tbuckley/cabot-search huggingface dataset:
A Humanized Anti-CD70 Monoclonal Antibody Targets CD70-Expressing Multiple Myeloma.
Authors: Julie A. McEarchern, Charlotte McDonagh, Allen Ho, Yu-Tzu Tai, Leigh Francisco, Kerry Klussman, Carol Morris-Tilden, Kristine Gordon, Ezogelin Oflazoglu, Kim Kissler, Nikhil Munshi, Kenneth C. Anderson, Steven P. Treon, Paul Carter, Alan F. Wahl, Iqbal S. Grewal, Che-Leung Law
Journal: Blood (2005)
Effectiveness of Fluticasone Furoate–Vilanterol for COPD in Clinical Practice
Authors: Jørgen Vestbo, David Leather, Nawar Diar Bakerly, John New, J. Martin Gibson, Sheila McCorkindale, Susan Collier, Jodie Crawford, Lucy Frith, Catherine Harvey, Henrik Svedsater, Ashley Woodcock
Journal: New England Journal of Medicine (2016)

Evidence for the management of chronic obstructive pulmonary disease (COPD) comes from closely monitored efficacy trials involving groups of patients who were selected on the basis of restricted entry criteria. There is a need for randomized trials to be conducted in conditions that are closer to usual clinical practice.In a controlled effectiveness trial conducted in 75 general practices, we randomly assigned 2799 patients with COPD to a once-daily inhaled combination of fluticasone furoate at a dose of 100 μg and vilanterol at a dose of 25 μg (the fluticasone furoate-vilanterol group) or to usual care (the usual-care group). The primary outcome was the rate of moderate or severe exacerbations among patients who had had an exacerbation within 1 year before the trial. Secondary outcomes were the rates of primary care contact (contact with a general practitioner, nurse, or other health care professional) and secondary care contact (inpatient admission, outpatient visit with a specialist, or visit to the emergency department), modification of the initial trial treatment for COPD, and the rate of exacerbations among patients who had had an exacerbation within 3 years before the trial, as assessed in a time-to-event analysis.The rate of moderate or severe exacerbations was significantly lower, by 8.4% (95% confidence interval, 1.1 to 15.2), with fluticasone furoate-vilanterol therapy than with usual care (P=0.02). There was no significant difference in the annual rate of COPD-related contacts to primary or secondary care. There were no significant between-group differences in the rates of the first moderate or severe exacerbation and the first severe exacerbation in the time-to-event analyses. There were no excess serious adverse events of pneumonia in the fluticasone furoate-vilanterol group. The numbers of other serious adverse events were similar in the two groups.In patients with COPD and a history of exacerbations, a once-daily treatment regimen of combined fluticasone furoate and vilanterol was associated with a lower rate of exacerbations than usual care, without a greater risk of serious adverse events. (Funded by GlaxoSmithKline; Salford Lung Study ClinicalTrials.gov number, NCT01551758 .).
Study on Membrane Fluidity and Oxidative Stress of Platelets with Function Abnormalities in Myelodysplastic Syndromes
Authors: Ana Maria Vladareanu, Viola Maria Popov, Horia Bumbea, Radu Gologan, Eugenia Kovacs, Mihaela Georgeta Moisescu, Minodora Onisai, Maria Minodora Iordache, Tudor Savopol
Journal: Blood (2011)
Comparison of neurobehavioral outcomes in survivors of childhood acute lymphoblastic leukemia (ALL) previously randomized to intrathecal methotrexate vs. intrathecal methotrexate/hydrocortisone/cytarabine
Authors: N. S. Kadan-Lottick, P. Brouwers, T. A. Kaleita, D. Breiger, L. C. Stork, B. C. Bostrom, J. P. Neglia
Journal: Journal of Clinical Oncology (2008)

