Éditeur(s) : Paris : Morizot
Résumé : Nouvelle édition
Description : Nouvelle édition continuée jusqu'à nos jours, d'après les documents scientifiques les plus récents, les derniers voyages et les dernières découvertes par V.-A. Malte-Brun fils,...

Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11197
FRA11197

Éditeur(s) : HAL CCSD American Association for the Advancement of Science
Résumé :  
Amazon forests are a key but poorly understood component of the global carbon cycle. If, as anticipated, they dry this century, they might accelerate climate change through carbon losses and changed surface energy balances. We used records from multiple long-term monitoring plots across Amazonia to assess forest responses to the intense 2005 drought, a possible analog of future events. Affected forest lost biomass, reversing a large long-term carbon sink, with the greatest impacts observed where the dry season was unusually intense. Relative to pre-2005 conditions, forest subjected to a 100-millimeter increase in water deficit lost 5.3 megagrams of aboveground biomass of carbon per hectare. The drought had a total biomass carbon impact of 1.2 to 1.6 petagrams (1.2 × 1015 to 1.6 × 1015 grams). Amazon forests therefore appear vulnerable to increasing moisture stress, with the potential for large carbon losses to exert feedback on climate change.
ISSN: 0036-8075

hal-01032111
https://hal.archives-ouvertes.fr/hal-01032111
DOI : 10.1126/science.1164033

Éditeur(s) : Leipzig : Duncker und Humblot
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Université Toulouse 1 Capitole. Service Commun de la Documentation
Permalien : http://www.manioc.org/patrimon/TLS17022
TLS17022

Éditeur(s) : HAL CCSD
Résumé : International audience
BACKGROUND: The aryl hydrocarbon receptor (AhR) has gradually emerged as a regulator of inflammation in the lung and other tissues. AhR may interact with the p65-subunit of the nuclear factor (NF)-κB transcription factors, but reported outcomes of AhR/NF-κB-interactions are conflicting. Some studies suggest that AhR possess pro-inflammatory activities while others suggest that AhR may be anti-inflammatory. The present study explored the impact of AhR and its binding partner AhR nuclear translocator (Arnt) on p65-activation and two differentially regulated chemokines, CXCL8 (IL-8) and CCL5 (RANTES), in human bronchial epithelial cells (BEAS-2B). RESULTS: Cells were exposed to CXCL8- and CCL5-inducing chemicals, 1-nitropyrene (1-NP) and 1-aminopyrene (1-AP) respectively, or the synthetic double-stranded RNA analogue, polyinosinic-polycytidylic acid (Poly I:C) which induced both chemokines. Only CXCL8, and not CCL5, appeared to be p65-dependent. Yet, constitutively active unligated AhR suppressed both CXCL8 and CCL5, as shown by siRNA knock-down and the AhR antagonist α-naphthoflavone. Moreover, AhR suppressed activation of p65 by TNF-α and Poly I:C as assessed by luciferase-assay and p65-phosphorylation at serine 536, without affecting basal p65-activity. In contrast, Arnt suppressed only CXCL8, but did not prevent the p65-activation directly. However, Arnt suppressed expression of the NF-κB-subunit RelB which is under transcriptional regulation by p65. Furthermore, AhR-ligands alone at high concentrations induced a moderate CXCL8-response, without affecting CCL5, but suppressed both CXCL8 and CCL5-responses by Poly I:C. CONCLUSION: AhR and Arnt may differentially and independently regulate chemokine-responses induced by both inhaled pollutants and pulmonary infections. Constitutively active, unligated AhR suppressed the activation of p65, while Arnt may possibly interfere with the action of activated p65. Moreover, ligand-activated AhR suppressed CXCL8 and CCL5 responses by other agents, but AhR ligands alone induced CXCL8 responses when given at sufficiently high concentrations, thus underscoring the duality of AhR in regulation of inflammation. We propose that AhR-signaling may be a weak activator of p65-signaling that suppresses p65-activity induced by strong activators of NF-κB, but that its anti-inflammatory properties also are due to interference with additional pathways.
Cell communication and signaling: CCS

hal-01063555
https://hal.archives-ouvertes.fr/hal-01063555
DOI : 10.1186/s12964-014-0048-8

