tbuckley/cabot-search huggingface dataset:
Association of Intensive Care Unit Patient-to-Intensivist Ratios With Hospital Mortality
Authors: Hayley B. Gershengorn, David A. Harrison, Allan Garland, M. Elizabeth Wilcox, Kathryn M. Rowan, Hannah Wunsch
Journal: JAMA Internal Medicine (2017)

The patient-to-intensivist ratio (PIR) across intensive care units (ICUs) is not standardized and the association of PIR with patient outcome is not well established. Understanding the impact of PIR on outcomes is necessary to optimize senior medical staffing and deliver high-quality care.To test the hypotheses that: (1) there is significant variation in the PIR across ICUs and (2) higher PIRs are associated with higher hospital mortality for ICU patients.Retrospective cohort analysis of patients (≥16 years) admitted to ICUs staffed by a single intensivist during daytime hours in the United Kingdom from 2010 to 2013.Patient-to-intensivist ratios, which we defined for each patient as the number of patients cared for by the intensivist each day averaged over the patient's stay.Using standard summary statistics, we evaluated PIR variation across ICUs. We used multivariable, mixed-effect, logistic regression analysis to evaluate the association between PIR and hospital mortality at ultimate discharge from acute hospital (primary outcome) and at ICU discharge.Among 49 686 adults in 94 ICUs, median age was 66 (interquartile range [IQR], 52-76) years, and 45.1% were women. The ultimate hospital mortality was 25.7%. The median PIR for patients was 8.5 (IQR, 6.9-10.8; full range, 1.0-23.5), and varied substantially among individual ICUs. The association between PIR and ultimate hospital mortality was U-shaped; there was a reduction in the odds of mortality associated with an increasing PIR up to 7.5 after which the odds of mortality increased again significantly (average patient mortality for lowest PIR, 22%; PIR of 7.5, 15%; highest PIR, 19%; P = .003). A similar U-shaped association was seen for PIR and mortality in the ICU (nadir of mortality at a PIR of 7.8, P < .001).PIR varied across UK ICUs. The optimal PIR in this cohort of UK ICU patients was 7.5, with significantly increased ICU and hospital mortality above and below this ratio. The number of patients cared for by 1 intensivist may impact patient outcomes.
Treatment Failure Is Strongly Predicted by P-Glycoprotein (Pgp) Function but Not by Multidrug Resistance Protein (MRP-1), Breast Cancer Resistance Protein (BCRP) or Lung Resistance Protein (LRP) in Acute Myeloid Leukemia (AML) Patients 60 Years and Older Receiving Intensive Chemotherapy (CALGB 9720/9760).
Authors: Maria R. Baer, Nicholas W. Cuviello, Jennifer S. Shoemaker, Robert C. Barrier, Michael A. Caligiuri, Jonathan E. Kolitz, Bayard L. Powell, Richard A. Larson, Clara D. Bloomfield
Journal: Blood (2005)
Genetic Drivers of Kidney Defects in the DiGeorge Syndrome
Authors: Esther Lopez-Rivera, Yangfan P. Liu, Miguel Verbitsky, Blair R. Anderson, Valentina P. Capone, Edgar A. Otto, Zhonghai Yan, Adele Mitrotti, Jeremiah Martino, Nicholas J. Steers, David A. Fasel, Katarina Vukojevic, Rong Deng, Silvia E. Racedo, Qingxue Liu, Max Werth, Rik Westland, Asaf Vivante, Gabriel S. Makar, Monica Bodria, Matthew G. Sampson, Christopher E. Gillies, Virginia Vega-Warner, Mariarosa Maiorana, Donald S. Petrey, Barry Honig, Vladimir J. Lozanovski, Rémi Salomon, Laurence Heidet, Wassila Carpentier, Dominique Gaillard, Alba Carrea, Loreto Gesualdo, Daniele Cusi, Claudia Izzi, Francesco Scolari, Joanna A.E. van Wijk, Adela Arapovic, Mirna Saraga-Babic, Marijan Saraga, Nenad Kunac, Ali Samii, Donna M. McDonald-McGinn, Terrence B. Crowley, Elaine H. Zackai, Dorota Drozdz, Monika Miklaszewska, Marcin Tkaczyk, Przemyslaw Sikora, Maria Szczepanska, Malgorzata Mizerska-Wasiak, Grazyna Krzemien, Agnieszka Szmigielska, Marcin Zaniew, John M. Darlow, Prem Puri, David Barton, Emilio Casolari, Susan L. Furth, Bradley A. Warady, Zoran Gucev, Hakon Hakonarson, Hana Flogelova, Velibor Tasic, Anna Latos-Bielenska, Anna Materna-Kiryluk, Landino Allegri, Craig S. Wong, Iain A. Drummond, Vivette D’Agati, Akira Imamoto, Jonathan M. Barasch, Friedhelm Hildebrandt, Krzysztof Kiryluk, Richard P. Lifton, Bernice E. Morrow, Cecile Jeanpierre, Virginia E. Papaioannou, Gian Marco Ghiggeri, Ali G. Gharavi, Nicholas Katsanis, Simone Sanna-Cherchi
Journal: New England Journal of Medicine (2017)

The DiGeorge syndrome, the most common of the microdeletion syndromes, affects multiple organs, including the heart, the nervous system, and the kidney. It is caused by deletions on chromosome 22q11.2; the genetic driver of the kidney defects is unknown.
