8 results on '"Véronique Baud"'
Search Results
2. HIGH ADIPOSE TISSUE DENSITY IS A NEGATIVE PROGNOSTIC FACTOR IN DLBCL PATIENTS TREATED BY R‐CHOP, INDEPENDENT FROM TMTV AND PS –FROM THE REMARC STUDY
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Hervé Tilly, O. Casasnovas, L. Vercellino, Michel Meignan, Loïc Chartier, A. Cottereau, Catherine Thieblemont, J.-F. Deux, Véronique Baud, and A. Judet
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Oncology ,Cancer Research ,medicine.medical_specialty ,Prognostic factor ,business.industry ,Internal medicine ,Medicine ,Adipose tissue ,Hematology ,General Medicine ,business - Published
- 2021
3. DEFINING ULTRA‐HIGH‐RISK DLBCL PATIENTS PRIOR TO INITIAL TREATMENT BASED ON AN INTEGRATIVE HOST AND DISEASE PROGNOSTIC SCORE (FROM REMARC STUDY)
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Catherine Thieblemont, Loïc Chartier, A. Cottereau, O. Casasnovas, Michel Meignan, Véronique Baud, A. Judet, Hervé Tilly, Laetitia Vercellino, and J.-F. Deux
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Oncology ,Cancer Research ,medicine.medical_specialty ,business.industry ,Hematology ,General Medicine ,Disease ,Ultra high risk ,Prognostic score ,Internal medicine ,medicine ,Initial treatment ,business ,Host (network) - Published
- 2021
4. Author response for 'Tumor necrosis factor receptor family co‐stimulation increases regulatory T cell activation and function via NF‐κB'
- Author
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Véronique Baud, Harald Wajant, Tomás Gomes, Martina Lubrano di Ricco, Gilles Marodon, Davi Collares, Emilie Ronin, Jordane Divoux, Yenkel Grinberg-Bleyer, Sylvie Grégoire, and Benoît L. Salomon
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chemistry.chemical_compound ,medicine.anatomical_structure ,chemistry ,Co-stimulation ,Regulatory T cell ,medicine ,Cancer research ,NF-κB ,Tumor Necrosis Factor Receptor Family ,Biology ,Function (biology) - Published
- 2019
5. Prevalence and factors associated with academic burnout risk among nursing and midwifery students during the COVID‐19 pandemic: A cross‐sectional study
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Véronique Baudewyns, Arnaud Bruyneel, Pierre Smith, Jean‐Christophe Servotte, and Jacinthe Dancot
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burnout ,COVID‐19 (SARS‐CoV‐2) ,education ,midwives ,nursing ,prevalence ,Nursing ,RT1-120 - Abstract
Abstract Aim The aim of the study was to assess the prevalence of academic burnout (AB) and its associated factors among nursing and midwifery students during the COVID‐19 pandemic. Design A correlational cross‐sectional study. Methods An online survey was distributed from November to December 2020 to nursing and midwifery students in Belgium. The risk of AB was assessed using the MBI‐SS Academic Burnout Inventory scale. Factors associated with AB were related to the personal life and level of education of the student and to the COVID‐19 pandemic. Results The prevalence of overall AB risk was 50.0% (95% CI 48.5–53.1). Factors significantly associated with higher risk of AB were having a child, having a job, the level of academic training, working overtime, insufficient personal protective equipment against viral contamination during the last internship, work overload due to the pandemic, personal proven or possible SARS‐CoV‐2 infection and having a relative who died related to COVID‐19.
