2020
|
Briand-M{é}sange, Fabienne ; Pons, V{é}ronique ; Allart, Sophie ; Masquelier, Julien ; Chicanne, Ga{ë}tan ; Beton, Nicolas ; Payrastre, Bernard ; Muccioli, Giulio G; Ausseil, J{é}r{ô}me ; Davignon, Jean Luc ; Salles, Jean Pierre ; Chap, Hugues Glycerophosphodiesterase 3 (GDE3) is a lysophosphatidylinositol-specific ectophospholipase C acting as an endocannabinoid signaling switch Journal Article Journal of Biological Chemistry, 295 (46), pp. 15767–15781, 2020, ISSN: 1083351X. Abstract | Links | BibTeX @article{Briand-Mesange2020,
title = {Glycerophosphodiesterase 3 (GDE3) is a lysophosphatidylinositol-specific ectophospholipase C acting as an endocannabinoid signaling switch},
author = {Briand-M{é}sange, Fabienne and Pons, V{é}ronique and Allart, Sophie and Masquelier, Julien and Chicanne, Ga{ë}tan and Beton, Nicolas and Payrastre, Bernard and Muccioli, Giulio G. and Ausseil, J{é}r{ô}me and Davignon, Jean Luc and Salles, Jean Pierre and Chap, Hugues},
doi = {10.1074/jbc.RA120.015278},
issn = {1083351X},
year = {2020},
date = {2020-11-01},
journal = {Journal of Biological Chemistry},
volume = {295},
number = {46},
pages = {15767--15781},
publisher = {American Society for Biochemistry and Molecular Biology Inc.},
abstract = {Endocannabinoid signaling plays a regulatory role in various (neuro)biological functions. 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid, and although its canonical biosynthetic pathway involving phosphoinositide-specific phospholipase C and diacylglycerol lipase a is known, alternative pathways remain unsettled. Here, we characterize a non-canonical pathway implicating glycerophosphodiesterase 3 (GDE3, from GDPD2 gene). Human GDE3 expressed in HEK293T cell membranes catalyzed the conversion of lysophosphatidylinositol (LPI) into monoacylglycerol and inositol-1-phosphate. The enzyme was equally active against 1-acyl and 2-acyl LPI. When using 2-acyl LPI, where arachidonic acid is the predominant fatty acid, LC-MS analysis identified 2-AG as the main product of LPI hydrolysis by GDE3. Furthermore, inositol-1-phosphate release into the medium occurred upon addition of LPI to intact cells, suggesting that GDE3 is actually an ecto-lysophospholipase C. In cells expressing G-protein–coupled receptor GPR55, GDE3 abolished 1-acyl LPI–induced signaling. In contrast, upon simultaneous expression of GDE3 and cannabinoid receptor CB2, 2-acyl LPI evoked the same signal as that induced by 2-AG. These data strongly suggest that, in addition to degrading the GPR55 LPI ligand, GDE3 can act as a switch between GPR55 and CB2 signaling. Coincident with a major expression of both GDE3 and CB2 in the spleen, spleens from transgenic mice lacking GDE3 displayed doubling of LPI content compared with WT mice. Decreased production of 2-AG in whole spleen was also observed, supporting the in vivo relevance of our findings. These data thus open a new research avenue in the field of endocannabinoid generation and reinforce the view of GPR55 and LPI being genuine actors of the endocannabinoid system.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Endocannabinoid signaling plays a regulatory role in various (neuro)biological functions. 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid, and although its canonical biosynthetic pathway involving phosphoinositide-specific phospholipase C and diacylglycerol lipase a is known, alternative pathways remain unsettled. Here, we characterize a non-canonical pathway implicating glycerophosphodiesterase 3 (GDE3, from GDPD2 gene). Human GDE3 expressed in HEK293T cell membranes catalyzed the conversion of lysophosphatidylinositol (LPI) into monoacylglycerol and inositol-1-phosphate. The enzyme was equally active against 1-acyl and 2-acyl LPI. When using 2-acyl LPI, where arachidonic acid is the predominant fatty acid, LC-MS analysis identified 2-AG as the main product of LPI hydrolysis by GDE3. Furthermore, inositol-1-phosphate release into the medium occurred upon addition of LPI to intact cells, suggesting that GDE3 is actually an ecto-lysophospholipase C. In cells expressing G-protein–coupled receptor GPR55, GDE3 abolished 1-acyl LPI–induced signaling. In contrast, upon simultaneous expression of GDE3 and cannabinoid receptor CB2, 2-acyl LPI evoked the same signal as that induced by 2-AG. These data strongly suggest that, in addition to degrading the GPR55 LPI ligand, GDE3 can act as a switch between GPR55 and CB2 signaling. Coincident with a major expression of both GDE3 and CB2 in the spleen, spleens from transgenic mice lacking GDE3 displayed doubling of LPI content compared with WT mice. Decreased production of 2-AG in whole spleen was also observed, supporting the in vivo relevance of our findings. These data thus open a new research avenue in the field of endocannabinoid generation and reinforce the view of GPR55 and LPI being genuine actors of the endocannabinoid system. |
Briand-M{é}sange, Fabienne ; Trudel, St{é}phanie ; Salles, Juliette ; Ausseil, J{é}r{ô}me ; Salles, Jean Pierre ; Chap, Hugues Possible Role of Adipose Tissue and the Endocannabinoid System in Coronavirus Disease 2019 Pathogenesis: Can Rimonabant Return? Journal Article Obesity, 28 (9), pp. 1580–1581, 2020, ISSN: 1930739X. Links | BibTeX @article{Briand-Mesange2020b,
title = {Possible Role of Adipose Tissue and the Endocannabinoid System in Coronavirus Disease 2019 Pathogenesis: Can Rimonabant Return?},
author = {Briand-M{é}sange, Fabienne and Trudel, St{é}phanie and Salles, Juliette and Ausseil, J{é}r{ô}me and Salles, Jean Pierre and Chap, Hugues},
doi = {10.1002/oby.22916},
issn = {1930739X},
year = {2020},
date = {2020-01-01},
journal = {Obesity},
volume = {28},
number = {9},
pages = {1580--1581},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Couture, G; Degboe, Y; Baujat, G; Cormier-Daire, V; Laroche, M Juvenile osteoporosis with calvarial doughnuts: Progressive high-turnover bone loss responsive to bisphosphonate therapy Journal Article Joint Bone Spine, 87 (3), pp. 271-272, 2020, ISSN: 1778-7254 (Electronic)
1297-319X (Linking). Links | BibTeX @article{RN999,
title = {Juvenile osteoporosis with calvarial doughnuts: Progressive high-turnover bone loss responsive to bisphosphonate therapy},
author = {Couture, G. and Degboe, Y. and Baujat, G. and Cormier-Daire, V. and Laroche, M.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31678657},
doi = {10.1016/j.jbspin.2019.10.006},
issn = {1778-7254 (Electronic)
1297-319X (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Joint Bone Spine},
volume = {87},
number = {3},
pages = {271-272},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Couture, G; Degboe, Y; Geniez, C; Tack, I; Vallet, M; Laroche, M Comment on: Diagnosis of fibromyalgia: comparison of the 2011/2016 ACR and AAPT criteria and validation of the modified Fibromyalgia Assessment Status Journal Article Rheumatology (Oxford), 59 (10), pp. e79-e80, 2020, ISSN: 1462-0332 (Electronic)
1462-0324 (Linking). Links | BibTeX @article{RN998,
title = {Comment on: Diagnosis of fibromyalgia: comparison of the 2011/2016 ACR and AAPT criteria and validation of the modified Fibromyalgia Assessment Status},
author = {Couture, G. and Degboe, Y. and Geniez, C. and Tack, I. and Vallet, M. and Laroche, M.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/32793954},
doi = {10.1093/rheumatology/keaa339},
issn = {1462-0332 (Electronic)
1462-0324 (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Rheumatology (Oxford)},
volume = {59},
number = {10},
pages = {e79-e80},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Degboe, Y Pre-rheumatoid arthritis and ACPA: Contribution of ACPAs in the pathogeny of pre-disease stage Journal Article Joint Bone Spine, 88 (3), pp. 105098, 2020, ISSN: 1778-7254 (Electronic)
1297-319X (Linking). Links | BibTeX @article{RN997,
title = {Pre-rheumatoid arthritis and ACPA: Contribution of ACPAs in the pathogeny of pre-disease stage},
author = {Degboe, Y.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/33157231},
doi = {10.1016/j.jbspin.2020.105098},
issn = {1778-7254 (Electronic)
1297-319X (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Joint Bone Spine},
volume = {88},
number = {3},
pages = {105098},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Degboe, Y; Schiff, M; Weinblatt, M; Fleischmann, R; Ahmad, H A; Constantin, A Background Glucocorticoid Therapy Has No Impact on Efficacy and Safety of Abatacept or Adalimumab in Patients with Rheumatoid Arthritis Journal Article J Clin Med, 9 (6), 2020, ISSN: 2077-0383 (Print)
2077-0383 (Linking). Links | BibTeX @article{RN996,
title = {Background Glucocorticoid Therapy Has No Impact on Efficacy and Safety of Abatacept or Adalimumab in Patients with Rheumatoid Arthritis},
author = {Degboe, Y. and Schiff, M. and Weinblatt, M. and Fleischmann, R. and Ahmad, H. A. and Constantin, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/32604962},
doi = {10.3390/jcm9062017},
issn = {2077-0383 (Print)
2077-0383 (Linking)},
year = {2020},
date = {2020-01-01},
journal = {J Clin Med},
volume = {9},
number = {6},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Ferrieres, L; Degboe, Y; Laroche, M; Constantin, A; Ruyssen-Witrand, A No impact of anti-Rank ligand and PTH analogs on cardiovascular risk in postmenopausal osteoporosis: a systematic literature review and meta-analysis Journal Article Arch Osteoporos, 15 (1), pp. 10, 2020, ISSN: 1862-3514 (Electronic). Links | BibTeX @article{RN995,
title = {No impact of anti-Rank ligand and PTH analogs on cardiovascular risk in postmenopausal osteoporosis: a systematic literature review and meta-analysis},
author = {Ferrieres, L. and Degboe, Y. and Laroche, M. and Constantin, A. and Ruyssen-Witrand, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31897759},
doi = {10.1007/s11657-019-0672-4},
issn = {1862-3514 (Electronic)},
year = {2020},
date = {2020-01-01},
journal = {Arch Osteoporos},
volume = {15},
number = {1},
pages = {10},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Garcia, P; Revet, A; Yrondi, A; Rousseau, V; Degboe, Y; Montastruc, F Psychiatric Disorders and Hydroxychloroquine for Coronavirus Disease 2019 (COVID-19): A VigiBase Study Journal Article Drug Saf, 43 (12), pp. 1315-1322, 2020, ISSN: 1179-1942 (Electronic)
0114-5916 (Linking). Links | BibTeX @article{RN994,
title = {Psychiatric Disorders and Hydroxychloroquine for Coronavirus Disease 2019 (COVID-19): A VigiBase Study},
author = {Garcia, P. and Revet, A. and Yrondi, A. and Rousseau, V. and Degboe, Y. and Montastruc, F.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/33078372},
doi = {10.1007/s40264-020-01013-3},
issn = {1179-1942 (Electronic)
0114-5916 (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Drug Saf},
volume = {43},
number = {12},
pages = {1315-1322},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Laroche, M; Champs, B; Couture, G; Degboe, Y Consequence of vertebral fracture cascades: about a cohort of 79 patients Journal Article Osteoporos Int, 31 (12), pp. 2497-2498, 2020, ISSN: 1433-2965 (Electronic)
0937-941X (Linking). Links | BibTeX @article{RN993,
title = {Consequence of vertebral fracture cascades: about a cohort of 79 patients},
author = {Laroche, M. and Champs, B. and Couture, G. and Degboe, Y.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/33052438},
doi = {10.1007/s00198-020-05581-z},
issn = {1433-2965 (Electronic)
0937-941X (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Osteoporos Int},
volume = {31},
number = {12},
pages = {2497-2498},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Laroche, M; Couture, G; Ruyssen-Witrand, A; Constantin, A; Degboe, Y Effect of risedronate on bone loss at discontinuation of denosumab Journal Article Bone Rep, 13 , pp. 100290, 2020, ISSN: 2352-1872 (Print)
2352-1872 (Linking). Links | BibTeX @article{RN992,
title = {Effect of risedronate on bone loss at discontinuation of denosumab},
author = {Laroche, M. and Couture, G. and Ruyssen-Witrand, A. and Constantin, A. and Degboe, Y.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/32715031},
doi = {10.1016/j.bonr.2020.100290},
issn = {2352-1872 (Print)
2352-1872 (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Bone Rep},
volume = {13},
pages = {100290},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Rauwel, B; Degboe, Y; Diallo, K; Sayegh, S; Baron, M; Boyer, J F; Constantin, A; Cantagrel, A; Davignon, J L Inhibition of Osteoclastogenesis by the RNA-Binding Protein QKI5: a Novel Approach to Protect from Bone Resorption Journal Article J Bone Miner Res, 35 (4), pp. 753-765, 2020, ISSN: 1523-4681 (Electronic)
0884-0431 (Linking). Links | BibTeX @article{RN991,
title = {Inhibition of Osteoclastogenesis by the RNA-Binding Protein QKI5: a Novel Approach to Protect from Bone Resorption},
author = {Rauwel, B. and Degboe, Y. and Diallo, K. and Sayegh, S. and Baron, M. and Boyer, J. F. and Constantin, A. and Cantagrel, A. and Davignon, J. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31834954},
doi = {10.1002/jbmr.3943},
issn = {1523-4681 (Electronic)
0884-0431 (Linking)},
year = {2020},
date = {2020-01-01},
journal = {J Bone Miner Res},
volume = {35},
number = {4},
pages = {753-765},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Rauwel, B; Degboe, Y; Nigon, D; Boyer, J F; Abravanel, F; Izopet, J; Combe, B; Ruyssen-Witrand, A; Constantin, A; Cantagrel, A; Davignon, J L Reduced progression of bone erosion in cytomegalovirus seropositive rheumatoid arthritis patients Journal Article Arthritis Res Ther, 22 (1), pp. 13, 2020, ISSN: 1478-6362 (Electronic)
1478-6354 (Linking). Links | BibTeX @article{RN990,
title = {Reduced progression of bone erosion in cytomegalovirus seropositive rheumatoid arthritis patients},
author = {Rauwel, B. and Degboe, Y. and Nigon, D. and Boyer, J. F. and Abravanel, F. and Izopet, J. and Combe, B. and Ruyssen-Witrand, A. and Constantin, A. and Cantagrel, A. and Davignon, J. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31959222},
doi = {10.1186/s13075-020-2098-1},
issn = {1478-6362 (Electronic)
1478-6354 (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Arthritis Res Ther},
volume = {22},
number = {1},
pages = {13},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Simons, N; Degboe, Y; Barnetche, T; Cantagrel, A; Ruyssen-Witrand, A; Constantin, A Biological DMARD efficacy in psoriatic arthritis: a systematic literature review and meta-analysis on articular, enthesitis, dactylitis, skin and functional outcomes Journal Article Clin Exp Rheumatol, 38 (3), pp. 508-515, 2020, ISSN: 0392-856X (Print)
0392-856X (Linking). Links | BibTeX @article{RN989,
title = {Biological DMARD efficacy in psoriatic arthritis: a systematic literature review and meta-analysis on articular, enthesitis, dactylitis, skin and functional outcomes},
author = {Simons, N. and Degboe, Y. and Barnetche, T. and Cantagrel, A. and Ruyssen-Witrand, A. and Constantin, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31969228},
issn = {0392-856X (Print)
0392-856X (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Clin Exp Rheumatol},
volume = {38},
number = {3},
pages = {508-515},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Vinson, D; Molet-Benhamou, L; Degboe, Y; den Broeder, A; Ibrahim, F; Pontes, C; Westhovens, R; Zavada, J; Pham, T; Barnetche, T; Constantin, A; Ruyssen-Witrand, A Impact of tapering targeted therapies (bDMARDs or JAKis) on the risk of serious infections and adverse events of special interest in patients with rheumatoid arthritis or spondyloarthritis: a systematic analysis of the literature and meta-analysis Journal Article Arthritis Res Ther, 22 (1), pp. 97, 2020, ISSN: 1478-6362 (Electronic)
1478-6354 (Linking). Links | BibTeX @article{RN988,
title = {Impact of tapering targeted therapies (bDMARDs or JAKis) on the risk of serious infections and adverse events of special interest in patients with rheumatoid arthritis or spondyloarthritis: a systematic analysis of the literature and meta-analysis},
author = {Vinson, D. and Molet-Benhamou, L. and Degboe, Y. and den Broeder, A. and Ibrahim, F. and Pontes, C. and Westhovens, R. and Zavada, J. and Pham, T. and Barnetche, T. and Constantin, A. and Ruyssen-Witrand, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/32349791},
doi = {10.1186/s13075-020-02188-x},
issn = {1478-6362 (Electronic)
1478-6354 (Linking)},
year = {2020},
date = {2020-01-01},
journal = {Arthritis Res Ther},
volume = {22},
number = {1},
pages = {97},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Kraus, Francois ; Dremaux, Julie ; Altakfi, Wajd ; Goux, Magalie ; Pontois, Léa; Sevestre, Henri ; Trudel, Stéphanie FOXL2 homozygous genotype and chromosome instability are associated with recurrence in adult granulosa cell tumors of the ovary Journal Article Oncotarget, 11 (4), pp. 419–428, 2020, ISSN: 1949-2553. Abstract | Links | BibTeX @article{kraus_foxl2_2020,
title = {FOXL2 homozygous genotype and chromosome instability are associated with recurrence in adult granulosa cell tumors of the ovary},
author = {Kraus, Francois and Dremaux, Julie and Altakfi, Wajd and Goux, Magalie and Pontois, Léa and Sevestre, Henri and Trudel, Stéphanie},
doi = {10.18632/oncotarget.27447},
issn = {1949-2553},
year = {2020},
date = {2020-01-01},
journal = {Oncotarget},
volume = {11},
number = {4},
pages = {419--428},
abstract = {INTRODUCTION: Adult granulosa cell tumors (aGCTs) are extremely rare tumors characterized by the presence of the single missense mutation (c.402 CtextgreaterG, p. C134W) in the FOXL2 gene. These tumors are frequently associated with a slow, indolent disease progression and a high probability of aggressive tumor recurrence. Hence, the identification of molecular markers that are predictive of recurrence and/or aggressive behavior would be a great asset in the management of aGCT. The present study focused on the influence of the FOXL2 genotype (heterozygous or homozygous) and copy number variations (CNVs) in recurrence by comparing the primary tumor with recurrent lesions in the same patient. We performed array comparative genomic hybridization (CGH) experiments and FOXL2 genotyping by allelic discrimination on 40 tumor samples.