Defibrotide for the Treatment of Hepatic Veno-Occlusive Disease/Sinusoidal Obstruction Syndrome with Multi-Organ Dysfunction: Final Results from a Pivotal, Historically Controlled, Phase 3 Trial
Authors: Paul G. Richardson, Marcie Riches, Nancy A. Kernan, Joel A. Brochstein, Shin Mineishi, Amanda M. Termuhlen, Sally Arai, Stephan A. Grupp, Eva C. Guinan, Paul L. Martin, Gideon Steinbach, Amrita Krishnan, Eneida R. Nemecek, Sergio A. Giralt, Tulio E. Rodriguez, Reggie Duerst, John J. Doyle, Joseph H. Antin, Angela R. Smith, Leslie E. Lehmann, Richard E. Champlin, Alfred Gillio, Rajinder Bajwa, Ralph B. D'Agostino, Joseph Massaro, Maja Miloslavsky, Robin L. Hume, Massimo Iacobelli, Bijan Nejadnik, Alison L. Hannah, Robert J. Soiffer
Journal: Blood (2015)
Calmodulin Inhibition Rescues the Effects of Ribosomal Protein Deficiency in in Vitro and In Vivo Diamond Blackfan Anemia Models
Authors: Elizabeth R Macari, Alison Taylor, David Raiser, Kavitha Siva, Katherine McGrath, Jessica M Humphries, Johan Flygare, Benjamin L Ebert, Leonard I. Zon
Journal: Blood (2015)
NUP98/JARID1A Is a New Recurrent Genetic Abnormality in Pediatric Acute Megakaryoblastic Leukemia with a Distinct HOX-Gene Expression Pattern
Authors: Jasmijn D.E. de Rooij, Marry M. van den Heuvel-Eibrink, Iris H.I.M. Hollink, Susan T.C.J.M. Arentsen-Peters, H. Berna Beverloo, Janneke F. van Galen, Andre Baruchel, Jan Trka, Dirk Reinhardt, Edwin Sonneveld, Martin Zimmermann, Todd A. Alonzo, Rob Pieters, Soheil Meshinchi, C. Michel Zwaan
Journal: Blood (2012)
A High Long-Term Survival Were Produced by Early Sequential Intensive Consolidation Chemotherapy Followed by Autologous Stem Cell Transplantation in First Complete Remission in Patients with Adult Acute Lymphoblastic Leukemia.
Authors: Dehui Zou, Lugui Qiu, Yenan Li, Yaozhong Zhao, Mingzhe Han, Sizhou Feng
Journal: Blood (2008)
Characterization of HDACI OSU42 as a Novel Histone Deacetylase Inhibitor in AML Cell Lines.
