation between CITTA and PD-L1 were observed, difference in immunohistochemistry with two different anti-bodies was observed. In intracranial SFTs/HPCs, tumor immunity mechanism associated with PD-1/PD-L1 may play an important role in their extracranial metastases, and mutation in 3’-UTR may be a cause of PD-L1 activation in SFT/HPC.
Interim Results from the Phase I Deplethink Trial Evaluating the Infusion of a NKG2D CAR T-Cell Therapy Post a Non-Myeloablative Conditioning in Relapse or Refractory Acute Myeloid Leukemia and Myelodysplastic Syndrome Patients
Authors: A. Samer Al-Homsi, Enkhtsetseg Purev, Philippe Lewalle, Maher Abdul-Hay, Daniel A Pollyea, Adriano Salaroli, Thomas Lequertier, Erik Alcantar-Orozco, Fabian Borghese, Caroline Lonez, Nathalie Braun, Florence Renard, Anne Flament, Ine Moors, Tessa Kerre
Journal: Blood (2019)
CK2 Inhibitor CX4945 Shows Strong In Vivo Synergistic Anti-Leukemia Activity with Rapamycin in B-ALL Due to Enhanced Ikaros Mediated Repression of mTOR Pathway
Authors: Chandrika Gowda, Chunhua Song, Yali Ding, Pavan kumar Dhanyamraju, Soumya Iyer, Jonathon Payne, Yevgeniya Bamme, Arati Sharma, Kimberly J. Payne, Sinisa Dovat
Journal: Blood (2019)
Absolute Lymphocyte Count (ALC) Less Than 100 Predicts Adverse Transplant Outcomes with Rabbit Thymoglobulin in Patients Undergoing Matched Unrelated Allogeneic Hematopoietic Stem Cell Transplantation
Authors: Dipenkumar Modi, Malini Surapaneni, Seongho Kim, Lois Ayash, Asif Alavi, Andrew Kin, Voravit Ratanatharathorn, Joseph P. Uberti, Abhinav Deol
Journal: Blood (2019)
Bendamustine and Rituximab Plus Venetoclax in Untreated Mantle Cell Lymphoma over 60 Years of Age (PrE0405): A Phase II Study
Authors: Craig A. Portell, N. Nora Bennani, Opeyemi Jegede, Seema Naik, Benjamin M Parsons, Priyank P Patel, Christopher M. Reynolds, Brad S. Kahl
Journal: Blood (2019)
TMIC-38. CLINICAL AND IMMUNOLOGICAL CHARACTERIZATION OF HERPES VIRUS ENTRY MEDIATOR IN HUMAN GLIOMAS
Authors: Ming-Zhi Han, Shuai Wang, Dong-Hai Wang
Journal: Neuro-Oncology (2019)

Abstract BACKGROUND Dysregulation of immune checkpoint members within tumors, including glioblastoma (GBM), is related to immune evasion. Herpes virus entry mediator (HVEM) is a novel identified immune checkpoint molecule which plays essential roles in both innate and acquired immunity. Despite recent advances in exploring the function HVEM in a variety cancer types, the clinical and immunological importance of HVEM in human gliomas remain largely unknown. METHODS Molecular and clinical data was obtained from publicly genomic databases. Immunohistochemistry was applied to assess the protein level of HVEM. Matlab software as well as R language were used for statistical analysis. RESULTS HVEM was found to be elevated in aggressive gliomas, especially in isocitrate dehydrogenase (IDH) wild-type GBM. High expression of HVEM was associated with Mesenchymal subtype and showed promising prognostic values based on Cox regression model and nomogram model. HVEM showed intra-tumor heterogeneity with abundant in peri-necrotic zone and microvascular region. In addition, HVEM high patients were more frequent with genomic aberrations of oncogenic events. Gene ontology and pathway analysis uncovered the enrichment of HVEM in multiple immune regulation process, especially in the suppression of T cell mediated immunity in GBM. Moreover, HVEM was tightly associated with several infiltrating immune and stromal cell lineages in microenvironment, and showed high correlation with other immune checkpoints. CONCLUSIONS Our data highlights the importance of HVEM in GBM progression and that targeting HVEM combined with current immune checkpoint blockades might be a novel therapeutic strategy for GBM.
