Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
The high proportion of crystallized apatite forming the bones and teeth should theoretically allow the use of fission track analysis to date vertebrate fossils when burying of the fossiliferous series did not subject them to temperatures exceeding 60 degrees C. However several major obstacles arise such as the complexity of fossils' internal structures, diagenetic modifications and substitutions of the hydroxyapatite by other minerals, and massive U uptake or loss during diagenesis. In this work, those various problems are addressed combining optical microscope observation of the fossils, a systematic fission track analysis of the best samples, alpha and gamma spectrometry and Secondary Ion Mass Spectrometry. Even if the problems caused by internal structures and mineral substitutions can be solved, U movements in and out of the fossils are generally too complex to allow fission track analysis dating of the fossils.
ISSN: 0009-2541

hal-00411880
https://hal.archives-ouvertes.fr/hal-00411880
DOI : 10.1016/j.chemgeo.2007.10.009

Éditeur(s) : [S.l.] : [s.n.]
Siècle(s) traité(s) : 20
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/ADG18171
ADG18171

Éditeur(s) : HAL CCSD Wiley-Blackwell
Résumé : International audience
Archaea may be involved in global energy cycles, and are known for their ability to interact with eukaryotic species (sponges, corals and ascidians) or as archaeal-bacterial consortia. The recently proposed phylum Thaumarchaeota may represent the deepest branching lineage in the archaeal phylogeny emerging before the divergence between Euryarchaeota and Crenarchaeota. Here we report the first characterization of two marine thaumarchaeal species from shallow waters that consist of multiple giant cells. One species is coated with sulfur-oxidizing g-Proteobacteria. These new uncultured thaumarchaeal species are able to live in the sulfide-rich environments of a tropical mangrove swamp, either on living tissues such as roots or on various kinds of materials such as stones, sunken woods, etc. These archaea and archaea/bacteria associations have been studied using light microscopy, transmission electron microscopy and scanning electron microscopy. Species identification of archaeons and the putative bacterial symbiont have been assessed by 16S small subunit ribosomal RNA analysis. The sulfur-oxidizing ability of the bacteria has been assessed by genetic investigation on alpha-subunit of the adenosine-5_- phosphosulfate reductase/oxidase's (AprA). Species identifications have been confirmed by fluorescence in situ hybridization using specific probes designed in this study. In this article, we describe two new giant archaeal species that form the biggest archaeal filaments ever observed. One of these species is covered by a specific biofilm of sulfur-oxidizing g-Proteobacteria. This study highlights an unexpected morphological and genetic diversity of the phylum Thaumarchaeota.
ISSN: 1462-2912

hal-00715219
https://hal.univ-antilles.fr/hal-00715219
DOI : 10.1111/j.1462-2920.2010.02309.x

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
The early apoptotic events induced by environmental pollutants with carcinogenic properties are poorly understood. Here, we focus on the early cytotoxic effects of benzo[a]pyrene (B[a]P). In F258 rat hepatic epithelial cells, B[a]P induces intrinsic apoptosis via a mitochondrial dysfunction characterized by the release of hexokinase II (HKII) from the mitochondria. Cancer cells often have an anomalous cell energy metabolism; since HKII dysfunction regulates B[a]P-induced apoptosis in F258 cells, but may also alter cell energy metabolism, HKII release from the mitochondria may represent an important B[a]P-related carcinogenic issue. Thus in the present study, we aimed at deciphering the mechanisms underlying HKII dysfunction upon B[a]P exposure. We show that while glycogen synthase kinase 3 beta (GSK3β) regulated the expression of HKII at the transcriptional level, glycogen synthase kinase 3 alpha (GSK3α) was involved in B[a]P-induced apoptosis via a decrease in c-Myc expression. The reduced level of c-Myc caused the relocation of HKII from the mitochondria to the cytosol, thereby being involved in the formation of reactive oxygen species and apoptosis. In conclusion, we show that the couple GSK3α/c-Myc plays a key role in B[a]P-induced early apoptotic cell signaling via HKII dysfunction.
ISSN: 0887-2333

hal-00682104
https://hal.archives-ouvertes.fr/hal-00682104
https://hal.archives-ouvertes.fr/hal-00682104/document
https://hal.archives-ouvertes.fr/hal-00682104/file/1-s2.0-S0887233311003018-main%20Dendel%C3%A9_%7B75929874-2DF9-47C3-92F6-92AF398668E5%7D.pdf
DOI : 10.1016/j.tiv.2011.11.001