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- 2023
- Full Text
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6. Dichotomy between factors inducing the immunosuppressive enzyme IL-4-induced gene 1 (IL4I1) in B lymphocytes and mononuclear phagocytes
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Nadine Martin-Garcia, Marie-Line Puiffe, Véronique Baud, Jean-Pierre Farcet, Céline Cousin, Fanny Chereau, Valérie Molinier-Frenkel, Fanette Lasoudris, Jeanine Marquet, Flavia Castellano, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service d'immunologie biologique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Guellaen, Georges, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Institut National de la Santé et de la Recherche Médicale (INSERM) - IFR10 - Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut Cochin (UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), and Assistance publique - Hôpitaux de Paris (AP-HP) - Hôpital Henri Mondor - Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)
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MESH: Inflammation ,MESH: NF-kappa B ,Immune tolerance ,0302 clinical medicine ,MESH: RNA, Small Interfering ,Immunology and Allergy ,RNA, Small Interfering ,MESH: Flavoproteins ,granuloma ,Mononuclear Phagocyte System ,Tissue homeostasis ,STAT6 ,B-Lymphocytes ,0303 health sciences ,STAT ,NF-kappa B ,3. Good health ,Cell biology ,STAT1 Transcription Factor ,MESH: STAT6 Transcription Factor ,030220 oncology & carcinogenesis ,medicine.symptom ,immunosuppressive enzyme ,MESH: Immune Tolerance ,MESH: Interferon-gamma ,CD40 Ligand ,Immunology ,Inflammation ,Biology ,L-Amino Acid Oxidase ,Article ,NFkB ,Cell Line ,Proinflammatory cytokine ,MESH: Coculture Techniques ,Interferon-gamma ,03 medical and health sciences ,Th2 Cells ,MESH: Th2 Cells ,MESH: B-Lymphocytes ,MESH: Cell Proliferation ,[SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Immune Tolerance ,medicine ,Humans ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,Interleukin 4 ,Cell Proliferation ,MESH: CD40 Ligand ,030304 developmental biology ,MESH: Mononuclear Phagocyte System ,MESH: Humans ,CD40 ,Flavoproteins ,Th1 Cells ,MESH: Interleukin-4 ,Coculture Techniques ,MESH: Cell Line ,MESH: Th1 Cells ,inflammation ,Cell culture ,biology.protein ,Interleukin-4 ,MESH: STAT1 Transcription Factor ,STAT6 Transcription Factor - Abstract
International audience; MPhi and DC are key elements in the control of tissue homeostasis and response to insult. In this work, we demonstrate that MPhi and DC are the major producers of the phenylalanine catabolizing enzyme IL-4-induced gene 1 (IL4I1) under inflammatory conditions. IL4I1 was first described in B cells, which indeed can produce IL4I1 in vitro, although at much lower levels. In vivo, IL4I1 is highly expressed by MPhi and DC of Th1 granulomas (sarcoidosis, tuberculosis) but poorly detected in Th2 granulomas (schistosomiasis). In vitro, expression of the enzyme is induced in mononuclear phagocytes by various pro-inflammatory stimuli through the activation of the transcription factors NF-kappaB and/or STAT1. B cells also express IL4I1 in response to NF-kappaB-activating stimuli such as CD40L; however, in contrast to myeloid cells, B cells are insensitive to IFN-gamma but respond to stimulation of the IL-4/STAT6 axis. As we show that the expression of IL4I1 by a monocytic cell line inhibits T-cell proliferation and production of IFN-gamma and inflammatory cytokines, we propose that IL4I1 participates in the downregulation of Th1 inflammation in vivo.
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- 2010
7. The IKK complex contributes to the induction of autophagy
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Ezgi Tasdemir, Alfredo Criollo, Alain Israël, Amena Ben Younes, Maximilien Tailler, Guido Kroemer, Eugenia Morselli, Oliver Kepp, Daniela De Stefano, Hélène Authier, Laurence Zitvogel, Maria Chiara Maiuri, Laura Senovilla, Gérard Pierron, Ilio Vitale, Shensi Shen, Véronique Baud, Nicolas F. Delahaye, Sergio Lavandero, Francis Harper, Lorenzo Galluzzi, Antoine Tesniere, Criollo, A, Senovilla, L, Authier, H, Maiuri, MARIA CHIARA, Morselli, E, Vitale, I, Kepp, O, Tasdemir, E, Galluzzi, L, Shen, S, Tailler, M, Delahaye, N, Tesniere, A, DE STEFANO, Daniela, Younes, Ab, Harper, F, Pierron, G, Lavandero, S, Zitvogel, L, Israel, A, Baud, V, and Kroemer, G.