EXTH-63. LIPOSOMAL DELIVERY OF FERRITIN HEAVY CHAIN (FTH1) siRNA RESULTS IN INCREASED RADIATION SENSITIVITY IN PATIENT DERIVED GLIOMA INITIATING CELLS
Authors: Vagisha Ravi, Thomas Abraham, Achuthamangalam Madhankumar, Becky Slagle-Webb, Bhavyata Pandya, James Connor
Journal: Neuro-Oncology (2019)

Abstract Glioblastoma (GBM) is the most lethal and incurable brain cancer. Despite maximum treatment, high recurrence rates result in median survival of less than 2 years. A subset of treatment resistant cells within GBM known as glioma initiating cells (GICs) are implicated in recurrence and exhibit ferritin overexpression. High expression of ferritin is known to be associated with poor overall survival in GBM patients. Our previous finding showed that downregulation of the ferritin heavy chain subunit (FTH1) enhanced treatment sensitivity in astrocytoma cells. Recently, functional importance of FTH1 in GICs was demonstrated by shRNA silencing leading to ablation of tumorigenic ability. We therefore posited that disrupting iron metabolism through FTH1 knockdown would radiosensitize GICs. Thus we developed multivalent cationic liposomes that enabled delivery of FTH1 siRNA to patient derived GICs isolated from pro-neural (PN) and mesenchymal (Mes) GBM. In both subtypes, FTH1 loss led to increased apoptosis and reduced cell viability. When exposed to radiation, PN GICs were unable to repair and recover from DNA damage, leading to a further decrease in cell viability and a complete loss of reproductive clonogenic potential unlike their more radioresistant Mes counterparts. Moreover, expression of stem cell marker Nestin was markedly reduced in PN but not Mes GICs. Thus, FTH1 loss is detrimental to both GIC subtypes, it seems to be critical for maintaining stemness and radiation resistance of PN GICs. These findings further support the viability of FTH1 as a therapeutic target in GBM.
Cross-Intolerance with Bosutinib after Prior Tyrosine Kinase Inhibitors in Patients with Chronic Phase Chronic Myeloid Leukemia: BYOND Phase 4 Study
Authors: Bjørn T. Gjertsen, Andreas Hochhaus, Gianantonio Rosti, Justin M. Watts, Guillermo Ortí, Philipp le Coutre, Eric Leip, Andrea Viqueira, Jorge E. Cortes, Frank Giles, Carlo Gambacorti-Passerini
Journal: Blood (2019)
Involvement of RUNX1 Pathway Is a Common Event in the Leukemic Transformation of Chronic Myeloproliferative Neoplasms (MPNs)
Authors: Paola Guglielmelli, Niccolò Bartalucci, Elisa Contini, Giada Rotunno, Annalisa Pacilli, Simone Romagnoli, Lara Mannelli, Francesco Mannelli, Giacomo Coltro, Alessandro Pancrazzi, Valentina Ariu, Sara Fiaccabrino, Roberto Semeraro, Alberto Magi, Carmela Mannarelli, Francesca Gesullo, Chiara Paoli, Alessandro M. Vannucchi
Journal: Blood (2019)
Correcting Rare Blood Disorders Using Coagulation Factors Produced In Vivo By Shielded Living TherapeuticsTM Products
Authors: Guillaume Carmona, Lauren Barney, Jared Sewell, Ryan Newman, Christine Carroll, Michael Beauregard, Janet Huang, Richard W Heidebrecht, Deya Corzo, David Moller, Devyn Smith, David Peritt, Rogerio Vivaldi
Journal: Blood (2019)
NIMG-04. MRI CHARACTERISTICS, TREATMENT APPROACH, PATTERN OF RELAPSE AND SURVIVAL FOR MULTICENTRIC GLIOBLASTOMA. A RETROSPECTIVE MONOCENTRIC STUDY
Authors: Alexandra Benouaich-amiel, Vadim Khasminsky, Omer Gal, Tamara Weiss, Suzana Fichman, Tali Siegal, Shlomit Yust-Katz
Journal: Neuro-Oncology (2019)

