tbuckley/cabot-search huggingface dataset:
Integration of Genomic and Genetic Approaches Highlight a Novel Validated Gene Signature for Pulmonary Hypertension Associated with Sickle Cell Disease
Authors: Ankit A Desai, Homaa Ahmad, Tong Zhou, Wei Zhang, Sharon Trevino, Michael Wade, Nalini Raghavachari, Gregory J. Kato, Tejasi Thiruvoipati, Kristin Turner, Nicole Artz, Amit R Patel, Jason × Yuan, Victor R. Gordeuk, Roberto M Lang, Joe GN Garcia, Roberto F. Machado
Journal: Blood (2011)
Phase II Trial of WT1 Analog Peptide Vaccine in Patients with Acute Myeloid Leukemia (AML) in Complete Remission (CR)
Authors: Todd L. Rosenblat, Mark G. Frattini, Suzanne M. Chanel, Tao Dao, Yvette Bernal, Joseph G. Jurcic, Rhong Zhang, Pamela Simancek, Martin S Tallman, David A. Scheinberg, Peter G. Maslak
Journal: Blood (2012)
Aspirin After Oral Anticoagulants for Prevention of Recurrence in Patients with Unprovoked Venous Thromboembolism. the Warfasa STUDY
Authors: Cecilia Becattini, Giancarlo Agnelli, Renzo Poggio, Sabine Eichinger, Eugenio Bucherini, Mauro Silingardi, Marina Bianchi, Marco Moia, Walter Ageno, Maria Rita Vandelli, Elvira Grandone, Sergio Siragusa, Rosamaria Salvi, Luigi Ria, Nello Zanatta, Daniela Poli, Giuseppe Camporese, Aldo Salvi, Roberto Santi, Claudio Cimminiello, Gianluigi Scannapieco, Giovanni Barillari, Egidio De Gaudenzi, Roberto Cappelli, Giovanni di Minno, Gabriele Frausini, Carlo Bova, Paolo Prandoni
Journal: Blood (2011)
A Novel and Efficient Induction Approach for Accelerated Differentiation and Rapid Hematopoietic Recovery in Acute Promyelocytic Leukemia (APL) Patients by Combining All-Trans Retinoic Acid (ATRA) with Granulocyte-Colony Stimulating Factor (G-CSF).
Authors: Shripad D. Banavali, Lovenish Goyal, Reena Nair, Prasad Narayan, Brijesh Arora, Pratibha Amre-Kadam, Chanda Baisane, Shashikant Mahadik, Sumit Gujral, Purna A. Kurkure, Purvish M. Parikh
Journal: Blood (2006)
Compare The Outcome Of Patients With Hematological Malignancies Treated With Allogeneic Stem Cell Transplant In Patients Age Over 50 Conditioned With Reduce Intensity Regimens With Those Under 50 Conditioned With Standard Intensity Regimen In a Rural University Hospital – A Single Institution Experience
Authors: Luke N. D'Cunha, Nicholas C. D'Cunha, Deanna Harville, Everardo Cobos
Journal: Blood (2013)
P0262 : Inhibition of regulatory T cells using the FOXP3-inhibitory peptide P60 improves antitumoural effect of a vaccination with mAFP-expressing DC in subcutaneous and orthotopic murine HCC model
Authors: J. Waysczak, A. Vogt, N. Casares, J.J. Lasarte, J. Prieto, I. Schmidt-Wolf, C.P. Strassburg, M.A. Gonzalez-Carmona
Journal: Journal of Hepatology (2015)
AB0012 Genetic Signatures in Rheumatoid Arthritis: Changes upon Anti-TNF Therapy and Association with Response To Biological Treatment
Authors: S. Poliska, E. Végh, A. Váncsa, S. Szamosi, M. Csumita, G. Zahuczky, G. Szücs, S. Szántό, L. Nagy, Z. Szekanecz
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Genetic signatures may be involved in the pathogenesis of rheumatoid arthritis (RA) and ankylosing spondylitis (AS). In addition, such genetic patterns may change overtime upon treatment with anti-TNF biologics. With respect to pharmacogenomics, pre-treatment genomics may predict response or non-response to biological therapy. <h3>Objectives</h3> In the present study, we wished to determine gene expression changes due to anti-TNF therapy. Furthermore, we wished to study associations between baseline genetic signature and response to TNF blockade. <h3>Methods</h3> Altogether 23 RA and 17 AS patients were recruited for the study. Among RA patients, 10 received certolizumab pegol (CZP), and 13 etanercept (ETN). All AS patients were treated with ETN. Gene expression analysis using Affymetrix microarray and PrimeView array was performed at baseline and after 2 weeks of treatment. EULAR response criteria were used to differentiate responders (R) from non-responders (NR) after 12 weeks of treatment using GeneSpring software. Principal Component Analysis (PCA) was also performed. Changes in gene expression patterns were also determined between baseline and 2 weeks. <h3>Results</h3> In the CZP-treated RA group, 4 patients were R and 6 were NR. Altogether 453 genes showed significantly differential expression between N and NR. In the RA-ETN group, 10 patients were R, and 3 were NR. Here, 836 genes exerted differential expression. When a CZP- and ETN-treated patients, were pooled, 165 genes separated R from NR. In the AS population, 14 patients were R and 3 were NR. 177 genes differentiated between R and NR. When changes in gene expression patterns from baseline to week 2 were determined, in the RA-CZP, RA-ETN, RA-all and AS groups 370, 79, 24 and 76 genes showed significant changes in expression. <h3>Conclusions</h3> Using microarray, genetic signatures may differentiate RA patients responding or not responding to anti-TNF therapy. Furthermore, a large set of genes show differential expression before versus 2 weeks after biologic treatment. <h3>Disclosure of Interest</h3> None declared
SP0015 Pain Trajectory Groups in Persons with Osteoarthritis
Authors: G.M. Peat
Journal: Annals of the Rheumatic Diseases (2016)

Pain in persons with osteoarthritis does not follow a simple, single, immutable 9natural history9. In recent years several prospective cohorts using repeated measures of patient-reported health states have matured and there has been a flurry of publications on the existence of discrete developmental trajectories of reported pain severity and other states. What does it all add up to? And what does it teach us about concepts of time, heterogeneity, and prognosis in OA? This presentation will (i) briefly introduce the rationale and assumptions underlying these methods, (ii) review published findings when applied to pain and other patient-reported health states in osteoarthritis, (iii) discuss implications of these findings for research and clinical practice, (iv) contemplate productive directions for future investigation in this field. <h3>Disclosure of Interest</h3> None declared
Antioxidant Vitamins C and E Supplementation Does Not Improve the Hemolytic Profile of Sickle Cell Anemia Patients: A Randomized, Double-Blind, Placebo-Controlled Trial
Authors: Martha Mariana A S Arruda, Grazielle Mecabo, Celso Arrais Rodrigues, Sandra S Matsuda, Iara Baldim Rabelo, Maria Stella Figueiredo
Journal: Blood (2011)
Plk4 Promotes Cancer Invasion and Metastasis through Arp2/3 Complex Regulation of the Actin Cytoskeleton
Authors: Karineh Kazazian, Christopher Go, Hannah Wu, Olga Brashavitskaya, Roland Xu, James W. Dennis, Anne-Claude Gingras, Carol J. Swallow
Journal: Cancer Research (2016)

Abstract The polo family serine threonine kinase Plk4 has been proposed as a therapeutic target in advanced cancers based on increased expression in primary human cancers, facilitation of tumor growth in murine xenograft models, and centrosomal amplification induced by its overexpression. However, both the causal link between these phenomena and the feasibility of selective Plk4 inhibition remain unclear. Here we characterize Plk4-dependent cancer cell migration and invasion as well as local invasion and metastasis of cancer xenografts. Plk4 depletion suppressed cancer invasion and induced an epithelial phenotype in poorly differentiated breast cancer cells. In an unbiased BioID screen for Plk4 interactors, we identified members of the Arp2/3 complex and confirmed a physical and functional interaction between Plk4 and Arp2 in mediating Plk4-driven cancer cell movement. This interaction is mediated through the Plk4 Polo-box 1-Polo-box 2 domain and results in phosphorylation of Arp2 at the T237/T238 activation site, which is required for Plk4-driven cell movement. Our results validate Plk4 as a therapeutic target in cancer patients and reveal a new role for Plk4 in regulating Arp2/3-mediated actin cytoskeletal rearrangement. Cancer Res; 77(2); 434–47. ©2016 AACR.
“Hep C, where art thou”: What are the remaining (fundable) questions in hepatitis C virus research?
