tbuckley/cabot-search huggingface dataset:
Collar Osteophytes Mimicking Osteonecrosis in Planar Bone Scintigraphy and Usefulness of SPECT/CT Images
Authors: Jr-Jian Juang, Yi-Hsing Chen, Shih-Chuan Tsai, Wan-Yu Lin
Journal: Clinical Nuclear Medicine (2016)

The use of prednisolone is one major risk factor for osteonecrosis in patients with systemic lupus erythematosus. Bone scintigraphy can be a diagnostic tool for early diagnosis. We present a case who had collar osteophytes at the bilateral femoral heads, which mimicked osteonecrosis in the planar bone scintigram. An SPECT/CT scan avoided this pitfall and increased the diagnostic accuracy for osteonecrosis.
Expectations for Physicians Prescribing Marijuana
Authors: Jeffrey Hergenrather, Stephen S. Robinson, Fred Gardner
Journal: JAMA (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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Significance of Residual Mitral Regurgitation After Continuous Flow Left Ventricular Assist Device Implantation
Authors: Hayah Kassis, Krishna Cherukuri, Richa Agarwal, Manreet Kanwar, Subbarao Elapavaluru, George G. Sokos, Robert J. Moraca, Stephen H. Bailey, Srinivas Murali, Raymond L. Benza, Amresh Raina
Journal: JACC Heart Failure (2016)
Surgical Aspects of Dysentery, Including Liver-Abscess.
Journal: JAMA (1921)

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
MicroRNAs as the Target of Deletions on der(9) in Chronic Myeloid Leukemia.
Authors: Francesco Albano, Luisa Anelli, Antonella Zagaria, Alessandra Pannunzio, Antonella Russo Rossi, Floriana Manodoro, Vincenzo Liso, Mariano Rocchi, Giorgina Specchia
Journal: Blood (2007)
Prognostic Implications of WT1 and BAALC in Adult Patients with Core-Binding Factor Positive or Normal Karyotype AML: Consecutive Analyses From Diagnosis to Hematopoietic Stem Cell Transplantation
Authors: Jae-Ho Yoon, Heeje Kim, Seung-Hwan Shin, Seung-Ah Yahng, Byung-Sik Cho, Ki-Seong Eom, Yoo-Jin Kim, Seok Lee, Chang-Ki Min, Seok-Goo Cho, Dong-Wook Kim, Jong-Wook Lee, Woo-Sung Min, Chong-Won Park
Journal: Blood (2012)
GMCLI, Goelams Mantle Cell Lymphoma Index, a New Prognostic Index of Survival for MCL Patients Treated with VAD-C and Autologous PBSCT.
Authors: Remy Gressin, Sylvie Caulet Maugendre, Eric Deconinck, Olivier Tournilhac, Martine Dartigeas, Marie Pierre Moles, Gerard Lepeu, Denis Guyotat, Eric Legouffe, Jacqueline Dugay, Claude Martin, Philippe Casassus, Jean Pierre, Christiane Ghandour, Isabelle Grulois, Frederic Maloisel, Christine Le Maignan, Jean Pierre De Jaureguiberry, Antoine Thyss, Virginie Lucas, Sylvie Cailleres, Philippe Rodon, Jean Luc Dutel, Philippe Colombat, Emmanuel Gyan
Journal: Blood (2006)
Disease-modifying treatment in rheumatoid arthritis: treat early and do not forget to try to taper and stop
Authors: S Ajeganova, AHM van der Helm-van Mil
Journal: Annals of the Rheumatic Diseases (2016)

We thank Professor Zeidler1 for the interest in our study, in which we showed an increased chance and a shorter time to achieve disease-modifying antirheumatic drug (DMARD)-free sustained remission in patients with rheumatoid arthritis (RA) treated with present strategies (early start of methotrexate and treat-to-target approach) compared with treatment strategies that were applied 10 years ago.2 DMARD-free sustained remission in the study was defined as the sustained absence of synovitis (by physical examination) after discontinuation of DMARD therapy (including biologics and systemic or intra-articular corticosteroids) for the entire follow-up and at least for 1 year after DMARD …
MK-0457, a Novel Aurora Kinase and BCR-ABL Inhibitor, Is Active Against BCR-ABL T315I Mutant Chronic Myelogenous Leukemia (CML).
Authors: Francis Giles, Jorge Cortes, Donald A. Bergstrom, Alan Xiao, Penny Bristow, Dan Jones, Srdan Verstovsek, Deborah Thomas, Hagop Kantarjian, Steven J. Freedman
Journal: Blood (2006)
Annals for Hospitalists Inpatient Notes - Mistakes in the Hospital—Communicating, Apologizing, and Beyond
Authors: Allen Kachalia
Journal: Annals of Internal Medicine (2016)

