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151. International management platform for children’s interstitial lung disease (chILD-EU)

Author

Griese, Matthias, Seidl, Elias, Hengst, Meike, Reu, Simone, Rock, Hans, Anthony, Gisela, Kiper, Nural, Emiralioğlu, Nagehan, Snijders, Deborah, Goldbeck, Lutz, Leidl, Reiner, Ley-Zaporozhan, Julia, Kruger-Stollfuss, Ingrid, Kammer, Birgit, Wesselak, Traudl, Eismann, Claudia, Schams, Andrea, Neuner, Doerthe, MacLean, Morag, Nicholson, Andrew G, Lauren, McCann, Clement, Annick, Epaud, Ralph, de Blic, Jacques, Ashworth, Michael, Aurora, Paul, Calder, Alistair, Wetzke, Martin, Kappler, Matthias, Cunningham, Steve, Schwerk, Nicolaus, and Bush, Andy

Abstract

BackgroundChildren’s interstitial lung diseases (chILD) cover many rare entities, frequently not diagnosed or studied in detail. There is a great need for specialised advice and for internationally agreed subclassification of entities collected in a register.Our objective was to implement an international management platform with independent multidisciplinary review of cases at presentation for long-term follow-up and to test if this would allow for more accurate diagnosis. Also, quality and reproducibility of a diagnostic subclassification system were assessed using a collection of 25 complex chILD cases.MethodsA web-based chILD management platform with a registry and biobank was successfully designed and implemented.ResultsOver a 3-year period, 575 patients were included for observation spanning a wide spectrum of chILD. In 346 patients, multidisciplinary reviews were completed by teams at five international sites (Munich 51%, London 12%, Hannover 31%, Ankara 1% and Paris 5%). In 13%, the diagnosis reached by the referring team was not confirmed by peer review. Among these, the diagnosis initially given was wrong (27%), imprecise (50%) or significant information was added (23%).The ability of nine expert clinicians to subcategorise the final diagnosis into the chILD-EU register classification had an overall exact inter-rater agreement of 59% on first assessment and after training, 64%. Only 10% of the ‘wrong’ answers resulted in allocation to an incorrect category. Subcategorisation proved useful but training is needed for optimal implementation.ConclusionsWe have shown that chILD-EU has generated a platform to help the clinical assessment of chILD.Trial registration numberResults, NCT02852928.

Published
2018
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152. Anoctamin 1 dysregulation alters bronchial epithelial repair in cystic fibrosis

Author

Ruffin, Manon, primary, Voland, Mélanie, additional, Marie, Solenne, additional, Bonora, Monique, additional, Blanchard, Elise, additional, Blouquit-Laye, Sabine, additional, Naline, Emmanuel, additional, Puyo, Philippe, additional, Le Rouzic, Philippe, additional, Guillot, Loic, additional, Corvol, Harriet, additional, Clement, Annick, additional, and Tabary, Olivier, additional

Published
2013
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153. Liver disease in pediatric patients with cystic fibrosis is associated with glutathione S-transferase P1 polymorphism

Author

Henrion-Caude, Alexandra, Flamant, Cyril, Roussey, Michel, Housset, Chantal, Flahault, Antoine, Fryer, Anthony A., Chadelat, Katarina, Strange, Richard C., and Clement, Annick

Subjects
Male, Cystic Fibrosis/*epidemiology/*genetics, Glutathione Transferase/*genetics, Adolescent, Genotype, Liver Diseases/*epidemiology/*genetics, Polymorphism, Single Nucleotide, Glutathione S-Transferase pi, Isoenzymes/*genetics, Risk Factors, Genetic Predisposition to Disease/epidemiology, Humans, Female, Child
Published
2002