RESULTS AND DISCUSSION: In array CGH results of recurrent tumors, few samples presented the multiple chromosome losses and gains characteristic of chromosome instability (CIN). We also observed that three recurrent tumors and one primary tumor appeared to be homozygous for the FOXL2 c.402CtextgreaterG mutation. Interestingly, the homozygous FOXL2 genotype was correlated with a shorter time to relapse. A change in the FOXL2 genotype in cases of recurrence was correlated with the appearance of CIN.
CONCLUSION: Despite the small number of matching primary and recurrent tumors analyzed here, the present study is the first to have shown that the FOXL2 homozygous genotype and CIN are prevalent in recurrent aGCTs. The two mechanisms are probably linked, and both almost certainly have a role in the molecular transformation of aGCTs.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
INTRODUCTION: Adult granulosa cell tumors (aGCTs) are extremely rare tumors characterized by the presence of the single missense mutation (c.402 CtextgreaterG, p. C134W) in the FOXL2 gene. These tumors are frequently associated with a slow, indolent disease progression and a high probability of aggressive tumor recurrence. Hence, the identification of molecular markers that are predictive of recurrence and/or aggressive behavior would be a great asset in the management of aGCT. The present study focused on the influence of the FOXL2 genotype (heterozygous or homozygous) and copy number variations (CNVs) in recurrence by comparing the primary tumor with recurrent lesions in the same patient. We performed array comparative genomic hybridization (CGH) experiments and FOXL2 genotyping by allelic discrimination on 40 tumor samples.
RESULTS AND DISCUSSION: In array CGH results of recurrent tumors, few samples presented the multiple chromosome losses and gains characteristic of chromosome instability (CIN). We also observed that three recurrent tumors and one primary tumor appeared to be homozygous for the FOXL2 c.402CtextgreaterG mutation. Interestingly, the homozygous FOXL2 genotype was correlated with a shorter time to relapse. A change in the FOXL2 genotype in cases of recurrence was correlated with the appearance of CIN.
CONCLUSION: Despite the small number of matching primary and recurrent tumors analyzed here, the present study is the first to have shown that the FOXL2 homozygous genotype and CIN are prevalent in recurrent aGCTs. The two mechanisms are probably linked, and both almost certainly have a role in the molecular transformation of aGCTs. |
Mansour, Ali ; Darwiche, Walaa ; Yaker, Linda ; {Da Nascimento}, Sophie ; Gomila, Cathy ; Rossi, Claire ; Jung, Vincent ; Sonnet, Pascal ; Kamel, Sa{ï}d ; Guerrera, Ida Chiara ; Boullier, Agn{è}s ; Ausseil, J{é}r{ô}me GFOGER Peptide Modifies the Protein Content of Extracellular Vesicles and Inhibits Vascular Calcification Journal Article Frontiers in Cell and Developmental Biology, 8 (November), pp. 1–11, 2020, ISSN: 2296634X. Abstract | Links | BibTeX @article{Mansour2020,
title = {GFOGER Peptide Modifies the Protein Content of Extracellular Vesicles and Inhibits Vascular Calcification},
author = {Mansour, Ali and Darwiche, Walaa and Yaker, Linda and {Da Nascimento}, Sophie and Gomila, Cathy and Rossi, Claire and Jung, Vincent and Sonnet, Pascal and Kamel, Sa{ï}d and Guerrera, Ida Chiara and Boullier, Agn{è}s and Ausseil, J{é}r{ô}me},
doi = {10.3389/fcell.2020.589761},
issn = {2296634X},
year = {2020},
date = {2020-01-01},
journal = {Frontiers in Cell and Developmental Biology},
volume = {8},
number = {November},
pages = {1--11},
abstract = {Objective: Vascular calcification (VC) is an active process during which vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and release extracellular vesicles (EVs). In turn, the EVs serve as calcification foci via interaction with type 1 collagen (COL1). We recently showed that a specific, six-amino-acid repeat (GFOGER) in the sequence of COL1 was involved in the latter's interaction with integrins expressed on EVs. Our main objective was to test the GFOGER ability to inhibit VC. Approach: We synthesized the GFOGER peptide and tested its ability to inhibit the inorganic phosphate (Pi)-induced calcification of VSMCs and aortic rings. Using mass spectrometry, we studied GFOGER's effect on the protein composition of EVs released from Pi-treated VSMCs. Results: Calcification of mouse VSMCs (MOVAS-1 cells), primary human VSMCs, and rat aortic rings was lower in the presence of GFOGER than with Pi alone (with relative decreases of 66, 58, and 91%, respectively; p < 0.001 for all) (no effect was observed with the scramble peptide GOERFG). A comparative proteomic analysis of EVs released from MOVAS-1 cells in the presence or absence of Pi highlighted significant differences in EVs' protein content. Interestingly, the expression of some of the EVs' proteins involved in the calcification process (such as osteogenic markers, TANK-binding kinase 1, and casein kinase II) was diminished in the presence of GFOGER peptide (data are available via ProteomeXchange with identifier PXD018169∗). The decrease of osteogenic marker expression observed in the presence of GFOGER was confirmed by q-RT-PCR analysis. Conclusion: GFOGER peptide reduces vascular calcification by modifying the protein content of the subsequently released EVs, in particular by decreasing osteogenicswitching in VSMCs.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Objective: Vascular calcification (VC) is an active process during which vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and release extracellular vesicles (EVs). In turn, the EVs serve as calcification foci via interaction with type 1 collagen (COL1). We recently showed that a specific, six-amino-acid repeat (GFOGER) in the sequence of COL1 was involved in the latter's interaction with integrins expressed on EVs. Our main objective was to test the GFOGER ability to inhibit VC. Approach: We synthesized the GFOGER peptide and tested its ability to inhibit the inorganic phosphate (Pi)-induced calcification of VSMCs and aortic rings. Using mass spectrometry, we studied GFOGER's effect on the protein composition of EVs released from Pi-treated VSMCs. Results: Calcification of mouse VSMCs (MOVAS-1 cells), primary human VSMCs, and rat aortic rings was lower in the presence of GFOGER than with Pi alone (with relative decreases of 66, 58, and 91%, respectively; p < 0.001 for all) (no effect was observed with the scramble peptide GOERFG). A comparative proteomic analysis of EVs released from MOVAS-1 cells in the presence or absence of Pi highlighted significant differences in EVs' protein content. Interestingly, the expression of some of the EVs' proteins involved in the calcification process (such as osteogenic markers, TANK-binding kinase 1, and casein kinase II) was diminished in the presence of GFOGER peptide (data are available via ProteomeXchange with identifier PXD018169∗). The decrease of osteogenic marker expression observed in the presence of GFOGER was confirmed by q-RT-PCR analysis. Conclusion: GFOGER peptide reduces vascular calcification by modifying the protein content of the subsequently released EVs, in particular by decreasing osteogenicswitching in VSMCs. |
Beauvieux, Marie Christine ; B{é}rard, Annie M; Aimone-Gastin, Isabelle ; Barb{é}, Fran{ç}oise ; Barguil, Yann ; Collin-Chavagnac, Delphine ; Delacour, Herv{é} ; Delevall{é}e, C{é}line ; Nivet-Antoine, Val{é}rie ; Peoc'h, Katell ; Poupon, Carole ; Schmitt, Fran{ç}ois ; Pi{é}roni, Laurence ; Sapin, Vincent SFBC working group "Biochemical markers of COVID-19" Journal Article Annales de Biologie Clinique, 78 (3), pp. 269–277, 2020, ISSN: 19506112. Abstract | Links | BibTeX @article{Beauvieux2020,
title = {SFBC working group "Biochemical markers of COVID-19"},
author = {Beauvieux, Marie Christine and B{é}rard, Annie M. and Aimone-Gastin, Isabelle and Barb{é}, Fran{ç}oise and Barguil, Yann and Collin-Chavagnac, Delphine and Delacour, Herv{é} and Delevall{é}e, C{é}line and Nivet-Antoine, Val{é}rie and Peoc'h, Katell and Poupon, Carole and Schmitt, Fran{ç}ois and Pi{é}roni, Laurence and Sapin, Vincent},
doi = {10.1684/abc.2020.1563},
issn = {19506112},
year = {2020},
date = {2020-01-01},
journal = {Annales de Biologie Clinique},
volume = {78},
number = {3},
pages = {269--277},
abstract = {The SARS-CoV-2 virus is responsible for an epidemic disease called COVID-19, which was initially evidenced in Wuhan, China, and spread very rapidly in China and around the world. In France, the first isolated case seems now to be reported in December 2019, stage 3 of the COVID-19 epidemic was triggered on March 14th, the start of the planned containment exit from May 11th. Healthcare services have faced a large influx of patients who may be beyond their capacity to receive and care, particularly in the Large-East and Ile-de-France regions. Some patients show an evolution of the disease never observed before with other coronaviruses and develop in a few days a very important inflammatory reaction, which can lead to death of patients. A working group of the French Society of Clinical Biology (SFBC) was set up with the objective of providing updated information on the current status of the biological prescriptions (focusing on biochemistry ones) and their evolution during the epidemic, and of analyzing the biological parameters associated with comorbidities and patient evolution in order to link biological results with medical events. The expanded working group covers all sectors of medical biology in France and extends to the French-speaking world: hospital sectors (CHU and CH, Army Training Hospitals) and the private sector opening a field of view on the biological situation in establishments for dependent elderly, social establishments and clinical medical institutions. The purpose of this article is the presentation of this working group and its immediate and future actions.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The SARS-CoV-2 virus is responsible for an epidemic disease called COVID-19, which was initially evidenced in Wuhan, China, and spread very rapidly in China and around the world. In France, the first isolated case seems now to be reported in December 2019, stage 3 of the COVID-19 epidemic was triggered on March 14th, the start of the planned containment exit from May 11th. Healthcare services have faced a large influx of patients who may be beyond their capacity to receive and care, particularly in the Large-East and Ile-de-France regions. Some patients show an evolution of the disease never observed before with other coronaviruses and develop in a few days a very important inflammatory reaction, which can lead to death of patients. A working group of the French Society of Clinical Biology (SFBC) was set up with the objective of providing updated information on the current status of the biological prescriptions (focusing on biochemistry ones) and their evolution during the epidemic, and of analyzing the biological parameters associated with comorbidities and patient evolution in order to link biological results with medical events. The expanded working group covers all sectors of medical biology in France and extends to the French-speaking world: hospital sectors (CHU and CH, Army Training Hospitals) and the private sector opening a field of view on the biological situation in establishments for dependent elderly, social establishments and clinical medical institutions. The purpose of this article is the presentation of this working group and its immediate and future actions. |
Hocquemiller, Micha{ë}l ; Hemsley, Kim M; Douglass, Meghan L; Tamang, Sarah J; Neumann, Daniel ; King, Barbara M; Beard, Helen ; Trim, Paul J; Winner, Leanne K; Lau, Adeline A; Snel, Marten F; Gomila, Cathy ; Ausseil, J{é}r{ô}me ; Mei, Xin ; Giersch, Laura ; Plavsic, Mark ; Laufer, Ralph AAVrh10 Vector Corrects Disease Pathology in MPS IIIA Mice and Achieves Widespread Distribution of SGSH in Large Animal Brains Journal Article Molecular Therapy - Methods and Clinical Development, 17 (June), pp. 174–187, 2020, ISSN: 23290501. Abstract | Links | BibTeX @article{Hocquemiller2020,
title = {AAVrh10 Vector Corrects Disease Pathology in MPS IIIA Mice and Achieves Widespread Distribution of SGSH in Large Animal Brains},
author = {Hocquemiller, Micha{ë}l and Hemsley, Kim M. and Douglass, Meghan L. and Tamang, Sarah J. and Neumann, Daniel and King, Barbara M. and Beard, Helen and Trim, Paul J. and Winner, Leanne K. and Lau, Adeline A. and Snel, Marten F. and Gomila, Cathy and Ausseil, J{é}r{ô}me and Mei, Xin and Giersch, Laura and Plavsic, Mark and Laufer, Ralph},
doi = {10.1016/j.omtm.2019.12.001},
issn = {23290501},
year = {2020},
date = {2020-01-01},
journal = {Molecular Therapy - Methods and Clinical Development},
volume = {17},
number = {June},
pages = {174--187},
abstract = {Patients with mucopolysaccharidosis type IIIA (MPS IIIA) lack the lysosomal enzyme sulfamidase (SGSH), which is responsible for the degradation of heparan sulfate (HS). Build-up of undegraded HS results in severe progressive neurodegeneration for which there is currently no treatment. The ability of the vector adeno-associated virus (AAV)rh.10-CAG-SGSH (LYS-SAF302) to correct disease pathology was evaluated in a mouse model for MPS IIIA. LYS-SAF302 was administered to 5-week-old MPS IIIA mice at three different doses (8.6E+08, 4.1E+10, and 9.0E+10 vector genomes [vg]/animal) injected into the caudate putamen/striatum and thalamus. LYS-SAF302 was able to dose-dependently correct or significantly reduce HS storage, secondary accumulation of GM2 and GM3 gangliosides, ubiquitin-reactive axonal spheroid lesions, lysosomal expansion, and neuroinflammation at 12 weeks and 25 weeks post-dosing. To study SGSH distribution in the brain of large animals, LYS-SAF302 was injected into the subcortical white matter of dogs (1.0E+12 or 2.0E+12 vg/animal) and cynomolgus monkeys (7.2E+11 vg/animal). Increases of SGSH enzyme activity of at least 20% above endogenous levels were detected in 78% (dogs 4 weeks after injection) and 97% (monkeys 6 weeks after injection) of the total brain volume. Taken together, these data validate intraparenchymal AAV administration as a promising method to achieve widespread enzyme distribution and correction of disease pathology in MPS IIIA.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Patients with mucopolysaccharidosis type IIIA (MPS IIIA) lack the lysosomal enzyme sulfamidase (SGSH), which is responsible for the degradation of heparan sulfate (HS). Build-up of undegraded HS results in severe progressive neurodegeneration for which there is currently no treatment. The ability of the vector adeno-associated virus (AAV)rh.10-CAG-SGSH (LYS-SAF302) to correct disease pathology was evaluated in a mouse model for MPS IIIA. LYS-SAF302 was administered to 5-week-old MPS IIIA mice at three different doses (8.6E+08, 4.1E+10, and 9.0E+10 vector genomes [vg]/animal) injected into the caudate putamen/striatum and thalamus. LYS-SAF302 was able to dose-dependently correct or significantly reduce HS storage, secondary accumulation of GM2 and GM3 gangliosides, ubiquitin-reactive axonal spheroid lesions, lysosomal expansion, and neuroinflammation at 12 weeks and 25 weeks post-dosing. To study SGSH distribution in the brain of large animals, LYS-SAF302 was injected into the subcortical white matter of dogs (1.0E+12 or 2.0E+12 vg/animal) and cynomolgus monkeys (7.2E+11 vg/animal). Increases of SGSH enzyme activity of at least 20% above endogenous levels were detected in 78% (dogs 4 weeks after injection) and 97% (monkeys 6 weeks after injection) of the total brain volume. Taken together, these data validate intraparenchymal AAV administration as a promising method to achieve widespread enzyme distribution and correction of disease pathology in MPS IIIA. |
Yaker, Linda ; Kamel, Sa{ï}d ; Ausseil, J{é}r{ô}me ; Boullier, Agn{è}s Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology Journal Article Toxins, 12 (12), pp. 1–28, 2020, ISSN: 20726651. Abstract | Links | BibTeX @article{Yaker2020,
title = {Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology},
author = {Yaker, Linda and Kamel, Sa{ï}d and Ausseil, J{é}r{ô}me and Boullier, Agn{è}s},
doi = {10.3390/toxins12120811},
issn = {20726651},
year = {2020},
date = {2020-01-01},
journal = {Toxins},
volume = {12},
number = {12},
pages = {1--28},
