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 Article de journal Int J Mol Sci, 20 (2), 2019, ISSN: 1422-0067 (Electronic)
1422-0067 (Linking). Liens | 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}
}
|
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 Article de journal European Journal of Endocrinology, 179 (6), p. 409–418, 2018. Résumé | Liens | 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. Article de journal International journal of nanomedicine, 13 , p. 5511–5521, 2018, ISSN: 1178-2013. Résumé | Liens | 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. Article de journal Pediatric endocrinology reviews : PER, 16 (Suppl 1), p. 91–99, 2018, ISSN: 1565-4753. Résumé | Liens | 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 Article de journal Human Molecular Genetics, 27 (13), p. 2276–2289, 2018. Résumé | Liens | 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. Article de journal Molecules (Basel, Switzerland), 23 (6), 2018. Résumé | Liens | 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 Article de journal Endocrine Connections, 7 (5), p. 663–672, 2018. Résumé | Liens | 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. Article de journal Biomacromolecules, 19 (3), p. 712–720, 2018, ISSN: 1526-4602. Résumé | Liens | 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. Article de journal Materials (Basel, Switzerland), 11 (2), p. 270, 2018, ISSN: 1996-1944. Résumé | Liens | 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 Article de journal PLoS ONE, 13 (1), p. 1–19, 2018, ISSN: 19326203. Résumé | Liens | 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 Article de journal American Journal of Medical Genetics, Part A, 176 (1), p. 41–47, 2018, ISSN: 15524833. Résumé | Liens | 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 Article de journal Glia, 66 (8), p. 1709-1723, 2018, ISSN: 1098-1136 (Electronic)
0894-1491 (Linking). Liens | 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 Article de journal Neuromuscul Disord, 28 (7), p. 564-571, 2018, ISSN: 1873-2364 (Electronic)
0960-8966 (Linking). Liens | 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 Article de journal J Transl Med, 16 (1), p. 248, 2018, ISSN: 1479-5876 (Electronic)
1479-5876 (Linking). Liens | 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. Article de journal Nanomaterials (Basel, Switzerland), 7 (9), p. 251, 2017, ISSN: 2079-4991. Résumé | Liens | 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 Article de journal J Clin Invest, 127 (1), p. 293-305, 2017, ISSN: 1558-8238 (Electronic)
0021-9738 (Linking). Liens | 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 Article de journal PEDIATRICS, 139 (2), p. 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 Article de journal Anal Bioanal Chem, 409 (5), p. 1257-1269, 2017, ISSN: 1618-2650 (Electronic)
1618-2642 (Linking). Liens | 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 Article de journal J Neuropathol Exp Neurol, 76 (10), p. 883-897, 2017, ISSN: 1554-6578 (Electronic)
0022-3069 (Linking). Liens | 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 Article de journal Arterioscler Thromb Vasc Biol, 37 (7), p. 1391-1401, 2017, ISSN: 1524-4636 (Electronic)
1079-5642 (Linking). Liens | 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 Article de journal Lancet Neurol, 16 (9), p. 712-720, 2017, ISSN: 1474-4465 (Electronic)
1474-4422 (Linking). Liens | 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 Article de journal Clin Chim Acta, 475 , p. 7-14, 2017, ISSN: 1873-3492 (Electronic)
0009-8981 (Linking). Liens | 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 Article de journal Stem Cell Res, 17 (3), p. 526-530, 2016, ISSN: 1876-7753 (Electronic)
1873-5061 (Linking). Liens | 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 Article de journal Arthritis Res Ther, 18 , p. 56, 2016, ISSN: 1478-6362 (Electronic)
1478-6354 (Linking). Liens | 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 Article de journal Phys Chem Chem Phys, 18 (31), p. 21871-80, 2016, ISSN: 1463-9084 (Electronic)
1463-9076 (Linking). Liens | 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 Article de journal Nanomedicine, 12 (8), p. 2321-2330, 2016, ISSN: 1549-9642 (Electronic)
1549-9634 (Linking). Liens | 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 Article de journal Front Aging Neurosci, 8 , p. 154, 2016, ISSN: 1663-4365 (Print)
1663-4365 (Linking). Liens | 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 Article de journal Eur J Hum Genet, 23 (2), p. 252-5, 2015, ISSN: 1476-5438 (Electronic)
1018-4813 (Linking). Liens | 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 Article de journal J Bone Miner Res, 30 (8), p. 1369-76, 2015, ISSN: 1523-4681 (Electronic)
0884-0431 (Linking). Liens | 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 Article de journal Scoliosis, 10 , p. 33, 2015, ISSN: 1748-7161 (Print)
1748-7161 (Linking). Liens | 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 Article de journal Nat Commun, 6 , p. 7722, 2015, ISSN: 2041-1723 (Electronic)
2041-1723 (Linking). Liens | 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 Article de journal Nanotoxicology, 9 (4), p. 433-41, 2015, ISSN: 1743-5404 (Electronic)
1743-5390 (Linking). Liens | 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 Article de journal Journal of Polymer Science Part A: Polymer Chemistry, 53 (6), p. 761-774, 2015, ISSN: 0887624X. Liens | 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 Article de journal Nanoscale, 7 (42), p. 17672-84, 2015, ISSN: 2040-3372 (Electronic)
2040-3364 (Linking). Liens | 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 Article de journal J Mol Biol, 427 (4), p. 775-791, 2015, ISSN: 1089-8638 (Electronic)
0022-2836 (Linking). Liens | 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 Article de journal Brain, 138 (Pt 2), p. 336-55, 2015, ISSN: 1460-2156 (Electronic)
0006-8950 (Linking). Liens | 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 Article de journal J Neurosci Res, 93 (3), p. 424-32, 2015, ISSN: 1097-4547 (Electronic)
0360-4012 (Linking). Liens | 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 Article de journal Int J Obes (Lond), 38 (9), p. 1234-40, 2014, ISSN: 1476-5497 (Electronic)
0307-0565 (Linking). Liens | 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 Article de journal 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 Article de journal Biochim Biophys Acta, 1831 (1), p. 93-8, 2013, ISSN: 0006-3002 (Print)
0006-3002 (Linking). Liens | 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 Article de journal Rheumatology (Oxford), 52 (4), p. 590-8, 2013, ISSN: 1462-0332 (Electronic)
1462-0324 (Linking). Liens | 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 Article de journal Molecules, 18 (8), p. 9305-16, 2013, ISSN: 1420-3049 (Electronic)
1420-3049 (Linking). Liens | 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 Article de journal Proc Natl Acad Sci U S A, 109 (11), p. 4257-62, 2012, ISSN: 1091-6490 (Electronic)
0027-8424 (Linking). Liens | 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 Article de journal Arthritis Care Res (Hoboken), 64 (6), p. 872-80, 2012, ISSN: 2151-4658 (Electronic)
2151-464X (Linking). Liens | 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 Article de journal Bone, 49 (3), p. 395-403, 2011, ISSN: 1873-2763 (Electronic)
1873-2763 (Linking). Liens | 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 Article de journal Joint Bone Spine, 78 (2), p. 179-83, 2011, ISSN: 1778-7254 (Electronic)
1297-319X (Linking). Liens | 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 Article de journal Arthritis Rheum, 63 (3), p. 681-90, 2011, ISSN: 1529-0131 (Electronic)
0004-3591 (Linking). Liens | 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 Article de journal 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 Article de journal 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
|
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 Article de journal Arthritis Res Ther, 12 (4), p. R142, 2010, ISSN: 1478-6362 (Electronic)
1478-6354 (Linking). Liens | 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}
}
|
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.