154. Delineation of CCDC39/CCDC40 mutation spectrum and associated phenotypes in primary: Ciliary dyskinesia

Author

Blanchon, Sylvain, Legendre, Marie, Copin, Bruno, Duquesnoy, Philippe, Montantin, Guy, Kott, Esther, Dastot, Florence, Jeanson, Ludovic, Cachanado, Marine, Rousseau, Alexandra, Papon, Jean François, Beydon, Nicole, Brouard, Jacques, Crestani, Bruno, Deschildre, Antoine, Désir, Julie, Dollfus, Héle'ne, Leheup, Bruno, Tamalet, Aline, Thumerelle, Caroline, Vojtek, Anne-Marie, Escalier, Denise, Coste, André, de Blic, Jacques, Clement, Annick, Escudier, Estelle, Amselem, Serge, Blanchon, Sylvain, Legendre, Marie, Copin, Bruno, Duquesnoy, Philippe, Montantin, Guy, Kott, Esther, Dastot, Florence, Jeanson, Ludovic, Cachanado, Marine, Rousseau, Alexandra, Papon, Jean François, Beydon, Nicole, Brouard, Jacques, Crestani, Bruno, Deschildre, Antoine, Désir, Julie, Dollfus, Héle'ne, Leheup, Bruno, Tamalet, Aline, Thumerelle, Caroline, Vojtek, Anne-Marie, Escalier, Denise, Coste, André, de Blic, Jacques, Clement, Annick, Escudier, Estelle, and Amselem, Serge

Abstract

Background CCDC39 and CCDC40 genes have recently been implicated in primary ciliary dyskinesia (PCD) with inner dynein arm (IDA) defects and axonemal disorganisation; their contribution to the disease is, however, unknown. Aiming to delineate the CCDC39/ CCDC40 mutation spectrum and associated phenotypes, this study screened a large cohort of patients with IDA defects, in whom clinical and ciliary phenotypes were accurately described. Methods All CCDC39 and CCDC40 exons and intronic boundaries were sequenced in 43 patients from 40 unrelated families. The study recorded and compared clinical features (sex, origin, consanguinity, laterality defects, ages at first symptoms and at phenotype evaluation, neonatal respiratory distress, airway infections, nasal polyposis, otitis media, bronchiectasis, infertility), ciliary beat frequency, and quantitative ultrastructural analyses of cilia and sperm flagella. Results Biallelic CCDC39 or CCDC40 mutations were identified in 30/34 (88.2%) unrelated families with IDA defects associated with axonemal disorganisation (22 and eight families, respectively). Fourteen of the 28 identified mutations are novel. No mutation was found in the six families with isolated IDA defects. Patients with identified mutations shared a similar phenotype, in terms of both clinical features and ciliary structure and function. The sperm flagellar ultrastructure, analysed in 4/7 infertile males, showed evidence of abnormalities similar to the ciliary ones. Conclusions CCDC39 and CCDC40 mutations represent the major cause of PCD with IDA defects and axonemal disorganisation. Patients carrying CCDC39 or CCDC40 mutations are phenotypically indistinguishable. CCDC39 and CCDC40 analyses in selected patients ensure mutations are found with high probability, even if clinical or ciliary phenotypes cannot prioritise one analysis over the other., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2012

155. Proinflammatory effect of sodium 4-phenylbutyrate in deltaF508-cystic fibrosis transmembrane conductance regulator lung epithelial cells: involvement of extracellular signal-regulated protein kinase 1/2 and c-Jun-NH2-terminal kinase signaling.

Author

Roque, Telma, Boncoeur, Emilie, Saint-Criq, Vinciane, Bonvin, Elise, Clement, Annick, Tabary, Olivier, Jacquot, Jacky, Roque, Telma, Boncoeur, Emilie, Saint-Criq, Vinciane, Bonvin, Elise, Clement, Annick, Tabary, Olivier, and Jacquot, Jacky

Abstract

Sodium 4-phenylbutyrate (4-PBA) has attracted a great deal of attention in cystic fibrosis (CF) pathology due to its capacity to traffic DeltaF508-cystic fibrosis transmembrane conductance regulator (CFTR) to the cell membrane and restore CFTR chloride function at the plasma membrane of CF lung cells in vitro and in vivo. Using two different DeltaF508-CFTR lung epithelial cell lines (CFBE41o- and IB3-1 cells, characterized with DeltaF508-homozygous and heterozygous genotype, respectively) in vitro, 4-PBA induced an increase of proinflammatory cytokine interleukin (IL)-8 production in a concentration-dependent manner. This 4-PBA-induced IL-8 production was associated with a strong reduction of proteasome and nuclear factor-kappaB transcriptional activities in the two DeltaF508-CFTR lung cells either in a resting state or after tumor necrosis factor-alpha stimulation. In contrast, a strong increase of activator protein-1 transcriptional activity was observed. The inhibition of extracellular signal-regulated protein kinase 1/2 (ERK1/2) by 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio] butadiene (U0126) and 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) and c-Jun-NH(2)-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) by anthra[1,9-cd] pyrazol-6 (2H)-one (SP600125), respectively, was associated with a reduction (2-3.5-fold) of IL-8 production in both DeltaF508-CFTR lung cell lines treated with 4-PBA. No significant change of IL-8 production was observed after an inhibition of p38 MAPK with 4-[4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazol-2-yl] phenol (SB202190). Therefore, we suggest that inhibition of both ERK1/2 and JNK signaling may be a means to strongly reduce 4-PBA-induced IL-8 production in combination with 4-PBA treatment to restore CFTR Cl(-) channel function in lung epithelial cells of patients with CF., Comparative Study, Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Published
2008