Éditeur(s) : Cayenne : Imprimerie du gouvernement
Résumé : 531-fin
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11221-6
FRA11221-6

Éditeur(s) : HAL CCSD Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists
Résumé : International audience
Schistosome infection is a major public health concern affecting millions of people living in tropical regions of Africa, Asia, and South America. Schistosomes cause mild clinical symptoms in most subjects, whereas a small proportion of individuals presents severe clinical disease (as periportal fibrosis (PPF)) that may lead to death. Severe PPF results from an abnormal deposition of extracellular matrix proteins in the periportal spaces due to a chronic inflammation triggered by eggs and schistosome Ags. Extracellular matrix protein production is regulated by a number of cytokines, including IFN-gamma. We have now screened putative polymorphic sites within this gene in a population living in an endemic area for Schistosoma mansoni. Two polymorphisms located in the third intron of the IFN-gamma gene are associated with PPF. The IFN-gamma +2109 A/G polymorphism is associated with a higher risk for developing PPF, whereas the IFN-gamma +3810 G/A polymorphism is associated with less PPF. The polymorphisms result in changes in nuclear protein interactions with the intronic regions of the gene, suggesting that they may modify IFN-gamma mRNA expression. These results are consistent with the results of previous studies. Indeed, PPF is controlled by a major locus located on chromosome 6q22-q23, closely linked to the gene encoding the alpha-chain of the IFN-gamma receptor, and low IFN-gamma producers have been shown to have an increased risk of severe PPF. Together, these observations support the view that IFN-gamma expression and subsequent signal transduction play a critical role in the control of PPF in human hepatic schistosome infection (S. mansoni).
ISSN: 0022-1767

Droits : http://creativecommons.org/licenses/by-nc-nd/
hal-01211760
https://hal.archives-ouvertes.fr/hal-01211760
https://hal.archives-ouvertes.fr/hal-01211760/document
https://hal.archives-ouvertes.fr/hal-01211760/file/J%20Immunol-2003-Chevillard-5596-601.pdf
DOI : 10.4049/jimmunol.171.10.5596

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
The effects of some progestins on fish reproduction have been recently reported revealing the hazard of this class of steroidal pharmaceuticals. However, their effects at the central nervous system level have been poorly studied until now. Notwithstanding, progesterone, although still widely considered primarily a sex hormone, is an important agent affecting many central nervous system functions. Herein, we investigated the effects of a large set of synthetic ligands of the nuclear progesterone receptor on the glial-specific expression of the zebrafish brain aromatase (cyp19a1b) using zebrafish mechanism-based assays. Progesterone and 24 progestins were first screened on transgenic cyp19a1b-GFP zebrafish embryos. We showed that progesterone, dydrogesterone, drospirenone and all the progesterone-derived progestins had no effect on GFP expression. Conversely, all progestins derived from 19-nortesterone induced GFP in a concentration-dependent manner with EC50 ranging from the low nM range to hundreds nM. The 19-nortestosterone derived progestins levonorgestrel (LNG) and norethindrone (NET) were further tested in a radial glial cell context using U251-MG cells co-transfected with zebrafish ER subtypes (zfER alpha, zfER beta 1 or zfER beta 2) and cyp19a1b promoter linked to luciferase. Progesterone had no effect on luciferase activity while NET and LNG induced luciferase activity that was blocked by ICI 182,780. Zebrafish-ERs competition assays showed that NET and LNG were unable to bind to ERs, suggesting that the effects of these compounds on cyp19a1b require metabolic activation prior to elicit estrogenic activity. Overall, we demonstrate that 19-nortestosterone derived progestins elicit estrogenic activity by inducing cyp19a1b expression in radial glial cells. Given the crucial role of radial glial cells and neuro-estrogens in early development of brain, the consequences of exposure of fish to these compounds require further investigation.
ISSN: 0041-008X

hal-01366373
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01366373
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01366373/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01366373/file/Several%20synthetic%20progestins%20disrupt%20the%20glial%20cell.pdf
DOI : 10.1016/j.taap.2016.05.019

