474 research outputs found

    Bonne nouvelle : les enseignants du fondamental estiment qu’il est important d’enseigner l’oral en classe et se sentent compétents pour le faire ! Mais certains ne le font quand même pas…

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    L'objectif de cette contribution est de prolonger un Ă©tat des lieux rĂ©alisĂ© en 2019 sur l'enseignement de l'oral. Plus particulièrement, nous abordons ici : (1) les croyances des enseignants concernant l’oral et son enseignement ; (2) leur sentiment de compĂ©tence pour le faire ; (3) les situations orales pour lesquelles les enseignants estiment que les Ă©lèves doivent ĂŞtre compĂ©tents en langage orale ; (4) ce qu'ils disent faire concernant l'oral en classe et (5) les freins qui pourraient les empĂŞcher de mener Ă  bien des activitĂ©s oĂą l'oral est enseignĂ©. En plus, nous avons voulu savoir si les rĂ©ponses Ă  ces questionnements divergeaient entre les enseignants du maternel et du primaire. Il ressort des analyses quantitatives et qualitatives menĂ©es certaines diffĂ©rences existent entre les enseignants des deux "groupes", mais aussi des ressemblances : ils trouvent que c'est important de travailler et enseigner l'oral en classe et ils se disent confiants dans leur capacitĂ© Ă  l'enseigner. Leur top 4 des situations qu'il faudrait privilĂ©gier en classe est "donner une explication, expliquer un raisonnement, exprimer ses Ă©motions et reformuler une idĂ©e". On remarque aussi un Ă©cart entre ce que les enseignants pensent, leurs conceptions de l’enseignement de l’oral en classe et leurs pratiques rapportĂ©es qui renseignent finalement peu d'oral enseignĂ©. Cinq freins pour l'enseignement de l'oral ressortent de nos analyses

    Symptom Clusters in Acute Myocardial Infarction: A Secondary Data Analysis

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    Background: Early recognition of acute myocardial infarction (AMI) symptoms and reduced time to treatment may reduce morbidity and mortality. People having AMI experience a constellation of symptoms, but the common constellations or clusters of symptoms have yet to be identified. Objectives: To identify clusters of symptoms that represent AMI. Methods: This was a secondary data analysis of nine descriptive, cross-sectional studies that included data from 1,073 people having AMI in the United States and England. Data were analyzed using latent class cluster analysis, an atheoretical method that uses only information contained in the data. Results: Five distinct clusters of symptoms were identified. Age, race, and sex were statistically significant in predicting cluster membership. None of the symptom clusters described in this analysis included all of the symptoms that are considered typical. In one cluster, subjects had only a moderate to low probability of experiencing any of the symptoms analyzed. Discussion: Symptoms of AMI occur in clusters, and these clusters vary among persons. None of the clusters identified in this study included all of the symptoms that are included typically as symptoms of AMI (chest discomfort, diaphoresis, shortness of breath, nausea, and lightheadedness). These AMI symptom clusters must be communicated clearly to the public in a way that will assist them in assessing their symptoms more efficiently and will guide their treatment-seeking behavior. Symptom clusters for AMI must also be communicated to the professional community in a way that will facilitate assessment and rapid intervention for AMI

    What Can a Pilot Congestive Heart Failure Disease Management Program Tell Us about Likely Return on Investment?: A Case Study from a Program Offered to Federal Employees

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    In 1999, the Blue Cross and Blue Shield Federal Employee Program (FEP) implemented a pilot disease management program to manage congestive heart failure (CHF) among members. The purpose of this project was to estimate the financial return on investment in the pilot CHF program, prior to a full program rollout. A cohort of 457 participants from the state of Maryland was matched to a cohort of 803 nonparticipants from a neighboring state where the CHF program was not offered. Each cohort was followed for 12 months before the program began and 12 months afterward. The outcome measures of primary interest were the differences over time in medical care expenditures paid by FEP and by all payers. Independent variables included indicators of program participation, type of heart disease, comorbidity measures, and demographics. From the perspective of the funding organization (FEP), the estimated return on investment for the pilot CHF disease management program was a savings of 1.08inmedicalexpenditureforeverydollarspentontheprogram.Addingsavingstootherpayersaswell,thereturnoninvestmentwasasavingsof1.08 in medical expenditure for every dollar spent on the program. Adding savings to other payers as well, the return on investment was a savings of 1.15 in medical expenditures per dollar spent on the program. The amount of savings depended upon CHF risk levels. The value of a pilot initiative and evaluation is that lessons for larger-scale efforts can be learned prior to full-scale rollout. (Disease Management 2005;8:346-360)Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/63402/1/dis.2005.8.346.pd