156. Oxidative stress induces extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase in cystic fibrosis lung epithelial cells: Potential mechanism for excessive IL-8 expression.

Author

Boncoeur, Emilie, Criq, Vinciane Saint, Bonvin, Elise, Roque, Telma, Henrion-Caude, Alexandra, Gruenert, Dieter C, Clement, Annick, Jacquot, Jacky, Tabary, Olivier, Boncoeur, Emilie, Criq, Vinciane Saint, Bonvin, Elise, Roque, Telma, Henrion-Caude, Alexandra, Gruenert, Dieter C, Clement, Annick, Jacquot, Jacky, and Tabary, Olivier

Abstract

Cystic fibrosis (CF) is a lethal disease caused by defective function of the cftr gene product, the CF transmembrane conductance regulator (CFTR) that leads to oxidative damage and excessive inflammatory response in lungs of CF patients. We here report the effects of oxidative stress (hyperoxia, 95% O(2)) on the expression of pro-inflammatory interleukin (IL)-8 and CXCR1/2 receptors in two human CF lung epithelial cell lines (IB3-1, with the heterozygous F508del/W1282X mutation and CFBE41o- with the homozygous F508del/F508del mutation) and two control non-CF lung epithelial cell lines (S9 cell line derived from IB3-1 after correction with wtCFTR and the normal bronchial cell line 16HBE14o-). Under oxidative stress, the expression of IL-8 and CXCR1/2 receptors was increased in CF, corrected and normal lung cell lines. The effects of oxidative stress were also investigated by measuring the transcription nuclear factor kappaB (NF-kappaB) and activator protein-1 (AP-1) activities. Under oxidative stress, no increase of NF-kappaB activation was observed in CF lung cells in contrast to that observed in normal and corrected CF lung cells. The signalling of mitogen-activated protein (MAP) kinases was further studied. We demonstrated that extracellular signal-regulated kinase (ERK1/2) and AP-1 activity was markedly enhanced in CF but not non-CF lung cells under oxidative stress. Consistently, inhibition of ERK1/2 in oxidative stress-exposed CF lung cells strongly decreased both the IL-8 production and CXCR1/2 expression. Therefore, targeting of ERK1/2 MAP kinase may be critical to reduce oxidative stress-mediated inflammation in lungs of CF patients., Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Published
2008

157. Cystic fibrosis transmembrane conductance regulator controls lung proteasomal degradation and nuclear factor-kappaB activity in conditions of oxidative stress.

Author

Boncoeur, Emilie, Roque, Telma, Bonvin, Elise, Saint-Criq, Vinciane, Bonora, Monique, Clement, Annick, Tabary, Olivier, Henrion-Caude, Alexandra, Jacquot, Jacky, Boncoeur, Emilie, Roque, Telma, Bonvin, Elise, Saint-Criq, Vinciane, Bonora, Monique, Clement, Annick, Tabary, Olivier, Henrion-Caude, Alexandra, and Jacquot, Jacky