Web Exclusives20 December 2016Annals for Hospitalists Inpatient Notes - Mistakes in the Hospital—Communicating, Apologizing, and BeyondAllen Kachalia, MD, JDAllen Kachalia, MD, JDFrom Brigham and Women's Hospital, Boston, Massachusetts.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M16-2545 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Hospital medicine is often cited as a field that can help drive improvements in health care quality and safety (1). Hospitalists, however, are not immune from making mistakes. It is easy to imagine situations in which a hospitalist might make an error that has adverse consequences—for example, forgetting to prescribe venous thromboembolism (VTE) prophylaxis for a patient at high risk for a blood clot. If this happens and the patient later develops a pulmonary embolism (PE), what should the hospitalist tell the patient?When addressing adverse events, most quality and safety experts agree that transparency should be a guiding principle. ...References1. Wachter RM, Goldman L. Zero to 50,000—The 20th anniversary of the hospitalist. N Engl J Med. 2016;375:1009-11. [PMID: 27508924] doi:10.1056/NEJMp1607958 CrossrefMedlineGoogle Scholar2. Agency for Healthcare Research and Quality. Communication and optimal resolution (CANDOR) toolkit. Accessed at www.ahrq.gov/professionals/quality-patient-safety/patient-safety-resources/resources/candor/introduction.html on 5 September 2016. Google Scholar3. Schaffer AC, Puopolo AL, Raman S, Kachalia A. Liability impact of the hospitalist model of care. J Hosp Med. 2014;9:750-5. [PMID: 25331989] doi:10.1002/jhm.2244 CrossrefMedlineGoogle Scholar4. Kachalia A, Kaufman SR, Boothman R, Anderson S, Welch K, Saint S, et al. Liability claims and costs before and after implementation of a medical error disclosure program. Ann Intern Med. 2010;153:213-21. [PMID: 20713789]. doi:10.7326/0003-4819-153-4-201008170-00002 LinkGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From Brigham and Women's Hospital, Boston, Massachusetts.Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M16-2545.Requests for Single Reprints: Allen Kachalia, MD, JD, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115; e-mail, [email protected]org. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoAnnals for Hospitalists - 20 December 2016 David H. Wesorick and Vineet Chopra Metrics 20 December 2016Volume 165, Issue 12Page: HO2-HO3KeywordsAdverse eventsDisclosureEmotionsFearHealth care qualityHospitalistsProphylaxisRisk managementSafetyVenous thromboembolism ePublished: 20 December 2016 Issue Published: 20 December 2016 Copyright & PermissionsCopyright © 2016 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Inflammatory pre-conditioning restricts the seeded induction of α-synuclein pathology in wild type mice
Authors: Emily J. Koller, Mieu M. T. Brooks, Todd E. Golde, Benoit I. Giasson, Paramita Chakrabarty
Journal: Molecular Neurodegeneration (2017)