Abstract INTRODUCTION Multicentric glioblastoma (m-GBM) is a rare GBM variant (6–13% of all GBM cases). Published data is scarce and focus largely on enhancing foci. We performed a retrospective study to determine the incidence, imaging characteristics, treatment, pattern of relapse and prognosis of m-GBM. METHODS The neuropathological database of our institution was surveyed for histological diagnosis of adult GBM diagnosed between 01/01/2015 and 31/05/2018. All pre-operative MRI were reviewed to identify patients with m-GBM (defined as well separated enhancing and non-enhancing tumor foci). Medical records and follow-up MRI studies were reviewed to retrieve the data. RESULTS Of the 167 patients with newly diagnosed GBM, 14 (8%) presented with m-GBM. All of them had at least one enhancing lesion. The total number of lesions was 37 (19 enhancing and 18 non-enhancing) with a median number of lesions per patient of 2 (range 2 to 4). Median age at diagnosis was 66 (range: 49–79) years. MGMT status was known for 10 patients (5 methylated and 5 un-methylated). Nine patients underwent resection of the enhancing component whereas 5 patients had a biopsy. Median follow up was 14.3 (range: 2–30) months. All but one patient were treated by concurrent radiotherapy with temozolomide. All enhancing lesions were included in radiation field, whereas 4 of the 18 Flair lesions were not. Median progression free survival was 6.2 (range: 0–13.3) months. Six of the 18 non-enhancing tumor foci eventually displayed contrast enhancement during the follow-up. At last follow up, 12 patients died, with an overall survival of 12.3 months. Information regarding radiation fields, pattern of progression and molecular profile will be presented at the meeting. CONCLUSION m-GBM presents therapeutic dilemmas regarding the optimal therapeutical approach. Better understanding of the disease course and pattern of progression may help to optimize the therapeutic approach implying particularly to non-enhancing tumor foci.
Old People and Mental Hospitals
Authors: P. R. H. Davis
Journal: BMJ (1965)

Charter will do anything to help us with this impossible work load."With the present net loss of principals running at a rate of over 200 in five months, the general practitioner is faced with an in- evitable increase in this load which seems likely to be a geometric progression.On the other hand, as a result of these losses the Pool will be £600,000 the poorer.The pro- fession must decide whether the Minister's suggestions for a publicity campaign are likely to be more effective in reducing un- necessary demand than a discretionary charge
NKTR-255, a Polymer-Conjugated IL-15 Enhances Antibody-Dependent Cellular Cytotoxicity Mediated By NK Cells in a B Cell Lymphoma Model
Authors: Takahiro Miyazaki, Saul Kivimäe, Marlene Hennessy, Rhoneil Pena, Phi Quach, Andrew Moffet, Wildaliz Nieves, Ping Zhang, Mario Q. Marcondes, Loui Madakamutil, Jonathan Zalevsky
Journal: Blood (2019)
Clinical outcome of personalised treatment guided by genome and transcriptome sequencing in patients with neuroendocrine neoplasms: Updated results from the German NCT/DKTK MASTER trial
Authors: S. Kreutzfeldt, L. Apostolidis, M. Oles, P. Horak, C.E. Heilig, C. Heining, B. Hutter, B. Klink, M. Lamping, S. Uhrig, A. Stenzinger, E.C. Winkler, B. Wiedenmann, D. Jäger, B. Brors, E. Schröck, U. Keilholz, M.E. Pavel, H. Glimm, S. Fröhling
Journal: Annals of Oncology (2019)
GENE-32. SYNTHETIC LETHAL INTERACTIONS WITH IDH1R132H IN GLIOMA STEM-LIKE CELLS
Authors: Maria Ventosa, Padma Kadiyala, Stephen Carney, Maria Castro, Pedro Lowenstein
Journal: Neuro-Oncology (2019)