Abstract

Cystic fibrosis is a lethal inherited disorder caused by mutations in a single gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein, resulting in progressive oxidative lung damage. In this study, we evaluated the role of CFTR in the control of ubiquitin-proteasome activity and nuclear factor (NF)-kappaB/IkappaB-alpha signaling after lung oxidative stress. After a 64-hour exposure to hyperoxia-mediated oxidative stress, CFTR-deficient (cftr(-/-)) mice exhibited significantly elevated lung proteasomal activity compared with wild-type (cftr(+/+)) animals. This was accompanied by reduced lung caspase-3 activity and defective degradation of NF-kappaB inhibitor IkappaB-alpha. In vitro, human CFTR-deficient lung cells exposed to oxidative stress exhibited increased proteasomal activity and decreased NF-kappaB-dependent transcriptional activity compared with CFTR-sufficient lung cells. Inhibition of the CFTR Cl(-) channel by CFTR(inh-172) in the normal bronchial immortalized cell line 16HBE14o- increased proteasomal degradation after exposure to oxidative stress. Caspase-3 inhibition by Z-DQMD in CFTR-sufficient lung cells mimicked the response profile of increased proteasomal degradation and reduced NF-kappaB activity observed in CFTR-deficient lung cells exposed to oxidative stress. Taken together, these results suggest that functional CFTR Cl(-) channel activity is crucial for regulation of lung proteasomal degradation and NF-kappaB activity in conditions of oxidative stress., Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Published
2008

159. Loss-of-Function Mutations in RSPH1 Cause Primary Ciliary Dyskinesia with Central-Complex and Radial-Spoke Defects

Author

Kott, Esther, primary, Legendre, Marie, additional, Copin, Bruno, additional, Papon, Jean-François, additional, Dastot-Le Moal, Florence, additional, Montantin, Guy, additional, Duquesnoy, Philippe, additional, Piterboth, William, additional, Amram, Daniel, additional, Bassinet, Laurence, additional, Beucher, Julie, additional, Beydon, Nicole, additional, Deneuville, Eric, additional, Houdouin, Véronique, additional, Journel, Hubert, additional, Just, Jocelyne, additional, Nathan, Nadia, additional, Tamalet, Aline, additional, Collot, Nathalie, additional, Jeanson, Ludovic, additional, Le Gouez, Morgane, additional, Vallette, Benoit, additional, Vojtek, Anne-Marie, additional, Epaud, Ralph, additional, Coste, André, additional, Clement, Annick, additional, Housset, Bruno, additional, Louis, Bruno, additional, Escudier, Estelle, additional, and Amselem, Serge, additional

Published
2013
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160. Impact of nutrition on phenotype in CFTR-deficient mice.

Author

Cottart, Charles-Henry, Bonvin, Elise, Rey, Colette, Wendum, Dominique, Bernaudin, Jean-François, Dumont, Sylvie, Lasnier, Elisabeth, Debray, Dominique, Clement, Annick, Housset, Chantal, Bonora, Monique, Cottart, Charles-Henry, Bonvin, Elise, Rey, Colette, Wendum, Dominique, Bernaudin, Jean-François, Dumont, Sylvie, Lasnier, Elisabeth, Debray, Dominique, Clement, Annick, Housset, Chantal, and Bonora, Monique

Abstract

To elucidate the impact of nutrition in cystic fibrosis (CF), we compared the phenotypic traits of Cftr -/- mice fed either a lipid-enriched liquid diet (Peptamen) or a standard chow combined with polyethylenglycol osmotic laxative (PEG), two strategies commonly used to prevent intestinal obstruction in CF mice. Survival, growth, liver, and ventilatory status were determined in Cftr -/- and Cftr +/+ mice, followed-up until 120 d. Ventilation was recorded in conscious animals using whole-body plethysmography. We found that the survival rate was similar in Peptamen and PEG Cftr -/- mice. Cftr -/- mice had lower minute ventilation than Cftr +/+ mice, whatever the diet. Both Cftr -/- and Cftr +/+ mice fed Peptamen displayed preadult growth delay compared with PEG-treated animals. Despite subsequent growth catch-up, Cftr -/- mice remained smaller than Cftr +/+ mice, whatever the diet. All Peptamen fed Cftr -/- mice showed hepatomegaly and liver steatosis, which also occurred but to a lesser extent in Peptamen fed Cftr +/+ animals. Therefore, while both treatment strategies are similarly efficient to avoid high mortality at weaning, Peptamen induces preadult growth delay and liver steatosis. These effects of diet are important to consider in future animal studies and also prompt to evaluate high-energy diets in CF patients., Comparative Study, Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Published
2007

161. Mutations in GAS8, a Gene Encoding a Nexin-Dynein Regulatory Complex Subunit, Cause Primary Ciliary Dyskinesia with Axonemal Disorganization.

