tbuckley/cabot-search huggingface dataset:
Correspondence: Osteonecrosis in childhood acute lymphoblastic leukemia: a retrospective cohort study of the Italian Association of Pediatric Haemato-Oncology (AIEOP)
Authors: Rosanna Parasole, Maria G. Valsecchi, Daniela Silvestri, Franco Locatelli, Elena Barisone, Fara Petruzziello, M. Caterina Putti, Concetta Micalizzi, Antonella Colombini, Rossella Mura, Tommaso Mina, Anna M. Testi, Lucia D. Notarangelo, Nicola Santoro, Tommaso Casini, Caterina Consarino, Luca Lo Nigro, Ottavio Ziino, Giovanna Giagnuolo, Carmelo Rizzari, Valentino Conter
Journal: Blood Cancer Journal (2018)

Osteonecrosis (ON) is a well-known, disabling complication that can occur in pediatric acute lymphoblastic leukemia (ALL), either during treatment or after its discontinuation 1 .Severity of ON may range from asymptomatic to debilitating, causing severe pain, limited motion of joints, and finally joint destruction, thus negatively affecting patients' quality of life (QoL) 2 .Prevalence and risk factors varied widely in published papers 3 .This wide variability might be related to differences in definition of ON or in detection methods, but also to difference in age of investigated cohorts (e.g. percentage of adolescents) and in type/cumulative doses of steroids employed during treatment 4 .ON pathogenesis in patients with childhood ALL is not fully elucidated 5 , being presumably multifactorial.Although corticosteroids, both prednisone (PRED) and dexamethasone (DEXA), have been identified as the main cause of ON in children with ALL, causing increased intramedullary pressure and subsequent blood stasis, other drugs, including methotrexate and asparaginase, may contribute to the development of this complication 3,6,7 .ON incidence correlates with age at diagnosis and female gender, suggesting a contribution of growth and hormonal factors in ON pathogenesis 8 .Hyperlipidemia/ hypercholesterolemia, were also observed in patients with ON, but the real meaning of this association requires further investigations 1,9 .Other proposed risk factors include Caucasian race 4 , higher BMI, genetic polymorphisms involving PAI-1 4G/5G, VDR, TYM, CYP3A, ACP1 genes 7 .In this multicenter study, we assessed incidence of ON, its risk factors and outcome in children with ALL enrolled in two clinical trials conducted in centers affiliated to the Italian Association of Pediatric Hematology and Oncology (AIEOP) 10 .A cohort of 3691 ALL patients (aged 1-17 years at diagnosis), diagnosed from September 2000 to December 2011 and treated according to either the AIEOP-BFM-ALL-2000 protocol (clinicaltrials.gov/NCT00613457) 10 or subsequent guidelines (AIEOP-ALL-R2006), was analyzed.Complete information on ON-related symptoms, radiological findings, treatment, and outcome of ON were retrospectively retrieved with ad hoc forms.Infants and Philadelphia positive ALL were excluded from the study because they were enrolled in ad hoc trials.Cases of ON
Food sources of fructose-containing sugars and glycaemic control: systematic review and meta-analysis of controlled intervention studies
Authors: Vivian L Choo, Effie Viguiliouk, Sonia Blanco Mejia, Adrian I Cozma, Tauseef A Khan, Vanessa Ha, Thomas M S Wolever, Lawrence A Leiter, Vladimir Vuksan, Cyril W C Kendall, Russell J de Souza, David J A Jenkins, John L Sievenpiper
Journal: BMJ (2018)