Abstract Gliomas are the most frequently diagnosed human primary brain tumors. Mutations in Isocitrate Dehydrogenase (IDH) 1 occur in the vast majority of low grade gliomas and secondary high grade glioblastomas. A single amino acid missense mutation in IDH1 at arginine 132 (R132H) is an early event in tumor development. IDH1R132H leads to the production of the oncometabolite 2-R-2-hydroxyglutarate. However the exact roles played by IDH1R132H in the development and malignant transformation of the tumors remain unclear. Further studies are required to determine optimal therapeutic strategies to target the IDH1 mutated subsets of gliomas. New generation high-throughput genetic perturbation technologies make it possible to systematically identify the genes and pathways required for the survival and proliferation of mammalian cells. Herein, we present preliminary results from a CRISPR-dCas9 derived activation to drive the transcriptional activation of more than 23,000 coding genes in both wild type and mutant IDH1 patient-derived pediatric glioma cells. Based on an average of three viability screens per cell type, we analyzed the sgRNA library representation in the IDH1 mutated and non-mutated glioma cultures after the genome wide activation. We identified 1553 candidate genes that upon gain of function trigger the death of glioma cells harboring the IDH1 mutation. The analysis of these results further pinpoints the activation of the Cyclin E1 (CCNE1), the BCL2 Antagonist/Killer 1 (BAK1) and the Homeobox B13 (HOXB13) as the most significant synthetic lethal targets in IDH1R132H glioma cells. Interestingly, results from RNAseq showed a decreased expression of these genes in IDH1 mutated compared to non-mutated glioma cells. Thus, this viability screening aims to elucidate genes that interact with IDH1R123H and play a role in tumor cell fitness. The functional analysis of these candidate genes will allow us to uncover their contribution to the progression of IDH1 mutated gliomas.
INNV-43. IMPROVING POST OPERATIVE FOLLOW-UP AND TIME TO ADJUVANT TREATMENT FOR HIGH GRADE GLIOMA
Authors: Michael Catalino, Daniel Zeitouni, Sonja Henretty, Anqi Zhu, Simon Khagi
Journal: Neuro-Oncology (2019)

Abstract BACKGROUND High grade glioma patients are prone to lapses in treatment due to the complexities related to coordination of care, the timing of adjuvant treatment, and insurance barriers. The purpose of this study was to determine the impact of an institutional multidisciplinary protocol on transitions of care after surgery for high grade gliomas between 2015 and 2018. METHODS A retrospective cohort study was conducted using CPT codes for enrolled glioma patients between 2015–2018 with unplanned surgery. Historical controls were compared to the intervention group which began enrollment in November 2016. We used time-to-event analysis to compare time to neuro-oncology follow up and time to adjuvant treatment (radiation and/or chemotherapy). The effect of discharge disposition and insurance status was also assessed. The study incorporated an ad hoc analysis of survival outcomes. RESULTS The intervention and control groups had similar baseline characteristics. The intervention was associated with more patients following up with neuro-oncology within 2 weeks (51.1% in intervention group compared to 30.0% in control group), more patients starting radiation within 30 days (43.6% and 25.0%, respectively) and more patients starting chemotherapy within 30 days (59.0% and 35.0%, respectively). Time-to-event analysis revealed that the intervention trended toward earlier initiation of chemotherapy (p=0.076). Only 16.7% of patients discharge to a skilled nursing facility were able to initiate chemotherapy at the 30-day mark. Time-to-event analysis revealed that insurance status was significantly associated with initiating chemotherapy at the 30-day mark (p=0.023). Survival analysis is planned and will be reported in a future manuscript. CONCLUSION A multidisciplinary approach to capturing patients after surgery decreases time to follow up with neuro-oncology and initiation of adjuvant treatment. Timely follow up is associated with insurance status, discharge disposition, and multidisciplinary discussions between the treatment team and ancillary staff. Survival outcomes are being assessed and will be reported.