Author

Jeanson, Ludovic, Thomas, Lucie, Copin, Bruno, Coste, André, Sermet‐Gaudelus, Isabelle, Dastot‐Le Moal, Florence, Duquesnoy, Philippe, Montantin, Guy, Collot, Nathalie, Tissier, Sylvie, Papon, Jean‐François, Clement, Annick, Louis, Bruno, Escudier, Estelle, Amselem, Serge, and Legendre, Marie

Abstract

ABSTRACT Primary ciliary dyskinesia (PCD) is an autosomal recessive disease characterized by chronic respiratory infections of the upper and lower airways, hypofertility, and, in approximately half of the cases, situs inversus. This complex phenotype results from defects in motile cilia and sperm flagella. Among the numerous genes involved in PCD, very few-including CCDC39 and CCDC40-carry mutations that lead to a disorganization of ciliary axonemes with microtubule misalignment. Focusing on this particular phenotype, we identified bi-allelic loss-of-function mutations in GAS8, a gene that encodes a subunit of the nexin-dynein regulatory complex (N-DRC) orthologous to DRC4 of the flagellated alga Chlamydomonas reinhardtii. Unlike the majority of PCD patients, individuals with GAS8 mutations have motile cilia, which, as documented by high-speed videomicroscopy, display a subtle beating pattern defect characterized by slightly reduced bending amplitude. Immunofluorescence studies performed on patients' respiratory cilia revealed that GAS8 is not required for the proper expression of CCDC39 and CCDC40. Rather, mutations in GAS8 affect the subcellular localization of another N-DRC subunit called DRC3. Overall, this study, which identifies GAS8 as a PCD gene, unveils the key importance of the corresponding protein in N-DRC integrity and in the proper alignment of axonemal microtubules in humans. [ABSTRACT FROM AUTHOR]

Published
2016
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162. Intracellular colocalization and interaction of IGF-binding protein-2 with the cyclin-dependent kinase inhibitor p21CIP1/WAF1 during growth inhibition.

Author

Terrien, Xavier, Bonvin, Elise, Corroyer, Sophie, Tabary, Olivier, Clement, Annick, Henrion-Caude, Alexandra, Terrien, Xavier, Bonvin, Elise, Corroyer, Sophie, Tabary, Olivier, Clement, Annick, and Henrion-Caude, Alexandra

Abstract

It is presently unknown whether any member of the IGFBP (insulin-like growth factor binding protein) family directly participates in the control of cell proliferation. We have previously documented that induction of IGFBP-2 was associated with inhibition of DNA synthesis in lung alveolar epithelial cells. In the present study, we investigated the relationship between IGFBP-2 and the cell cycle inhibitor p21CIP1/WAF1 further. We used serum deprivation to inhibit the proliferation of MLE (mouse lung epithelial)-12 cells, and characterized the spatial localization of IGFBP-2. We found that growth inhibition, which was supported by the strong induction of p21CIP1/WAF1, was correlated with increased secretion of IGFBP-2 and, unexpectedly, with its increased localization in the nucleus and particularly in the cytoplasm. By coimmunoprecipitation, we discovered that IGFBP-2 is capable of binding to p21CIP1/WAF1. Interaction between these two proteins was further supported by colocalization of the proteins within growth-arrested cells, as visualized by confocal microscopy. Furthermore, this interaction increased with the duration of the stress, but was suppressed when proliferation was restimulated by the addition of serum. The recombinant expression of GFP (green fluorescent protein)-tagged IGFBP-2 in transfected MLE-12 cells demonstrated its ability to bind specifically to p21CIP1/WAF1. Taken together, these results provide a link between IGFBP-2 and p21CIP1/WAF1 in the regulation of alveolar lung cell proliferation., Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Published
2005

163. Knockout of Insulin-Like Growth Factor-1 Receptor Impairs Distal Lung Morphogenesis

Author

Epaud, Ralph, primary, Aubey, Flore, additional, Xu, Jie, additional, Chaker, Zayna, additional, Clemessy, Maud, additional, Dautin, Alexandre, additional, Ahamed, Karmène, additional, Bonora, Monique, additional, Hoyeau, Nadia, additional, Fléjou, Jean-François, additional, Mailleux, Arnaud, additional, Clement, Annick, additional, Henrion-Caude, Alexandra, additional, and Holzenberger, Martin, additional

Published
2012
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164. Loss-of-Function Mutations in LRRC6 , a Gene Essential for Proper Axonemal Assembly of Inner and Outer Dynein Arms, Cause Primary Ciliary Dyskinesia

