Institution
Collège de France
Education•Paris, France•
About: Collège de France is a education organization based out in Paris, France. It is known for research contribution in the topics: Population & Dopamine. The organization has 6541 authors who have published 11983 publications receiving 648742 citations. The organization is also known as: College de France.
Topics: Population, Dopamine, Dopaminergic, Receptor, Neural crest
Papers published on a yearly basis
Papers
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Max Planck Society1, Durham University2, Hoffmann-La Roche3, Collège de France4, Centre national de la recherche scientifique5, Humboldt University of Berlin6, University of Montpellier7, École Polytechnique8, Dublin Institute for Advanced Studies9, DSM10, University of Hamburg11, Joseph Fourier University12, North-West University13, Ruhr University Bochum14, Charles University in Prague15, Yerevan Physics Institute16, University of Namibia17
TL;DR: A first sensitive survey of the inner part of the Milky Way with the High Energy Stereoscopic System (HESS) reveals a population of eight previously unknown firmly detected sources of very high energy γ-rays.
Abstract: Very high energy gamma-rays probe the long-standing mystery of the origin of cosmic rays. Produced in the interactions of accelerated particles in astrophysical objects, they can be used to image cosmic particle accelerators. A first sensitive survey of the inner part of the Milky Way with the High Energy Stereoscopic System (HESS) reveals a population of eight previously unknown firmly detected sources of very high energy gamma-rays. At least two have no known radio or x-ray counterpart and may be representative of a new class of "dark" nucleonic cosmic ray sources.
317 citations
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Pierre-and-Marie-Curie University1, Nottingham City Hospital2, Erasmus University Rotterdam3, University Hospital of Lausanne4, Medical University of Vienna5, University of Turin6, Ruhr University Bochum7, Rabin Medical Center8, Collège de France9, Curie Institute10, University of Cologne11, Umeå University12, University of Bonn13, VU University Amsterdam14, University of Zurich15
TL;DR: These guidelines provide consensus considerations and recommendations for diagnosis, assessment, staging, and treatment of primary CNS lymphoma and should aid clinicians in their daily practice and decision making, and serve as a basis for future investigations in neuro-oncology.
Abstract: The management of primary CNS lymphoma is one of the most controversial topics in neuro-oncology because of the complexity of the disease and the very few controlled studies available. In 2013, the European Association of Neuro-Oncology created a multidisciplinary task force to establish evidence-based guidelines for immunocompetent adults with primary CNS lymphoma. In this Review, we present these guidelines, which provide consensus considerations and recommendations for diagnosis, assessment, staging, and treatment of primary CNS lymphoma. Specifically, we address aspects of care related to surgery, systemic and intrathecal chemotherapy, intensive chemotherapy with autologous stem-cell transplantation, radiotherapy, intraocular manifestations, and management of elderly patients. The guidelines should aid clinicians in their daily practice and decision making, and serve as a basis for future investigations in neuro-oncology.
315 citations
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TL;DR: Results indicated that Mash1 and Math3 direct neuronal versus glial fate determination in the CNS and raised the possibility that downregulation of these bHLH genes is one of the mechanisms to initiate gliogenesis.
Abstract: Whereas vertebrate achaete–scute complex (as-c) and atonal (ato) homologs are required for neurogenesis, their neuronal determination activities in the central nervous system (CNS) are not yet supported by loss-of-function studies, probably because of genetic redundancy. Here, to address this problem, we generated mice double mutant for the as-c homolog Mash1 and the ato homolog Math3. Whereas in Mash1 or Math3 single mutants neurogenesis is only weakly affected, in the double mutants tectal neurons, two longitudinal columns of hindbrain neurons and retinal bipolar cells were missing and, instead, those cells that normally differentiate into neurons adopted the glial fate. These results indicated that Mash1 and Math3 direct neuronal versus glial fate determination in the CNS and raised the possibility that downregulation of these bHLH genes is one of the mechanisms to initiate gliogenesis.
315 citations
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TL;DR: ANGPTL4, originally identified as a peroxisome proliferator-activated receptor alpha and gamma target gene, has potential for use as a new diagnostic tool and a potential therapeutic target, modulating angiogenesis both in tumors and in ischemic tissues.
Abstract: Ischemic and solid tumor tissues are less well perfused than normal tissue, leading to metabolic changes and chronic hypoxia, which in turn promotes angiogenesis. We identified human angiopoietin-like 4 (angptl4) as a gene with hypoxia-induced expression in endothelial cells. We showed that the levels of both mRNA and protein for ANGPTL4 increased in response to hypoxia. When tested in the chicken chorioallantoic membrane assay, ANGPTL4 induced a strong proangiogenic response, independently of vascular endothelial growth factor. In human pathology, ANGPTL4 mRNA is produced in ischemic tissues, in conditions such as critical leg ischemia. In tumors, ANGPTL4 is produced in the hypoxic areas surrounding necrotic regions. We observed particularly high levels of ANGPTL4 mRNA in tumor cells of conventional renal cell carcinoma. Other benign and malignant renal tumor cells do not produce ANGPTL4 mRNA. This molecule therefore seems to be a marker of conventional renal cell carcinoma. ANGPTL4, originally identified as a peroxisome proliferator-activated receptor α and γ target gene, has potential for use as a new diagnostic tool and a potential therapeutic target, modulating angiogenesis both in tumors and in ischemic tissues. This study also suggests that ANGPTL4 may provide a link between metabolic disorders and hypoxia-induced angiogenesis.
315 citations
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TL;DR: The selective expression of RXR beta in Sertoli cells, together with the timing of appearance of the histological abnormalities, suggests that the primary defect resulting from the mutation resides in these cells.
Abstract: We have generated mouse lines in which the RXR beta gene was disrupted by homologous recombination. Approximately 50% of the RXR beta homozygous mutants died before or at birth, but those that survived appeared normal except that the males were sterile, owing to oligo-astheno-teratozoospermia. Failure of spermatid release occurred within the germinal epithelium, and the epididymis contained very few spermatozoa that, in addition, exhibited abnormal acrosomes and tails. There was a progressive accumulation of lipids within the mutant Sertoli cells, which were histochemically characterized as unsaturated triglycerides. In old mutant males, progressive degeneration of the germinal epithelium occurred, ending with the formation of acellular lipid-filled tubules. The selective expression of RXR beta in Sertoli cells, together with the timing of appearance of the histological abnormalities, suggests that the primary defect resulting from the mutation resides in these cells.
314 citations
Authors
Showing all 6597 results
Name | H-index | Papers | Citations |
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Pierre Chambon | 211 | 884 | 161565 |
Irving L. Weissman | 201 | 1141 | 172504 |
David R. Williams | 178 | 2034 | 138789 |
Kari Alitalo | 174 | 817 | 114231 |
Pierre Bourdieu | 153 | 592 | 194586 |
Stanislas Dehaene | 149 | 456 | 86539 |
Howard L. Weiner | 144 | 1047 | 91424 |
Alain Fischer | 143 | 770 | 81680 |
Yves Agid | 141 | 669 | 74441 |
Michel Foucault | 140 | 499 | 191296 |
Jean-Pierre Changeux | 138 | 672 | 76462 |
Jean-Marie Tarascon | 136 | 853 | 137673 |
K. Ganga | 132 | 272 | 99004 |
Jacques Delabrouille | 131 | 354 | 94923 |
G. Patanchon | 128 | 241 | 87233 |