Authors: Hugo Ramón Rosen
Journal: Hepatology (2016)

Hepatitis C virus (HCV) has dominated the field of hepatology for the past 25 years, and its cure in the majority of treated patients is one of the greatest achievements in all of medicine. However, the latter has led to the belief by some that HCV research should be shelved for other, more pressing areas. The mission for HCV eradication is far from accomplished. As a historical reference, we should consider that disease elimination has required vaccination with all previously controlled infections including smallpox and polio and that simple, effective treatment is not sufficient in most infections to lead to substantial control. Syphilis is the best example, for which a single dose of penicillin (which literally costs pennies and that we have had since 1945) is curative in early stages. Not only have we not eradicated syphilis, rates of infection have increased in many places within the United States in recent years. Most HCV-infected subjects are unaware of their infection, remaining at risk for transmission to others and disease progression, including cirrhosis and hepatocellular carcinoma. In the era of highly effective direct-acting antivirals (DAAs), many questions pertaining to HCV remain, but they are more complex and difficult to answer. Here, I provide my perspective on some of these salient issues: the residual risk for disease progression after sustained virologic response, the optimal approach to current DAA failures, the impact of targeting people who inject drugs with DAAs, vaccine prospects, and application of neutralizing HCV glycoprotein antibodies. (Hepatology 2017;65:341-349).
THU0563 Characterization of A Group of 6 Patients with Mevalonate Kinase Deficiency: Symptoms and Treatment with IL-1 Inhibitors
Authors: A. Kozlova, N. Kuzmenko, S. Zimin, T. Varlamova, A. Shcherbina
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Mevalonate kinase deficiency (MKD) is a rare autosomal recessive autoinflammatory disease caused by mutations in MVK gene. MKD patients typically have an early onset of symptoms including recurrent episodes of high fever, abdominal pain, diarrhea and vomiting, arthralgia and lymphadenopathy. However not all patients have typical clinical picture of MKD. <h3>Methods</h3> We conducted a retrospective analysis of clinical features of six patients (4 females, 2 males) with MKD (confirmed by identification of MVK gene mutations). Four patients received therapy with inhibitors of IL-1 (Anakinra and/or Canakinumab). One of the patients died from amyloidosis and macrophage activation syndrome (MAS) prior to treatment initiation, her diagnosis was verified <i>post mortem</i>. <h3>Results</h3> All patients had the first symptoms of disease within the first 6 months of life. During the course of the disease all patients had periodic fever and peripheral lymphadenopathy (mainly cervical group), as well as abdominal pain, nausea/vomiting. Five patients had diarrhea, sometimes with blood, one patient suffered from severe constipation. Rash was seen in five patients, myalgia, artralgia were observed only in four. Oral ulcers were noted in two children. Two patients had neurological involvement. Interestingly, five out of six patients had rhinitis during attacks. One patient during the attack had periorbital edema and hyperemia, which; to our knowledge, have not been reported previously in MKD. One patient developed amyloidosis and MAS before treatment initiation, which led to her death. In patients receiving anti-IL-1 therapy AIDAI index decreased from 49.5±14,6 before to 1,75±1,3 after 6 month of therapy (p=0.003). <h3>Conclusions</h3> MKD symptoms can be variable and sometimes atypical, which requires physician9s awareness. In our small cohort of MKD patients anti IL-1 therapy was highly effective. <h3>Disclosure of Interest</h3> None declared
CBL, CBLB, TET2, ASXL1, and IDH1/2 Mutations as Well as Additional Chromosomal Aberrations Constitute Molecular Events Contributing to Malignant Progression In Advanced Philadelphia Chromosome-Positive Disorders.
Authors: Hideki Makishima, Anna Jankowska, Michael A McDevitt, Simon Dujardin, Heather Cazzolli, Bartlomiej Przychodzen, Courtney Prince, John Nicoll, Siddaiah Harish, Mohammed Shaik, Eric Hsi, Anjali Advani, Ronald Paquette, Jaroslaw P Maciejewski
Journal: Blood (2010)
Hepatitis E Virus and Guillain-Barré Syndrome
Authors: Kenneth L. Tyler, Daniel M. Pastula
Journal: JAMA Neurology (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
Risk of HHV6-Associated Post-Transplant Acute Limbic Encephalitis (PALE) after Umbilical Cord Blood Stem Cell Transplantation: A Cohort Analysis.