abstract = {Vascular calcification (VC) is a cardiovascular complication associated with a high mortality rate, especially in patients with diabetes, atherosclerosis or chronic kidney disease (CKD). In CKD patients, VC is associated with the accumulation of uremic toxins, such as indoxyl sulphate or inorganic phosphate, which can have a major impact in vascular remodeling. During VC, vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and secrete extracellular vesicles (EVs) that are heterogeneous in terms of their origin and composition. Under physiological conditions, EVs are involved in cell-cell communication and the maintenance of cellular homeostasis. They contain high levels of calcification inhibitors, such as fetuin-A and matrix Gla protein. Under pathological conditions (and particularly in the presence of uremic toxins), the secreted EVs acquire a pro-calcifying profile and thereby act as nucleating foci for the crystallization of hydroxyapatite and the propagation of calcification. Here, we review the most recent findings on the EVs' pathophysiological role in VC, the impact of uremic toxins on EV biogenesis and functions, the use of EVs as diagnostic biomarkers and the EVs' therapeutic potential in CKD.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Vascular calcification (VC) is a cardiovascular complication associated with a high mortality rate, especially in patients with diabetes, atherosclerosis or chronic kidney disease (CKD). In CKD patients, VC is associated with the accumulation of uremic toxins, such as indoxyl sulphate or inorganic phosphate, which can have a major impact in vascular remodeling. During VC, vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and secrete extracellular vesicles (EVs) that are heterogeneous in terms of their origin and composition. Under physiological conditions, EVs are involved in cell-cell communication and the maintenance of cellular homeostasis. They contain high levels of calcification inhibitors, such as fetuin-A and matrix Gla protein. Under pathological conditions (and particularly in the presence of uremic toxins), the secreted EVs acquire a pro-calcifying profile and thereby act as nucleating foci for the crystallization of hydroxyapatite and the propagation of calcification. Here, we review the most recent findings on the EVs' pathophysiological role in VC, the impact of uremic toxins on EV biogenesis and functions, the use of EVs as diagnostic biomarkers and the EVs' therapeutic potential in CKD. |
2019
|
Tebani, A; Abily-Donval, L; Schmitz-Afonso, I; Piraud, M; Ausseil, J; Zerimech, F; Pilon, C; Pereira, T; Marret, S; Afonso, C; Bekri, S Analysis of Mucopolysaccharidosis Type VI through Integrative Functional Metabolomics Journal Article Int J Mol Sci, 20 (2), 2019, ISSN: 1422-0067 (Electronic)
1422-0067 (Linking). Links | BibTeX @article{RN1000,
title = {Analysis of Mucopolysaccharidosis Type VI through Integrative Functional Metabolomics},
author = {Tebani, A. and Abily-Donval, L. and Schmitz-Afonso, I. and Piraud, M. and Ausseil, J. and Zerimech, F. and Pilon, C. and Pereira, T. and Marret, S. and Afonso, C. and Bekri, S.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30669586},
doi = {10.3390/ijms20020446},
issn = {1422-0067 (Electronic)
1422-0067 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Int J Mol Sci},
volume = {20},
number = {2},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Braun, H; Geniez, C; Degboe, Y; Constantin, A; Cantagrel, A; Nigon, D; Sans, N; Faruch-Bilfeld, M; Ruyssen-Witrand, A Prevalence of inflammatory posterior arch abnormalities on lumbar spine MRI in spondyloarthritis patients compared with low back pain patients Journal Article Eur Radiol, 29 (12), pp. 6405-6415, 2019, ISSN: 1432-1084 (Electronic)
0938-7994 (Linking). Links | BibTeX @article{RN1010,
title = {Prevalence of inflammatory posterior arch abnormalities on lumbar spine MRI in spondyloarthritis patients compared with low back pain patients},
author = {Braun, H. and Geniez, C. and Degboe, Y. and Constantin, A. and Cantagrel, A. and Nigon, D. and Sans, N. and Faruch-Bilfeld, M. and Ruyssen-Witrand, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31119417},
doi = {10.1007/s00330-019-06231-7},
issn = {1432-1084 (Electronic)
0938-7994 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Eur Radiol},
volume = {29},
number = {12},
pages = {6405-6415},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Casassa, E A; Mailhol, C; Tournier, E; Laurent, C; Degboe, Y; Eischen, M; Kirsten, N; Moreau, J; Evrard, S M; Mansat-De Mas, V; Lamant, L; Dubreuil, P; Apoil, P A; Hermine, O; Paul, C; Bulai Livideanu, C Mast cell activation syndrome: High frequency of skin manifestations and anaphylactic shock Journal Article Allergol Int, 68 (1), pp. 119-121, 2019, ISSN: 1440-1592 (Electronic)
1323-8930 (Linking). Links | BibTeX @article{RN1009b,
title = {Mast cell activation syndrome: High frequency of skin manifestations and anaphylactic shock},
author = {Casassa, E. A. and Mailhol, C. and Tournier, E. and Laurent, C. and Degboe, Y. and Eischen, M. and Kirsten, N. and Moreau, J. and Evrard, S. M. and Mansat-De Mas, V. and Lamant, L. and Dubreuil, P. and Apoil, P. A. and Hermine, O. and Paul, C. and Bulai Livideanu, C.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30097253},
doi = {10.1016/j.alit.2018.07.003},
issn = {1440-1592 (Electronic)
1323-8930 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Allergol Int},
volume = {68},
number = {1},
pages = {119-121},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Champs, B; Degboe, Y; Barnetche, T; Cantagrel, A; Ruyssen-Witrand, A; Constantin, A Short-term risk of major adverse cardiovascular events or congestive heart failure in patients with psoriatic arthritis or psoriasis initiating a biological therapy: a meta-analysis of randomised controlled trials Journal Article RMD Open, 5 (1), pp. e000763, 2019, ISSN: 2056-5933 (Print)
2056-5933 (Linking). Links | BibTeX @article{RN1008b,
title = {Short-term risk of major adverse cardiovascular events or congestive heart failure in patients with psoriatic arthritis or psoriasis initiating a biological therapy: a meta-analysis of randomised controlled trials},
author = {Champs, B. and Degboe, Y. and Barnetche, T. and Cantagrel, A. and Ruyssen-Witrand, A. and Constantin, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30792887},
doi = {10.1136/rmdopen-2018-000763},
issn = {2056-5933 (Print)
2056-5933 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {RMD Open},
volume = {5},
number = {1},
pages = {e000763},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Degboe, Y; Eischen, M; Apoil, P A; Mailhol, C; Dubreuil, P; Hermine, O; Paul, C; Bulai Livideanu, C; Laroche, M Higher prevalence of vertebral fractures in systemic mastocytosis, but not in cutaneous mastocytosis and idiopathic mast cell activation syndrome Journal Article Osteoporos Int, 30 (6), pp. 1235-1241, 2019, ISSN: 1433-2965 (Electronic)
0937-941X (Linking). Links | BibTeX @article{RN1007b,
title = {Higher prevalence of vertebral fractures in systemic mastocytosis, but not in cutaneous mastocytosis and idiopathic mast cell activation syndrome},
author = {Degboe, Y. and Eischen, M. and Apoil, P. A. and Mailhol, C. and Dubreuil, P. and Hermine, O. and Paul, C. and Bulai Livideanu, C. and Laroche, M.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30847528},
doi = {10.1007/s00198-019-04918-7},
issn = {1433-2965 (Electronic)
0937-941X (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Osteoporos Int},
volume = {30},
number = {6},
pages = {1235-1241},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Degboe, Y; Rauwel, B; Baron, M; Boyer, J F; Ruyssen-Witrand, A; Constantin, A; Davignon, J L Polarization of Rheumatoid Macrophages by TNF Targeting Through an IL-10/STAT3 Mechanism Journal Article Front Immunol, 10 , pp. 3, 2019, ISSN: 1664-3224 (Electronic)
1664-3224 (Linking). Links | BibTeX @article{RN1006b,
title = {Polarization of Rheumatoid Macrophages by TNF Targeting Through an IL-10/STAT3 Mechanism},
author = {Degboe, Y. and Rauwel, B. and Baron, M. and Boyer, J. F. and Ruyssen-Witrand, A. and Constantin, A. and Davignon, J. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30713533},
doi = {10.3389/fimmu.2019.00003},
issn = {1664-3224 (Electronic)
1664-3224 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Front Immunol},
volume = {10},
pages = {3},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Fradet, M; Negretto, M; Tournier, E; Laurent, C; Apoil, P A; Evrard, S; Degboe, Y; Del Mas, V; Lamant, L; Dubreuil, P; Laroche, M; Mailhol, C; Hermine, O; Paul, C; Bulai Livideanu, C Frequency of isolated cutaneous involvement in adult mastocytosis: a cohort study Journal Article J Eur Acad Dermatol Venereol, 33 (9), pp. 1713-1718, 2019, ISSN: 1468-3083 (Electronic)
0926-9959 (Linking). Links | BibTeX @article{RN1005,
title = {Frequency of isolated cutaneous involvement in adult mastocytosis: a cohort study},
author = {Fradet, M. and Negretto, M. and Tournier, E. and Laurent, C. and Apoil, P. A. and Evrard, S. and Degboe, Y. and Del Mas, V. and Lamant, L. and Dubreuil, P. and Laroche, M. and Mailhol, C. and Hermine, O. and Paul, C. and Bulai Livideanu, C.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31009132},
doi = {10.1111/jdv.15638},
issn = {1468-3083 (Electronic)
0926-9959 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {J Eur Acad Dermatol Venereol},
volume = {33},
number = {9},
pages = {1713-1718},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Luxembourger, C; Ruyssen-Witrand, A; Ladhari, C; Rittore, C; Degboe, Y; Maillefert, J F; Gaudin, P; Marotte, H; Wendling, D; Jorgensen, C; Cantagrel, A; Constantin, A; Nigon, D; Touitou, I; Gottenberg, J E; Pers, Y M A single nucleotide polymorphism of IL6-receptor is associated with response to tocilizumab in rheumatoid arthritis patients Journal Article Pharmacogenomics J, 19 (4), pp. 368-374, 2019, ISSN: 1473-1150 (Electronic)
1470-269X (Linking). Links | BibTeX @article{RN1004,
title = {A single nucleotide polymorphism of IL6-receptor is associated with response to tocilizumab in rheumatoid arthritis patients},
author = {Luxembourger, C. and Ruyssen-Witrand, A. and Ladhari, C. and Rittore, C. and Degboe, Y. and Maillefert, J. F. and Gaudin, P. and Marotte, H. and Wendling, D. and Jorgensen, C. and Cantagrel, A. and Constantin, A. and Nigon, D. and Touitou, I. and Gottenberg, J. E. and Pers, Y. M.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30647443},
doi = {10.1038/s41397-019-0072-6},
issn = {1473-1150 (Electronic)
1470-269X (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Pharmacogenomics J},
volume = {19},
number = {4},
pages = {368-374},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Magnol, M; Degboe, Y; Couture, G; Constantin, A; Laroche, M Complex regional pain syndrome secondary to everolimus: Two cases Journal Article Joint Bone Spine, 86 (5), pp. 659-660, 2019, ISSN: 1778-7254 (Electronic)
1297-319X (Linking). Links | BibTeX @article{RN1003b,
title = {Complex regional pain syndrome secondary to everolimus: Two cases},
author = {Magnol, M. and Degboe, Y. and Couture, G. and Constantin, A. and Laroche, M.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30776491},
doi = {10.1016/j.jbspin.2019.02.003},
issn = {1778-7254 (Electronic)
1297-319X (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Joint Bone Spine},
volume = {86},
number = {5},
pages = {659-660},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Ruyssen-Witrand, A; Luxembourger, C; Cantagrel, A; Nigon, D; Claudepierre, P; Degboe, Y; Constantin, A Association between IL23R and ERAP1 polymorphisms and sacroiliac or spinal MRI inflammation in spondyloarthritis: DESIR cohort data Journal Article Arthritis Res Ther, 21 (1), pp. 22, 2019, ISSN: 1478-6362 (Electronic)
1478-6354 (Linking). Links | BibTeX @article{RN1002b,
title = {Association between IL23R and ERAP1 polymorphisms and sacroiliac or spinal MRI inflammation in spondyloarthritis: DESIR cohort data},
author = {Ruyssen-Witrand, A. and Luxembourger, C. and Cantagrel, A. and Nigon, D. and Claudepierre, P. and Degboe, Y. and Constantin, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30646942},
doi = {10.1186/s13075-018-1807-5},
issn = {1478-6362 (Electronic)
1478-6354 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Arthritis Res Ther},
volume = {21},
number = {1},
pages = {22},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Sayegh, S; El Atat, O; Diallo, K; Rauwel, B; Degboe, Y; Cavaignac, E; Constantin, A; Cantagrel, A; Trak-Smayra, V; Alaaeddine, N; Davignon, J L Corrigendum: Rheumatoid Synovial Fluids Regulate the Immunomodulatory Potential of Adipose-Derived Mesenchymal Stem Cells Through a TNF/NF-kappaB-Dependent Mechanism Journal Article Front Immunol, 10 , pp. 1961, 2019, ISSN: 1664-3224 (Electronic)
1664-3224 (Linking). Links | BibTeX @article{RN1001b,
title = {Corrigendum: Rheumatoid Synovial Fluids Regulate the Immunomodulatory Potential of Adipose-Derived Mesenchymal Stem Cells Through a TNF/NF-kappaB-Dependent Mechanism},
author = {Sayegh, S. and El Atat, O. and Diallo, K. and Rauwel, B. and Degboe, Y. and Cavaignac, E. and Constantin, A. and Cantagrel, A. and Trak-Smayra, V. and Alaaeddine, N. and Davignon, J. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31475016},
doi = {10.3389/fimmu.2019.01961},
issn = {1664-3224 (Electronic)
1664-3224 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Front Immunol},
volume = {10},
pages = {1961},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Sayegh, S; El Atat, O; Diallo, K; Rauwel, B; Degboe, Y; Cavaignac, E; Constantin, A; Cantagrel, A; Trak-Smayra, V; Alaaeddine, N; Davignon, J L Rheumatoid Synovial Fluids Regulate the Immunomodulatory Potential of Adipose-Derived Mesenchymal Stem Cells Through a TNF/NF-kappaB-Dependent Mechanism Journal Article Front Immunol, 10 , pp. 1482, 2019, ISSN: 1664-3224 (Electronic)
1664-3224 (Linking). Links | BibTeX @article{RN1000b,
title = {Rheumatoid Synovial Fluids Regulate the Immunomodulatory Potential of Adipose-Derived Mesenchymal Stem Cells Through a TNF/NF-kappaB-Dependent Mechanism},
author = {Sayegh, S. and El Atat, O. and Diallo, K. and Rauwel, B. and Degboe, Y. and Cavaignac, E. and Constantin, A. and Cantagrel, A. and Trak-Smayra, V. and Alaaeddine, N. and Davignon, J. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/31316519},
doi = {10.3389/fimmu.2019.01482},
issn = {1664-3224 (Electronic)
1664-3224 (Linking)},
year = {2019},
date = {2019-01-01},
journal = {Front Immunol},
volume = {10},
pages = {1482},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2018
|
Moniez, Sophie ; Pienkowski, Catherine ; Lepage, Benoit ; Hamdi, Safouane ; Daudin, Myriam ; Oliver, Isabelle ; Jouret, B{é}atrice ; Cartault, Audrey ; Diene, Gwenaelle ; Verloes, Alain ; Cav{é}, H{é}l{è}ne ; Salles, Jean-Pierre ; Tauber, Maith{é} ; Yart, Armelle ; Edouard, Thomas Noonan syndrome males display Sertoli cell-specific primary testicular insufficiency Journal Article European Journal of Endocrinology, 179 (6), pp. 409–418, 2018. Abstract | Links | BibTeX @article{Moniez2018,
title = {Noonan syndrome males display Sertoli cell-specific primary testicular insufficiency},
author = {Moniez, Sophie and Pienkowski, Catherine and Lepage, Benoit and Hamdi, Safouane and Daudin, Myriam and Oliver, Isabelle and Jouret, B{é}atrice and Cartault, Audrey and Diene, Gwenaelle and Verloes, Alain and Cav{é}, H{é}l{è}ne and Salles, Jean-Pierre and Tauber, Maith{é} and Yart, Armelle and Edouard, Thomas},
url = {http://www.ncbi.nlm.nih.gov/pubmed/30325180 http://www.ncbi.nlm.nih.gov/pubmed/30325180},
doi = {10.1530/EJE-18-0582},
year = {2018},
date = {2018-12-01},
journal = {European Journal of Endocrinology},
volume = {179},
number = {6},
pages = {409--418},