Abstract Objective To assess the effect of different food sources of fructose-containing sugars on glycaemic control at different levels of energy control. Design Systematic review and meta-analysis of controlled intervention studies. Data sources Medine, Embase, and the Cochrane Library up to 25 April 2018. Eligibility criteria for selecting studies Controlled intervention studies of at least seven days’ duration and assessing the effect of different food sources of fructose-containing sugars on glycaemic control in people with and without diabetes were included. Four study designs were prespecified on the basis of energy control: substitution studies (sugars in energy matched comparisons with other macronutrients), addition studies (excess energy from sugars added to diets), subtraction studies (energy from sugars subtracted from diets), and ad libitum studies (sugars freely replaced by other macronutrients without control for energy). Outcomes were glycated haemoglobin (HbA1c), fasting blood glucose, and fasting blood glucose insulin. Data extraction and synthesis Four independent reviewers extracted relevant data and assessed risk of bias. Data were pooled by random effects models and overall certainty of the evidence assessed by the GRADE approach (grading of recommendations assessment, development, and evaluation). Results 155 study comparisons (n=5086) were included. Total fructose-containing sugars had no harmful effect on any outcome in substitution or subtraction studies, with a decrease seen in HbA1c in substitution studies (mean difference −0.22% (95% confidence interval to −0.35% to −0.08%), −25.9 mmol/mol (−27.3 to −24.4)), but a harmful effect was seen on fasting insulin in addition studies (4.68 pmol/L (1.40 to 7.96)) and ad libitum studies (7.24 pmol/L (0.47 to 14.00)). There was interaction by food source, with specific food sources showing beneficial effects (fruit and fruit juice) or harmful effects (sweetened milk and mixed sources) in substitution studies and harmful effects (sugars-sweetened beverages and fruit juice) in addition studies on at least one outcome. Most of the evidence was low quality. Conclusions Energy control and food source appear to mediate the effect of fructose-containing sugars on glycaemic control. Although most food sources of these sugars (especially fruit) do not have a harmful effect in energy matched substitutions with other macronutrients, several food sources of fructose-containing sugars (especially sugars-sweetened beverages) adding excess energy to diets have harmful effects. However, certainty in these estimates is low, and more high quality randomised controlled trials are needed. Study registration Clinicaltrials.gov ( NCT02716870 ).
Abstract P039: Lipid Rich Plaque by Coronary CT Angiography Associates With Cholesterol Efflux Capacity Independent of Traditional Cardiovascular Risk Factors in Those at Risk for Myocardial Infarction
Authors: Jonathan H Chung, Amit K Dey, Abhishek Chaturvedi, Joshua P Rivers, Joseph B Lerman, Charlotte L Harrington, Mark Ahlman, Martin P Playford, Scott M Gordon, Aditya A Joshi, Alan T Remaley, Marcus Chen, David A Bluemke, Nehal N Mehta
Journal: Circulation (2017)

Introduction: Cholesterol efflux capacity (CEC), a measure of high density lipoprotein (HDL) function, has been shown to be associated with future cardiovascular (CV) events. Lipid rich plaque is associated with higher plaque rupture and future CV events, and can be readily phenotyped by coronary CT angiography (CCTA). Whether CEC associates with lipid rich plaque is not known. Hypothesis: We hypothesize that CEC associates with lipid rich plaque in those at risk for myocardial infarction (MI). Methods: Consecutively recruited patients (N=94) underwent CCTA (Toshiba 320 slice) to assess plaque burden within the coronary arteries by QAngio CT (Medis, The Netherlands); history was obtained and statin use was recorded. CEC was measured using an ex vivo validated assay. Results: The study population mean age was 61 and had normal cholesterol, HDL, low density lipoprotein (LDL), and triglyceride levels (Table 1). CEC was 1.03 ± 0.17 while total plaque and lipid rich plaque were 1.05 (0.79-1.37) mm 2 and 1.00 (0.77-1.33) mm 2 , respectively. Lipid rich plaque inversely associated with CEC beyond adjustment for age, gender, systolic blood pressure, statin treatment, total cholesterol, LDL, and HDL (β= -0.18, p=0.002). Conclusion: CEC associated with lipid rich plaque independent of CV risk factors to provide additional risk stratification in those at risk for MI and early atherogenesis. Clinical Implications: My study will help cardiovascular clinicians to better understand that HDL function may capture additional CV risk in those at risk for future MI.
A model based on a new inflammation–nutrition score and TNM stage for predicting overall survival of patients with colorectal cancer
Authors: S. Fujino, N. Miyoshi, K. Saso, M. Sasaki, S. Ishikawa, Y. Takahashi, M. Yasui, M. Ohue, T. Hata, C. Matsuda, T. Mizushima, Y. Doki, M. Mori
Journal: Annals of Oncology (2018)
Abstract 14486: Bariatric Surgery is Associated With Reduced Risk of Hospitalizations for Stable Angina Pectoris in Obese Adults
Authors: Yuichi J Shimada, Yusuke Tsugawa, Hiroyasu Iso, David F Brown, Kohei Hasegawa
Journal: Circulation (2016)