Authors: Francisco M. Marty, Vincent T. Ho, William W. Seeley, Corey S. Cutler, John Koreth, Edwin P. Alyea, Robert J. Soiffer, Joseph H. Antin, Lindsey R. Baden
Journal: Blood (2006)
Trans-Atlantic Consensus on the Medical Management of Radiation Accident Victims
Authors: Bhawna Sirohi, Raymond Powles, Dietger Niederweiser, Norm Coleman, Nelson J. Chao, Judith Bader, Cullen Case, John Chute, Dennis L. Confer, Patrick Gourmelon, Norbert C Gorin, Arnold Ganser, Matthias Port, Viktor Meineke, Robert Krawisz, David M Weinstock, Albert Wiley, Ted Fliedner
Journal: Blood (2008)
TET2 Mutations Revealed by Whole Genome Sequencing in Adult T-Cell Leukemia.
Authors: Yasunobu Nagata, Aiko Sato, Ayana Kon, Yusuke Okuno, Kenichi Chiba, Hiroko Tanaka, Yuichi Shiraishi, Kenichi Yoshida, Masashi Sanada, Atae Utsunomiya, Kazunari Yamaguchi, Kouichi Oshima, Shuichi Miyawaki, Akira Kitanaka, Satoru Miyano, Toshiki Watanabe, Seishi Ogawa
Journal: Blood (2012)
Pocket-sized epidemiology
Authors: David D Celentano
Journal: The Lancet Infectious Diseases (2016)

The Oxford Specialist Handbooks seek to provide concise references for trainees and practitioners in a host of specialities; this recent volume, Infectious Disease Epidemiology, was designed as a quick reference guide to comprehensively review the topic for students and practicing infectious disease specialists. The handbook has two sections: section 1 covers the basic epidemiological methods common to all investigations, with special emphasis on recent methodological approaches relevant to infectious disease investigations; section 2 reviews the epidemiological features of the most commonly confronted infections internationally.
Endothelial Microparticles From Acute Coronary Syndrome Patients Induce Premature Coronary Artery Endothelial Cell Aging and Thrombogenicity
Authors: Malak Abbas, Laurence Jesel, Cyril Auger, Lamia Amoura, Nathan Messas, Guillaume Manin, Cordula Rumig, Antonio J. León-González, Thais P. Ribeiro, Grazielle C. Silva, Raghida Abou-Merhi, Eva Hamade, Markus Hecker, Yannick Georg, Nabil Chakfe, Patrick Ohlmann, Valérie B. Schini-Kerth, Florence Toti, Olivier Morel
Journal: Circulation (2016)

Microparticles (MPs) have emerged as a surrogate marker of endothelial dysfunction and cardiovascular risk. This study examined the potential of MPs from senescent endothelial cells (ECs) or from patients with acute coronary syndrome (ACS) to promote premature EC aging and thrombogenicity.Primary porcine coronary ECs were isolated from the left circumflex coronary artery. MPs were prepared from ECs and venous blood from patients with ACS (n=30) and from healthy volunteers (n=4) by sequential centrifugation. The level of endothelial senescence was assessed as senescence-associated β-galactosidase activity using flow cytometry, oxidative stress using the redox-sensitive probe dihydroethidium, tissue factor activity using an enzymatic Tenase assay, the level of target protein expression by Western blot analysis, platelet aggregation using an aggregometer, and shear stress using a cone-and-plate viscometer.Senescence, as assessed by senescence-associated β-galactosidase activity, was induced by the passaging of porcine coronary artery ECs from passage P1 to P4, and was associated with a progressive shedding of procoagulant MPs. Exposure of P1 ECs to MPs shed from senescent P3 cells or circulating MPs from ACS patients induced increased senescence-associated β-galactosidase activity, oxidative stress, early phosphorylation of mitogen-activated protein kinases and Akt, and upregulation of p53, p21, and p16. Ex vivo, the prosenescent effect of circulating MPs from ACS patients was evidenced only under conditions of low shear stress. Depletion of endothelial-derived MPs from ACS patients reduced the induction of senescence. Prosenescent MPs promoted EC thrombogenicity through tissue factor upregulation, shedding of procoagulant MPs, endothelial nitric oxide synthase downregulation, and reduced nitric oxide-mediated inhibition of platelet aggregation. These MPs exhibited angiotensin-converting enzyme activity and upregulated AT1 receptors and angiotensin-converting enzyme in P1 ECs. Losartan, an AT1 receptor antagonist, and inhibitors of either mitogen-activated protein kinases or phosphoinositide 3-kinase prevented the MP-induced endothelial senescence.These findings indicate that endothelial-derived MPs from ACS patients induce premature endothelial senescence under atheroprone low shear stress and thrombogenicity through angiotensin II-induced redox-sensitive activation of mitogen-activated protein kinases and phosphoinositide 3-kinase/Akt. They further suggest that targeting endothelial-derived MP shedding and their bioactivity may be a promising therapeutic strategy to limit the development of an endothelial dysfunction post-ACS.