Cell-to-cell transmission of α-synuclein (αSyn) is hypothesized to play an important role in disease progression in synucleinopathies. This process involves cellular uptake of extracellular amyloidogenic αSyn seeds followed by seeding of endogenous αSyn. Though it is well known that αSyn is an immunogenic protein that can interact with immune receptors, the role of innate immunity in regulating induction of αSyn pathology in vivo is unknown. Herein, we explored whether altering innate immune activation affects induction of αSyn pathology in wild type mice. We have previously demonstrated that recombinant adeno-associated virus (AAV) mediated expression of the inflammatory cytokine, Interleukin (IL)-6, in neonatal wild type mice brains leads to widespread immune activation in the brain without overt neurodegeneration. To investigate how IL-6 expression affects induction of αSyn pathology, we injected mouse wild type αSyn fibrils in the hippocampus of AAV-IL-6 expressing mice. Control mice received AAV containing an Empty vector (EV) construct. Two separate cohorts of AAV-IL-6 and AAV-EV mice were analyzed in this study: 4 months or 2 months following intrahippocampal αSyn seeding. Here, we show that IL-6 expression resulted in widespread gliosis and concurrently reduced αSyn inclusion pathology induced by a single intra-hippocampal injection of exogenous amyloidogenic αSyn. The reduction in αSyn inclusion pathology in IL-6 expressing mice was time-dependent. Suppression of αSyn pathology was accompanied by reductions in both argyrophilic and p62 immunoreactive inclusions. Our data supports a beneficial role of inflammatory priming of the CNS in wild type mice challenged with exogenous αSyn. A likely mechanism is efficient astroglial scavenging of exogenous αSyn, at least early in the disease process, and in the absence of human αSyn transgene overexpression. Given evidence that a pro-inflammatory environment may restrict seeding of αSyn pathology, this can be used to design anti-αSyn immunobiotherapies by harnessing innate immune function.
Abstract 739: Tumor cell plasticity with transition to a mesenchymal phenotype is a mechanism of chemoresistance that is reversed by Notch pathway inhibition in lung adenocarcinoma
Authors: Khaled A. Hassan
Journal: Cancer Research (2015)

Abstract Background: Lung cancer is the leading cause of cancer death in the world, mainly due to complex genetic events that characterize lung cancer, tumor heterogeneity and resistance to traditional and targeted treatments. Resistance may be explained by passive clonal selectivity, however, the propensity and variability of resistance suggests an active process of tumor plasticity. We hypothesize that tumor cells undergo an epithelial to mesenchymal transition as a mechanism of resistance to chemotherapy. Results: The lung adenocarcinoma cell lines NCI-H1299, NCI-H358, and NCI-H441 were exposed to gradually increasing doses of docetaxel over 12-16 weeks. Chemoresistance emerged with a 10-15X increase in IC50 as compared to parental cells. With each treatment dose increase more than 50% of cells remained alive, suggesting bulk cell transformation. This resistance has been maintained for more than 20 generations after withdrawal of docetaxel. Morphologically, NCI-H358 and NCI-H441 chemoresistant cell lines lost their cobblestone architecture becoming more spindle-shaped. Using RT-PCR assays, there was increased expression of mesenchymal-related genes, vimentin (2.5-3.5X), twist (2-4X) and decreased expression of epithelial-related genes such as E-CAD (2-5X). Our previous data suggested that Notch activity plays a significant role in the EMT process, thus we evaluated Notch downstream genes expression by RT-PCR. We detected increase expression of Hey2 (2.5-3.5X), in NCI-H358 and NCI-H441 resistant cell lines as compared to parental cells. When chemoresistant cell lines were exposed to gamma secretase inhibitor, a Notch inhibitor, they became less invasive, epithelial-like and sensitive to docetaxel. Conclusion: These data suggest that tumor cell plasticity with transition to a mesenchymal phenotype is a mechanism of chemotherapy resistance that is controlled through the Notch pathway. Inhibiting Notch activity induces mesenchymal to epithelial transition and re-sensitizes cells to chemotherapy. Notch inhibition in combination with standard chemotherapy represents a potential approach to achieve better disease control. Citation Format: Khaled A. Hassan. Tumor cell plasticity with transition to a mesenchymal phenotype is a mechanism of chemoresistance that is reversed by Notch pathway inhibition in lung adenocarcinoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 739. doi:10.1158/1538-7445.AM2015-739
Histone Deacetylase 3 Inhibition Overcomes <i>BIM</i> Deletion Polymorphism–Mediated Osimertinib Resistance in <i>EGFR-</i>Mutant Lung Cancer
Authors: Azusa Tanimoto, Shinji Takeuchi, Sachiko Arai, Koji Fukuda, Tadaaki Yamada, Xavier Roca, S. Tiong Ong, Seiji Yano
Journal: Clinical Cancer Research (2016)