Introduction: Obesity and stable angina pectoris (SAP) are important public health problems in the U.S. There are potential pathophysiologic mechanisms that connect obesity to increased morbidity i...
Mifepristone inhibits ovarian cancer cell growth in vitro and in vivo
Authors: Alicia Goyeneche, Carlos Telleria
Journal: Cancer Research (2007)

4344  A major clinical problem in the treatment of ovarian cancer is the resistance to current chemotherapy, the high toxicity of standard chemotherapeutic drugs, and the repopulation of cells escaping chemotherapy. Therefore, the development of novel strategies to treat ovarian cancer is of significant importance. The purpose of this study was to determine whether the synthetic steroid mifepristone inhibits ovarian cancer growth in vitro and in vivo and the molecular mechanism involved. The effect of mifepristone on ovarian cancer cell growth in vitro was studied in ovarian cancer cell lines of different genetic backgrounds (SK-OV-3, Caov-3, OV2008, and IGROV-1). In addition, the growth inhibition capacity of mifepristone on ovarian carcinoma xenografts was tested in nude mice. Dose-response and time-course experiments revealed that mifepristone inhibited ovarian cancer cell proliferation in a dose-dependent manner, and, at the highest dose tested, it completely abrogated proliferation within 24 h of treatment. The cytostatic effect of mifepristone was confirmed in a clonogenic survival assay, and was not linked to loss of viability as revealed in a two-color fluorescence cell viability assay. Mifepristone blocked DNA synthesis demonstrated by decreased bromodeoxyuridine incorporation, and arrested the cell cycle at the G1-to-S transition as shown by flow cytometry. Western blot analysis demonstrated that mifepristone up-regulated cyclin-dependent kinase (cdk) inhibitors p21cip1and p27kip1, down-regulated transcription factor E2F1, decreased expression of the E2F1 regulated genes, cdk1 (cdc2) and cyclin A, and to some extent declined cdk2 abundance. The abrupt arrest in cell growth induced by mifepristone correlated with reduced cdk2 activity assessed in an in vitro kinase assay, whereas immunoprecipitation of whole protein extracts from mifepristone-treated cells with an anti-cdk2 antibody revealed an increased association of cdk2 with p21cip1 and p27kip1. Finally, mifepristone significantly delayed the growth of ovarian carcinoma xenografts in a dose-dependent manner and without apparent toxic effects for the animals. In conclusion, these preclinical studies demonstrate that mifepristone is effective as a single agent in vitro and in vivo inhibiting growth of human epithelial ovarian cancer cells. Mifepristone markedly reduces cdk2 activity likely due to increased association of cdk2 with the cdk inhibitors p21cip1 and p27kip1. Acting as a cytostatic agent mifepristone promises to be of translational significance in ovarian cancer therapeutics.
Up-regulation of connexin26 and gap junctional intracellular communication by celecoxib might mediate outstanding anti-cancer effect of celecoxib in HNSCC cell lines
Authors: Seok-Woo Park, Myung-Whun Sung, Seon-Hui Shim
Journal: Cancer Research (2008)

