243 master-"https:" "https:" "https:" "https:" "UCL" "UCL" research jobs at CNRS in France
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interact with researchers from diverse backgrounds to develop innovative approaches for studying lipid metabolism. This environment fosters the development of original projects combining cell biology
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The expert will participate in the necessary methodological developments and analyses of airborne data recorded by the IAGOS research infrastructure (https://www.iagos.org ) and from other networks, to provide
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laboratories such as the ENS Physics Laboratory in Paris or the Albert Fert Laboratory in Palaiseau for THz emission measurements. Where to apply Website https://emploi.cnrs.fr/Offres/CDD/UMR8191-MATJAM-002
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responsible for a research project aimed at understanding how macrophages and their tissue niches influence homeostasis and tissue repair in vivo, using original and innovative models. The position is based
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A, Campus Illkirch station) from Strasbourg train station or by car (parking available). Public transportation costs are partially covered. Where to apply Website https://emploi.cnrs.fr/Offres/CDD
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campus with meal subsidies from the CNRS. Where to apply Website https://emploi.cnrs.fr/Candidat/Offre/UMR7515-JULBER-106/Candidater.aspx Requirements Research FieldChemistryEducation LevelPhD
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Chernodub's group in Tours, Adolfo Grushin's group in San Sebastian, Spain, and Andrei Fedorenko, Edmond Orignac and David Carpentier at LPENSL. Where to apply Website https://emploi.cnrs.fr/Candidat/Offre
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Research Framework Programme? Not funded by a EU programme Is the Job related to staff position within a Research Infrastructure? No Offer Description The postdoctoral researcher will have the primary
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atmospheric models WRF-Chem and/or CHIMERE, developing new descriptions of primary ice formation from sources such as aviation, wildfire emissions, and mineral dust. High-resolution simulations of selected case
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abnormal scarring of the liver in which healthy tissue is replaced by a rigid and dysfunctional extracellular matrix (ECM). It results from chronic damage, activating myofibroblasts, the main agents