abstract = {Context Abnormalities in the hypothalamo-pituitary-gonadal axis have long been reported in Noonan syndrome (NS) males with only few data available in prepubertal children. Objective The aim of this study was to describe the gonadal function of NS males from childhood to adulthood. Design It is a retrospective chart review. Patients and methods A total of 37 males with a genetically confirmed diagnosis of NS were included. Clinical and genetic features, as well as serum hormone levels (LH, FSH, testosterone, anti-Müllerian hormone (AMH), and inhibin B) were analysed. Results Of the 37 patients, 16 (43%) children had entered puberty at a median age of 13.5 years (range: 11.4-15.0 years); age at pubertal onset was negatively correlated with BMI SDS (r = -0.541; P = 0.022). In pubertal boys, testosterone levels were normal suggesting a normal Leydig cell function. In contrast, NS patients had significant lower levels of AMH (mean SDS: -0.6 ± 1.1; P = 0.003) and inhibin B (mean SDS: -1.1 ± 1.2; P textless 0.001) compared with the general population, suggesting a Sertoli cell dysfunction. Lower AMH and inhibin B levels were found in NS-PTPN11 patients, whereas these markers did not differ from healthy children in SOS1 patients. No difference was found between cryptorchid and non-cryptorchid patients for AMH and inhibin B levels (P = 0.43 and 0.62 respectively). Four NS-PTPN11 patients had a severe primary hypogonadism with azoospermia/cryptozoospermia. Conclusions NS males display Sertoli cell-specific primary testicular insufficiency, whereas Leydig cell function seems to be unaffected.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Context Abnormalities in the hypothalamo-pituitary-gonadal axis have long been reported in Noonan syndrome (NS) males with only few data available in prepubertal children. Objective The aim of this study was to describe the gonadal function of NS males from childhood to adulthood. Design It is a retrospective chart review. Patients and methods A total of 37 males with a genetically confirmed diagnosis of NS were included. Clinical and genetic features, as well as serum hormone levels (LH, FSH, testosterone, anti-Müllerian hormone (AMH), and inhibin B) were analysed. Results Of the 37 patients, 16 (43%) children had entered puberty at a median age of 13.5 years (range: 11.4-15.0 years); age at pubertal onset was negatively correlated with BMI SDS (r = -0.541; P = 0.022). In pubertal boys, testosterone levels were normal suggesting a normal Leydig cell function. In contrast, NS patients had significant lower levels of AMH (mean SDS: -0.6 ± 1.1; P = 0.003) and inhibin B (mean SDS: -1.1 ± 1.2; P textless 0.001) compared with the general population, suggesting a Sertoli cell dysfunction. Lower AMH and inhibin B levels were found in NS-PTPN11 patients, whereas these markers did not differ from healthy children in SOS1 patients. No difference was found between cryptorchid and non-cryptorchid patients for AMH and inhibin B levels (P = 0.43 and 0.62 respectively). Four NS-PTPN11 patients had a severe primary hypogonadism with azoospermia/cryptozoospermia. Conclusions NS males display Sertoli cell-specific primary testicular insufficiency, whereas Leydig cell function seems to be unaffected. |
Poupot, R{é}my ; Goursat, C{é}cile ; Fruchon, S{é}verine Multivalent nanosystems: targeting monocytes/macrophages. Journal Article International journal of nanomedicine, 13 , pp. 5511–5521, 2018, ISSN: 1178-2013. Abstract | Links | BibTeX @article{Poupot2018,
title = {Multivalent nanosystems: targeting monocytes/macrophages.},
author = {Poupot, R{é}my and Goursat, C{é}cile and Fruchon, S{é}verine},
url = {https://www.dovepress.com/multivalent-nanosystems-targeting-monocytesmacrophages-peer-reviewed-article-IJN http://www.ncbi.nlm.nih.gov/pubmed/30271144 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC6154704},
doi = {10.2147/IJN.S146192},
issn = {1178-2013},
year = {2018},
date = {2018-09-01},
journal = {International journal of nanomedicine},
volume = {13},
pages = {5511--5521},
abstract = {Among all the cellular partners involved in inflammatory processes, monocytes and macrophages are the master regulators of inflammation. They are found in almost all the tissues and are nearly the only cells capable of performing each step of inflammation. Consequently, they stand as major relevant therapeutic targets to treat inflammatory disorders and diseases. The physiological phagocytic activity of macrophages prompts them to detect, to recognize, and eventually to engulf any nanosystem cruising in their neighborhood. Interestingly, nanosystems can be rationally engineered to afford multivalent, and multifunctional if needed, entities with multiplexed and/or reinforced biological activities. Indeed, engineered nanosystems bearing moieties specifically targeting macrophages, and loaded with or bound to drugs are promising candidates to modulate, or even eradicate, deleterious macrophages in vivo. In this review we highlight recent articles and concepts of multivalent nanosystems targeting monocytes and macrophages to treat inflammatory disorders.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Among all the cellular partners involved in inflammatory processes, monocytes and macrophages are the master regulators of inflammation. They are found in almost all the tissues and are nearly the only cells capable of performing each step of inflammation. Consequently, they stand as major relevant therapeutic targets to treat inflammatory disorders and diseases. The physiological phagocytic activity of macrophages prompts them to detect, to recognize, and eventually to engulf any nanosystem cruising in their neighborhood. Interestingly, nanosystems can be rationally engineered to afford multivalent, and multifunctional if needed, entities with multiplexed and/or reinforced biological activities. Indeed, engineered nanosystems bearing moieties specifically targeting macrophages, and loaded with or bound to drugs are promising candidates to modulate, or even eradicate, deleterious macrophages in vivo. In this review we highlight recent articles and concepts of multivalent nanosystems targeting monocytes and macrophages to treat inflammatory disorders. |
Tauber, Ma{ï}th{é} ; Diene, Gwenaelle ; Molinas, Catherine Growth Hormone Treatment for Prader-Willi Syndrome. Journal Article Pediatric endocrinology reviews : PER, 16 (Suppl 1), pp. 91–99, 2018, ISSN: 1565-4753. Abstract | Links | BibTeX @article{Tauber2018,
title = {Growth Hormone Treatment for Prader-Willi Syndrome.},
author = {Tauber, Ma{ï}th{é} and Diene, Gwenaelle and Molinas, Catherine},
url = {http://www.ncbi.nlm.nih.gov/pubmed/30378786},
doi = {10.17458/per.vol16.2018.tdm.ghpraderwilli},
issn = {1565-4753},
year = {2018},
date = {2018-09-01},
journal = {Pediatric endocrinology reviews : PER},
volume = {16},
number = {Suppl 1},
pages = {91--99},
abstract = {The European Marketing Authorization for recombinant human growth hormone (rhGH) in children with Prader-Willi syndrome was the first indication for metabolic and body composition effects in children. In the US it is indicated for short stature associated with PWS. Recombinant hGH is the first treatment for the PWS population and radically changed the care of these children by facilitating access to physicians who prescribe rhGH, mainly paediatric endocrinologists, and manage the organization of multidisciplinary care. Recombinant hGH treatment improved linear growth, body composition, and socialization not only in children but also in young adults. The pathophysiology of combined hormonal deficiencies including GH is starting to be unravelled. We now have to focus on co-morbidities that are not modified by rhGH treatment, such as feeding disorders and behaviour problems, to truly change the life of patients. The transition of care from adolescents to young adults also remains a challenge.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The European Marketing Authorization for recombinant human growth hormone (rhGH) in children with Prader-Willi syndrome was the first indication for metabolic and body composition effects in children. In the US it is indicated for short stature associated with PWS. Recombinant hGH is the first treatment for the PWS population and radically changed the care of these children by facilitating access to physicians who prescribe rhGH, mainly paediatric endocrinologists, and manage the organization of multidisciplinary care. Recombinant hGH treatment improved linear growth, body composition, and socialization not only in children but also in young adults. The pathophysiology of combined hormonal deficiencies including GH is starting to be unravelled. We now have to focus on co-morbidities that are not modified by rhGH treatment, such as feeding disorders and behaviour problems, to truly change the life of patients. The transition of care from adolescents to young adults also remains a challenge. |
Tajan, Myl{è}ne ; Pernin-Grandjean, Julie ; Beton, Nicolas ; Gennero, Isabelle ; Capilla, Florence ; Neel, Benjamin G; Araki, Toshiyuki ; Valet, Philippe ; Tauber, Maith{é} ; Salles, Jean-Pierre ; Yart, Armelle ; Edouard, Thomas Noonan syndrome-causing SHP2 mutants impair ERK-dependent chondrocyte differentiation during endochondral bone growth Journal Article Human Molecular Genetics, 27 (13), pp. 2276–2289, 2018. Abstract | Links | BibTeX @article{Tajan2018,
title = {Noonan syndrome-causing SHP2 mutants impair ERK-dependent chondrocyte differentiation during endochondral bone growth},
author = {Tajan, Myl{è}ne and Pernin-Grandjean, Julie and Beton, Nicolas and Gennero, Isabelle and Capilla, Florence and Neel, Benjamin G and Araki, Toshiyuki and Valet, Philippe and Tauber, Maith{é} and Salles, Jean-Pierre and Yart, Armelle and Edouard, Thomas},
url = {http://www.ncbi.nlm.nih.gov/pubmed/29659837 http://www.ncbi.nlm.nih.gov/pubmed/29659837 http://www.ncbi.nlm.nih.gov/pubmed/29659837},
doi = {10.1093/hmg/ddy133},
year = {2018},
date = {2018-07-01},
journal = {Human Molecular Genetics},
volume = {27},
number = {13},
pages = {2276--2289},
abstract = {Growth retardation is a constant feature of Noonan syndrome (NS) but its physiopathology remains poorly understood. We previously reported that hyperactive NS-causing SHP2 mutants impair the systemic production of insulin-like growth factor 1 (IGF1) through hyperactivation of the RAS/extracellular signal-regulated kinases (ERK) signalling pathway. Besides endocrine defects, a direct effect of these mutants on growth plate has not been explored, although recent studies have revealed an important physiological role for SHP2 in endochondral bone growth. We demonstrated that growth plate length was reduced in NS mice, mostly due to a shortening of the hypertrophic zone and to a lesser extent of the proliferating zone. These histological features were correlated with decreased expression of early chondrocyte differentiation markers, and with reduced alkaline phosphatase staining and activity, in NS murine primary chondrocytes. Although IGF1 treatment improved growth of NS mice, it did not fully reverse growth plate abnormalities, notably the decreased hypertrophic zone. In contrast, we documented a role of RAS/ERK hyperactivation at the growth plate level since 1) NS-causing SHP2 mutants enhance RAS/ERK activation in chondrocytes in vivo (NS mice) and in vitro (ATDC5 cells) and 2) inhibition of RAS/ERK hyperactivation by U0126 treatment alleviated growth plate abnormalities and enhanced chondrocyte differentiation. Similar effects were obtained by chronic treatment of NS mice with statins. In conclusion, we demonstrated that hyperactive NS-causing SHP2 mutants impair chondrocyte differentiation during endochondral bone growth through a local hyperactivation of the RAS/ERK signalling pathway, and that statin treatment may be a possible therapeutic approach in NS.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Growth retardation is a constant feature of Noonan syndrome (NS) but its physiopathology remains poorly understood. We previously reported that hyperactive NS-causing SHP2 mutants impair the systemic production of insulin-like growth factor 1 (IGF1) through hyperactivation of the RAS/extracellular signal-regulated kinases (ERK) signalling pathway. Besides endocrine defects, a direct effect of these mutants on growth plate has not been explored, although recent studies have revealed an important physiological role for SHP2 in endochondral bone growth. We demonstrated that growth plate length was reduced in NS mice, mostly due to a shortening of the hypertrophic zone and to a lesser extent of the proliferating zone. These histological features were correlated with decreased expression of early chondrocyte differentiation markers, and with reduced alkaline phosphatase staining and activity, in NS murine primary chondrocytes. Although IGF1 treatment improved growth of NS mice, it did not fully reverse growth plate abnormalities, notably the decreased hypertrophic zone. In contrast, we documented a role of RAS/ERK hyperactivation at the growth plate level since 1) NS-causing SHP2 mutants enhance RAS/ERK activation in chondrocytes in vivo (NS mice) and in vitro (ATDC5 cells) and 2) inhibition of RAS/ERK hyperactivation by U0126 treatment alleviated growth plate abnormalities and enhanced chondrocyte differentiation. Similar effects were obtained by chronic treatment of NS mice with statins. In conclusion, we demonstrated that hyperactive NS-causing SHP2 mutants impair chondrocyte differentiation during endochondral bone growth through a local hyperactivation of the RAS/ERK signalling pathway, and that statin treatment may be a possible therapeutic approach in NS. |
Fruchon, S{é}verine ; Poupot, R{é}my The ABP Dendrimer, a Drug-Candidate against Inflammatory Diseases That Triggers the Activation of Interleukin-10 Producing Immune Cells. Journal Article Molecules (Basel, Switzerland), 23 (6), 2018. Abstract | Links | BibTeX @article{Fruchon2018,
title = {The ABP Dendrimer, a Drug-Candidate against Inflammatory Diseases That Triggers the Activation of Interleukin-10 Producing Immune Cells.},
author = {Fruchon, S{é}verine and Poupot, R{é}my},
url = {http://www.ncbi.nlm.nih.gov/pubmed/29799517 http://www.ncbi.nlm.nih.gov/pubmed/29799517},
doi = {10.3390/molecules23061272},
year = {2018},
date = {2018-05-01},
journal = {Molecules (Basel, Switzerland)},
volume = {23},
number = {6},
publisher = {Multidisciplinary Digital Publishing Institute (MDPI)},
abstract = {The ABP dendrimer, which is built on a phosphorus-based scaffold and bears twelve azabisphosphonate groups at its surface, is one of the dendrimers that has been shown to display immuno-modulatory and anti-inflammatory effects towards the human immune system. Its anti-inflammatory properties have been successfully challenged in animal models of inflammatory disorders. In this review, we trace the discovery and the evaluation of the therapeutic effects of the ABP dendrimer in three different animal models of both acute and chronic inflammatory diseases. We emphasize that its therapeutic effects rely on the enhancement of the production of Interleukin-10, the paradigm of anti-inflammatory cytokines, by different subsets of immune cells, such as monocytes/macrophages and CD4+ T lymphocytes.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The ABP dendrimer, which is built on a phosphorus-based scaffold and bears twelve azabisphosphonate groups at its surface, is one of the dendrimers that has been shown to display immuno-modulatory and anti-inflammatory effects towards the human immune system. Its anti-inflammatory properties have been successfully challenged in animal models of inflammatory disorders. In this review, we trace the discovery and the evaluation of the therapeutic effects of the ABP dendrimer in three different animal models of both acute and chronic inflammatory diseases. We emphasize that its therapeutic effects rely on the enhancement of the production of Interleukin-10, the paradigm of anti-inflammatory cytokines, by different subsets of immune cells, such as monocytes/macrophages and CD4+ T lymphocytes. |
Paepegaey, A C; Coupaye, M; Jaziri, A; M{é}nesguen, F; Dubern, B; Polak, M; Oppert, J M; Tauber, M; Pinto, G; Poitou, C Impact of transitional care on endocrine and anthropometric parameters in Prader–Willi syndrome Journal Article Endocrine Connections, 7 (5), pp. 663–672, 2018. Abstract | Links | BibTeX @article{Paepegaey2018,
title = {Impact of transitional care on endocrine and anthropometric parameters in Prader–Willi syndrome},
author = {Paepegaey, A C and Coupaye, M and Jaziri, A and M{é}nesguen, F and Dubern, B and Polak, M and Oppert, J M and Tauber, M and Pinto, G and Poitou, C},
url = {http://www.ncbi.nlm.nih.gov/pubmed/29666169 http://www.ncbi.nlm.nih.gov/pubmed/29666169 http://www.ncbi.nlm.nih.gov/pubmed/29666169},
doi = {10.1530/EC-18-0089},
year = {2018},
date = {2018-05-01},
journal = {Endocrine Connections},
volume = {7},
number = {5},
pages = {663--672},