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Estrogen receptors (ERs) α and β are distributed in most tissues of women and men. ERs are bound by estradiol (E2), a natural hormone, and mediate the pleiotropic and tissue-specific effects of E2, such as proliferation of breast epithelial cells or protection and differentiation of neuronal cells. Numerous environmental molecules, called endocrine disrupting compounds, also interact with ERs. Phytoestrogens belong to this large family and are considered potent therapeutic molecules that act through their selective estrogen receptor modulator (SERM) activity. Using breast cancer cell lines as a model of estrogen-dependent proliferation and a stably ER-expressing PC12 cell line as a model of neuronal differentiating cells, we studied the SERM activity of major dietary compounds, such as apigenin, liquiritigenin, daidzein, genistein, coumestrol, resveratrol and zearalenone. The ability of these compounds to induce ER-transactivation and breast cancer cell proliferation and enhance Nerve Growth Factor (NGF) -induced neuritogenesis was assessed. Surprisingly, although all compounds were able to activate the ER through an estrogen responsive element reporter gene, they showed differential activity toward proliferation or differentiation. Apigenin and resveratrol showed a partial or no proliferative effect on breast cancer cells but fully contributed to the neuritogenesis effect of NGF. However, daidzein and zearalenone showed full effects on cellular proliferation but did not induce cellular differentiation. In summary, our results suggest that the therapeutic potential of phytoestrogens can diverge depending on the molecule and the phenotype considered. Hence, apigenin and resveratrol might be used in the development of therapeutics for breast cancer and brain diseases.
ISSN: 0041-008X

hal-01558816
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01558816
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01558816/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01558816/file/Lecomte%20et%20al.%20-%20Assessment%20of%20the%20potential%20activity%20of%20major%20diet.pdf
DOI : 10.1016/j.taap.2017.04.005

Extrait de : La science et la vie, n°78, pp452-459
Résumé : Article 8 p., 2 gravures, 7 photographies
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : ORkidé|Fonds privé Pierre Rostan
Permalien : http://www.manioc.org/patrimon/ORK12199
ORK12199

Éditeur(s) : Paris : F. Alcan
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Archives territoriales de Guyane
Permalien : http://www.manioc.org/patrimon/FRA11188
FRA11188

Éditeur(s) : Paris : Barba
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11123
FRA11123

Éditeur(s) : Paris : Imprimerie de E. Martinet
Résumé : Extrait du bulletin de la société botanique de France. Tome 18
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11227-5
FRA11227-5

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Although many studies reported mechanisms involved in the positive regulation of estrogens (E2) target genes, very little is known concerning the repressive effect of E2. In this study, we explored the molecular mechanisms by which E2 regulates CXCR7 expression in breast cancer cells. Our results show that E2-mediated down-regulation of CXCR7 occurs at the transcriptional level as demonstrated using actinomycin D and requires estrogen receptor alpha (ERα). In addition, CXCR7 is a primary ERα-target gene because the effect of E2 does not require the synthesis of an intermediary protein as revealed by the translational inhibitor cycloheximide treatment. Using an inhibitor of the NFκB pathway and chromatin immunoprecipitation assays, we demonstrated that NFκB is necessary for the high expression of CXCR7 gene and is recruited to the proximal promoter of the CXCR7 gene. Interestingly, the chromatin immunoprecipitation analyses also showed that E2-treatment significantly prevented the recruitment of NFκB to the promoter. Altogether, our results demonstrate that E2, through ERα, directly down-regulates CXCR7 expression by interfering with NFκB transcription factor at the promoter level.
ISSN: 0006-291X

inserm-00808966
http://www.hal.inserm.fr/inserm-00808966
DOI : 10.1016/j.bbrc.2013.01.050
PUBMED : 23352615