2660   Firstly, in head and neck squamous cell carcinoma (HNSCC) cell lines, we had tried to identify if there is any relationship between up-regulated cyclooxygenase-2 (COX-2) and abnormal gap junctional intracellular communication (GJIC). Although it was observed the possibility that expression of some connexins might be abnormally regulated in HNSCC cells, any positive relationship between COX-2-induced prostaglandins and GJIC was not identified. Instead, we found that among several COX-2 specific inhibitors, the only celecoxib seemed to activate GJIC through COX-2-independent mechanism in tested HNSCC cells. Next, considering our previous findings, we tested the effect of celecoxib on connexin26 (Cx26) and connexin43 (Cx43) which were identified to be expressed in our cell models and found that celecoxib activated GJIC through up-regulation of Cx26 expression but not Cx43. Celecoxib-induced Cx26 expression and GJIC activation seemed to be mediated through ERK and p38 activation. The pre-treatment of ERK and/or p38 inhibitor(s) as well as Cx26 siRNA inhibited celecoxib-induced GJIC activation. Also, the Cx26 siRNA treatment reversed the growth-inhibitory effect of celecoxib by 30-50%. These imply that Cx26-up-regulated GJIC activation might be one of cancer killing mechanisms of celecoxib in HNSCC cells. In conclusion, our study suggests that celecoxib might show outstanding anti-cancer effects in cancer cells through unexpected mechanisms of a variety of COX-2-independent actions like our findings.
Serum Free Methylated Glutathione S-transferase 1 DNA Levels, Survival, and Response to Docetaxel in Metastatic, Castration-resistant Prostate Cancer: Post Hoc Analyses of Data from a Phase 3 Trial
Authors: Kate L. Mahon, Wenjia Qu, Hui-Ming Lin, Calan Spielman, Daniel Cain, Cindy Jacobs, Martin R. Stockler, Celestia S. Higano, Johann S. de Bono, Kim N. Chi, Susan J. Clark, Lisa Glen Horvath
Journal: European Urology (2018)
H2O2 accumulation is a crucial step for the cytotoxicity of Paclitaxel
Authors: Jerome Alexandre, Frédéric Batteux, Carole Nicco, Christiane Chereau, Alexis Laurent, Bernard Weill, François Goldwasser
Journal: Cancer Research (2004)