10033 Background: Intrathecal medications have replaced cranial radiation for central nervous system (CNS) prophylaxis in most patients with ALL. The relative long-term toxicities of different intrathecal preparations are uncertain. The objective of this study is to compare neurobehavioral outcomes of children with ALL randomized on a legacy Children’s Oncology Group study to either intrathecal methotrexate (MTX) or methotrexate/hydrocortisone/cytarabine (ITT). Methods: Cross-sectional study at 32 sites. The neurobehavioral evaluation included: Wechsler Intelligence Scale for Children-IV (WISC-IV), Wechsler Individual Achievement Test-2nd Ed. Abbrev. (WIAT-II-A), Behavior Rating Inventory of Executive Function (BRIEF), FAS Fluency (FAS), and the Beery Developmental Test of Visual Motor Integration (VMI). Results: Data were received on 147 patients (46% F); 46% received MTX and 54% ITT. Mean age = 11.9 years, age at diagnosis = 4.3 years, and interval since diagnosis = 7.6 years. The groups were similar in age, gender, and time since diagnosis. Mean Full Scale IQ was similar in both groups (99.1±11.4 vs 99.7± 13.3). WIAT-II-A scores were average in word reading, mathematics, and spelling for both subgroups, as were mean BRIEF and FAS scores for executive function. The MTX group had a lower mean score on the Processing Speed Index (93.8±10.9 vs 97.2±10.7, p=0.07); 18% in the MTX group scored >1 standard deviation (SD) below the normative mean compared with 7% of the ITT group (p=0.04). Mean scores on Beery VMI were significantly lower than the normative mean of 100. (91.3±13.6 for MTX group, p<0.0001 and 94.5±13.2 for ITT group, p=0.0007), but did not differ by treatment subgroup. Conclusions: Patients treated with ITT had neurobehavioral functioning similar to those who received MTX alone, except for mildly reduced processing speed in MTX patients. Both groups of patients performed in the average range except for a relative weakness in visual motor integration. No significant financial relationships to disclose.
The Need to Improve Care and Research on Sexual Functioning in Cardiology
Authors: Kevin P. Weinfurt
Journal: JAMA Cardiology (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 Cardiology 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 Cardiology journal
Роль ентеропатогенних кишкових паличок у розвитку і перебігу хронічного невиразкового коліту
Authors: L.I. Sydorchuk, D.V. Rotar, A.V. Humenna, I.Y. Sydorchuk
Journal: GASTROENTEROLOGY (2016)

Мета. Проведений аналіз даних літератури показав, що у хворих на хронічний невиразковий коліт ізолюють E. сoli, які викликають дизентерієподібні, холероподібні захворювання та ешерихіози. Тому метою наших досліджень було встановити рівень персистенції у товстій кишці хворих на хронічний невиразковий коліт енте ропатогенних ешерихій та їх значення в екологічній системі «макроорганізм — мікробіота». Матеріали та методи. Протягом 2000–2015 рр. проведено бактеріологічне обстеження вмісту порожнини товстої кишки хворих на хронічний невиразковий коліт віком 27–41 рік (середній вік 37,74 ± 3,62 року). Отримані культури перевіряли в орієнтовній реакції аглютинації з полівалентною сироваткою ОКА. Позитивні культури піддавались дослідженню з полівалентною сироваткою вузького спектра ОКВ, ОКС, ОКД та ОКЕ. Результати. У хворих, у порожнині товстої кишки яких виявлені E. сoli О18ас:К77; О26:К60; О55:К59; О128ав:К67, захворювання мало перебіг за нозологічною формою коліентериту. У тих пацієнтів, в кого виділили сероваріанти О25:К11; О144:К; О124:К72, захворювання перебігало як бактеріальна дизентерія, а О25:К11 і О128:К67 — у холероподібній формі. Обговорення. У 94,50 % хворих виявляються звичайні E. сoli, але у 55 (35,03 %) персистують ентеропатогенні ешерихії, у 41 (26,11 %) — E. сoli Hly+, у 37 (23,57 %) — E. сoli Lac–, у 18 (11,46 %) — ентеротоксигенні E. сoli, у 14 (8,42 %) — ентероінвазивні та в 11 (7,01 %) — ентерогеморагічні ешерихії. Висновки. Визначено, що основними сероваріантами умовно-патогенних ешерихій, що колонізують товсту кишку хворих на хронічний невиразковий коліт і персистують в її порожнині, є О114:К90; О25:К11; О124:К72; О128:К67; О18ас:К77, персистенція яких впливає на клінічну маніфестацію від коліту до дизентерієподібного або до холероподібного захворювання.