Authors: Jin Sun, Shujun Liu, Jianhua Yu, Min Wei, Charlene Mao, Haiming Ding, Jessica Kearney, LeNguyen Huynh, Peter Paschka, Dachun Wang, Rebecca B. Klisovic, Danilo Perrotti, Ching-shih Chen, Williom George Blum, Guido Marcucci
Journal: Blood (2006)
Discovery and functional prioritization of Parkinson’s disease candidate genes from large-scale whole exome sequencing
Authors: Iris E. Jansen, Hui Ye, Sasja Heetveld, Marie C. Lechler, Helen Michels, Renée I. Seinstra, Steven J. Lubbe, Valérie Drouet, Suzanne Lesage, Elisa Majounie, J. Raphael Gibbs, Mike A. Nalls, Mina Ryten, Juan A. Botia, Jana Vandrovcova, Javier Simon-Sanchez, Melissa Castillo-Lizardo, Patrizia Rizzu, Cornelis Blauwendraat, Amit K. Chouhan, Yarong Li, Puja Yogi, Najaf Amin, Cornelia M. van Duijn, Huw R. Morris, Alexis Brice, Andrew B. Singleton, Della C. David, Ellen A. Nollen, Shushant Jain, Joshua M. Shulman, Peter Heutink
Journal: Genome biology (2017)

Whole-exome sequencing (WES) has been successful in identifying genes that cause familial Parkinson's disease (PD). However, until now this approach has not been deployed to study large cohorts of unrelated participants. To discover rare PD susceptibility variants, we performed WES in 1148 unrelated cases and 503 control participants. Candidate genes were subsequently validated for functions relevant to PD based on parallel RNA-interference (RNAi) screens in human cell culture and Drosophila and C. elegans models. Assuming autosomal recessive inheritance, we identify 27 genes that have homozygous or compound heterozygous loss-of-function variants in PD cases. Definitive replication and confirmation of these findings were hindered by potential heterogeneity and by the rarity of the implicated alleles. We therefore looked for potential genetic interactions with established PD mechanisms. Following RNAi-mediated knockdown, 15 of the genes modulated mitochondrial dynamics in human neuronal cultures and four candidates enhanced α-synuclein-induced neurodegeneration in Drosophila. Based on complementary analyses in independent human datasets, five functionally validated genes—GPATCH2L, UHRF1BP1L, PTPRH, ARSB, and VPS13C—also showed evidence consistent with genetic replication. By integrating human genetic and functional evidence, we identify several PD susceptibility gene candidates for further investigation. Our approach highlights a powerful experimental strategy with broad applicability for future studies of disorders with complex genetic etiologies.
High Efficiency of ICE (Ifosfamide-Carboplatin-Etoposide) in Relapse/Refractory Primary Central-Nervous System and Intra-Ocular Non Hodgkin Lymphoma, After First Line Treatment Containing High Doses of Methotrexate and Cytarabine. A Monocentric Retrospective Study From 2010 to 2012 On 17 Cases
Authors: Sylvain Choquet, Damien roos Weil, Khe Hoang Xuan, Nathalie Cassoux, Helene Merle-Beral, Veronique Leblond
Journal: Blood (2012)
Downs Syndrome Patients with Acute Lymphoblastic Leukemia; an Intermediate Outcome with a High Infectious Morbidity.
Authors: Mahasen Saleh, Ashraf R. Khairy, Hassan El-Solh, Mohammed Al-Mahr, Abdulrahman Al-Musa, Amel Al-Seraihy, Ali Al-Ahmari, Asim F. Belgaumi
Journal: Blood (2006)
Dysregulated Distribution of Naïve and Memory FoxP3 Positive Regulatory T-Cells Associated with Anemia in Myelodysplastic Syndrome (MDS)
Authors: Chiharu Sugimori, JianXiang Zou, Christine O’Keefe, Michael Clemente, Tie-Ying Wei, Jaroslaw Maciejewski, Thomas P. Loughran, Ron Paquette, Alan F. List, P.K. Epling-Burnette
Journal: Blood (2008)
IMMUNITY IN MUMPS
Authors: Elizabeth P. Maris, John F. Enders, Joseph Stokes, Lewis W. Kane
Journal: The Journal of Experimental Medicine (1946)

Of 163 persons giving positive complement fixation tests who were exposed to mumps, 1 afterwards developed the disease; of 285 negative reactors similarly exposed, 56 afterwards came down with mumps. Of 78 individuals subjected to intimate exposure to mumps whose tests were originally negative and who failed to develop the disease, 41 per cent gave positive reactions when tested 1 month later. Seventy-seven per cent of complement fixation tests done on the sera of 565 normal adults who admitted a previous attack of mumps were positive. A similar correlation was recorded in tests on the sera of a small group of children with positive histories. Of 356 medical students admitting previous attacks, 80 per cent gave positive tests. Of 386 normal adults who denied previous attacks, 42 per cent gave positive tests; of 85 children giving negative histories, 38 per cent reacted positively. The results of complement fixation tests on the sera of 1665 normal adults (over 17 years) and 679 children (1 to 17 years) are recorded. It has been shown that 63 per cent of the adults and 57 per cent of the children had antibody in their blood which reacted with the virus of mumps. In groups in which exceptionally intense exposure was not known to have occurred in the past, the proportions of positive reactors were: adults, 61 per cent; children, 49 per cent. In contrast to these normal persons, the incidence of positive reactors among permanently institutionalized mental defectives was 38 per cent of 356 adults and 32 per cent of 475 children. In only 2 per cent of 320 normal adults and children did the titer of complement-fixing antibody reach 1–192. In no instance in which the endpoint was determined was a higher titer recorded. The results of complement fixation tests on the sera of mother and newborn infant were essentially the same in 5 instances.