Author

Kott, Esther, primary, Duquesnoy, Philippe, additional, Copin, Bruno, additional, Legendre, Marie, additional, Dastot-Le Moal, Florence, additional, Montantin, Guy, additional, Jeanson, Ludovic, additional, Tamalet, Aline, additional, Papon, Jean-François, additional, Siffroi, Jean-Pierre, additional, Rives, Nathalie, additional, Mitchell, Valérie, additional, de Blic, Jacques, additional, Coste, André, additional, Clement, Annick, additional, Escalier, Denise, additional, Touré, Aminata, additional, Escudier, Estelle, additional, and Amselem, Serge, additional

Published
2012
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168. Multiple apical plasma membrane constituents are associated with susceptibility to meconium ileus in individuals with cystic fibrosis

Author

Sun, Lei, primary, Rommens, Johanna M, additional, Corvol, Harriet, additional, Li, Weili, additional, Li, Xin, additional, Chiang, Theodore A, additional, Lin, Fan, additional, Dorfman, Ruslan, additional, Busson, Pierre-François, additional, Parekh, Rashmi V, additional, Zelenika, Diana, additional, Blackman, Scott M, additional, Corey, Mary, additional, Doshi, Vishal K, additional, Henderson, Lindsay, additional, Naughton, Kathleen M, additional, O'Neal, Wanda K, additional, Pace, Rhonda G, additional, Stonebraker, Jaclyn R, additional, Wood, Sally D, additional, Wright, Fred A, additional, Zielenski, Julian, additional, Clement, Annick, additional, Drumm, Mitchell L, additional, Boëlle, Pierre-Yves, additional, Cutting, Garry R, additional, Knowles, Michael R, additional, Durie, Peter R, additional, and Strug, Lisa J, additional

Published
2012
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169. Multiplex Ligation-Dependent Probe Amplification Improves the Detection Rate of NKX2.1 Mutations in Patients Affected by Brain-Lung-Thyroid Syndrome

Author

Teissier, Raphaël, primary, Guillot, Loïc, additional, Carré, Aurore, additional, Morandini, Melina, additional, Stuckens, Chantal, additional, Ythier, Hubert, additional, Munnich, Arnold, additional, Szinnai, Gabor, additional, de Blic, Jacques, additional, Clement, Annick, additional, Leger, Juliane, additional, Castanet, Mireille, additional, Epaud, Ralph, additional, and Polak, Michel, additional

Published
2012
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170. Molecular and cellular characteristics of ABCA3 mutations associated with diffuse parenchymal lung diseases in children

Author

Flamein, Florence, primary, Riffault, Laure, additional, Muselet-Charlier, Céline, additional, Pernelle, Julie, additional, Feldmann, Delphine, additional, Jonard, Laurence, additional, Durand-Schneider, Anne-Marie, additional, Coulomb, Aurore, additional, Maurice, Michèle, additional, Nogee, Lawrence M., additional, Inagaki, Nobuya, additional, Amselem, Serge, additional, Dubus, Jean Christophe, additional, Rigourd, Virginie, additional, Brémont, François, additional, Marguet, Christophe, additional, Brouard, Jacques, additional, de Blic, Jacques, additional, Clement, Annick, additional, Epaud, Ralph, additional, and Guillot, Loïc, additional

Published
2011
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178. NKX2-1mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in “Brain-Lung-Thyroid Syndrome”

Author

Guillot, Loïc, primary, Carré, Aurore, additional, Szinnai, Gabor, additional, Castanet, Mireille, additional, Tron, Elodie, additional, Jaubert, Francis, additional, Broutin, Isabelle, additional, Counil, François, additional, Feldmann, Delphine, additional, Clement, Annick, additional, Polak, Michel, additional, and Epaud, Ralph, additional

Published
2010
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184. Therapeutic strategies for idiopathic chylothorax

Author

Epaud, Ralph, primary, Dubern, Beatrice, additional, Larroquet, Michele, additional, Tamalet, Aline, additional, Guillemot, Nathalie, additional, Maurage, Chantal, additional, Clement, Annick, additional, and Fauroux, Brigitte, additional

Published
2008
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185. Oxidative stress induces extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase in cystic fibrosis lung epithelial cells: Potential mechanism for excessive IL-8 expression