Induction of Scleroderma Fibrosis in Skin‐Humanized Mice by Administration of Anti−Platelet‐Derived Growth Factor Receptor Agonistic Autoantibodies
Authors: Michele M. Luchetti, Gianluca Moroncini, Maria Jose Escamez, Silvia Svegliati Baroni, Tatiana Spadoni, Antonella Grieco, Chiara Paolini, Ada Funaro, Enrico V. Avvedimento, Fernando Larcher, Marcela Del Rio, Armando Gabrielli
Journal: Arthritis & Rheumatology (2016)

To describe a skin-SCID mouse chimeric model of systemic sclerosis (SSc; scleroderma) fibrosis based on engraftment of ex vivo-bioengineered skin using skin cells derived either from scleroderma patients or from healthy donors.Three-dimensional bioengineered skin containing human keratinocytes and fibroblasts isolated from skin biopsy specimens from healthy donors or SSc patients was generated ex vivo and then grafted onto the backs of SCID mice. The features of the skin grafts were analyzed by immunohistochemistry, and the functional profile of the graft fibroblasts was defined before and after treatment with IgG from healthy controls or SSc patients. Two procedures were used to investigate the involvement of platelet-derived growth factor receptor (PDGFR): 1) nilotinib, a tyrosine kinase inhibitor, was administered to mice before injection of IgG from SSc patient sera (SSc IgG) into the grafts, and 2) human anti-PDGFR monoclonal antibodies were injected into the grafts.Depending on the type of bioengineered skin grafted, the regenerated human skin exhibited either the typical scleroderma phenotype or the healthy human skin architecture. Treatment of animals carrying healthy donor skin grafts with SSc IgG resulted in the appearance of a bona fide scleroderma phenotype, as confirmed by increased collagen deposition and fibroblast activation markers. Results of the experiments involving administration of nilotinib or monoclonal antibodies confirmed the involvement of PDGFR.Our results provide the first in vivo demonstration of the fibrotic properties of anti-PDGFR agonistic antibodies. This bioengineered skin-humanized mouse model can be used to test in vivo the progression of the disease and to monitor response to antifibrotic drugs.
Drug Company Ethics
Authors: Allan S. Detsky
Journal: JAMA (2006)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Reductions in Funding for Medical Research
Authors: Jack L. Arbiser
Journal: JAMA (2013)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
A Novel Inhibitor of Mutant IDH1 Induces Differentiation in Vivo and Prolongs Survival in a Mouse Model of Leukemia
Authors: Anuhar Chaturvedi, Michelle Maria Araujo Cruz, Ramya Goparaju, Nidhi Jyotsana, Heike Baehre, Kerstin Goerlich, Renate Schottmann, Matthias Preller, Eduard A. Struys, Arnold Kloos, Volkhard Kaever, Arnold Ganser, Felicitas Thol, Michael Heuser
Journal: Blood (2014)
Inflammatory monocytes and NK cells play a crucial role in DNAM-1–dependent control of cytomegalovirus infection
Authors: Tihana Lenac Rovis, Paola Kucan Brlic, Noa Kaynan, Vanda Juranic Lisnic, Ilija Brizic, Stefan Jordan, Adriana Tomic, Daria Kvestak, Marina Babic, Pinchas Tsukerman, Marco Colonna, Ulrich Koszinowski, Martin Messerle, Ofer Mandelboim, Astrid Krmpotic, Stipan Jonjic
Journal: The Journal of Experimental Medicine (2016)

The poliovirus receptor (PVR) is a ubiquitously expressed glycoprotein involved in cellular adhesion and immune response. It engages the activating receptor DNAX accessory molecule (DNAM)-1, the inhibitory receptor TIGIT, and the CD96 receptor with both activating and inhibitory functions. Human cytomegalovirus (HCMV) down-regulates PVR expression, but the significance of this viral function in vivo remains unknown. Here, we demonstrate that mouse CMV (MCMV) also down-regulates the surface PVR. The m20.1 protein of MCMV retains PVR in the endoplasmic reticulum and promotes its degradation. A MCMV mutant lacking the PVR inhibitor was attenuated in normal mice but not in mice lacking DNAM-1. This attenuation was partially reversed by NK cell depletion, whereas the simultaneous depletion of mononuclear phagocytes abolished the virus control. This effect was associated with the increased expression of DNAM-1, whereas TIGIT and CD96 were absent on these cells. An increased level of proinflammatory cytokines in sera of mice infected with the virus lacking the m20.1 and an increased production of iNOS by inflammatory monocytes was observed. Blocking of CCL2 or the inhibition of iNOS significantly increased titer of the virus lacking m20.1. In this study, we have demonstrated that inflammatory monocytes, together with NK cells, are essential in the early control of CMV through the DNAM-1–PVR pathway.