Dendritic Cells Recovery and Chimerism after Reduced Intensity Hematopoietic Stem Cell Transplantation.
Authors: Reza Tabrizi, Francis Belloc, Xavier Lafarge, Virginie Perreau, Krimo Bouabdallah, Gerald Marit, Fontanet Bijou, Thibaut Leguay, Francis Lacombe, Arnaud Pigneux, Cyril Melot, François Comeau, Jean-Michel Boiron
Journal: Blood (2005)
Analysis of Cytogenetic Abnormalities and Their Prognostic Impact in a Series of 145 Mantle Cell Lymphoma Cases with An Abnormal Karyotype.
Authors: Blanca Espinet, Salaverría Itziar, Sílvia Beà, Neus Ruiz-Xivillé, Olga Balagué, Marta Salido, Dolors Costa, Ana E Rodriguez, Juan LuíS. García, JesúS. M.ª Hernández-Rivas, M.ª José Calasanz, Ana M Ferrer, Antonio Salar, Ana Carrió, Natividad Polo, Jose Antonio García-Marco, Alicia Domingo, Eva González-Barca, Vicenç Romagosa, Isabel Marugán, Armando López-Guillermo, Fuensanta Millá, José Luís Mate, Elisa Luño, Carmen Sanzo, Rosa Collado, Isabel Oliver, Sebastià Monzó, Antonio Palacín, Teresa González, Francesc Sant, Ramon Salinas, Mª Teresa Ardanaz, Llorenç Font, Lourdes Escoda, Lourdes Florensa, Elias Campo, Sergi Serrano, Francesc Solé
Journal: Blood (2008)
Thrombospondin-2 promotes prostate cancer bone metastasis by the up-regulation of matrix metalloproteinase-2 through down-regulating miR-376c expression
Authors: Po-Chun Chen, Chih-Hsin Tang, Liang-Wei Lin, Chun-Hao Tsai, Cheng-Ying Chu, Tien-Huang Lin, Yuan-Li Huang
Journal: Journal of Hematology & Oncology (2017)

Thrombospondin-2 (TSP-2) is a secreted matricellular glycoprotein that is found to mediate cell-to-extracellular matrix attachment and participates in many physiological and pathological processes. The expression profile of TSP-2 on tumors is controversial, and it up-regulates in some cancers, whereas it down-regulates in others, suggesting that the functional role of TSP-2 on tumors is still uncertain. The expression of TSP-2 on prostate cancer progression was determined in the tissue array by the immunohistochemistry. The molecular mechanism of TSP-2 on prostate cancer (PCa) metastasis was investigated through pharmaceutical inhibitors, siRNAs, and miRNAs analyses. The role of TSP-2 on PCa metastasis in vivo was verified through xenograft in vivo imaging system. Based on the gene expression omnibus database and immunohistochemistry, we found that TSP-2 increased with the progression of PCa, especially in metastatic PCa and is correlated with the matrix metalloproteinase-2 (MMP-2) expression. Additionally, through binding to CD36 and integrin ανβ3, TSP-2 increased cell migration and MMP-2 expression. With inhibition of p38, ERK, and JNK, the TSP-2-induced cell migration and MMP-2 expression were abolished, indicating that the TSP-2's effect on PCa is MAPK dependent. Moreover, the microRNA-376c (miR-376c) was significantly decreased by the TSP-2 treatment. Furthermore, the TSP-2-induced MMP-2 expression and the subsequent cell motility were suppressed upon miR-376c mimic stimulation. On the other hand, the animal studies revealed that the bone metastasis was abolished when TSP-2 was stably knocked down in PCa cells. Taken together, our results indicate that TSP-2 enhances the migration of PCa cells by increasing MMP-2 expression through down-regulation of miR-376c expression. Therefore, TSP-2 may represent a promising new target for treating PCa.