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Mice, Transgenic ,IκB kinase ,Biology ,BAG3 ,environment and public health ,Article ,General Biochemistry, Genetics and Molecular Biology ,Mice ,chemistry.chemical_compound ,Autophagy ,Animals ,Humans ,CHUK ,Molecular Biology ,Transcription factor ,Cells, Cultured ,General Immunology and Microbiology ,General Neuroscience ,NF-kappa B ,NF-κB ,NFKB1 ,I-kappa B Kinase ,Cell biology ,Mice, Inbred C57BL ,enzymes and coenzymes (carbohydrates) ,chemistry ,Multiprotein Complexes ,NIH 3T3 Cells ,biological phenomena, cell phenomena, and immunity ,Signal transduction ,HeLa Cells ,Signal Transduction - Abstract
In response to stress, cells start transcriptional and transcription-independent programs that can lead to adaptation or death. Here, we show that multiple inducers of autophagy, including nutrient depletion, trigger the activation of the IKK (IkappaB kinase) complex that is best known for its essential role in the activation of the transcription factor NF-kappaB by stress. Constitutively active IKK subunits stimulated autophagy and transduced multiple signals that operate in starvation-induced autophagy, including the phosphorylation of AMPK and JNK1. Genetic inhibition of the nuclear translocation of NF-kappaB or ablation of the p65/RelA NF-kappaB subunit failed to suppress IKK-induced autophagy, indicating that IKK can promote the autophagic pathway in an NF-kappaB-independent manner. In murine and human cells, knockout and/or knockdown of IKK subunits (but not that of p65) prevented the induction of autophagy in response to multiple stimuli. Moreover, the knockout of IKK-beta suppressed the activation of autophagy by food deprivation or rapamycin injections in vivo, in mice. Altogether, these results indicate that IKK has a cardinal role in the stimulation of autophagy by physiological and pharmacological stimuli.
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- 2009
8. PAK4, a novel effector for Cdc42Hs, is implicated in the reorganization of the actin cytoskeleton and in the formation of filopodia
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Véronique Baud, Audrey Minden, Alexandra Fritsch, Barbara Belisle, Arie Abo, Marta S. Cammarano, Chuntao Dan, and Jian Qu
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DNA, Complementary ,Molecular Sequence Data ,Golgi Apparatus ,Arp2/3 complex ,Cell Cycle Proteins ,macromolecular substances ,Protein Serine-Threonine Kinases ,General Biochemistry, Genetics and Molecular Biology ,Cell Line ,Substrate Specificity ,Jurkat Cells ,Actin remodeling of neurons ,Biopolymers ,GTP-Binding Proteins ,Humans ,Amino Acid Sequence ,Pseudopodia ,Phosphorylation ,cdc42 GTP-Binding Protein ,Molecular Biology ,Cytoskeleton ,Base Sequence ,Sequence Homology, Amino Acid ,General Immunology and Microbiology ,biology ,General Neuroscience ,JNK Mitogen-Activated Protein Kinases ,Actin remodeling ,Actin cytoskeleton ,Actins ,Cell biology ,p21-Activated Kinases ,Cdc42 GTP-Binding Protein ,Paracytophagy ,Calcium-Calmodulin-Dependent Protein Kinases ,Mutation ,biology.protein ,Guanosine Triphosphate ,MDia1 ,Mitogen-Activated Protein Kinases ,Filopodia ,Protein Binding ,Research Article - Abstract
The GTPases Rac and Cdc42Hs control diverse cellular functions. In addition to being mediators of intracellular signaling cascades, they have important roles in cell morphogenesis and mitogenesis. We have identified a novel PAK-related kinase, PAK4, as a new effector molecule for Cdc42Hs. PAK4 interacts only with the activated form of Cdc42Hs through its GTPase-binding domain (GBD). Co-expression of PAK4 and the constitutively active Cdc42HsV12 causes the redistribution of PAK4 to the brefeldin A-sensitive compartment of the Golgi membrane and the subsequent induction of filopodia and actin polymerization. Importantly, the reorganization of the actin cytoskeleton is dependent on PAK4 kinase activity and on its interaction with Cdc42Hs. Thus, unlike other members of the PAK family, PAK4 provides a novel link between Cdc42Hs and the actin cytoskeleton. The cellular locations of PAK4 and Cdc42Hs suggest a role for the Golgi in cell morphogenesis.
- Published
- 1998
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