In Myeloma, the Prognostic Impact of Hyperdiploidy Is Mainly Related to the Gain of Chromosome 5
Authors: Herve Avet Loiseau, Cheng Li, Florence Magrangeas, Catherine Guerin, Wilfried Gouraud, Jean-Luc Harousseau, Michel Attal, Gerald Marit, Claire Mathiot, Thierry Facon, Philippe Moreau, Kenneth C Anderson, Loic Campion, Nikhil C. Munshi, Stephane Minvielle
Journal: Blood (2008)
A New Stratification Strategy That Identifies a Subset of Class III Patients among Children with β Thalassemia Major Undergoing a Matched Related Allogeneic Stem Cell Transplantation.
Authors: Vikram Mathews, Biju George, Kavitha M. Lakshmi, Auro Viswabandya, Mammen Chandy, Alok Srivastava
Journal: Blood (2006)
FRI0053 Amelioration of Experimental Arthritis by Dissociating The Binding of P53 Family Members with Inhibitory Apoptosis Stimulating Protein of P53 To Induce Apoptosis in Synovial Fibroblast
Authors: C.-R. Wang, S.-Y. Chen, A.-L. Shiau, I.-M. Jou, M.-F. Liu, C.-L. Wu
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> In rheumatoid arthritis (RA), apoptosis-resistant synovial fibroblasts (SFs) constitute the major cell component of pannus tissues [1]. 37 amino acid (37AA), a hybrid small peptide corresponding to p53 residues, inhibits the binding of p53 family members with inhibitory apoptosis stimulating protein of p53 (iASPP), thus activating the downstream apoptosis signaling pathway in tumor cells [2]. <h3>Objectives</h3> We hypothesized that iASPP is involved in the RA pathogenesis, and examined whether dissociating the binding of p53 family members with this molecule can ameliorate experimental arthritis. <h3>Methods</h3> Synovial tissues and SFs from RA and osteoarthritis patients were subjected to immunohistochemical (IHC) and immunofluorescent staining, respectively, for expression of iASPP and p73, a p53 family member molecule. Synovial tissues from male Sprague-Dawley rats immunized with type II collagen, were analyzed by IHC staining and real-time RT-PCR for expression of iASPP and p73. SFs transfected with adenoviral vectors encoding 37AA (Ad37AA), were subjected to TUNEL assay for apoptotic status and real-time RT-PCR for expression of p53 upregulated modulator of apoptosis (PUMA), a downstream apoptosis signaling molecule. The association of iASPP with p73 in Ad37AA-transfected SFs was identified by immunoprecipitation with anti-iASPP, followed by immunoblot with anti-p73. Therapeutic effects of intra-articular (i.a.) injection with Ad37AA on arthritis rats were evaluated by articular index and histological score. IHC staining was performed to analyze synovial expression of cadherin-11 (a specific SF marker), PUMA and IL-6, and apoptotic cells were detected by the TUNEL assay. <h3>Results</h3> There were increased levels of iASPP with co-localized p73 expression in synovial lining layers and purified SFs from RA patients and arthritis rats. Enhanced cell apoptosis and increased PUMA expression were identified in Ad37AA-transfected SFs with lower iASPP-associated p73 levels. Articular indexes and histologic scores were reduced in Ad37AA-injected joints with decreased SF densities, increased apoptotic cells, higher PUMA expression and lower IL-6 levels. <h3>Conclusions</h3> Our results demonstrate amelioration of experimental arthritis by dissociating the i.a. binding of p53 family members with iASPP to induce apoptosis in SFs, implicating this molecule as a potential therapeutic target in RA patients. <h3>References</h3> Bottini N et al. Nat Rev Rheumatol 2013;9:24–33. Bell HS et al. J Clin Invest 2007;117:1008–18. <h3>Acknowledgement</h3> We thank Dr. Kevin M. Ryan (Cancer Research UK Beatson Institute, Glasgow, UK) for providing pShuttleCMV-37AA adenoviral plasmids. <h3>Disclosure of Interest</h3> None declared