BESOIN D’AIDE POUR ANALYSER ET INTERPRÉTER VOS DONNÉES ?
AltraBio est une société de recherche contractuelle spécialisée dans l’analyse de données biologiques et médicales grâce à l’utilisation de méthodes statistiques et d’intelligence artificielle.
Elle est reconnue mondialement comme un partenaire de confiance pour les projets de recherche et développement menés par de grandes entreprises et des hôpitaux universitaires de premier plan évoluant dans divers secteurs tels que les produits pharmaceutiques, les dispositifs médicaux, le diagnostic et les dermato-cosmétiques.
COMMENT TRAVAILLER ENSEMBLE?
Partenariat
Développement d’outils informatiques pour l’analyse de données au sein de consortiums régionaux / nationaux / internationaux.
Exemples de projets réalisés ou en cours:
Sous-traitance
Analyse de données pour des entreprises ou des instituts hospitalo-universitaires.
-
Des centaines de projets réalisés
-
Des clients réguliers incluant les plus grandes pharmas et les leaders de la cosmétique
FINANCEMENTS
NOUVELLES
mars 2023
AltraBio partenaire d’un réseau européen pour la formation de chercheurs doctorants
AltraBio participe à cette initiative qui réunit 15 partenaires [...]
Meilleure entreprise pour l’analyse de données biologiques et médicales 2023 – Europe de l’Ouest
Nous sommes fiers d'avoir reçu le titre de "Meilleure [...]
janvier 2023
XXXI Cosmet’in Lyon Skin Science Days
AltraBio sera présent au XXXI Cosmet'in Lyon Skin Science [...]
septembre 2021
CYTO Virtual Interactive Event
Pourquoi perdre votre temps à analyser vos données de [...]
DERNIERES PUBLICATIONS
2015
Bauer, Yasmina; Tedrow, John; de Bernard, Simon; Birker-Robaczewska, Magdalena; Gibson, Kevin F; Guardela, Brenda Juan; Hess, Patrick; Klenk, Axel; Lindell, Kathleen O; Poirey, Sylvie; Renault, Bérengère; Rey, Markus; Weber, Edgar; Nayler, Oliver; Kaminski, Naftali
A novel genomic signature with translational significance for human idiopathic pulmonary fibrosis Article de journal
Dans: Am J Respir Cell Mol Biol, vol. 52, no. 2, p. 217–231, 2015, ISSN: 1535-4989.
@article{pmid25029475,
title = {A novel genomic signature with translational significance for human idiopathic pulmonary fibrosis},
author = {Yasmina Bauer and John Tedrow and Simon de Bernard and Magdalena Birker-Robaczewska and Kevin F Gibson and Brenda Juan Guardela and Patrick Hess and Axel Klenk and Kathleen O Lindell and Sylvie Poirey and Bérengère Renault and Markus Rey and Edgar Weber and Oliver Nayler and Naftali Kaminski},
doi = {10.1165/rcmb.2013-0310OC},
issn = {1535-4989},
year = {2015},
date = {2015-02-01},
urldate = {2015-02-01},
journal = {Am J Respir Cell Mol Biol},
volume = {52},
number = {2},
pages = {217--231},
abstract = {The bleomycin-induced rodent lung fibrosis model is commonly used to study mechanisms of lung fibrosis and to test potential therapeutic interventions, despite the well recognized dissimilarities to human idiopathic pulmonary fibrosis (IPF). Therefore, in this study, we sought to identify genomic commonalities between the gene expression profiles from 100 IPF lungs and 108 control lungs that were obtained from the Lung Tissue Research Consortium, and rat lungs harvested at Days 3, 7, 14, 21, 28, 42, and 56 after bleomycin instillation. Surprisingly, the highest gene expression similarity between bleomycin-treated rat and IPF lungs was observed at Day 7. At this point of maximal rat-human commonality, we identified a novel set of 12 disease-relevant translational gene markers (C6, CTHRC1, CTSE, FHL2, GAL, GREM1, LCN2, MMP7, NELL1, PCSK1, PLA2G2A, and SLC2A5) that was able to separate almost all patients with IPF from control subjects in our cohort and in two additional IPF/control cohorts (GSE10667 and GSE24206). Furthermore, in combination with diffusing capacity of carbon monoxide measurements, four members of the translational gene marker set contributed to stratify patients with IPF according to disease severity. Significantly, pirfenidone attenuated the expression change of one (CTHRC1) translational gene marker in the bleomycin-induced lung fibrosis model, in transforming growth factor-β1-treated primary human lung fibroblasts and transforming growth factor-β1-treated human epithelial A549 cells. Our results suggest that a strategy focused on rodent model-human disease commonalities may identify genes that could be used to predict the pharmacological impact of therapeutic interventions, and thus facilitate the development of novel treatments for this devastating lung disease.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
2014
Faugaret, Delphine; Amara, Amira Ben; Alingrin, Julie; Daumas, Aurélie; Delaby, Amélie; Lépolard, Catherine; Raoult, Didier; Textoris, Julien; M`ege, Jean-Louis
Granulomatous response to Coxiella burnetii, the agent of Q fever: the lessons from gene expression analysis Article de journal
Dans: Front. Cell. Infect. Microbiol., vol. 4, p. 172, 2014.