Stage-Specific Switches in Alternative Pre-mRNA Splicing during Late Erythropoiesis Are Conserved from Mouse to Human
Authors: Sherry Gee, Jonathan Villalobos, Miki Yamamoto, Tyson A. Clark, Jeong-Ah Kang, Amittha Wickrema, Joel Anne Chasis, john G. Conboy
Journal: Blood (2008)
De novo and rare mutations in the HSPA1L heat shock gene associated with inflammatory bowel disease
Authors: Shinichi Takahashi, Gaia Andreoletti, Rui Chen, Yoichi Munehira, Akshay Batra, Nadeem A. Afzal, R. Mark Beattie, Jonathan A. Bernstein, Sarah Ennis, Michael Snyder
Journal: Genome Medicine (2017)

Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disease of the gastrointestinal tract which includes ulcerative colitis and Crohn's disease. Genetic risk factors for IBD are not well understood. We performed a family-based whole exome sequencing (WES) analysis on a core family (Family A) to identify potential causal mutations and then analyzed exome data from a Caucasian pediatric cohort (136 patients and 106 controls) to validate the presence of mutations in the candidate gene, heat shock 70 kDa protein 1-like (HSPA1L). Biochemical assays of the de novo and rare (minor allele frequency, MAF < 0.01) mutation variant proteins further validated the predicted deleterious effects of the identified alleles. In the proband of Family A, we found a heterozygous de novo mutation (c.830C > T; p.Ser277Leu) in HSPA1L. Through analysis of WES data of 136 patients, we identified five additional rare HSPA1L mutations (p.Gly77Ser, p.Leu172del, p.Thr267Ile, p.Ala268Thr, p.Glu558Asp) in six patients. In contrast, rare HSPA1L mutations were not observed in controls, and were significantly enriched in patients (P = 0.02). Interestingly, we did not find non-synonymous rare mutations in the HSP70 isoforms HSPA1A and HSPA1B. Biochemical assays revealed that all six rare HSPA1L variant proteins showed decreased chaperone activity in vitro. Moreover, three variants demonstrated dominant negative effects on HSPA1L and HSPA1A protein activity. Our results indicate that de novo and rare mutations in HSPA1L are associated with IBD and provide insights into the pathogenesis of IBD, and also expand our understanding of the roles of HSP70s in human disease.
Preliminary SAR study on a novel inhibitor of the apoptosis suppressor Bcl proteins
Authors: Giorgio Attardo, Laurent Belec, Kenza Dairi, Lionel Dumas, Gerson Gonzales, Jean-Francois Lavallee, Mathieu Lemay, Valerie Perron, Elise Rioux, Sasmita Tripathy, Angela Babineau, Helen Chan, Gang Chen, Gaetan Gagnon, Anne Jang, Abdelkrim Khadir, Richard Marcellus, Denis Paquette, Anne Roulston, Nancy Steenaart, Mark Watson, Zhiying Zhang, Daniel Goulet, Pierre Beauparlant, Gordon Shore
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

1207 

GX15 is a naturally occuring substance that was recently reported to be a novel inhibitor of the Bcl-2 family of apoptosis suppressor proteins. Furthermore, it exhibited cytotoxicity in several cancer cell lines. Structure-activity-relationship (SAR) studies were initiated by preparing semi-synthetic derivatives from the natural product and by total synthesis. A series of structurally simple analogs of GX15 was found to be potently cytotoxic in vitro. A good inhibitory profile towards Bcl antiapoptotic proteins was obtained with several analogs.
Histone Profiling of Normal B-Precursors and Primary Pre-B Acute Lymphoblastic Leukemia Reveals Distinct Aberrant Histone Codes In MLL-Rearranged Vs. Wild Type MLL Leukemias That Correlate with Differential Expression of Key MLL Target Genes
Authors: Sandeep S. Negi, Eric S. Schafer, Donald Small, Patrick Brown
Journal: Blood (2010)
Primary Waldesntrom Macroglobulinemia Cells Harbor Constitutive Activation of Akt, mTOR, Rictor and Raptor: Rational for Testing a Dual Inhibitor of the PI3K/Akt and mTOR Pathways in This Disease.
