Institution
University of Grenoble
Education•Saint-Martin-d'Hères, France•
About: University of Grenoble is a education organization based out in Saint-Martin-d'Hères, France. It is known for research contribution in the topics: Population & Context (language use). The organization has 25658 authors who have published 45143 publications receiving 909760 citations.
Papers published on a yearly basis
Papers
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TL;DR: Since no evidence of third-generation squarks is found, exclusion limits are derived by combining several analyses and are presented in both a simplified model framework, assuming simple decay chains, as well as within the context of more elaborate phenomenological supersymmetric models.
Abstract: This paper reviews and extends searches for the direct pair production of the scalar supersymmetric partners of the top and bottom quarks in proton-proton collisions collected by the ATLAS collaboration during the LHC Run 1. Most of the analyses use 20 [Formula: see text] of collisions at a centre-of-mass energy of [Formula: see text] TeV, although in some case an additional [Formula: see text] of collision data at [Formula: see text] TeV are used. New analyses are introduced to improve the sensitivity to specific regions of the model parameter space. Since no evidence of third-generation squarks is found, exclusion limits are derived by combining several analyses and are presented in both a simplified model framework, assuming simple decay chains, as well as within the context of more elaborate phenomenological supersymmetric models.
225 citations
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TL;DR: Thrombus formation on the device is not uncommon in patients with AF who are treated by LAA closure, and such events are strongly associated with a higher risk of ischemic stroke during follow-up.
225 citations
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TL;DR: CD74-NRG1 gene fusions are activating genomic alterations in invasive mucinous adenocarcinomas and may offer a therapeutic opportunity for a lung tumor subtype with, so far, no effective treatment.
Abstract: We discovered a novel somatic gene fusion, CD74-NRG1 , by transcriptome sequenc- ing of 25 lung adenocarcinomas of never smokers. By screening 102 lung adenocar- cinomas negative for known oncogenic alterations, we found four additional fusion-positive tumors, all of which were of the invasive mucinous subtype. Mechanistically, CD74-NRG1 leads to extracellular expression of the EGF-like domain of NRG1 III-β3, thereby providing the ligand for ERBB2-ERBB3 receptor complexes. Accordingly, ERBB2 and ERBB3 expression was high in the index case, and expres- sion of phospho-ERBB3 was specifi cally found in tumors bearing the fusion ( P < 0.0001). Ectopic expression of CD74-NRG1 in lung cancer cell lines expressing ERBB2 and ERBB3 activated ERBB3 and the PI3K-AKT pathway, and led to increased colony formation in soft agar. Thus, CD74-NRG1 gene fusions are activating genomic alterations in invasive mucinous adenocarcinomas and may offer a therapeutic opportunity for a lung tumor subtype with, so far, no effective treatment. SIGNIFICANCE: CD74-NRG1 fusions may represent a therapeutic opportunity for invasive mucinous lung adenocarcinomas, a tumor with no effective treatment that frequently presents with multifocal unresectable disease. Cancer Discov; 4(4); 415-22. ©2014 AACR.
224 citations
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Ludwig Maximilian University of Munich1, Maastricht University2, University of California, San Francisco3, University of Grenoble4, Centro Nacional de Investigaciones Cardiovasculares5, University of Hamburg6, Scripps Research Institute7, Karolinska Institutet8, Technische Universität München9, Max Planck Society10
TL;DR: This work demonstrates that extracellular histone H4-mediated membrane lysis of smooth muscle cells (SMCs) triggers arterial tissue damage and inflammation, and identifies a form of cell death found at the core of chronic vascular disease that is instigated by leukocytes and can be targeted therapeutically.
Abstract: The perpetuation of inflammation is an important pathophysiological contributor to the global medical burden. Chronic inflammation is promoted by non-programmed cell death; however, how inflammation is instigated, its cellular and molecular mediators, and its therapeutic value are poorly defined. Here we use mouse models of atherosclerosis-a major underlying cause of mortality worldwide-to demonstrate that extracellular histone H4-mediated membrane lysis of smooth muscle cells (SMCs) triggers arterial tissue damage and inflammation. We show that activated lesional SMCs attract neutrophils, triggering the ejection of neutrophil extracellular traps that contain nuclear proteins. Among them, histone H4 binds to and lyses SMCs, leading to the destabilization of plaques; conversely, the neutralization of histone H4 prevents cell death of SMCs and stabilizes atherosclerotic lesions. Our data identify a form of cell death found at the core of chronic vascular disease that is instigated by leukocytes and can be targeted therapeutically.
224 citations
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Paris Diderot University1, Boehringer Ingelheim2, University of Perugia3, French Institute of Health and Medical Research4, Dresden University of Technology5, University of Grenoble6, University of Western Brittany7, University of Göttingen8, University of Freiburg9, Greifswald University Hospital10, University of Bologna11, Medical University of Warsaw12, Ljubljana University Medical Centre13, Technische Universität München14, Medical University of Vienna15
TL;DR: Thrombolytic treatment did not affect long-term mortality rates, and it did not appear to reduce residual dyspnea or RV dysfunction in patients with intermediate-risk PE.
224 citations
Authors
Showing all 25961 results
Name | H-index | Papers | Citations |
---|---|---|---|
Dieter Lutz | 139 | 671 | 67414 |
Marcella Bona | 137 | 1391 | 92162 |
Nicolas Berger | 137 | 1581 | 96529 |
Cordelia Schmid | 135 | 464 | 103925 |
J. F. Macías-Pérez | 134 | 486 | 94715 |
Marina Cobal | 132 | 1078 | 85437 |
Lydia Roos | 132 | 1284 | 89435 |
Tetiana Hryn'ova | 131 | 1059 | 84260 |
Johann Collot | 131 | 1018 | 82865 |
Remi Lafaye | 131 | 1012 | 83281 |
Jan Stark | 131 | 1186 | 87025 |
Sabine Crépé-Renaudin | 129 | 1142 | 82741 |
Isabelle Wingerter-Seez | 129 | 930 | 79689 |
James Alexander | 129 | 886 | 75096 |
Jessica Levêque | 129 | 1006 | 70208 |