    The Transcription Factor GLI1 Mediates TGFb1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism

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    The role of the epithelial-to-mesenchymal transition (EMT) during hepatocellular carcinoma (HCC) progression is well established, however the regulatory mechanisms modulating this phenomenon remain unclear. Here, we demonstrate that transcription factor glioma-associated oncogene 1 (GLI1) modulates EMT through direct up-regulation of SNAI1 and serves as a downstream effector of the transforming growth factor-b1 (TGFb1) pathway, a well-known regulator of EMT in cancer cells. Overexpression of GLI1 increased proliferation, viability, migration, invasion, and colony formation by HCC cells. Conversely, GLI1 knockdown led to a decrease in all the above-mentioned cancer-associated phenotypes in HCC cells. Further analysis of GLI1 regulated cellular functions showed that this transcription factor is able to induce EMT and identified SNAI1 as a transcriptional target of GLI1 mediating this cellular effect in HCC cells. Moreover, we demonstrated that an intact GLI1-SNAI1 axis is required by TGFb1 to induce EMT in these cells. Together, these findings define a novel cellular mechanism regulated by GLI1, which controls the growth and EMT phenotype in HCC.National Institutes of Health Grants CA100882 and CA128633 (to LRR) and CA165076; the Mayo Clinic Center for Cell Signaling in Gastroenterology (NIDDK P30DK084567) (to MEFZ); the Mayo Clinic Cancer Center (CA15083), the Mayo Clinic Center for Translational Science Activities (NIH/NCRR CTSA Grant Number KL2 RR024151), and an American Gastroenterological Association Foundation for Digestive Health and Nutrition Bridging Grant (to LRR)

    Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

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    Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

    Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

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    Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

    Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

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    This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

    Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

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    Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment

    Parenthood in survivors of Hodgkin lymphoma: an EORTC-GELA general population case-control study.

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    Contains fulltext : 108966.pdf (publisher's version ) (Open Access)PURPOSE: We investigated the impact of Hodgkin lymphoma (HL) on parenthood, including factors influencing parenthood probability, by comparing long-term HL survivors with matched general population controls. PATIENTS AND METHODS: A Life Situation Questionnaire was sent to 3,604 survivors treated from 1964 to 2004 in successive clinical trials. Responders were matched with controls (1:3 or 4) for sex, country, education, and year of birth (10-year groups). Controls were given an artificial date of start of treatment equal to that of their matched case. The main end point was presence of biologic children after treatment, which was evaluated by using conditional logistic regression analysis. Logistic regression analysis was used to analyze factors influencing spontaneous post-treatment parenthood. RESULTS: In all, 1,654 French and Dutch survivors were matched with 6,414 controls. Median follow-up was 14 years (range, 5 to 44 years). After treatment, the odds ratio (OR) for having children was 0.77 (95% CI, 0.68 to 0.87; P < .001) for survivors compared with controls. Of 898 survivors who were childless before treatment, 46.7% achieved post-treatment parenthood compared with 49.3% of 3,196 childless controls (OR, 0.87; P = .08). Among 756 survivors with children before treatment, 12.4% became parents after HL treatment compared with 22.2% of 3,218 controls with children before treatment (OR, 0.49; P < .001). Treatment with alkylating agents, second-line therapy, and age older than 35 years at treatment appeared to reduce the chances of spontaneous post-treatment parenthood. CONCLUSION: Survivors of HL had slightly but significantly fewer children after treatment than matched general population controls. The difference concerned only survivors who had children before treatment and appears to have more personal than biologic reasons. The chance of successful post-treatment parenthood was 76%

    Communications Biophysics

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    Contains reports on ten research projects.National Institutes of Health (Grant 5 P01 NS13126)National Institutes of Health (Training Grant 5 T32 NS0704)National Science Foundation (Grant BNS80-06369)National Institutes of Health (Grant 5 R01 NS11153)National Science Foundation (Grant BNS77-16861)National Institutes of Health (Grant 5 RO1 NS12846)National Science Foundation (Grant BNS77-21751)National Institutes of Health (Grant 1 P01 NS14092)Karmazin Foundation through the Council for the Arts at MITNational Institutes of Health (Fellowship 5 F32 NS06386)National Science Foundation (Fellowship SP179-14913)National Institutes of Health (Grant 5 RO1 NS11080
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