abstract = {CONTEXT The transition of patients with Prader-Willi syndrome (PWS) to adult life for medical care is challenging because of multiple comorbidities, including hormone deficiencies, obesity and cognitive and behavioral disabilities. OBJECTIVE To assess endocrine management, and metabolic and anthropometric parameters of PWS adults who received (n = 31) or not (n = 64) transitional care, defined as specialized pediatric care followed by a structured care pathway to a multidisciplinary adult team. PATIENTS AND STUDY DESIGN Hormonal and metabolic parameters were retrospectively recorded in 95 adults with PWS (mean ± s.d. age 24.7 ± 8.2 years, BMI: 39.8 ± 12.1 kg/m²) referred to our Reference Center and compared according to transition. RESULTS Among the entire cohort, 35.8% received growth hormone (GH) during childhood and 16.8% had a GH stimulation test after completion of growth. In adulthood, 14.7% were treated with GH, 56.8% received sex-hormone therapy, whereas 91.1% were hypogonadic and 37.9% had undergone valid screening of the corticotropic axis. The main reason for suboptimal endocrine management was marked behavioral disorders. Patients receiving transitional care were more likely to have had a GH stimulation test and hormonal substitutions in childhood. They also had a lower BMI, percentage of fat mass, improved metabolic parameters and fewer antidepressant treatments. Transitional care remained significantly associated with these parameters in multivariate analysis when adjusted on GH treatment. CONCLUSION A coordinated care pathway with specialized pediatric care and transition to a multidisciplinary adult team accustomed to managing complex disability including psychiatric troubles are associated with a better health status in adults with PWS.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
CONTEXT The transition of patients with Prader-Willi syndrome (PWS) to adult life for medical care is challenging because of multiple comorbidities, including hormone deficiencies, obesity and cognitive and behavioral disabilities. OBJECTIVE To assess endocrine management, and metabolic and anthropometric parameters of PWS adults who received (n = 31) or not (n = 64) transitional care, defined as specialized pediatric care followed by a structured care pathway to a multidisciplinary adult team. PATIENTS AND STUDY DESIGN Hormonal and metabolic parameters were retrospectively recorded in 95 adults with PWS (mean ± s.d. age 24.7 ± 8.2 years, BMI: 39.8 ± 12.1 kg/m²) referred to our Reference Center and compared according to transition. RESULTS Among the entire cohort, 35.8% received growth hormone (GH) during childhood and 16.8% had a GH stimulation test after completion of growth. In adulthood, 14.7% were treated with GH, 56.8% received sex-hormone therapy, whereas 91.1% were hypogonadic and 37.9% had undergone valid screening of the corticotropic axis. The main reason for suboptimal endocrine management was marked behavioral disorders. Patients receiving transitional care were more likely to have had a GH stimulation test and hormonal substitutions in childhood. They also had a lower BMI, percentage of fat mass, improved metabolic parameters and fewer antidepressant treatments. Transitional care remained significantly associated with these parameters in multivariate analysis when adjusted on GH treatment. CONCLUSION A coordinated care pathway with specialized pediatric care and transition to a multidisciplinary adult team accustomed to managing complex disability including psychiatric troubles are associated with a better health status in adults with PWS. |
Hayder, Myriam ; Garzoni, Matteo ; Bochicchio, Davide ; Caminade, Anne-Marie ; Couderc, Fran{ç}ois ; Ong-Meang, Varravaddheay ; Davignon, Jean-Luc ; Turrin, C{é}dric-Olivier ; Pavan, Giovanni M; Poupot, R{é}my Three-Dimensional Directionality Is a Pivotal Structural Feature for the Bioactivity of Azabisphosphonate-Capped Poly(PhosphorHydrazone) Nanodrug Dendrimers. Journal Article Biomacromolecules, 19 (3), pp. 712–720, 2018, ISSN: 1526-4602. Abstract | Links | BibTeX @article{Hayder2018,
title = {Three-Dimensional Directionality Is a Pivotal Structural Feature for the Bioactivity of Azabisphosphonate-Capped Poly(PhosphorHydrazone) Nanodrug Dendrimers.},
author = {Hayder, Myriam and Garzoni, Matteo and Bochicchio, Davide and Caminade, Anne-Marie and Couderc, Fran{ç}ois and Ong-Meang, Varravaddheay and Davignon, Jean-Luc and Turrin, C{é}dric-Olivier and Pavan, Giovanni M and Poupot, R{é}my},
url = {http://pubs.acs.org/doi/10.1021/acs.biomac.7b01398 http://www.ncbi.nlm.nih.gov/pubmed/29443507},
doi = {10.1021/acs.biomac.7b01398},
issn = {1526-4602},
year = {2018},
date = {2018-03-01},
journal = {Biomacromolecules},
volume = {19},
number = {3},
pages = {712--720},
abstract = {Dendrimers are nanosized, nonlinear, hyperbranched polymers whose overall 3D shape is key for their biological activity. Poly(PhosphorHydrazone) (PPH) dendrimers capped with aza-bisphosphonate (ABP) end groups are known to have anti-inflammatory properties enabling the control of inflammatory diseases in different mouse models. Here we screen the anti-inflammatory activity of a series of PPH dendrimers bearing between 2 and 16 ABP end groups in a mouse model of arthritis and confront the biological results with atomistic simulations of the dendrimers. We show that only the PPH dendrimers capped with 10 and 12 ABP end groups can control the flare of the inflammatory disease. All-atom accelerated molecular dynamics simulations show that dendrimers with a low number of ABP end groups are directional but highly flexible/dynamic and have thereby limited efficiency in establishing multivalent interactions. The largest dendrimer appears as nondirectional, having 16 ABP end groups forming patches all over the dendrimer surface. Conversely, intermediate dendrimers having 10 or 12 ABP end groups reach the best compromise between the number of surface groups and their stable directional gathering, a real maximization of multivalency.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Dendrimers are nanosized, nonlinear, hyperbranched polymers whose overall 3D shape is key for their biological activity. Poly(PhosphorHydrazone) (PPH) dendrimers capped with aza-bisphosphonate (ABP) end groups are known to have anti-inflammatory properties enabling the control of inflammatory diseases in different mouse models. Here we screen the anti-inflammatory activity of a series of PPH dendrimers bearing between 2 and 16 ABP end groups in a mouse model of arthritis and confront the biological results with atomistic simulations of the dendrimers. We show that only the PPH dendrimers capped with 10 and 12 ABP end groups can control the flare of the inflammatory disease. All-atom accelerated molecular dynamics simulations show that dendrimers with a low number of ABP end groups are directional but highly flexible/dynamic and have thereby limited efficiency in establishing multivalent interactions. The largest dendrimer appears as nondirectional, having 16 ABP end groups forming patches all over the dendrimer surface. Conversely, intermediate dendrimers having 10 or 12 ABP end groups reach the best compromise between the number of surface groups and their stable directional gathering, a real maximization of multivalency. |
Poupot, R{é}my ; Bergozza, Dylan ; Fruchon, S{é}verine Nanoparticle-Based Strategies to Treat Neuro-Inflammation. Journal Article Materials (Basel, Switzerland), 11 (2), pp. 270, 2018, ISSN: 1996-1944. Abstract | Links | BibTeX @article{Poupot2018a,
title = {Nanoparticle-Based Strategies to Treat Neuro-Inflammation.},
author = {Poupot, R{é}my and Bergozza, Dylan and Fruchon, S{é}verine},
url = {http://www.mdpi.com/1996-1944/11/2/270 http://www.ncbi.nlm.nih.gov/pubmed/29425146 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5848967},
doi = {10.3390/ma11020270},
issn = {1996-1944},
year = {2018},
date = {2018-02-01},
journal = {Materials (Basel, Switzerland)},
volume = {11},
number = {2},
pages = {270},
abstract = {Neuro-inflammation is a pivotal physio-pathological feature of brain disorders, including neurodegenerative diseases. As such, it is a relevant therapeutic target against which drugs have to be proposed. Targeting neuro-inflammation implies crossing the Blood-Brain Barrier (BBB) to reach the Central Nervous System (CNS). Engineered nanoparticles (ENPs) are promising candidates to carry and deliver drugs to the CNS by crossing the BBB. There are several strategies to design ENPs intended for crossing through the BBB. Herein, we first put nanotechnologies back in their historical context and introduce neuro-inflammation and its consequences in terms of public health. In a second part, we explain how ENPs can get access to the brain and review this area by highlighting recent papers in the field. Finally, after pointing out potential guidelines for preclinical studies involving ENPs, we conclude by opening the debate on the questions of nanosafety and toxicity of these ENPs and in particular on ecotoxicity related to regulatory issues and public concerns.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Neuro-inflammation is a pivotal physio-pathological feature of brain disorders, including neurodegenerative diseases. As such, it is a relevant therapeutic target against which drugs have to be proposed. Targeting neuro-inflammation implies crossing the Blood-Brain Barrier (BBB) to reach the Central Nervous System (CNS). Engineered nanoparticles (ENPs) are promising candidates to carry and deliver drugs to the CNS by crossing the BBB. There are several strategies to design ENPs intended for crossing through the BBB. Herein, we first put nanotechnologies back in their historical context and introduce neuro-inflammation and its consequences in terms of public health. In a second part, we explain how ENPs can get access to the brain and review this area by highlighting recent papers in the field. Finally, after pointing out potential guidelines for preclinical studies involving ENPs, we conclude by opening the debate on the questions of nanosafety and toxicity of these ENPs and in particular on ecotoxicity related to regulatory issues and public concerns. |
Allas, Soraya ; Caix{à}s, Assumpta ; Poitou, Christine ; Coupaye, Muriel ; Thuilleaux, Denise ; Lorenzini, Fran{ç}oise ; Diene, Gwena{ë}lle ; Crin{ò}, Antonino ; Illouz, Fr{é}d{é}ric ; Grugni, Graziano ; Potvin, Diane ; Bocchini, Sarah ; Delale, Thomas ; Abribat, Thierry ; Tauber, Maith{é} AZP-531, an unacylated ghrelin analog, improves food-related behavior in patients with Prader-Willi syndrome: A randomized placebo-controlled trial Journal Article PLoS ONE, 13 (1), pp. 1–19, 2018, ISSN: 19326203. Abstract | Links | BibTeX @article{Allas2018,
title = {AZP-531, an unacylated ghrelin analog, improves food-related behavior in patients with Prader-Willi syndrome: A randomized placebo-controlled trial},
author = {Allas, Soraya and Caix{à}s, Assumpta and Poitou, Christine and Coupaye, Muriel and Thuilleaux, Denise and Lorenzini, Fran{ç}oise and Diene, Gwena{ë}lle and Crin{ò}, Antonino and Illouz, Fr{é}d{é}ric and Grugni, Graziano and Potvin, Diane and Bocchini, Sarah and Delale, Thomas and Abribat, Thierry and Tauber, Maith{é}},
doi = {10.1371/journal.pone.0190849},
issn = {19326203},
year = {2018},
date = {2018-01-01},
journal = {PLoS ONE},
volume = {13},
number = {1},
pages = {1--19},
abstract = {CONTEXT AND OBJECTIVE Prader-Willi syndrome (PWS) is characterized by early-onset hyperphagia and increased circulating levels of the orexigenic Acylated Ghrelin (AG) hormone with a relative deficit of Unacylated Ghrelin (UAG). AZP-531, a first-in-class UAG analog, was shown to inhibit the orexigenic effect of AG in animals, to improve glycemic control and decrease body weight in humans. We aimed to investigate the safety and efficacy of AZP-531 in patients with PWS for whom no approved treatment for hyperphagia is currently available. METHODS AND DESIGN Multi-center, randomized, double-blind, placebo-controlled trial. Forty-seven patients with genetically confirmed PWS and evidence of hyperphagia received daily subcutaneous injections of AZP-531 (3 and 4 mg for 50-70 kg and textgreater70 kg body weight, respectively) or matching placebo for 14 days. Assessments included adverse events, vital signs, safety laboratory tests, the Hyperphagia Questionnaire (HQ), patient-reported appetite, body composition and glycemic measures. RESULTS AZP-531 was well tolerated. There was a significant improvement with AZP-531 versus placebo in the mean total score, the 9-item score and the severity domain score of the HQ (p textless .05). The highest reduction in the total and 9-item scores was observed in AZP-531 subjects with the highest hyperphagia score at baseline. Findings were supported by a reduction in appetite scores observed with AZP-531 only. Body weight did not change in both groups while a significant reduction in waist circumference and fat mass was observed only with AZP-531. AZP-531 significantly decreased post-prandial glucose levels in a baseline glucose dependent fashion. CONCLUSIONS AZP-531 may constitute a new treatment strategy to improve hyperphagia and metabolic issues in patients with PWS. These findings support further investigation in longer-term clinical trials.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
CONTEXT AND OBJECTIVE Prader-Willi syndrome (PWS) is characterized by early-onset hyperphagia and increased circulating levels of the orexigenic Acylated Ghrelin (AG) hormone with a relative deficit of Unacylated Ghrelin (UAG). AZP-531, a first-in-class UAG analog, was shown to inhibit the orexigenic effect of AG in animals, to improve glycemic control and decrease body weight in humans. We aimed to investigate the safety and efficacy of AZP-531 in patients with PWS for whom no approved treatment for hyperphagia is currently available. METHODS AND DESIGN Multi-center, randomized, double-blind, placebo-controlled trial. Forty-seven patients with genetically confirmed PWS and evidence of hyperphagia received daily subcutaneous injections of AZP-531 (3 and 4 mg for 50-70 kg and textgreater70 kg body weight, respectively) or matching placebo for 14 days. Assessments included adverse events, vital signs, safety laboratory tests, the Hyperphagia Questionnaire (HQ), patient-reported appetite, body composition and glycemic measures. RESULTS AZP-531 was well tolerated. There was a significant improvement with AZP-531 versus placebo in the mean total score, the 9-item score and the severity domain score of the HQ (p textless .05). The highest reduction in the total and 9-item scores was observed in AZP-531 subjects with the highest hyperphagia score at baseline. Findings were supported by a reduction in appetite scores observed with AZP-531 only. Body weight did not change in both groups while a significant reduction in waist circumference and fat mass was observed only with AZP-531. AZP-531 significantly decreased post-prandial glucose levels in a baseline glucose dependent fashion. CONCLUSIONS AZP-531 may constitute a new treatment strategy to improve hyperphagia and metabolic issues in patients with PWS. These findings support further investigation in longer-term clinical trials. |
Thuilleaux, Denise ; Laurier, Virginie ; Copet, Pierre ; Tricot, Julie ; Demeer, Genevi{è}ve ; Mourre, Fabien ; Tauber, Maith{é} ; Jauregi, Joseba A model to characterize psychopathological features in adults with Prader-Willi syndrome Journal Article American Journal of Medical Genetics, Part A, 176 (1), pp. 41–47, 2018, ISSN: 15524833. Abstract | Links | BibTeX @article{Thuilleaux2018,
title = {A model to characterize psychopathological features in adults with Prader-Willi syndrome},
author = {Thuilleaux, Denise and Laurier, Virginie and Copet, Pierre and Tricot, Julie and Demeer, Genevi{è}ve and Mourre, Fabien and Tauber, Maith{é} and Jauregi, Joseba},
doi = {10.1002/ajmg.a.38525},
issn = {15524833},
year = {2018},
date = {2018-01-01},
journal = {American Journal of Medical Genetics, Part A},
volume = {176},
number = {1},
pages = {41--47},
abstract = {High prevalence of behavioral and psychiatric disorders in adults with Prader-Willi Syndrome (PWS) has been reported in last few years. However, data are confusing and often contradictory. In this article, we propose a model to achieve a better understanding of the psychopathological features in adults with PWS. The study is based on clinical observations of 150 adult inpatients, males and females. Non-parametric statistics were performed to analyse the association of psychopathological profiles with genotype, gender and age. We propose a model of psychiatric disorders in adults with PWS based on cognitive, emotional and behavioural issues. This model defines four psychopathological profiles: Basic, Impulsive, Compulsive, and Psychotic. The Basic profile is defined by traits and symptoms that are present in varying degrees in all persons with PWS. In our cohort, this Basic profile corresponds to 55% of the patients. The rest show, in addition to these characteristics, salient features of impulsivity (Impulsive profile, 19%), compulsivity (Compulsive profile, 7%), or psychosis (Psychotic profile, 19%). The analysis of factors associated with different profiles reveals an effect of genotype on Basic and Psychotic profiles (Deletion: 70% Basic, 9% Psychotic; Non-deletion: 23% Basic, 43% Psychotic) and a positive correlation between male sex and impulsivity, unmediated by sex hormone treatment. This is a clinical study, based on observation proposing an original model to understand the psychiatric and behavioural disorders in adults with PWS. Further studies are needed in order to test the validity of this model.Copyright textcopyright 2017 Wiley Periodicals, Inc.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