@article{Faugaret2014-ap,
title = {Granulomatous response to Coxiella burnetii, the agent of Q fever: the lessons from gene expression analysis},
author = {Delphine Faugaret and Amira Ben Amara and Julie Alingrin and Aurélie Daumas and Amélie Delaby and Catherine Lépolard and Didier Raoult and Julien Textoris and Jean-Louis M`ege},
doi = {10.3389/fcimb.2014.00172},
year = {2014},
date = {2014-12-01},
urldate = {2014-12-01},
journal = {Front. Cell. Infect. Microbiol.},
volume = {4},
pages = {172},
publisher = {Frontiers Media SA},
abstract = {The formation of granulomas is associated with the resolution of
Q fever, a zoonosis due to Coxiella burnetii; however the
molecular mechanisms of granuloma formation remain poorly
understood. We generated human granulomas with peripheral blood
mononuclear cells (PBMCs) and beads coated with C. burnetii,
using BCG extracts as controls. A microarray analysis showed
dramatic changes in gene expression in granuloma cells of which
more than 50% were commonly modulated genes in response to C.
burnetii and BCG. They included M1-related genes and genes
related to chemotaxis. The inhibition of the chemokines, CCL2
and CCL5, directly interfered with granuloma formation. C.
burnetii granulomas also expressed a specific transcriptional
profile that was essentially enriched in genes associated with
type I interferon response. Our results showed that granuloma
formation is associated with a core of transcriptional response
based on inflammatory genes. The specific granulomatous response
to C. burnetii is characterized by the activation of type 1
interferon pathway.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Q fever, a zoonosis due to Coxiella burnetii; however the
molecular mechanisms of granuloma formation remain poorly
understood. We generated human granulomas with peripheral blood
mononuclear cells (PBMCs) and beads coated with C. burnetii,
using BCG extracts as controls. A microarray analysis showed
dramatic changes in gene expression in granuloma cells of which
more than 50% were commonly modulated genes in response to C.
burnetii and BCG. They included M1-related genes and genes
related to chemotaxis. The inhibition of the chemokines, CCL2
and CCL5, directly interfered with granuloma formation. C.
burnetii granulomas also expressed a specific transcriptional
profile that was essentially enriched in genes associated with
type I interferon response. Our results showed that granuloma
formation is associated with a core of transcriptional response
based on inflammatory genes. The specific granulomatous response
to C. burnetii is characterized by the activation of type 1
interferon pathway.
Idbaih, Ahmed; Mokhtari, Karima; cois Emile, Jean-Franc; Galanaud, Damien; Belaid, Hayat; Bernard, Simon; Benameur, Neila; Barlog, Vlad-Ciprian; Psimaras, Dimitri; Donadieu, Jean; Carpentier, Catherine; Martin-Duverneuil, Nadine; Haroche, Julien; Feuvret, Loic; Zahr, Noel; Delattre, Jean-Yves; Hoang-Xuan, Kh^e
Dramatic response of a BRAF V600E-mutated primary CNS histiocytic sarcoma to vemurafenib Article de journal
Dans: Neurology, vol. 83, no. 16, p. 1478–1480, 2014.
@article{Idbaih2014-pa,
title = {Dramatic response of a BRAF V600E-mutated primary CNS histiocytic sarcoma to vemurafenib},
author = {Ahmed Idbaih and Karima Mokhtari and Jean-Franc cois Emile and Damien Galanaud and Hayat Belaid and Simon Bernard and Neila Benameur and Vlad-Ciprian Barlog and Dimitri Psimaras and Jean Donadieu and Catherine Carpentier and Nadine Martin-Duverneuil and Julien Haroche and Loic Feuvret and Noel Zahr and Jean-Yves Delattre and Kh^e Hoang-Xuan},
doi = {10.1212/WNL.0000000000000880},
year = {2014},
date = {2014-10-01},
urldate = {2014-10-01},
journal = {Neurology},
volume = {83},
number = {16},
pages = {1478--1480},
publisher = {Ovid Technologies (Wolters Kluwer Health)},
keywords = {},
pubstate = {published},
tppubtype = {article}
}