Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Cécilie Dufour"'
Publikováno v:
Experimental Cell Research. 313:394-403
The mechanisms underlying the altered osteoblastogenesis and bone loss in response to disuse are incompletely understood. Using the rat tail suspension model, we studied the effect of skeletal unloading on osteoblast and osteocyte apoptosis. Tail sus
Autor:
Eric Billaud, Marie-Josée Wendling, Georges Haour, Fabrice Carrat, Philippe Sogni, Lionel Piroth, Patrick Miailhes, David Rey, Faiza Ajana, Alexandra Rohel, Jean-Michel Molina, Cécilie Dufour, Marie-Louise Michel, Odile Launay
Publikováno v:
The Lancet Infectious Diseases
The Lancet Infectious Diseases, New York, NY : Elsevier Science ; The Lancet Pub. Group, 2001-, 2015, 15 (11), pp.1283-1291. ⟨10.1016/s1473-3099(15)00220-0⟩
The Lancet Infectious Diseases, 2015, 15 (11), pp.1283-1291. ⟨10.1016/s1473-3099(15)00220-0⟩
The Lancet Infectious Diseases, New York, NY : Elsevier Science ; The Lancet Pub. Group, 2001-, 2015, 15 (11), pp.1283-1291. ⟨10.1016/s1473-3099(15)00220-0⟩
The Lancet Infectious Diseases, 2015, 15 (11), pp.1283-1291. ⟨10.1016/s1473-3099(15)00220-0⟩
Equipe CHU UB (EA) Pôle MERS CT3 Hors Enjeu ANRS HB04 B-BOOST study group : Hugues Aumaitre (Centre Hospitalier Marechal Joff re, Perpignan, France); Jean-Luc Berger (Centre Hospitalier Universitaire de Reims– Hopital Robert Debre, Reims, France);
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3e4d4182b02eb4877b01891100ae119c
https://www.hal.inserm.fr/inserm-01996236
https://www.hal.inserm.fr/inserm-01996236
Autor:
Fabrice Carrat, Fabien Zoulim, Dominique Larrey, Lawrence Serfaty, Christophe Hézode, Hélène Fontaine, Jean-Pierre Zarski, Véronique Loustaud-Ratti, François Bailly, Cécilie Dufour, Pierre Pradat, Jean-Pierre Bronowicki, Victor Virlogeux, Marc Bourlière, Sophie Metivier, Laurent Alric, Didier Samuel
Publikováno v:
Clinics and Research in Hepatology and Gastroenterology
Clinics and Research in Hepatology and Gastroenterology, 2015, 39 (4), pp.443-450. ⟨10.1016/j.clinre.2014.12.007⟩
Clinics and Research in Hepatology and Gastroenterology, Elsevier, 2015, 39 (4), pp.443-450. ⟨10.1016/j.clinre.2014.12.007⟩
Clinics and Research in Hepatology and Gastroenterology, 2015, 39 (4), pp.443-450. ⟨10.1016/j.clinre.2014.12.007⟩
Clinics and Research in Hepatology and Gastroenterology, Elsevier, 2015, 39 (4), pp.443-450. ⟨10.1016/j.clinre.2014.12.007⟩
Summary Background and objective To assess within the ANRS CO20-CUPIC cohort whether the viral load (VL) at week 2/week 6 for telaprevir/boceprevir-based triple therapy, respectively, was predictive of sustained virological response (SVR) in patients
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9dd59c4d123cafb31f116f5e39652393
https://hal.univ-lorraine.fr/hal-01669113
https://hal.univ-lorraine.fr/hal-01669113
Publikováno v:
The American Journal of Pathology. 169:1303-1311
Genetic mutations of Twist, a basic helix-loop-helix transcription factor, induce premature fusion of cranial sutures in Saethre-Chotzen syndrome (SCS). We report here a previously undescribed mechanism involved in the altered osteoblastogenesis in S
Publikováno v:
BONE
BONE, Elsevier, 2008, 42 (6), pp.1032-9. ⟨10.1016/j.bone.2008.02.009⟩
BONE, 2008, 42 (6), pp.1032-9. ⟨10.1016/j.bone.2008.02.009⟩
BONE, Elsevier, 2008, 42 (6), pp.1032-9. ⟨10.1016/j.bone.2008.02.009⟩
BONE, 2008, 42 (6), pp.1032-9. ⟨10.1016/j.bone.2008.02.009⟩
International audience; Fibroblast growth factor receptor (FGFR) signaling plays an important role in skeletogenesis. The molecular mechanisms triggered by activated FGFR in bone forming cells are however not fully understood. In this study, we ident
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::baebb583dad90f441a8ae9dfed7522fc
https://www.hal.inserm.fr/inserm-00346884
https://www.hal.inserm.fr/inserm-00346884
Publikováno v:
American journal of physiology. Endocrinology and metabolism. 294(4)
Loss of mechanical loading induces rapid bone loss resulting from reduced osteoblastogenesis and decreased bone formation. The signaling mechanisms involved in this deleterious effect on skeletal metabolism remain poorly understood. We have previousl
Publikováno v:
Bone. 42:S20