High prevalence of behavioral and psychiatric disorders in adults with Prader-Willi Syndrome (PWS) has been reported in last few years. However, data are confusing and often contradictory. In this article, we propose a model to achieve a better understanding of the psychopathological features in adults with PWS. The study is based on clinical observations of 150 adult inpatients, males and females. Non-parametric statistics were performed to analyse the association of psychopathological profiles with genotype, gender and age. We propose a model of psychiatric disorders in adults with PWS based on cognitive, emotional and behavioural issues. This model defines four psychopathological profiles: Basic, Impulsive, Compulsive, and Psychotic. The Basic profile is defined by traits and symptoms that are present in varying degrees in all persons with PWS. In our cohort, this Basic profile corresponds to 55% of the patients. The rest show, in addition to these characteristics, salient features of impulsivity (Impulsive profile, 19%), compulsivity (Compulsive profile, 7%), or psychosis (Psychotic profile, 19%). The analysis of factors associated with different profiles reveals an effect of genotype on Basic and Psychotic profiles (Deletion: 70% Basic, 9% Psychotic; Non-deletion: 23% Basic, 43% Psychotic) and a positive correlation between male sex and impulsivity, unmediated by sex hormone treatment. This is a clinical study, based on observation proposing an original model to understand the psychiatric and behavioural disorders in adults with PWS. Further studies are needed in order to test the validity of this model.Copyright textcopyright 2017 Wiley Periodicals, Inc. |
Puy, V; Darwiche, W; Trudel, S; Gomila, C; Lony, C; Puy, L; Lefebvre, T; Vitry, S; Boullier, A; Karim, Z; Ausseil, J Predominant role of microglia in brain iron retention in Sanfilippo syndrome, a pediatric neurodegenerative disease Journal Article Glia, 66 (8), pp. 1709-1723, 2018, ISSN: 1098-1136 (Electronic)
0894-1491 (Linking). Links | BibTeX @article{RN1003,
title = {Predominant role of microglia in brain iron retention in Sanfilippo syndrome, a pediatric neurodegenerative disease},
author = {Puy, V. and Darwiche, W. and Trudel, S. and Gomila, C. and Lony, C. and Puy, L. and Lefebvre, T. and Vitry, S. and Boullier, A. and Karim, Z. and Ausseil, J.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/29624734},
doi = {10.1002/glia.23335},
issn = {1098-1136 (Electronic)
0894-1491 (Linking)},
year = {2018},
date = {2018-01-01},
journal = {Glia},
volume = {66},
number = {8},
pages = {1709-1723},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Rouillon, J; Lefebvre, T; Denard, J; Puy, V; Daher, R; Ausseil, J; Zocevic, A; Fogel, P; Peoc'h, K; Wong, B; Servais, L; Voit, T; Puy, H; Karim, Z; Svinartchouk, F High urinary ferritin reflects myoglobin iron evacuation in DMD patients Journal Article Neuromuscul Disord, 28 (7), pp. 564-571, 2018, ISSN: 1873-2364 (Electronic)
0960-8966 (Linking). Links | BibTeX @article{RN1002,
title = {High urinary ferritin reflects myoglobin iron evacuation in DMD patients},
author = {Rouillon, J. and Lefebvre, T. and Denard, J. and Puy, V. and Daher, R. and Ausseil, J. and Zocevic, A. and Fogel, P. and Peoc'h, K. and Wong, B. and Servais, L. and Voit, T. and Puy, H. and Karim, Z. and Svinartchouk, F.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/29776718},
doi = {10.1016/j.nmd.2018.03.008},
issn = {1873-2364 (Electronic)
0960-8966 (Linking)},
year = {2018},
date = {2018-01-01},
journal = {Neuromuscul Disord},
volume = {28},
number = {7},
pages = {564-571},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Tebani, A; Abily-Donval, L; Schmitz-Afonso, I; Heron, B; Piraud, M; Ausseil, J; Zerimech, F; Gonzalez, B; Marret, S; Afonso, C; Bekri, S Unveiling metabolic remodeling in mucopolysaccharidosis type III through integrative metabolomics and pathway analysis Journal Article J Transl Med, 16 (1), pp. 248, 2018, ISSN: 1479-5876 (Electronic)
1479-5876 (Linking). Links | BibTeX @article{RN1001,
title = {Unveiling metabolic remodeling in mucopolysaccharidosis type III through integrative metabolomics and pathway analysis},
author = {Tebani, A. and Abily-Donval, L. and Schmitz-Afonso, I. and Heron, B. and Piraud, M. and Ausseil, J. and Zerimech, F. and Gonzalez, B. and Marret, S. and Afonso, C. and Bekri, S.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30180851},
doi = {10.1186/s12967-018-1625-1},
issn = {1479-5876 (Electronic)
1479-5876 (Linking)},
year = {2018},
date = {2018-01-01},
journal = {J Transl Med},
volume = {16},
number = {1},
pages = {248},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2017
|
Fruchon, S{é}verine ; Poupot, R{é}my Pro-Inflammatory Versus Anti-Inflammatory Effects of Dendrimers: The Two Faces of Immuno-Modulatory Nanoparticles. Journal Article Nanomaterials (Basel, Switzerland), 7 (9), pp. 251, 2017, ISSN: 2079-4991. Abstract | Links | BibTeX @article{Fruchon2017,
title = {Pro-Inflammatory Versus Anti-Inflammatory Effects of Dendrimers: The Two Faces of Immuno-Modulatory Nanoparticles.},
author = {Fruchon, S{é}verine and Poupot, R{é}my},
url = {http://www.mdpi.com/2079-4991/7/9/251 http://www.ncbi.nlm.nih.gov/pubmed/28862693 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5618362},
doi = {10.3390/nano7090251},
issn = {2079-4991},
year = {2017},
date = {2017-09-01},
journal = {Nanomaterials (Basel, Switzerland)},
volume = {7},
number = {9},
pages = {251},
abstract = {Dendrimers are soft matter, hyperbranched, and multivalent nanoparticles whose synthesis theoretically affords monodisperse compounds. They are built from a core on which one or several successive series of branches are engrafted in an arborescent way. At the end of the synthesis, the tunable addition of surface groups gives birth to multivalent nano-objects which are generally intended for a specific use. For these reasons, dendrimers have received a lot of attention from biomedical researchers. In particular, some of us have demonstrated that dendrimers can be intrinsically drug-candidate for the treatment of inflammatory disorders, amongst others, using relevant preclinical animal models. These anti-inflammatory dendrimers are innovative in the pharmaceutical field. More recently, it has appeared that some dendrimers (even among those which have been described as anti-inflammatory) can promote inflammatory responses in non-diseased animals. The main corpus of this concise review is focused on the reports which describe anti-inflammatory properties of dendrimers in vivo, following which we review the few recent articles that show pro-inflammatory effects of our favorite molecules, to finally discuss this duality in immuno-modulation which has to be taken into account for the preclinical and clinical developments of dendrimers.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Dendrimers are soft matter, hyperbranched, and multivalent nanoparticles whose synthesis theoretically affords monodisperse compounds. They are built from a core on which one or several successive series of branches are engrafted in an arborescent way. At the end of the synthesis, the tunable addition of surface groups gives birth to multivalent nano-objects which are generally intended for a specific use. For these reasons, dendrimers have received a lot of attention from biomedical researchers. In particular, some of us have demonstrated that dendrimers can be intrinsically drug-candidate for the treatment of inflammatory disorders, amongst others, using relevant preclinical animal models. These anti-inflammatory dendrimers are innovative in the pharmaceutical field. More recently, it has appeared that some dendrimers (even among those which have been described as anti-inflammatory) can promote inflammatory responses in non-diseased animals. The main corpus of this concise review is focused on the reports which describe anti-inflammatory properties of dendrimers in vivo, following which we review the few recent articles that show pro-inflammatory effects of our favorite molecules, to finally discuss this duality in immuno-modulation which has to be taken into account for the preclinical and clinical developments of dendrimers. |
Burnett, L C; LeDuc, C A; Sulsona, C R; Paull, D; Rausch, R; Eddiry, S; Carli, J F; Morabito, M V; Skowronski, A A; Hubner, G; Zimmer, M; Wang, L; Day, R; Levy, B; Fennoy, I; Dubern, B; Poitou, C; Clement, K; Butler, M G; Rosenbaum, M; Salles, J P; Tauber, M; Driscoll, D J; Egli, D; Leibel, R L Deficiency in prohormone convertase PC1 impairs prohormone processing in Prader-Willi syndrome Journal Article J Clin Invest, 127 (1), pp. 293-305, 2017, ISSN: 1558-8238 (Electronic)
0021-9738 (Linking). Links | BibTeX @article{RN2b,
title = {Deficiency in prohormone convertase PC1 impairs prohormone processing in Prader-Willi syndrome},
author = {Burnett, L. C. and LeDuc, C. A. and Sulsona, C. R. and Paull, D. and Rausch, R. and Eddiry, S. and Carli, J. F. and Morabito, M. V. and Skowronski, A. A. and Hubner, G. and Zimmer, M. and Wang, L. and Day, R. and Levy, B. and Fennoy, I. and Dubern, B. and Poitou, C. and Clement, K. and Butler, M. G. and Rosenbaum, M. and Salles, J. P. and Tauber, M. and Driscoll, D. J. and Egli, D. and Leibel, R. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/27941249},
doi = {10.1172/JCI88648},
issn = {1558-8238 (Electronic)
0021-9738 (Linking)},
year = {2017},
date = {2017-01-01},
journal = {J Clin Invest},
volume = {127},
number = {1},
pages = {293-305},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Tauber, Maïthé; Boulanouar, Kader; Diene, Gwenaelle; Çabal-Berthoumieu, Sophie; Ehlinger, Virginie; Fichaux-Bourin, Pascale; Molinas, Catherine; Faye, Sandy; Valette, Marion; Pourrinet, Jeanne; Cessans, Catie; Viaux-Sauvelon, Sylvie; Bascoul, Céline; Guedeney, Antoine; Delhanty, Patric; Geenen, Vincent; Martens, Henri; Muscatelli, Françoise; Cohen, David; Consoli, Angèle; Payoux, Pierre; Arnaud, Catherine; Salles, Jean-Pierre The Use of Oxytocin to Improve Feeding and Social Skills in Infants With Prader–Willi Syndrome Journal Article PEDIATRICS, 139 (2), pp. e2 0162976, 2017. BibTeX @article{RN10b,
title = {The Use of Oxytocin to Improve Feeding and Social Skills in Infants With Prader–Willi Syndrome},
author = {Maïthé Tauber and Kader Boulanouar and Gwenaelle Diene and Sophie Çabal-Berthoumieu and Virginie Ehlinger and Pascale Fichaux-Bourin and Catherine Molinas and Sandy Faye and Marion Valette and Jeanne Pourrinet and Catie Cessans and Sylvie Viaux-Sauvelon and Céline Bascoul and Antoine Guedeney and Patric Delhanty and Vincent Geenen and Henri Martens and Françoise Muscatelli and David Cohen and Angèle Consoli and Pierre Payoux and Catherine Arnaud and Salles, Jean-Pierre},
year = {2017},
date = {2017-01-01},
journal = {PEDIATRICS},
volume = {139},
number = {2},
pages = {e2 0162976},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Bodet, P E; Salard, I; Przybylski, C; Gonnet, F; Gomila, C; Ausseil, J; Daniel, R Efficient recovery of glycosaminoglycan oligosaccharides from polyacrylamide gel electrophoresis combined with mass spectrometry analysis Journal Article Anal Bioanal Chem, 409 (5), pp. 1257-1269, 2017, ISSN: 1618-2650 (Electronic)
1618-2642 (Linking). Links | BibTeX @article{RN1011,
title = {Efficient recovery of glycosaminoglycan oligosaccharides from polyacrylamide gel electrophoresis combined with mass spectrometry analysis},
author = {Bodet, P. E. and Salard, I. and Przybylski, C. and Gonnet, F. and Gomila, C. and Ausseil, J. and Daniel, R.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/27832303},
doi = {10.1007/s00216-016-0052-5},
issn = {1618-2650 (Electronic)
1618-2642 (Linking)},
year = {2017},
date = {2017-01-01},
journal = {Anal Bioanal Chem},
volume = {409},
number = {5},
pages = {1257-1269},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Daher, I; Le Dieu-Lugon, B; Dourmap, N; Lecuyer, M; Ramet, L; Gomila, C; Ausseil, J; Marret, S; Leroux, P; Roy, V; El Mestikawy, S; Daumas, S; Gonzalez, B; Leroux-Nicollet, I; Cleren, C Magnesium Sulfate Prevents Neurochemical and Long-Term Behavioral Consequences of Neonatal Excitotoxic Lesions: Comparison Between Male and Female Mice Journal Article J Neuropathol Exp Neurol, 76 (10), pp. 883-897, 2017, ISSN: 1554-6578 (Electronic)
0022-3069 (Linking). Links | BibTeX @article{RN1007,
title = {Magnesium Sulfate Prevents Neurochemical and Long-Term Behavioral Consequences of Neonatal Excitotoxic Lesions: Comparison Between Male and Female Mice},
author = {Daher, I. and Le Dieu-Lugon, B. and Dourmap, N. and Lecuyer, M. and Ramet, L. and Gomila, C. and Ausseil, J. and Marret, S. and Leroux, P. and Roy, V. and El Mestikawy, S. and Daumas, S. and Gonzalez, B. and Leroux-Nicollet, I. and Cleren, C.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/28922852},
doi = {10.1093/jnen/nlx073},
issn = {1554-6578 (Electronic)
0022-3069 (Linking)},
year = {2017},
date = {2017-01-01},
journal = {J Neuropathol Exp Neurol},
volume = {76},
number = {10},
pages = {883-897},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hodroge, A; Trecherel, E; Cornu, M; Darwiche, W; Mansour, A; Ait-Mohand, K; Verissimo, T; Gomila, C; Schembri, C; Da Nascimento, S; Elboutachfaiti, R; Boullier, A; Lorne, E; Courtois, J; Petit, E; Toumieux, S; Kovensky, J; Sonnet, P; Massy, Z A; Kamel, S; Rossi, C; Ausseil, J Oligogalacturonic Acid Inhibits Vascular Calcification by Two Mechanisms: Inhibition of Vascular Smooth Muscle Cell Osteogenic Conversion and Interaction With Collagen Journal Article Arterioscler Thromb Vasc Biol, 37 (7), pp. 1391-1401, 2017, ISSN: 1524-4636 (Electronic)
1079-5642 (Linking). Links | BibTeX @article{RN1009,
title = {Oligogalacturonic Acid Inhibits Vascular Calcification by Two Mechanisms: Inhibition of Vascular Smooth Muscle Cell Osteogenic Conversion and Interaction With Collagen},
author = {Hodroge, A. and Trecherel, E. and Cornu, M. and Darwiche, W. and Mansour, A. and Ait-Mohand, K. and Verissimo, T. and Gomila, C. and Schembri, C. and Da Nascimento, S. and Elboutachfaiti, R. and Boullier, A. and Lorne, E. and Courtois, J. and Petit, E. and Toumieux, S. and Kovensky, J. and Sonnet, P. and Massy, Z. A. and Kamel, S. and Rossi, C. and Ausseil, J.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/28522698},
doi = {10.1161/ATVBAHA.117.309513},
issn = {1524-4636 (Electronic)
1079-5642 (Linking)},
year = {2017},
date = {2017-01-01},
journal = {Arterioscler Thromb Vasc Biol},
volume = {37},
number = {7},
pages = {1391-1401},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Tardieu, M; Zerah, M; Gougeon, M L; Ausseil, J; de Bournonville, S; Husson, B; Zafeiriou, D; Parenti, G; Bourget, P; Poirier, B; Furlan, V; Artaud, C; Baugnon, T; Roujeau, T; Crystal, R G; Meyer, C; Deiva, K; Heard, J M Intracerebral gene therapy in children with mucopolysaccharidosis type IIIB syndrome: an uncontrolled phase 1/2 clinical trial Journal Article Lancet Neurol, 16 (9), pp. 712-720, 2017, ISSN: 1474-4465 (Electronic)
1474-4422 (Linking). Links | BibTeX @article{RN1008,
title = {Intracerebral gene therapy in children with mucopolysaccharidosis type IIIB syndrome: an uncontrolled phase 1/2 clinical trial},
author = {Tardieu, M. and Zerah, M. and Gougeon, M. L. and Ausseil, J. and de Bournonville, S. and Husson, B. and Zafeiriou, D. and Parenti, G. and Bourget, P. and Poirier, B. and Furlan, V. and Artaud, C. and Baugnon, T. and Roujeau, T. and Crystal, R. G. and Meyer, C. and Deiva, K. and Heard, J. M.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/28713035},
doi = {10.1016/S1474-4422(17)30169-2},
issn = {1474-4465 (Electronic)
1474-4422 (Linking)},
year = {2017},
date = {2017-01-01},
journal = {Lancet Neurol},
volume = {16},
number = {9},
pages = {712-720},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Tebani, A; Schmitz-Afonso, I; Abily-Donval, L; Heron, B; Piraud, M; Ausseil, J; Brassier, A; De Lonlay, P; Zerimech, F; Vaz, F M; Gonzalez, B J; Marret, S; Afonso, C; Bekri, S Urinary metabolic phenotyping of mucopolysaccharidosis type I combining untargeted and targeted strategies with data modeling Journal Article Clin Chim Acta, 475 , pp. 7-14, 2017, ISSN: 1873-3492 (Electronic)