Abstract Purpose: The BIM deletion polymorphism is associated with apoptosis resistance to EGFR tyrosine kinase inhibitors (EGFR-TKI), such as gefitinib and erlotinib, in non–small cell lung cancer (NSCLC) harboring EGFR mutations. Here, we investigated whether the BIM deletion polymorphism contributes to resistance against osimertinib, a third-generation EGFR-TKI. In addition, we determined the efficacy of a histone deacetylase (HDAC) inhibitor, vorinostat, against this form of resistance and elucidated the underlying mechanism. Experimental Design: We used EGFR-mutated NSCLC cell lines, which were either heterozygous or homozygous for the BIM deletion polymorphism, to evaluate the effect of osimertinib in vitro and in vivo. Protein expression was examined by Western blotting. Alternative splicing of BIM mRNA was analyzed by RT-PCR. Results: EGFR-mutated NSCLC cell lines with the BIM deletion polymorphism exhibited apoptosis resistance to osimertinib in a polymorphism dosage–dependent manner, and this resistance was overcome by combined use with vorinostat. Experiments with homozygous BIM deletion–positive cells revealed that vorinostat affected the alternative splicing of BIM mRNA in the deletion allele, increased the expression of active BIM protein, and thereby induced apoptosis in osimertinib-treated cells. These effects were mediated predominantly by HDAC3 inhibition. In xenograft models, combined use of vorinostat with osimertinib could regress tumors in EGFR-mutated NSCLC cells homozygous for the BIM deletion polymorphism. Moreover, this combination could induce apoptosis even when tumor cells acquired EGFR-T790M mutations. Conclusions: These findings indicate the importance of developing HDAC3-selective inhibitors, and their combined use with osimertinib, for treating EGFR-mutated lung cancers carrying the BIM deletion polymorphism. Clin Cancer Res; 23(12); 3139–49. ©2016 AACR.
Higher Plasma Cell Burden Predicts for Early Death In Patients with AL Amyloidosis
Authors: Cheng E. Chee, S. Vincent Rajkumar, Morie Abraham A Gertz, Martha Lacy, Steven Zeldenrust, Shaji Kumar, Suzanne R. Hayman, Francis Buadi, Stephen Russell, Robert Kyle, Philip R. Greipp, Angela Dispenzieri
Journal: Blood (2010)
Allogeneic Hematopoietic Cell Transplantation for Acute Myeloid Leukemia: Is It Time to Move Toward a Minimal Residual Disease-Based Definition of Complete Remission?
Authors: Daisuke Araki, Brent L Wood, Megan Othus, Jerald P. Radich, Anna B. Halpern, Yi Zhou, Marco Mielcarek, Elihu H. Estey, Frederick R. Appelbaum, Roland B. Walter
Journal: Blood (2015)
Survival analyses of pancreatic neuroendocrine tumors: Contrasting institutional databases with population-based studies.
Authors: J. R. Strosberg, T. R. Halfdanarson
Journal: Journal of Clinical Oncology (2011)

186 Background: Prognostic data in pancreatic neuroendocrine tumors derives from population-based studies as well as from institutional databases. Methods: The stage-stratified rates of 5-year survival derived from two institutional databases were contrasted with rates of 5-year survival derived from two national population-based studies (SEER 1973-2000 and National Cancer Data Base 1985-2004). Results: The 5-year survival rates derived from the two separate institutional databases were concordant with each other, but markedly higher than the 5-year survival rates derived from the population databases (Table). 5-year survival rates among stage IV patients were 55% and 57% in the institutional databases versus 15% and 19% in the population databases. Conclusions: Survival rates derived from institutional databases are substantially higher than survival rates derived from national population databases. The causes of these differences have yet to be clarified. [Table: see text] No significant financial relationships to disclose.
Autologous stem cell transplantation (ASCT) as upfront or salvage therapy for noncutaneous T-cell lymphoma (TCL): The University of Texas M. D. Anderson Cancer Center (MDACC) experience.
Authors: A. Beitinjaneh, R. Saliba, G. Okoroji, A. M. Alousi, U. R. Popat, M. Korbling, P. Anderlini, M. Qazilbash, P. Kebriaei, C. Hosing, R. E. Champlin, I. F. Khouri
Journal: Journal of Clinical Oncology (2011)