Authors: Aldo M. Roccaro, Antonio Sacco, Emanuel N. Husu, Costas M Pitsillides, Steven Vesole, Abdel Kareem Azab, Feda Azab, Molly Melhem, Hai Ngo, Phong Quang, Patricia Maiso, Judith M. Runnels, Charles P. Lin, Kenneth C. Anderson, Irene Ghobrial
Journal: Blood (2009)
Assessment of Early Evidence of Multiple Sclerosis in a Prospective Study of Asymptomatic High-Risk Family Members
Authors: Zongqi Xia, Sonya U. Steele, Anshika Bakshi, Sarah R. Clarkson, Charles C. White, Matthew K. Schindler, Govind Nair, Blake E. Dewey, Lauren R. Price, Joan Ohayon, Lori B. Chibnik, Irene C. M. Cortese, Philip L. De Jager, Daniel S. Reich
Journal: JAMA Neurology (2017)

<h3>Importance</h3> Subclinical inflammatory demyelination and neurodegeneration often precede symptom onset in multiple sclerosis (MS). <h3>Objective</h3> To investigate the prevalence of brain magnetic resonance imaging (MRI) and subclinical abnormalities among asymptomatic individuals at risk for MS. <h3>Design, Setting, and Participants</h3> The Genes and Environment in Multiple Sclerosis (GEMS) project is a prospective cohort study of first-degree relatives of people with MS. Each participant's risk for MS was assessed using a weighted score (Genetic and Environmental Risk Score for Multiple Sclerosis Susceptibility [GERS<sub>MS</sub>]) comprising an individual's genetic burden and environmental exposures. The study dates were August 2012 to July 2015. <h3>Main Outcomes and Measures</h3> Participants in the top and bottom 10% of the risk distribution underwent standard and quantitative neurological examination, including disability status, visual, cognitive, motor, and sensory testing, as well as qualitative and quantitative neuroimaging with 3-T brain MRI and optical coherence tomography. <h3>Results</h3> This study included 100 participants at risk for MS, with 41 at higher risk (40 women [98%]) and 59 at lower risk (25 women [42%]), at a mean (SD) age of 35.1 (8.7) years. Given the unequal sex distribution between the 2 groups, the analyses were restricted to women (n = 65). When considering all measured outcomes, higher-risk women differed from lower-risk women (<i>P</i> = .01 by omnibus test). Detailed testing with a vibration sensitivity testing device in a subgroup of 47 women showed that higher-risk women exhibited significantly poorer vibration perception in the distal lower extremities (<i>P</i> = .008, adjusting for age, height, and testing date). Furthermore, 5 of 65 women (8%) (4 at higher risk and 1 at lower risk) met the primary neuroimaging outcome of having T2-weighted hyperintense brain lesions consistent with the 2010 McDonald MRI criteria for dissemination in space. A subset of participants harbor many different neuroimaging features associated with MS, including perivenous T2-weighted hyperintense lesions and focal leptomeningeal enhancement, consistent with the hypothesis that these individuals are at higher risk of developing clinical symptoms of MS than the general population. <h3>Conclusions and Relevance</h3> Higher-risk asymptomatic family members of patients with MS are more likely to have early subclinical manifestations of MS. These findings underscore the importance of early detection in high-risk individuals. <h3>Trial Registration</h3> clinicaltrials.gov Identifier:NCT01353547
Therapy Related APL (tAPL). Prospective Analysis of Etiological Factors In Recent Cases, and Comparison with De Novo Cases
Authors: Sophie Cereja, Sylvie Chevret, Emmanuel Raffoux, Marie Beaumont, Laurence Detourmignies, Arnaud Pigneux, Xavier Thomas, Dominique Bordessoule, Norbert Vey, Agnès Guerci, Thierry Lamy, Christian Récher, Beatrice Mueller, Olivier Tournilhac, Cécile Pautas, Jean-Yves Cahn, Jacques Delaunay, Denis Guyotat, Eric Deconinck, Bruno Quesnel, Aspasia Stamatoullas, Christine Chomienne, Laurent Degos, Herve Dombret, Pierre Fenaux, Lionel Ades
Journal: Blood (2010)