0009-8981 (Linking). Links | BibTeX @article{RN1006,
title = {Urinary metabolic phenotyping of mucopolysaccharidosis type I combining untargeted and targeted strategies with data modeling},
author = {Tebani, A. and Schmitz-Afonso, I. and Abily-Donval, L. and Heron, B. and Piraud, M. and Ausseil, J. and Brassier, A. and De Lonlay, P. and Zerimech, F. and Vaz, F. M. and Gonzalez, B. J. and Marret, S. and Afonso, C. and Bekri, S.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/28982054},
doi = {10.1016/j.cca.2017.09.024},
issn = {1873-3492 (Electronic)
0009-8981 (Linking)},
year = {2017},
date = {2017-01-01},
journal = {Clin Chim Acta},
volume = {475},
pages = {7-14},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2016
|
Burnett, L C; LeDuc, C A; Sulsona, C R; Paull, D; Eddiry, S; Levy, B; Salles, J P; Tauber, M; Driscoll, D J; Egli, D; Leibel, R L Induced pluripotent stem cells (iPSC) created from skin fibroblasts of patients with Prader-Willi syndrome (PWS) retain the molecular signature of PWS Journal Article Stem Cell Res, 17 (3), pp. 526-530, 2016, ISSN: 1876-7753 (Electronic)
1873-5061 (Linking). Links | BibTeX @article{RN1b,
title = {Induced pluripotent stem cells (iPSC) created from skin fibroblasts of patients with Prader-Willi syndrome (PWS) retain the molecular signature of PWS},
author = {Burnett, L. C. and LeDuc, C. A. and Sulsona, C. R. and Paull, D. and Eddiry, S. and Levy, B. and Salles, J. P. and Tauber, M. and Driscoll, D. J. and Egli, D. and Leibel, R. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/27789403},
doi = {10.1016/j.scr.2016.08.008},
issn = {1876-7753 (Electronic)
1873-5061 (Linking)},
year = {2016},
date = {2016-01-01},
journal = {Stem Cell Res},
volume = {17},
number = {3},
pages = {526-530},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Boyer, J F; Baron, M; Constantin, A; Degboe, Y; Cantagrel, A; Davignon, J L Anti-TNF certolizumab pegol induces antioxidant response in human monocytes via reverse signaling Journal Article Arthritis Res Ther, 18 , pp. 56, 2016, ISSN: 1478-6362 (Electronic)
1478-6354 (Linking). Links | BibTeX @article{RN11b,
title = {Anti-TNF certolizumab pegol induces antioxidant response in human monocytes via reverse signaling},
author = {Boyer, J. F. and Baron, M. and Constantin, A. and Degboe, Y. and Cantagrel, A. and Davignon, J. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/26932562},
doi = {10.1186/s13075-016-0955-8},
issn = {1478-6362 (Electronic)
1478-6354 (Linking)},
year = {2016},
date = {2016-01-01},
journal = {Arthritis Res Ther},
volume = {18},
pages = {56},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Ielasi, F; Ledall, J; Anes, A P; Fruchon, S; Caminade, A M; Poupot, R; Turrin, C O; Blanzat, M Influence of PPH dendrimers' surface functions on the activation of human monocytes: a study of their interactions with pure lipid model systems Journal Article Phys Chem Chem Phys, 18 (31), pp. 21871-80, 2016, ISSN: 1463-9084 (Electronic)
1463-9076 (Linking). Links | BibTeX @article{RN24b,
title = {Influence of PPH dendrimers' surface functions on the activation of human monocytes: a study of their interactions with pure lipid model systems},
author = {Ielasi, F. and Ledall, J. and Anes, A. P. and Fruchon, S. and Caminade, A. M. and Poupot, R. and Turrin, C. O. and Blanzat, M.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/27435630},
doi = {10.1039/c6cp03536a},
issn = {1463-9084 (Electronic)
1463-9076 (Linking)},
year = {2016},
date = {2016-01-01},
journal = {Phys Chem Chem Phys},
volume = {18},
number = {31},
pages = {21871-80},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Poupot, M; Turrin, C O; Caminade, A M; Fournie, J J; Attal, M; Poupot, R; Fruchon, S Poly(phosphorhydrazone) dendrimers: yin and yang of monocyte activation for human NK cell amplification applied to immunotherapy against multiple myeloma Journal Article Nanomedicine, 12 (8), pp. 2321-2330, 2016, ISSN: 1549-9642 (Electronic)
1549-9634 (Linking). Links | BibTeX @article{RN36,
title = {Poly(phosphorhydrazone) dendrimers: yin and yang of monocyte activation for human NK cell amplification applied to immunotherapy against multiple myeloma},
author = {Poupot, M. and Turrin, C. O. and Caminade, A. M. and Fournie, J. J. and Attal, M. and Poupot, R. and Fruchon, S.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/27498187},
doi = {10.1016/j.nano.2016.07.009},
issn = {1549-9642 (Electronic)
1549-9634 (Linking)},
year = {2016},
date = {2016-01-01},
journal = {Nanomedicine},
volume = {12},
number = {8},
pages = {2321-2330},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Puy, V; Zmudka-Attier, J; Capel, C; Bouzerar, R; Serot, J M; Bourgeois, A M; Ausseil, J; Baledent, O Interactions between Flow Oscillations and Biochemical Parameters in the Cerebrospinal Fluid Journal Article Front Aging Neurosci, 8 , pp. 154, 2016, ISSN: 1663-4365 (Print)
1663-4365 (Linking). Links | BibTeX @article{RN1013,
title = {Interactions between Flow Oscillations and Biochemical Parameters in the Cerebrospinal Fluid},
author = {Puy, V. and Zmudka-Attier, J. and Capel, C. and Bouzerar, R. and Serot, J. M. and Bourgeois, A. M. and Ausseil, J. and Baledent, O.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/27445797},
doi = {10.3389/fnagi.2016.00154},
issn = {1663-4365 (Print)
1663-4365 (Linking)},
year = {2016},
date = {2016-01-01},
journal = {Front Aging Neurosci},
volume = {8},
pages = {154},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2015
|
Bieth, E; Eddiry, S; Gaston, V; Lorenzini, F; Buffet, A; Conte Auriol, F; Molinas, C; Cailley, D; Rooryck, C; Arveiler, B; Cavaille, J; Salles, J P; Tauber, M Highly restricted deletion of the SNORD116 region is implicated in Prader-Willi Syndrome Journal Article Eur J Hum Genet, 23 (2), pp. 252-5, 2015, ISSN: 1476-5438 (Electronic)
1018-4813 (Linking). Links | BibTeX @article{RN26,
title = {Highly restricted deletion of the SNORD116 region is implicated in Prader-Willi Syndrome},
author = {Bieth, E. and Eddiry, S. and Gaston, V. and Lorenzini, F. and Buffet, A. and Conte Auriol, F. and Molinas, C. and Cailley, D. and Rooryck, C. and Arveiler, B. and Cavaille, J. and Salles, J. P. and Tauber, M.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/24916642},
doi = {10.1038/ejhg.2014.103},
issn = {1476-5438 (Electronic)
1018-4813 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {Eur J Hum Genet},
volume = {23},
number = {2},
pages = {252-5},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Haine, E; Salles, J P; Khau Van Kien, P; Conte-Auriol, F; Gennero, I; Plancke, A; Julia, S; Dulac, Y; Tauber, M; Edouard, T Muscle and Bone Impairment in Children With Marfan Syndrome: Correlation With Age and FBN1 Genotype Journal Article J Bone Miner Res, 30 (8), pp. 1369-76, 2015, ISSN: 1523-4681 (Electronic)
0884-0431 (Linking). Links | BibTeX @article{RN22,
title = {Muscle and Bone Impairment in Children With Marfan Syndrome: Correlation With Age and FBN1 Genotype},
author = {Haine, E. and Salles, J. P. and Khau Van Kien, P. and Conte-Auriol, F. and Gennero, I. and Plancke, A. and Julia, S. and Dulac, Y. and Tauber, M. and Edouard, T.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/25656438},
doi = {10.1002/jbmr.2471},
issn = {1523-4681 (Electronic)
0884-0431 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {J Bone Miner Res},
volume = {30},
number = {8},
pages = {1369-76},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Sales de Gauzy, J; Gennero, I; Delrous, O; Salles, J P; Lepage, B; Accadbled, F Fasting total ghrelin levels are increased in patients with adolescent idiopathic scoliosis Journal Article Scoliosis, 10 , pp. 33, 2015, ISSN: 1748-7161 (Print)
1748-7161 (Linking). Links | BibTeX @article{RN23,
title = {Fasting total ghrelin levels are increased in patients with adolescent idiopathic scoliosis},
author = {Sales de Gauzy, J. and Gennero, I. and Delrous, O. and Salles, J. P. and Lepage, B. and Accadbled, F.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/26628906},
doi = {10.1186/s13013-015-0054-7},
issn = {1748-7161 (Print)
1748-7161 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {Scoliosis},
volume = {10},
pages = {33},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Caminade, A M; Fruchon, S; Turrin, C O; Poupot, M; Ouali, A; Maraval, A; Garzoni, M; Maly, M; Furer, V; Kovalenko, V; Majoral, J P; Pavan, G M; Poupot, R The key role of the scaffold on the efficiency of dendrimer nanodrugs Journal Article Nat Commun, 6 , pp. 7722, 2015, ISSN: 2041-1723 (Electronic)
2041-1723 (Linking). Links | BibTeX @article{RN29,
title = {The key role of the scaffold on the efficiency of dendrimer nanodrugs},
author = {Caminade, A. M. and Fruchon, S. and Turrin, C. O. and Poupot, M. and Ouali, A. and Maraval, A. and Garzoni, M. and Maly, M. and Furer, V. and Kovalenko, V. and Majoral, J. P. and Pavan, G. M. and Poupot, R.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/26169490},
doi = {10.1038/ncomms8722},
issn = {2041-1723 (Electronic)
2041-1723 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {Nat Commun},
volume = {6},
pages = {7722},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Fruchon, S; Mouriot, S; Thiollier, T; Grandin, C; Caminade, A M; Turrin, C O; Contamin, H; Poupot, R Repeated intravenous injections in non-human primates demonstrate preclinical safety of an anti-inflammatory phosphorus-based dendrimer Journal Article Nanotoxicology, 9 (4), pp. 433-41, 2015, ISSN: 1743-5404 (Electronic)
1743-5390 (Linking). Links | BibTeX @article{RN31,
title = {Repeated intravenous injections in non-human primates demonstrate preclinical safety of an anti-inflammatory phosphorus-based dendrimer},
author = {Fruchon, S. and Mouriot, S. and Thiollier, T. and Grandin, C. and Caminade, A. M. and Turrin, C. O. and Contamin, H. and Poupot, R.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/25051330},
doi = {10.3109/17435390.2014.940406},
issn = {1743-5404 (Electronic)
1743-5390 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {Nanotoxicology},
volume = {9},
number = {4},
pages = {433-41},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hameau, Aurélien ; Fruchon, Séverine ; Bijani, Christian ; Barducci, Alessandro ; Blanzat, Muriel ; Poupot, Rémy ; Pavan, Giovanni M; Caminade, Anne-Marie ; Turrin, Cédric-Olivier Theoretical and experimental characterization of amino-PEG-phosphonate-terminated Polyphosphorhydrazone dendrimers: Influence of size and PEG capping on cytotoxicity profiles Journal Article Journal of Polymer Science Part A: Polymer Chemistry, 53 (6), pp. 761-774, 2015, ISSN: 0887624X. Links | BibTeX @article{RN40,
title = {Theoretical and experimental characterization of amino-PEG-phosphonate-terminated Polyphosphorhydrazone dendrimers: Influence of size and PEG capping on cytotoxicity profiles},
author = {Hameau, Aurélien and Fruchon, Séverine and Bijani, Christian and Barducci, Alessandro and Blanzat, Muriel and Poupot, Rémy and Pavan, Giovanni M. and Caminade, Anne-Marie and Turrin, Cédric-Olivier},
doi = {10.1002/pola.27501},
issn = {0887624X},
year = {2015},
date = {2015-01-01},
journal = {Journal of Polymer Science Part A: Polymer Chemistry},
volume = {53},
number = {6},
pages = {761-774},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Ledall, J; Fruchon, S; Garzoni, M; Pavan, G M; Caminade, A M; Turrin, C O; Blanzat, M; Poupot, R Interaction studies reveal specific recognition of an anti-inflammatory polyphosphorhydrazone dendrimer by human monocytes Journal Article Nanoscale, 7 (42), pp. 17672-84, 2015, ISSN: 2040-3372 (Electronic)
2040-3364 (Linking). Links | BibTeX @article{RN35,
title = {Interaction studies reveal specific recognition of an anti-inflammatory polyphosphorhydrazone dendrimer by human monocytes},
author = {Ledall, J. and Fruchon, S. and Garzoni, M. and Pavan, G. M. and Caminade, A. M. and Turrin, C. O. and Blanzat, M. and Poupot, R.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/26335052},
doi = {10.1039/c5nr03884g},
issn = {2040-3372 (Electronic)
2040-3364 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {Nanoscale},
volume = {7},
number = {42},
pages = {17672-84},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Bruyere, J; Roy, E; Ausseil, J; Lemonnier, T; Teyre, G; Bohl, D; Etienne-Manneville, S; Lortat-Jacob, H; Heard, J M; Vitry, S Heparan sulfate saccharides modify focal adhesions: implication in mucopolysaccharidosis neuropathophysiology Journal Article J Mol Biol, 427 (4), pp. 775-791, 2015, ISSN: 1089-8638 (Electronic)
0022-2836 (Linking). Links | BibTeX @article{RN1024,
title = {Heparan sulfate saccharides modify focal adhesions: implication in mucopolysaccharidosis neuropathophysiology},
author = {Bruyere, J. and Roy, E. and Ausseil, J. and Lemonnier, T. and Teyre, G. and Bohl, D. and Etienne-Manneville, S. and Lortat-Jacob, H. and Heard, J. M. and Vitry, S.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/25268803},
doi = {10.1016/j.jmb.2014.09.012},
issn = {1089-8638 (Electronic)
0022-2836 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {J Mol Biol},
volume = {427},
number = {4},
pages = {775-791},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Martins, C; Hulkova, H; Dridi, L; Dormoy-Raclet, V; Grigoryeva, L; Choi, Y; Langford-Smith, A; Wilkinson, F L; Ohmi, K; DiCristo, G; Hamel, E; Ausseil, J; Cheillan, D; Moreau, A; Svobodova, E; Hajkova, Z; Tesarova, M; Hansikova, H; Bigger, B W; Hrebicek, M; Pshezhetsky, A V Neuroinflammation, mitochondrial defects and neurodegeneration in mucopolysaccharidosis III type C mouse model Journal Article Brain, 138 (Pt 2), pp. 336-55, 2015, ISSN: 1460-2156 (Electronic)
0006-8950 (Linking). Links | BibTeX @article{RN1021,
title = {Neuroinflammation, mitochondrial defects and neurodegeneration in mucopolysaccharidosis III type C mouse model},
author = {Martins, C. and Hulkova, H. and Dridi, L. and Dormoy-Raclet, V. and Grigoryeva, L. and Choi, Y. and Langford-Smith, A. and Wilkinson, F. L. and Ohmi, K. and DiCristo, G. and Hamel, E. and Ausseil, J. and Cheillan, D. and Moreau, A. and Svobodova, E. and Hajkova, Z. and Tesarova, M. and Hansikova, H. and Bigger, B. W. and Hrebicek, M. and Pshezhetsky, A. V.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/25567323},
doi = {10.1093/brain/awu355},
issn = {1460-2156 (Electronic)
0006-8950 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {Brain},
volume = {138},
number = {Pt 2},
pages = {336-55},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Trudel, S; Trecherel, E; Gomila, C; Peltier, M; Aubignat, M; Gubler, B; Morliere, P; Heard, J M; Ausseil, J Oxidative stress is independent of inflammation in the neurodegenerative Sanfilippo syndrome type B Journal Article J Neurosci Res, 93 (3), pp. 424-32, 2015, ISSN: 1097-4547 (Electronic)
0360-4012 (Linking). Links | BibTeX @article{RN1023,
title = {Oxidative stress is independent of inflammation in the neurodegenerative Sanfilippo syndrome type B},
author = {Trudel, S. and Trecherel, E. and Gomila, C. and Peltier, M. and Aubignat, M. and Gubler, B. and Morliere, P. and Heard, J. M. and Ausseil, J.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/25332157},
doi = {10.1002/jnr.23497},
issn = {1097-4547 (Electronic)
0360-4012 (Linking)},
year = {2015},
date = {2015-01-01},
journal = {J Neurosci Res},
volume = {93},
number = {3},
pages = {424-32},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2014
|
Cadoudal, T; Buleon, M; Sengenes, C; Diene, G; Desneulin, F; Molinas, C; Eddiry, S; Conte-Auriol, F; Daviaud, D; Martin, P G; Bouloumie, A; Salles, J P; Tauber, M; Valet, P Impairment of adipose tissue in Prader-Willi syndrome rescued by growth hormone treatment Journal Article Int J Obes (Lond), 38 (9), pp. 1234-40, 2014, ISSN: 1476-5497 (Electronic)
0307-0565 (Linking). Links | BibTeX @article{RN28,
title = {Impairment of adipose tissue in Prader-Willi syndrome rescued by growth hormone treatment},
author = {Cadoudal, T. and Buleon, M. and Sengenes, C. and Diene, G. and Desneulin, F. and Molinas, C. and Eddiry, S. and Conte-Auriol, F. and Daviaud, D. and Martin, P. G. and Bouloumie, A. and Salles, J. P. and Tauber, M. and Valet, P.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/24406482},
doi = {10.1038/ijo.2014.3},
issn = {1476-5497 (Electronic)
0307-0565 (Linking)},
year = {2014},
date = {2014-01-01},
journal = {Int J Obes (Lond)},
volume = {38},
number = {9},
pages = {1234-40},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Y, Degboé; S, Fruchon; M, Baron; D, Nigon; CO, Turrin; AM, Caminade; R, Poupot; A, Cantagrel; JL, Davignon Modulation of pro-inflammatory activation of monocytes and dendritic cells by aza-bis-phosphonate dendrimer as an experimental therapeutic agent Journal Article Arthritis Research and Therapy, 16 (R98), 2014. BibTeX @article{RN30,