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Chronic liver damage due to viral or chemical agents leads to a repair process resulting in hepatic fibrosis. Fibrosis may lead to cirrhosis, which may progress to liver cancer or a loss of liver function, with an associated risk of liver failure and death. Chlordecone is a chlorinated pesticide used in the 1990s. It is not itself hepatotoxic, but its metabolism in the liver triggers hepatomegaly and potentiates hepatotoxic agents. Chlordecone is now banned, but it persists in soil and water, resulting in an ongoing public health problem in the Caribbean area. We assessed the probable impact of chlordecone on the progression of liver fibrosis in the population of contaminated areas, by developing a mouse model of chronic co-exposure to chlordecone and a hepatotoxic agent, carbon tetrachloride (CCl4). After repeated administrations of chlordecone and CCl4 by gavage over a 12-week period, we checked for liver damage in the exposed mice, by determining serum liver transaminase (AST, ALT) levels, histological examinations of the liver and measuring the expression of genes encoding extracellular matrix components. The co-exposure of mice to CCl4 and chlordecone resulted in significant increases in ALT and AST levels. Chlordecone also increased expression of the Col1A2, MMP-2, TIMP-1 and PAI-1 genes in CCl4-treated mice. Finally, we demonstrated, by quantifying areas of collagen deposition and alpha-SMA gene expression, that chlordecone potentiated the hepatic fibrosis induced by CCl4. In conclusion, our data suggest that chlordecone potentiates hepatic fibrosis in mice with CCl4-induced chronic liver injury
ISSN: 0378-4274

hal-01274228
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01274228
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01274228/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01274228/file/Chlordecone%20potentiates%20hepatic%20fibrosis%20%281%29.pdf
DOI : 10.1016/j.toxlet.2016.02.005

Éditeur(s) : Paris : Pagnerre

Droits : Domaine public
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/HASH5940ff3e238f321491453f
HASH5940ff3e238f321491453f

Éditeur(s) : Paris : Calmann Lévy
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11110
FRA11110

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 : 1840-1906
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/TLS17055
TLS17055

Extrait de : Le Globe trotter, n°71, p. 377-378
Résumé : Article 2 p., 5 photographies
Siècle(s) traité(s) : 20
Droits : Domaine public
Provenance : ORkidé|Fonds privé Pierre Rostan
Permalien : http://www.manioc.org/patrimon/ORK12167
ORK12167

Extrait de : L'illustration, n°2114, p. 141 et p. 144
Résumé : Article 1 p. et 1 gravure
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : ORkidé|Fonds privé Pierre Rostan
Permalien : http://www.manioc.org/patrimon/ORK12169
ORK12169

Éditeur(s) : HAL CCSD Ivyspring International Publisher
Résumé : International audience
Mullerian duct regression is a complex process which involves the AMH signalling pathway. We have previously demonstrated that besides AMH and its specific type II receptor (AMHRII), BMPR-IA and Smad5 are two essential factors implicated in this mechanism. Mothers against decapentaplegic homolog 4 (Smad4) is a transcription factor and the common Smad (co-Smad) involved in transforming growth factor beta (TGF-beta) signalling pathway superfamily. Since Smad4 null mutants die early during gastrulation, we have inactivated Smad4 in the Mullerian duct mesenchyme. Specific inactivation of Smad4 in the urogenital ridge leads to the partial persistence of the Mullerian duct in adult male mice. Careful examination of the urogenital tract reveals that the Mullerian duct retention is randomly distributed either on one side or both sides. Histological analysis shows a uterus-like structure, which is confirmed by the expression of estrogen receptor alpha. As previously described in a beta-catenin conditional mutant mouse model, beta-catenin contributes to Mullerian duct regression. In our mutant male embryos, it appears that beta-catenin expression is locally reduced along the urogenital ridge as compared to control mice. Moreover, the expression pattern is similar to those observed in control female mice. This study shows that reduced Smad4 expression disrupts the Wnt/beta-catenin signalling leading to the partial persistence of Mullerian duct
ISSN: 1449-2288

hal-01319890
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01319890
DOI : 10.7150/ijbs.12300
PUBMED : 27194944