5607  The cytotoxicity of anticancer chemotherapy is largely conditioned by the molecular pathways involved following DNA damage, especially induction of apoptosis. Various anticancer agents, such as cisplatin and 5-FU, acting through independent molecular targets, were previously found able to enhance the production of reactive oxygen species (ROS). We hypothesized that the formation of ROS might play a critical role in the cellular response to taxanes-induced damages, downstream from microtubule assembly. We studied the cytotoxicity of paclitaxel (PCX) in presence and in absence of ROS modulators. The A549 human lung cancer cell line was exposed to various concentrations of PCX for 48h. Cell survival was measured using MTT assay. The IC50 of PCX was 5μM. The variations in H2O2 and O2.- production were monitored by oxidation of fluorescent probes H2DCFDA and DHE, respectively. Glutathione (GSH) concentration was determined by colorimetric micro-GSH assay. PCX induced a concentration-dependent ROS production : at IC50, a 1.8- and 1.3-fold increase in O2.- and H2O2 levels, respectively, were detected, while the GSH intracellular pool was depleted to 20% of baseline levels. The co-exposure to either 1.6 mM N-acetyl-cysteine (NAC), a GSH reductase mimetic, or 12 mM reduced GSH, resulted in a 2-fold decrease in H2O2 levels resulting in a 2-fold increase in PCX resistance. The protection of NAC was concentration-dependent and correlated with the extent of H2O2 depletion. Conversely, Buthionine Sulfoximine (1.1 μM), a GSH-reductase inhibitor, enhanced H2O2 accumulation and increased by 2 the sensitivity to PCX. CuDIPS (0.4 mM), a Superoxyde-Dismutase mimetic, which catalyses O2.- transformation into H2O2, induced 1.6-fold decrease in O2- concentration and enhanced PCX sensitivity, with a 1.6 fold- reduction in PCX IC50. The catalase inhibitor Amino-Triazole (6 mM), also increased by 2 PCX sensitivity. The intracellular location of PCX-induced ROS production was studied by measuring O2.- levels by FACS in presence or in absence of either inhibitors of mitochondrial respiratory chain (rotenone and antimycin), or an inhibitor of xanthine oxydase, (allopurinol), or an inhibitor of the cytoplasmic NADPH oxydase (DPI). DPI induced a 20% decrease in ROS levels in A549 cells exposed to PCX while the other inhibitors had no detectable effect. Experiments in mice with xenograft are ongoing to study the role of ROS production in vivo. In conclusion, PCX induces an intracytoplasmic production of O2.-, resulting in H2O2 accumulation, which appears as a crucial step for its cytotoxicity.
Interim Analysis Results from an International, Multi-Centre, Non-Interventional Retrospective Study to Describe Treatment Pathways, Outcomes, and Resource Use in Patients with Classical Hodgkin Lymphoma: B-CD30+ Hodgkin Lymphoma International Multi-Centre Retrospective Study of Treatment Practices and Outcomes (B-HOLISTIC)
Authors: Burhan Ferhanoglu, Tae Min Kim, Gayane Tumyan, Su-Peng Yeh, David Brittain, Amado Karduss, Yok Lam Kwong, Soon Thye Lim, Mubarak Al Mansour, Silvia Rivas-Vera, Yuqin Song, Marta Zerga, Julie Blair, Mehul Dalal, Hui Wan, Mark Hertzberg
Journal: Blood (2018)
Incidence of catheter-related thrombosis in patients with long-term indwelling central venous catheter who received chemotherapies for unresectable advanced digestive cancers
Authors: H. Tanioka, M. Asano, K. Kawasaki, R. Yoshida, N. Waki, F. Uno, M. Ishizaki, K. Yamashita, Y. Morishita, Y. Katata, T. Nagasaka
Journal: Annals of Oncology (2018)
Abstract 18647: Implications of Inconclusive Noninvasive Test Results in Stable Patients With Suspected Coronary Artery Disease: Insights From the PROMISE Trial
Authors: Neha Pagidipati, Larry Hill, Adrian Coles, James E Udelson, Michael H Picard, Patricia A Pellikka, Kerry L Lee, Udo Hoffmann, Pamela S Douglas
Journal: Circulation (2017)

Introduction: Clinically, inconclusive (IC) noninvasive diagnostic tests (NITs) are not infrequent in patients with suspected coronary artery disease, but the actual prevalence and impact of such t...
First-line cetuximab plus cisplatin and fluorouracil vs cisplatin and fluorouracil in Chinese patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck: The randomized, phase III CHANGE-2 trial
Authors: Y. Guo, Y. Luo, Q. Zhang, X. Huang, Z. Li, L. Shen, J. Feng, Y. Sun, K. Yang, M.-H. Ge, X. Zhu, L. Wang, Y. Liu, X. He, C. Bai, K. Xue, Y. Zeng, Y. Cao, W. Chen, T. Lin
Journal: Annals of Oncology (2018)
Impact of Upfront Stem Cell Transplantation in Newly Diagnosed Multiple Myeloma with Del(17) and t(4;14): A Report from the EBMT Chronic Malignancies Working Party
Authors: Nico Gagelmann, Dirk-Jan Eikema, Simona Iacobelli, Helene Schoemans, Linda Koster, Denis Caillot, Didier Blaise, Péter Reményi, Claude-Eric Bulabois, Jakob R. Passweg, Xavier Leleu, Samo Zver, Guido Kobbe, Alessandro Rambaldi, Patrice Chevallier, Mark Ringhoffer, Alexander M Martin, Urpu Salmenniemi, Xavier Poire, Stig Lenhoff, Pietro Pioltelli, Nicola Mordini, Hareth Nahi, Stefan Schönland, Laurent Garderet, Ibrahim Yakoub-Agha, Nicolaus Kroeger
Journal: Blood (2018)
Guidelines on Glycemic Targets for Persons With Type 2 Diabetes
Authors: Devan Kansagara, Amir Qaseem, Timothy J. Wilt
Journal: JAMA (2018)