6565 Background: Despite the advent of novel agents, outcomes of TCL with conventional chemotherapy are poor. We have previously reported encouraging results with ASCT (Rodriguez J, J Clin Oncol, 2001). Herein, we report our long-term experience in 126 patients (pts). Methods: This is a retrospective analysis of TCL pts treated at our institution between 1986 and 2009. Median age was 49 years and 65% were males. Histologies included 1)peripheral t-cell lymphoma not otherwise specified (PTCL -NOS=42, 2) anaplastic large cell lymphoma (ALCL=47) of which 9 pts were ALK(+), 3) angioimmunoblastic (AILT=15), 4) NK cell lymphomas (N=6), Hepatosplenic TCL (HS-TCL=6), others (n=10). Results: At transplant, 33% were in first remission (CR1), 51% had chemosensitive relapse, 16 % had refractory disease. Most pts received BEAM or BEAM like (82%) conditioning. With a median follow-up of 39 months, overall survival (OS) and progression-free-survival (PFS) estimates were 39% (95% CI, 28-50), and 30%(95% CI 20-41). Treatment related mortality rate was 3%. Pts with CR1 at ASCT had the best outcome regardless of histology. The 4-year OS and PFS rates for CR1 pts were 87% (95% CI 67-95), and 67% (95% CI 47-81), respectively, which compared favorably (p>0.05) to chemosensitive relapse pts(4-year OS and PFS rates of 39%, and 36%, and refractory disease (4-year OS and PFS rates of 24% and 15%). Risk factors for OS and PFS were evaluated within the largest histological subgroups (PTCL-NOS [n=42] and ACLC [n=40]). Among these 82 pts, IPI of >1, Prognostic Index for TCL (PIT) of >1, prior chemotherapy lines >3, and refractory disease were associated with a significantly (p>0.05) worse PFS and OS. In addition, age >50 was associated with significantly worse OS. We were not able to detect any difference in outcomes between ALK(-) and ALK (+) ACLC. The 4 yr PFS was 48% for PTCL-NOS, 38% for ALCL, 37% for AILT, 67% for NK TCL, and 14% for T-LBL. Conclusions: This largest single institution analysis of ASCT role for TCL demonstrates that it can produce long-term remissions when incorporated in an upfront strategy. Innovative strategies are needed for pts with relapsed disease.
Filgotinib (GLPG0634/GS-6034), an oral selective JAK1 inhibitor, is effective as monotherapy in patients with active rheumatoid arthritis: results from a randomised, dose-finding study (DARWIN 2)
Authors: A Kavanaugh, J Kremer, L Ponce, R Cseuz, O V Reshetko, M Stanislavchuk, M Greenwald, A Van der Aa, F Vanhoutte, C Tasset, P Harrison
Journal: Annals of the Rheumatic Diseases (2016)

Objectives To evaluate the efficacy and safety of different doses of filgotinib, an oral Janus kinase 1 inhibitor, as monotherapy in patients with active rheumatoid arthritis (RA) and previous inadequate response to methotrexate (MTX). Methods In this 24-week phase IIb study, patients with moderately to severely active RA were randomised (1:1:1:1) to receive 50, 100 or 200 mg filgotinib once daily, or placebo, after a ≥4-week washout from MTX. The primary end point was the percentage of patients achieving an American College of Rheumatology (ACR)20 response at week 12. Results Overall, 283 patients were randomised and treated. At week 12, significantly more patients receiving filgotinib at any dose achieved ACR20 responses versus placebo (≥65% vs 29%, p&lt;0.001). For other key end points at week 12 (ACR50, ACR70, ACR-N, Disease Activity Score based on 28 joints and C reactive protein, Clinical Disease Activity Index, Simplified Disease Activity Index and Health Assessment Questionnaire-Disability Index) significant differences from baseline in favour of filgotinib 100 and 200 mg versus placebo were seen; responses were maintained or improved through week 24. Rapid onset of action was observed for most efficacy end points. Dose-dependent increases in haemoglobin were observed. The percentage of patients with treatment-emergent adverse events (TEAE) was similar in the placebo and filgotinib groups (∼40%). Eight patients on filgotinib and one on placebo had a serious TEAE, and four patients, all of whom received filgotinib, experienced a serious infection. No tuberculosis or opportunistic infections were reported. Conclusions Over 24 weeks, filgotinib as monotherapy was efficacious in treating the signs and symptoms of active RA, with a rapid onset of action. Filgotinib was generally well tolerated. Trial registration number NCT01894516 .