Zinc Finger Nuclease-Mediated Disruption of the BCL11A Erythroid Enhancer Results in Enriched Biallelic Editing, Increased Fetal Hemoglobin, and Reduced Sickling in Erythroid Cells Derived from Sickle Cell Disease Patients
Authors: Samuel Lessard, Pauline Rimmele, Hui Ling, Kevin Moran, Benjamin Vieira, Yi-Dong Lin, Vu Hong, Andreas Reik, Denny Dang, Naoya Uchida, John F. Tisdale, Pablo Rendo, Ahmed Daak, Alexandra Hicks
Journal: Blood (2019)
Hypoxia and Hypoxia Inducible Factor (HIF)-1α in Multiple Myeloma: Effect on the Pro-Angiogenic Signature of Myeloma Cells and the Bone Marrow Microenvironment.
Authors: Simona Colla, Paola Storti, Gaetano Donofrio, Mirca Lazzaretti, Sabrina Bonomini, Paolo Lunghi, Monica Crugnola, Marina Bolzoni, Luisa Galla, Luigi Ippolito, Eugenia Martella, Gabriella Sammarelli, Luisa Craviotto, Cecilia Caramatti, Marcellina Mangoni, Antonio Bonati, Vittorio Rizzoli, Nicola Giuliani
Journal: Blood (2008)
Efficacy of the AS04-Adjuvanted HPV16/18 Vaccine: Pooled Analysis of the Costa Rica Vaccine and PATRICIA Randomized Controlled Trials
Authors: Joseph E Tota, Frank Struyf, Joshua N Sampson, Paula Gonzalez, Martin Ryser, Rolando Herrero, John Schussler, Naveen Karkada, Ana Cecilia Rodriguez, Nicolas Folschweiller, Carolina Porras, Mark Schiffman, John T Schiller, Wim Quint, Aimée R Kreimer, Cosette M Wheeler, Allan Hildesheim
Journal: JNCI Journal of the National Cancer Institute (2019)

The AS04-adjuvanted HPV16/18 (AS04-HPV16/18) vaccine provides excellent protection against targeted human papillomavirus (HPV) types and a variable degree of cross-protection against others, including types 6/11/31/33/45. High efficacy against any cervical intraepithelial neoplasia grade 3 or greater (CIN3+; >90%) suggests that lower levels of protection may exist for a wide range of oncogenic HPV types, which is difficult to quantify in individual trials. Pooling individual-level data from two randomized controlled trials, we aimed to evaluate AS04-HPV16/18 vaccine efficacy against incident HPV infections and cervical abnormalities .
Staff shortages are affecting cancer care in Scotland, cross party group warns
Authors: Bryan Christie
Journal: BMJ (2019)

Chronic staff shortages and inadequate funding are hindering efforts in Scotland to improve cancer survival rates, the Scottish parliament’s cross party group on cancer has warned. The group is made up of politicians and 76 member organisations involved in cancer research, treatment, care, and prevention.

A report,1 written by Cancer Research UK in its capacity as …
In Vivo Mobilization of Multiple Myeloma Cells Out of the Bone Marrow Using the CXCR4 Inhibitor AMD3100 and Bortezomib: Implications for Sensitization of Myeloma Cells to Apoptosis.