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
Some invasive inpatient and outpatient procedures were linked to infective endocarditis
Authors: John L. Brusch
Journal: Annals of Internal Medicine (2018)

ACP Journal Club20 November 2018Some invasive inpatient and outpatient procedures were linked to infective endocarditisJohn L. Brusch, MDJohn L. Brusch, MDDivision of Infectious Diseases, Cambridge Health Alliance, Cambridge, Massachusetts, USA (J.L.B.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/ACPJC-2018-169-10-058 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationJanszky I, Gémes K, Ahnve S, Asgeirsson H, Möller J. Invasive procedures associated with the development of infective endocarditis. J Am Coll Cardiol. 2018;71:2744-52. https://pubmed.ncbi.nlm.nih.gov/29903348Clinical Impact RatingsGIM/FP/GP: Cardiology: Infectious Disease: Nephrology: Pulmonology: References1 van den Brink FS, Swaans MJ, Hoogendijk MG, et al. Increased incidence of infective endocarditis after the 2009 European Society of Cardiology guideline update: a nationwide study in the Netherlands. Eur Heart J Qual Care Clin Outcomes. 2017;3:141-7. [PMID: 28927175] Google Scholar2 Sy RW, Kritharides L. Health care exposure and age in infective endocarditis: results of a contemporary population-based profile of 1536 patients in Australia. Eur Heart J 2010;31:1890-7. [PMID: 20453066]. Google Scholar3 Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2017;70:252-89.28315732. Google Scholar4 Issa VS, Fabri J Jr, Pomerantzeff PM, et al. Duration of symptoms in patients with infective endocarditis. Int J Cardiol. 2003;89:63-70. [PMID: 12727006] Google Scholar Author, Article, and Disclosure InformationAffiliations: Division of Infectious Diseases, Cambridge Health Alliance, Cambridge, Massachusetts, USA (J.L.B.)This article was published at Annals.org on 6 November 2018. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 20 November 2018Volume 169, Issue 10Page: JC58KeywordsAntibiotic prophylaxisBone marrowCardiac transplantationEndocarditisInpatientsOutpatient clinicsOutpatientsSepsisSigns and symptomsSpecificity ePublished: 20 November 2018 Issue Published: 20 November 2018 Copyright & PermissionsCopyright © 2018 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Increase in Acute Flaccid Myelitis — United States, 2018
Authors: Susannah L. McKay, Adria D. Lee, Adriana S. Lopez, W. Allan Nix, Kathleen L. Dooling, Amelia A. Keaton, Emily Spence-Davizon, Rachel Herlihy, Thomas A. Clark, Sarah E. Hopkins, Daniel M. Pastula, James Sejvar, M. Steven Oberste, Mark A. Pallansch, Manisha Patel, Janell A. Routh
Journal: MMWR Morbidity and Mortality Weekly Report (2018)

In August 2018, CDC noted an increased number of reports of patients having symptoms clinically compatible with acute flaccid myelitis (AFM), a rare condition characterized by rapid onset of flaccid weakness in one or more limbs and spinal cord gray matter lesions, compared with August 2017. Since 2014, CDC has conducted surveillance for AFM using a standardized case definition (1,2). An Epi-X* notice was issued on August 23, 2018, to increase clinician awareness and provide guidance for case reporting.