Correlation of Mir-155 Expression with Clinical Outcome in Childhood AML: A Report from Children’s Oncology Group
Authors: Ranjani Ramamurthy, Maya D Hughes, Hamid Bolouri, Robert B. Gerbing, Yi-Cheng Wang, Michael R Loken, Susana C. Raimondi, Betsy A. Hirsch, Richard Aplenc, Alan S. Gamis, Todd A. Alonzo, Soheil Meshinchi
Journal: Blood (2014)
Mammalian Innate Immune Response to a Leishmania -Resident RNA Virus Increases Macrophage Survival to Promote Parasite Persistence
Authors: Remzi Onur Eren, Marta Reverte, Matteo Rossi, Mary-Anne Hartley, Patrik Castiglioni, Florence Prevel, Ricardo Martin, Chantal Desponds, Lon-Fye Lye, Stefan K. Drexler, Walter Reith, Stephen M. Beverley, Catherine Ronet, Nicolas Fasel
Journal: Cell Host & Microbe (2016)
A clinico-genomic model of performance status in acute myeloid leukemia.
Authors: A. Rao, C. Acharya, H. J. Cohen, D. Rizzieri, A. Potti
Journal: Journal of Clinical Oncology (2010)

6558 Background: ECOG Performance Status (PS) is a well known clinical predictor of survival in patients with Acute Myeloid Leukemia (AML). Altered levels of certain cytokines e.g. IL-6, IL-1, IL-2, TNF-α, and CRP can lead to decreased functional status and increased mortality in cancer patients, suggestion a state of frailty. Methods: Clinically annotated microarray data from 377 patients with newly diagnosed AML from two publicly available datasets: GSE1159; and GSE12417 with ECOG PS, and Overall Survival (OS) data were analyzed. A “frailty profile” was developed by utilizing a set of previously characterized genesets/pathways that define the aforementioned cytokines. OS was used as the primary endpoint. Standard Kaplan-Meier survival curves were generated using the two-sided log-rank test. Results: The frailty profile was queried in the 377 patients, and by unsupervised clustering methods, two cohorts (n = 58) of patient samples that represented extremes of survival (cohort 1, median survival (MS) 4.9 months, cohort 2 MS 46.3 months; p < 0.0001) were identified. Standard Kaplan-Meier survival curves were also generated for these 58 patients based on ECOG PS, and there was no statistically significant difference in OS (MS for ECOG 0-1 was 14 months, ECOG ≥ 2 was 8.8 months; p = 0.29). We then developed a clinic-genomic classification of these patients into three risk groups: low, intermediate and high risk depending on a) cohort based on frailty profile and b) ECOG PS, to evaluate if the frailty profile adds any additional information to the clinically estimated ECOG PS. This combined analysis revealed that low-risk patients (cohort 2 plus ECOG 0-1) had a statistically significant higher MS of 56.1 months when compared to intermediate risk (MS 9.85 months) and high-risk (MS 8.35 months) patients; p = 0.02. Conclusions: A clinico-genomic model that combines the widely utilized ECOG PS, with a genomic frailty profile (representing genesets/pathways for cytokines associated with poor functional status) might represent a unique and more refined way of selecting AML patients for induction therapy. This may be especially valuable in elderly AML patients for whom the ECOG PS is not always an accurate measure of functional status. No significant financial relationships to disclose.
Ubap2l-Bmi-1-Rnf2 Define a Novel Polycomb Complex Essential For Self-Renewal Of Hematopoietic Stem Cells
Authors: Marie-Eve Bordeleau, Jalila Chagraoui, Romain Aucagne, Simon Girard, Éric Bonneil, Martin Sauvageau, Amélie Faubert, Pierre Thibault, Guy Sauvageau
Journal: Blood (2013)
CTC phenotype classifier to identify mCRPC patients (pts) with high genomic instability CTCs and to predict failure of androgen ecreptor signaling (AR Tx) and taxane (T) systemic therapies.