Author

Boncoeur, Emilie, primary, Criq, Vinciane Saint, additional, Bonvin, Elise, additional, Roque, Telma, additional, Henrion-Caude, Alexandra, additional, Gruenert, Dieter C., additional, Clement, Annick, additional, Jacquot, Jacky, additional, and Tabary, Olivier, additional

Published
2008
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187. Glucocorticoid receptor gene polymorphisms associated with progression of lung disease in young patients with cystic fibrosis

Author

Corvol, Harriet, primary, Nathan, Nadia, additional, Charlier, Celine, additional, Chadelat, Katarina, additional, Le Rouzic, Philippe, additional, Tabary, Olivier, additional, Fauroux, Brigitte, additional, Henrion-Caude, Alexandra, additional, Feingold, Josue, additional, Boelle, Pierre-Yves, additional, and Clement, Annick, additional

Published
2007
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190. Influence of Interleukin‐10 onAspergillus fumigatusInfection in Patients with Cystic Fibrosis

Author

Brouard, Jacques, primary, Knauer, Nicola, additional, Boelle, Pierre‐Yves, additional, Corvol, Harriet, additional, Henrion‐Caude, Alexandra, additional, Flamant, Cyril, additional, Bremont, François, additional, Delaisi, Bertrand, additional, Duhamel, Jean‐Francois, additional, Marguet, Christophe, additional, Roussey, Michel, additional, Miesch, Marie‐Claude, additional, Chadelat, Katarina, additional, Boule, Michele, additional, Fauroux, Brigitte, additional, Ratjen, Felix, additional, Grasemann, Hartmut, additional, and Clement, Annick, additional

Published
2005
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192. Glutathione-S-transferase M1, M3, P1 and T1 polymorphisms and severity of lung disease in children with cystic fibrosis

Author

Flamant, Cyril, primary, Henrion-Caude, Alexandra, additional, Bo??lle, Pierre-Yves, additional, Br??mont, Fran??ois, additional, Brouard, Jacques, additional, Delaisi, Bertrand, additional, Duhamel, Jean-Fran??ois, additional, Marguet, Christophe, additional, Roussey, Michel, additional, Miesch, Marie-Claude, additional, Boul??, Mich??le, additional, Strange, Richard C, additional, and Clement, Annick, additional

Published
2004
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193. Reply

Author

Caude, Alexandra Henrion, primary, Flamant, Cyril, additional, Housset, Chantal, additional, and Clement, Annick, additional

Published
2003
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198. Idiopathic eosinophilic pneumonia in children: the French experience.

Author

Giovannini-Chami, Lisa, Hadchouel, Alice, Nathan, Nadia, Brémont, Francois, Dubus, Jean-Christophe, Fayon, Michael, Houdouin, Véronique, Berlioz-Baudoin, Michèle, Feret, Virginie, Leblanc, Thierry, Morelle, Karine, Albertini, Marc, Clement, Annick, and de Blic, Jacques

Subjects
PULMONARY eosinophilia, IMMUNOSUPPRESSIVE agents, ADRENOCORTICAL hormones, CLASSIFICATION algorithms, PEDIATRIC therapy
Abstract

Background Idiopathic eosinophilic pneumonia is extremely rare in children and adults. We present herein the first series describing the specificities of idiopathic chronic (ICEP) and acute (IAEP) eosinophilic pneumonia in children. Methods We retrospectively analyzed all cases of ICEP and IAEP in children that were retrieved from French Reference Centers for rare pediatric lung diseases. Results Five cases of pediatric ICEP were identified. Corticosteroid or immunosuppressive therapy dramatically improved the outcome in three cases. The remaining two cases had a persistent interstitial pattern with progressive development of cystic airspace lesions. Three cases of IAEP in adolescents were reported, with one requiring four days of extracorporeal membrane oxygenation. Conclusion ICEP is a rare disease with a polymorphic clinical presentation in children. We identified patients with persistent interstitial patterns progressing to cystic airspace regions, for which the boundaries with idiopathic interstitial pneumonias are difficult to establish. We therefore propose a specific pediatric definition and classification algorithm. IAEP in children remains an inflammatory reaction of the lung to an acute toxic exposure, mainly tobacco, as in adults. International studies are required to comprehensively assess the various clinical forms of the disease as well as the appropriate therapeutic regimens. [ABSTRACT FROM AUTHOR]

Published
2014
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