title = {Modulation of pro-inflammatory activation of monocytes and dendritic cells by aza-bis-phosphonate dendrimer as an experimental therapeutic agent},
author = {Degboé Y and Fruchon S and Baron M and Nigon D and Turrin CO and Caminade AM and Poupot R and Cantagrel A and JL, Davignon},
year = {2014},
date = {2014-01-01},
journal = {Arthritis Research and Therapy},
volume = {16},
number = {R98},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2013
|
Salles, J P; Laurencin-Dalicieux, S; Conte-Auriol, F; Briand-Mesange, F; Gennero, I Bone defects in LPA receptor genetically modified mice Journal Article Biochim Biophys Acta, 1831 (1), pp. 93-8, 2013, ISSN: 0006-3002 (Print)
0006-3002 (Linking). Links | BibTeX @article{RN37,
title = {Bone defects in LPA receptor genetically modified mice},
author = {Salles, J. P. and Laurencin-Dalicieux, S. and Conte-Auriol, F. and Briand-Mesange, F. and Gennero, I.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/22867754},
doi = {10.1016/j.bbalip.2012.07.018},
issn = {0006-3002 (Print)
0006-3002 (Linking)},
year = {2013},
date = {2013-01-01},
journal = {Biochim Biophys Acta},
volume = {1831},
number = {1},
pages = {93-8},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Davignon, J L; Hayder, M; Baron, M; Boyer, J F; Constantin, A; Apparailly, F; Poupot, R; Cantagrel, A Targeting monocytes/macrophages in the treatment of rheumatoid arthritis Journal Article Rheumatology (Oxford), 52 (4), pp. 590-8, 2013, ISSN: 1462-0332 (Electronic)
1462-0324 (Linking). Links | BibTeX @article{RN15b,
title = {Targeting monocytes/macrophages in the treatment of rheumatoid arthritis},
author = {Davignon, J. L. and Hayder, M. and Baron, M. and Boyer, J. F. and Constantin, A. and Apparailly, F. and Poupot, R. and Cantagrel, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/23204551},
doi = {10.1093/rheumatology/kes304},
issn = {1462-0332 (Electronic)
1462-0324 (Linking)},
year = {2013},
date = {2013-01-01},
journal = {Rheumatology (Oxford)},
volume = {52},
number = {4},
pages = {590-8},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Fruchon, S; Caminade, A M; Abadie, C; Davignon, J L; Combette, J M; Turrin, C O; Poupot, R An azabisphosphonate-capped poly(phosphorhydrazone) dendrimer for the treatment of endotoxin-induced uveitis Journal Article Molecules, 18 (8), pp. 9305-16, 2013, ISSN: 1420-3049 (Electronic)
1420-3049 (Linking). Links | BibTeX @article{RN20,
title = {An azabisphosphonate-capped poly(phosphorhydrazone) dendrimer for the treatment of endotoxin-induced uveitis},
author = {Fruchon, S. and Caminade, A. M. and Abadie, C. and Davignon, J. L. and Combette, J. M. and Turrin, C. O. and Poupot, R.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/23921793},
doi = {10.3390/molecules18089305},
issn = {1420-3049 (Electronic)
1420-3049 (Linking)},
year = {2013},
date = {2013-01-01},
journal = {Molecules},
volume = {18},
number = {8},
pages = {9305-16},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2012
|
De Rocca Serra-Nedelec, A; Edouard, T; Treguer, K; Tajan, M; Araki, T; Dance, M; Mus, M; Montagner, A; Tauber, M; Salles, J P; Valet, P; Neel, B G; Raynal, P; Yart, A Noonan syndrome-causing SHP2 mutants inhibit insulin-like growth factor 1 release via growth hormone-induced ERK hyperactivation, which contributes to short stature Journal Article Proc Natl Acad Sci U S A, 109 (11), pp. 4257-62, 2012, ISSN: 1091-6490 (Electronic)
0027-8424 (Linking). Links | BibTeX @article{RN16b,
title = {Noonan syndrome-causing SHP2 mutants inhibit insulin-like growth factor 1 release via growth hormone-induced ERK hyperactivation, which contributes to short stature},
author = {De Rocca Serra-Nedelec, A. and Edouard, T. and Treguer, K. and Tajan, M. and Araki, T. and Dance, M. and Mus, M. and Montagner, A. and Tauber, M. and Salles, J. P. and Valet, P. and Neel, B. G. and Raynal, P. and Yart, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/22371576},
doi = {10.1073/pnas.1119803109},
issn = {1091-6490 (Electronic)
0027-8424 (Linking)},
year = {2012},
date = {2012-01-01},
journal = {Proc Natl Acad Sci U S A},
volume = {109},
number = {11},
pages = {4257-62},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Boyer, J F; Bongard, V; Cantagrel, A; Jamard, B; Gottenberg, J E; Mariette, X; Davignon, J L; Ferrieres, J; Ruidavets, J B; Dallongeville, J; Arveiler, D; Cambon-Thomsen, A; Constantin, A Link between traditional cardiovascular risk factors and inflammation in patients with early arthritis: results from a French multicenter cohort Journal Article Arthritis Care Res (Hoboken), 64 (6), pp. 872-80, 2012, ISSN: 2151-4658 (Electronic)
2151-464X (Linking). Links | BibTeX @article{RN12b,
title = {Link between traditional cardiovascular risk factors and inflammation in patients with early arthritis: results from a French multicenter cohort},
author = {Boyer, J. F. and Bongard, V. and Cantagrel, A. and Jamard, B. and Gottenberg, J. E. and Mariette, X. and Davignon, J. L. and Ferrieres, J. and Ruidavets, J. B. and Dallongeville, J. and Arveiler, D. and Cambon-Thomsen, A. and Constantin, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/22275176},
doi = {10.1002/acr.21623},
issn = {2151-4658 (Electronic)
2151-464X (Linking)},
year = {2012},
date = {2012-01-01},
journal = {Arthritis Care Res (Hoboken)},
volume = {64},
number = {6},
pages = {872-80},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2011
|
Gennero, I; Laurencin-Dalicieux, S; Conte-Auriol, F; Briand-Mesange, F; Laurencin, D; Rue, J; Beton, N; Malet, N; Mus, M; Tokumura, A; Bourin, P; Vico, L; Brunel, G; Oreffo, R O; Chun, J; Salles, J P Absence of the lysophosphatidic acid receptor LPA1 results in abnormal bone development and decreased bone mass Journal Article Bone, 49 (3), pp. 395-403, 2011, ISSN: 1873-2763 (Electronic)
1873-2763 (Linking). Links | BibTeX @article{RN21b,
title = {Absence of the lysophosphatidic acid receptor LPA1 results in abnormal bone development and decreased bone mass},
author = {Gennero, I. and Laurencin-Dalicieux, S. and Conte-Auriol, F. and Briand-Mesange, F. and Laurencin, D. and Rue, J. and Beton, N. and Malet, N. and Mus, M. and Tokumura, A. and Bourin, P. and Vico, L. and Brunel, G. and Oreffo, R. O. and Chun, J. and Salles, J. P.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/21569876},
doi = {10.1016/j.bone.2011.04.018},
issn = {1873-2763 (Electronic)
1873-2763 (Linking)},
year = {2011},
date = {2011-01-01},
journal = {Bone},
volume = {49},
number = {3},
pages = {395-403},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Boyer, J F; Gourraud, P A; Cantagrel, A; Davignon, J L; Constantin, A Traditional cardiovascular risk factors in rheumatoid arthritis: a meta-analysis Journal Article Joint Bone Spine, 78 (2), pp. 179-83, 2011, ISSN: 1778-7254 (Electronic)
1297-319X (Linking). Links | BibTeX @article{RN27,
title = {Traditional cardiovascular risk factors in rheumatoid arthritis: a meta-analysis},
author = {Boyer, J. F. and Gourraud, P. A. and Cantagrel, A. and Davignon, J. L. and Constantin, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/20851020},
doi = {10.1016/j.jbspin.2010.07.016},
issn = {1778-7254 (Electronic)
1297-319X (Linking)},
year = {2011},
date = {2011-01-01},
journal = {Joint Bone Spine},
volume = {78},
number = {2},
pages = {179-83},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Courties, G; Baron, M; Presumey, J; Escriou, V; van Lent, P; Scherman, D; Cantagrel, A; van den Berg, W B; Jorgensen, C; Apparailly, F; Davignon, J L Cytosolic phospholipase A2alpha gene silencing in the myeloid lineage alters development of Th1 responses and reduces disease severity in collagen-induced arthritis Journal Article Arthritis Rheum, 63 (3), pp. 681-90, 2011, ISSN: 1529-0131 (Electronic)
0004-3591 (Linking). Links | BibTeX @article{RN13b,
title = {Cytosolic phospholipase A2alpha gene silencing in the myeloid lineage alters development of Th1 responses and reduces disease severity in collagen-induced arthritis},
author = {Courties, G. and Baron, M. and Presumey, J. and Escriou, V. and van Lent, P. and Scherman, D. and Cantagrel, A. and van den Berg, W. B. and Jorgensen, C. and Apparailly, F. and Davignon, J. L.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/21360497},
doi = {10.1002/art.30174},
issn = {1529-0131 (Electronic)
0004-3591 (Linking)},
year = {2011},
date = {2011-01-01},
journal = {Arthritis Rheum},
volume = {63},
number = {3},
pages = {681-90},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hayder, Myriam; Poupot, Mary; Baron, Michel; Nigon, Delphine; Turrin, Cédric-Olivier; Caminade, Anne-Marie; Majoral, Jean-Pierre; Eisenberg, Robert A; Fournié, Jean-Jacques; Cantagrel, Alain; Poupot, Rémy; Davignon, Jean-Luc A Phosphorus-Based Dendrimer Targets Inflammation
and Osteoclastogenesis in Experimental Arthritis Journal Article Sci. Transl. Med, 3 (81 81ra35), 2011. BibTeX @article{RN34,
title = {A Phosphorus-Based Dendrimer Targets Inflammation
and Osteoclastogenesis in Experimental Arthritis},
author = {Myriam Hayder and Mary Poupot and Michel Baron and Delphine Nigon and Cédric-Olivier Turrin and Anne-Marie Caminade and Jean-Pierre Majoral and Robert A. Eisenberg and Jean-Jacques Fournié and Alain Cantagrel and Rémy Poupot and Davignon, Jean-Luc},
year = {2011},
date = {2011-01-01},
journal = {Sci. Transl. Med},
volume = {3},
number = {81 81ra35},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hayder, Myriam; Poupot, Mary; Baron, Michel; Nigon, Delphine; Turrin, Cédric-Olivier; Caminade, Anne-Marie; Majoral, Jean-Pierre; Eisenberg, Robert A; Fournié, Jean-Jacques; Cantagrel, Alain; Poupot, Rémy; Davignon, Jean-Luc A Phosphorus-Based Dendrimer Targets Inflammation
and Osteoclastogenesis in Experimental Arthritis Journal Article Sci. Transl. Med, 3 (81 81ra35), 2011. BibTeX @article{RN34b,
title = {A Phosphorus-Based Dendrimer Targets Inflammation
and Osteoclastogenesis in Experimental Arthritis},
author = {Myriam Hayder and Mary Poupot and Michel Baron and Delphine Nigon and Cédric-Olivier Turrin and Anne-Marie Caminade and Jean-Pierre Majoral and Robert A. Eisenberg and Jean-Jacques Fournié and Alain Cantagrel and Rémy Poupot and Davignon, Jean-Luc},
year = {2011},
date = {2011-01-01},
journal = {Sci. Transl. Med},
volume = {3},
number = {81 81ra35},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
2010
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Davignon, J L; Boyer, J F; Jamard, B; Nigon, D; Constantin, A; Cantagrel, A Maintenance of cytomegalovirus-specific CD4pos T-cell response in rheumatoid arthritis patients receiving anti-tumor necrosis factor treatments Journal Article Arthritis Res Ther, 12 (4), pp. R142, 2010, ISSN: 1478-6362 (Electronic)
1478-6354 (Linking). Links | BibTeX @article{RN14b,
title = {Maintenance of cytomegalovirus-specific CD4pos T-cell response in rheumatoid arthritis patients receiving anti-tumor necrosis factor treatments},
author = {Davignon, J. L. and Boyer, J. F. and Jamard, B. and Nigon, D. and Constantin, A. and Cantagrel, A.},
url = {https://www.ncbi.nlm.nih.gov/pubmed/20633267},
doi = {10.1186/ar3083},
issn = {1478-6362 (Electronic)
1478-6354 (Linking)},
year = {2010},
date = {2010-01-01},
journal = {Arthritis Res Ther},
volume = {12},
number = {4},
pages = {R142},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
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Le syndrome de Sanfilippo est caractérisé par une neuroinflammation sévère associée à une neurodégénérescence provoquée par l’absence d’une exoglycanase lysosomale conduisant à l’interruption de la dégradation de l’héparane sulfate (HS). L’accumulation progressive d’oligosaccharides d’HS (HSO) induit le développement d’un stress oxydatif, la production de cytokines et de chimiokines via une activation dépendante du récepteur TLR4 dans le système nerveux central (SNC) (Trudel, J Neurosci Res 2015) et dans le système ostéoarticulaire. L’activation du TLR4 a plusieurs conséquences dont l’induction d’une signalisation microgliale de STAT3 conduisant à une augmentation de l’expression de l’hepcidine et à une rétention de fer dans le cerveau (Puy, Glia 2018). Nous étudions actuellement les états fonctionnel et moléculaire de la microglie dans ce syndrome ainsi que l’implication de la microglie dans l’initiation et la propagation de l’inflammation conduisant aux processus neurodégénératifs (étude réalisée sur modèle cellulaire BV2 murine, microglie adulte primaire, microglie humaine CHME-5 et microglie primaire provenant de souris Sanfilippo B). Nos récents résultats indiquent que les vésicules extracellulaires (EVs) dérivées de la microglie seraient impliquées dans la propagation des signaux inflammatoires dans le cerveau. Cependant, on en sait peu sur la biogenèse et la régulation de cette production d’EVs. En utilisant des approches biochimiques et protéomiques, nous étudions la production, la composition et le rôle de ces EVs microgliales produites au cours de la neuroinflammation. Le système endocannabinoïde qui joue un rôle important dans la régulation de nombreuses pathologies infectieuses et inflammatoires, via le récepteur CB2 (le système immunitaire) et CB1 (fortement exprimé dans le système nerveux central) pourrait avoir un rôle protecteur important dans le syndrome de Sanfilippo. Nous avons récemment découvert une nouvelle voie de synthèse d’un agoniste puissant des deux récepteurs, le 2-arachidonoylglycérol (2-AG) (produit d’une manière endogène grâce à une enzyme GDE3, appelée AlterAG). Nous étudions l’implication de cette nouvelle voie dans le syndrome de Sanfilippo et dans d’autres pathologies inflammatoires et infectieuses, ce qui pourrait fournir de nouvelles cibles pharmacologiques intéressantes à explorer.
L’étude de l’effet anti-inflammatoire du « reverse signaling » du TNF transmembranaire (tmTNF) dans les monocytes a montré que des facteurs de transcription spécifiques sont impliqués par l’interaction des anti-TNF avec le tmTNF pour induire une action anti-inflammatoire. Nous étudions également le rôle du tmTNF dans l’inflammation des modèles murins d’arthrite.
Le fer présent dans toutes les cellules de l’organisme, est nécessaire à la vie (transport d’oxygène, réactions de transfert d’électrons ou synthèse d’ADN). Le fer physiologique est principalement utilisé pour produire de l’hème, le groupement prothétique des hémoprotéines telles que l’hémoglobine, la myoglobine et le cytochrome P450. Cependant, l’excès de fer représente une réelle menace pour la cellule car elle est capable de générer des radicaux libres (ou «réactifs oxygénés» (ROS)) lors de la réaction de Fenton (réaction chimique utilisant du fer et de l’eau oxygénée pour produire un radical hydroxyle: H2O2 + Fe2 + “OH- + OH • + Fe3 +). En plus, le fer peut également favoriser l’infection pathogène. Dans l’organisme, l’équilibre du fer est assuré par un équilibre strict entre son absorption par l’intestin et son stockage et recyclage par les macrophages suite à la phagocytose des globules rouges sénescents et à la dégradation de qui de l’hémoglobine et l’hème. L’absorption intestinale et la libération de fer des macrophages sont contrôlées par l’hepcidine, un petit peptide synthétisé et sécrété par le foie. L’expression de l’hepcidine est régulée par les variations du fer dans l’organisme (induites par une surcharge en fer et réprimée par une carence en fer et une érythropoïèse stimulée). De plus, étant une protéine de phase aiguë, l’hepcidine est induite par l’inflammation, ce qui en pathologie contribue à une carence en fer fonctionnelle et à une anémie inflammatoire. L’hepcidine est également exprimée dans de nombreux autres organes, bien qu’à un niveau beaucoup plus bas (rein, cerveau, os, monocytes / macrophages). L’objectif principal de cet axe 3 est de développer des recherches conduisant à élucider le rôle de l’hepcidine extra-hépatique dans le processus d’infection / inflammation et dans les pathologies confrontées au stress oxydatif dû à l’accumulation incontrôlée de fer inflammatoire, tant chez les modèles murins que chez les patients. Actuellement, nos priorités sont les maladies rénales (anémie inflammatoire, infection des voies urinaires), la neuroinflammation (syndrome de Sanfilippo) et l’os / articulations (maladie rhumatismale).
Les cellules myéloïdes (monocytes, cellules dendritiques, macrophages et ostéoclastes) jouent un rôle central dans la physiopathologie des maladies inflammatoires ostéoarticulaires telles que la Polyarthrite rhumatoïde et le Rhumatisme psoriasique. Ces cellules sont notamment impliquées dans l’inflammation articulaire, les dommages structuraux osseux et la perte osseuse inflammatoire.