Authors: Howard I. Scher, Adam Jendrisak, Ryon Graf, Nicole A. Schreiber, Brigit McLaughlin, Stephanie Greene, Angel Rodriguez, Jessica Louw, Lyndsey Dugan, Laura Leitz, Martin Fleisher, Jerry Lee, Yipeng Wang, Mark Andrew Landers, Ryan Vance Dittamore
Journal: Journal of Clinical Oncology (2016)

5044 Background: Prediction of pt response to AR Tx or T is an unmet medical need, as pts may respond to both classes of drug, to one but not the other, or have no response to either. Molecular profiling studies of mCRPC tumor samples suggest an association between high genomic instability (GI) and lack of response to either class of drug. Our objective was to develop a method to predict GI using phenotypic features from individual CTCs without next generation sequencing (NGS), Methods: Training set: 608 CTCs from 26 samples from pts with progressing mCRPC were detected on the Epic Sciences platform and analyzed for 20 phenotypic digital pathology cell features (protein & cell morphology). CTCs were then single-cell sequenced and GI quantified by the number of large scale transitions (LSTs) present in each cell. A regression algorithm to predict LSTs by CTC phenotype was developed, cross validated, and utilized to create a CTC GI score. A pt score was derived by the presence of high GI CTCs and tested on an independent cohort. Validation: 195 pt blood samples were collected prior to starting AR Tx (n = 134) or T (n = 61) as the 1st, 2nd or 3rd+ line of therapy and CTCs characterized for patient GI prediction and associated with overall survival (OS). Results: A high GI phenotype based score identified high LSTs ( > 13), with an AUC = 0.85. In the independent validation cohort, 27% (53 of 195) of pt samples had high GI scores which was associated with inferior OS on AR Tx (HR: 9.83, p < 0.0001, median 8 mo vs. not reached) and T (HR: 3.31, p = 0.0012, med 8 mo vs. 13 mo) relative to those with a low GI score. Conclusions: CTC phenotypes can predict underlying genomic instability with high accuracy, and are associated with poor OS on AR Tx and T. The ability to identify Pts who need alternatives to AR Tx or T by predicting GI scores through phenotypes without NGS informs therapeutic decision making more rapidly at reduced cost, and accelerate novel drug development.
Second-generation inhibitors of Bruton tyrosine kinase
Authors: Jingjing Wu, Christina Liu, Stella T. Tsui, Delong Liu
Journal: Journal of Hematology & Oncology (2016)

Bruton tyrosine kinase (BTK) is a critical effector molecule for B cell development and plays a major role in lymphoma genesis. Ibrutinib is the first-generation BTK inhibitor. Ibrutinib has off-target effects on EGFR, ITK, and Tec family kinases, which explains the untoward effects of ibrutinib. Resistance to ibrutinib was also reported. The C481S mutation in the BTK kinase domain was reported to be a major mechanism of resistance to ibrutinib. This review summarizes the clinical development of novel BTK inhibitors, ACP-196 (acalabrutinib), ONO/GS-4059, and BGB-3111.
Left Main Coronary Artery Disease
Authors: Pil Hyung Lee, Jung-Min Ahn, Mineok Chang, Seunghee Baek, Sung-Han Yoon, Soo-Jin Kang, Seung-Whan Lee, Young-Hak Kim, Cheol Whan Lee, Seong-Wook Park, Duk-Woo Park, Seung-Jung Park
Journal: Journal of the American College of Cardiology (2016)
Active zone scaffolds differentially accumulate Unc13 isoforms to tune Ca2+ channel–vesicle coupling
Authors: Mathias A Böhme, Christina Beis, Suneel Reddy-Alla, Eric Reynolds, Malou M Mampell, Andreas T Grasskamp, Janine Lützkendorf, Dominique Dufour Bergeron, Jan H Driller, Husam Babikir, Fabian Göttfert, Iain M Robinson, Cahir J O'Kane, Stefan W Hell, Markus C Wahl, Ulrich Stelzl, Bernhard Loll, Alexander M Walter, Stephan J Sigrist
Journal: Nature Neuroscience (2016)