Éditeur(s) : HAL CCSD BioMed Central
Résumé : International audience
BACKGROUND: The aryl hydrocarbon receptor (AhR) has gradually emerged as a regulator of inflammation in the lung and other tissues. AhR may interact with the p65-subunit of the nuclear factor (NF)-κB transcription factors, but reported outcomes of AhR/NF-κB-interactions are conflicting. Some studies suggest that AhR possess pro-inflammatory activities while others suggest that AhR may be anti-inflammatory. The present study explored the impact of AhR and its binding partner AhR nuclear translocator (Arnt) on p65-activation and two differentially regulated chemokines, CXCL8 (IL-8) and CCL5 (RANTES), in human bronchial epithelial cells (BEAS-2B). RESULTS: Cells were exposed to CXCL8- and CCL5-inducing chemicals, 1-nitropyrene (1-NP) and 1-aminopyrene (1-AP) respectively, or the synthetic double-stranded RNA analogue, polyinosinic-polycytidylic acid (Poly I:C) which induced both chemokines. Only CXCL8, and not CCL5, appeared to be p65-dependent. Yet, constitutively active unligated AhR suppressed both CXCL8 and CCL5, as shown by siRNA knock-down and the AhR antagonist α-naphthoflavone. Moreover, AhR suppressed activation of p65 by TNF-α and Poly I:C as assessed by luciferase-assay and p65-phosphorylation at serine 536, without affecting basal p65-activity. In contrast, Arnt suppressed only CXCL8, but did not prevent the p65-activation directly. However, Arnt suppressed expression of the NF-κB-subunit RelB which is under transcriptional regulation by p65. Furthermore, AhR-ligands alone at high concentrations induced a moderate CXCL8-response, without affecting CCL5, but suppressed both CXCL8 and CCL5-responses by Poly I:C. CONCLUSION: AhR and Arnt may differentially and independently regulate chemokine-responses induced by both inhaled pollutants and pulmonary infections. Constitutively active, unligated AhR suppressed the activation of p65, while Arnt may possibly interfere with the action of activated p65. Moreover, ligand-activated AhR suppressed CXCL8 and CCL5 responses by other agents, but AhR ligands alone induced CXCL8 responses when given at sufficiently high concentrations, thus underscoring the duality of AhR in regulation of inflammation. We propose that AhR-signaling may be a weak activator of p65-signaling that suppresses p65-activity induced by strong activators of NF-κB, but that its anti-inflammatory properties also are due to interference with additional pathways.
ISSN: 1478-811X

inserm-01085082
http://www.hal.inserm.fr/inserm-01085082
http://www.hal.inserm.fr/inserm-01085082/document
http://www.hal.inserm.fr/inserm-01085082/file/s12964-014-0048-8.pdf
PUBMED : 25201625

Éditeur(s) : Cayenne : Imprimerie du gouvernement
Résumé : Année 1857
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11259
FRA11259

Résumé : Publiée dans le cadre du premier Congrès international d'histoire coloniale à Paris
Siècle(s) traité(s) : 20
Droits : Domaine public
Provenance : Ville de Pointe-à-Pitre. Réseau des bibliothèques
Permalien : http://www.manioc.org/patrimon/PAP11103
PAP11103

Éditeur(s) : Leipzig : in der Weidmannschen Buchhandlung
Siècle(s) traité(s) : 18
Droits : Domaine public
Provenance : Université Toulouse III - Paul Sabatier. Service Commun de la Documentation
Permalien : http://www.manioc.org/patrimon/TLS17115
TLS17115

Éditeur(s) : Monachii ; Lipsiae : apud R. Oldenbourg in comm.
Extrait de : Flora brasiliensis : enumeratio plantarum in Brasilia hactenus detectarum quas suis aliorumque botanicorum studiis descriptas et methodo naturali digestas partim icone illustratas
Résumé : Édition : 1874-1900
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Université Toulouse III - Paul Sabatier. Service Commun de la Documentation
Permalien : http://www.manioc.org/patrimon/TLS17088
TLS17088

Éditeur(s) : Paris : G. Lang
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA12067
FRA12067

Éditeur(s) : Cayenne : Imprimerie du gouvernement
Résumé : Année 1851
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11258
FRA11258

Éditeur(s) : Leipzig : Duncker & Humbolt
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Université Toulouse - Jean Jaurès. Service Commun de la Documentation
Permalien : http://www.manioc.org/patrimon/TLS17041
TLS17041

Éditeur(s) : Annecy : Imprimerie L. Dépollier

Droits : Domaine public
Provenance : Université de Nantes. Service commun de la documentation
Permalien : http://www.manioc.org/patrimon/NAN13049
NAN13049

Éditeur(s) : Monachii ; Lipsiae : apud Frid. Fleischer in comm.
Extrait de : Flora brasiliensis : enumeratio plantarum in Brasilia hactenus detectarum quas suis aliorumque botanicorum studiis descriptas et methodo naturali digestas partim icone illustratas
Résumé : Édition : 1896-1897
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Université Toulouse III - Paul Sabatier. Service Commun de la Documentation
Permalien : http://www.manioc.org/patrimon/TLS17078
TLS17078