Authors: Judith M. Runnels, Abdelkareem Azab, Costas Pitsillides, Anne-Sophie Moreau, Feda Azab, Joel A. Spencer, Xavier Leleu, Alicia L. Carlson, Beatriz E. Ospina, Renee Wright, Xiaoying Jia, Hai Ngo, Andrew L. Kung, Charles P. Lin, Irene M. Ghobrial
Journal: Blood (2007)
GENE-10. A SIMPLE AND EFFICIENT METHOD FOR GENERATING MULTI-ALLELIC INSERTION-DELETION MUTATIONS AND PRECISE DELETIONS IN PRIMARY HUMAN CELL CULTURES
Authors: Pia Hoellerbauer, Megan Kufeld, Sonali Arora, Hua-Jun Wu, Heather Feldman, Patrick Paddison
Journal: Neuro-Oncology (2019)

Abstract CRISPR-Cas9-based technologies have revolutionized experimental manipulation of the human genome by enabling generation of site-specific genetic alterations, such as insertion-deletion (indel) mutations. None-the-less, limitations of the delivery and efficacy of these technologies restrict their application in primary human cells. Here, we present a simple and effective method for fast and penetrant induction of multi-allelic indels and near-precise deletions (ranging from ~50bp to &gt;50kbp) in primary human neural stem/progenitor cell (NPC) and brain tumor-derived stem-like cell cultures using the CRISPR-Cas9 system. We report that mono-, bi-, or multi-allelic (depending on ploidy) indel efficiencies of &gt;90% can be routinely achieved within 3 days, without the need for pre-engineering cells to express Cas9 or isolating clones. As a result, this method enables the quick generation of a series of knockouts at different genomic loci, which we illustrate by successively targeting TP53, CDKN2A, PTEN, and NF1 in human NPC populations, where ³95% loss of protein expression is observed. RNA-seq analysis of these NPC knockout pools confirmed gene expression changes including p53 transcriptional and Rb-axis targets, as well as NF1-dependent repression of major histocompatibility complex class II gene expression. Given its simplicity, this method is readily adaptable to other primary mammalian cell types.
R-BAC Maintains High Response Rate in Mantle Cell Lymphoma Following Relapse on BTK Inhibitor Therapy
Authors: Rory McCulloch, Carlo Visco, Rebecca Frewin, Neil Phillips, Toby A. Eyre, David Tucker, Francesca M. Quaglia, Annabel McMillan, Jonathan Lambert, Nicola Crosbie, Simon Rule
Journal: Blood (2019)
Subsequent Treatments, Responses and Survival in the Real World for Patients with Relapsed Multiple Myeloma Following Treatment with Lenalidomide
Authors: Jessica B Taube, Catherine SY Lecat, Simon Cheesman, Gabriel Wallis, Charalampia Kyriakou, Lydia Lee, Shameem Mahmood, Xenofon Papanikolaou, Christopher Parrish, Neil K Rabin, Sajitha Sachchithananthan, Jonathan Sive, Ashutosh D. Wechalekar, Kwee Yong, Gordon Cook, Rakesh Popat
Journal: Blood (2019)
Combination of Anti-CD19 and Anti-CD20 Chimeric Antigen Receptor T Cells for Relapsed and Refractory Diffuse Larger B Cell Lymphoma: An Open-Label, Single-Arm, Phase Ⅰ/Ⅱ Trial
Authors: Wei Sang, Ming Shi, Jingjing Yang, Jiang Cao, Linyan Xu, Dongmei Yan, Xuguang Song, Cai Sun, Depeng Li, Feng Zhu, Zhenyu Li, Junnian Zheng, Jianlin Qiao, Kailin Xu
Journal: Blood (2019)
Dermatology Tactile Learning Tool: Development and student evaluation of an interactive 3-dimensional skin lesion model for medical student education
Authors: Cory A. Dunnick, Michael Lehrer, Hania Flaten, Melissa R. Laughter, Roya Mirhossani, Amanda Schultz, Paige Bennett, Kurt Ashack, Robert P. Dellavalle, David R. Pearson
Journal: Journal of the American Academy of Dermatology (2019)
Genetic and Molecular Basis of Cardiac Arrhythmias: Impact on Clinical Management Part III
Authors: Silvia G. Priori, Jacques Barhanin, Richard N. W. Hauer, Wilhelm Haverkamp, Habo J. Jongsma, André G. Kleber, William J. McKenna, Dan M. Roden, Yoram Rudy, Ketty Schwartz, Peter J. Schwartz, Jeffrey A. Towbin, Arthur M. Wilde
Journal: Circulation (1999)