Éditeur(s) : Paris : chez l'auteur Paris : imprimerie Quillau Paris : Mequignon
Siècle(s) traité(s) : 18
Droits : Domaine public
Permalien : http://www.manioc.org/patrimon/MMC16057-1
MMC16057-1

Éditeur(s) : HAL CCSD Lippincott, Williams & Wilkins
Résumé : International audience
Objective Large-scale prospective studies do not support an association between neuroticism and extroversion with cancer incidence. However, research on other personality constructs is inconclusive. This longitudinal study examined the associations between four personality measures, Type 1, "suppressed emotional expression"; Type 5, "rational/antiemotional"; hostility; and Type A with cancer incidence. Methods Personality measures were available for 13,768 members in the GAZEL cohort study (baseline assessment in 1993). Follow-up for diagnoses of primary cancers was obtained from January 1, 1994 to December 31, 2009. Associations between personality and cancer incidence were evaluated using Cox proportional hazards analyses and adjusted for potential confounders. Results During a median follow-up of 16.0 years (range, 9 days-16 years), 1139 participants were diagnosed as having a primary cancer. The mean duration between baseline and cancer diagnosis was 9.3 years. Type 1 personality was associated with a decreased risk of breast cancer (hazard ratio per standard deviation = 0.81, 95% confidence interval = 0.68-0.97, p = .02). Type 5 personality was not associated with prostate, breast, colorectal, or smoking-related cancers, but was associated with other cancers (hazard ratio per standard deviation = 1.17, 95% confidence interval = 1.04-1.31, p = .01). Hostility was associated with an increased risk of smoking-related cancers, which was explained by smoking habits, and Type A was not associated with any of the cancer endpoints. Conclusions Several personality measures were prospectively associated with the incidence of selected cancers. These links may warrant further epidemiological studies and investigations about potential biobehavioral mechanisms.
ISSN: 0033-3174

inserm-00813178
http://www.hal.inserm.fr/inserm-00813178
http://www.hal.inserm.fr/inserm-00813178/document
http://www.hal.inserm.fr/inserm-00813178/file/PersonalityCancer_Lemogne_Psychosom_Med_2013.pdf
http://www.hal.inserm.fr/inserm-00813178/file/inserm-00813178_edited.pdf

Éditeur(s) : HAL CCSD Endocrine Society
Résumé : International audience
Transcriptional regulation by the estrogen receptor-alpha(ER) has been investigated mainly in breast cancer cell lines, but estrogens such as 17 beta-estradiol (E2) exert numerous extrareproductive effects, particularly in the liver, where E2 exhibits both protective metabolic and deleterious thrombotic actions. To analyze the direct and early transcriptional effects of estrogens in the liver, we determined the E2-sensitive transcriptome and ER cistrome in mice after acute administration of E2 or placebo. These analyses revealed the early induction of genes involved in lipid metabolism, which fits with the crucial role of ER in the prevention of liver steatosis. Characterization of the chromatin state of ER binding sites (BSs) in mice expressing or not ER demonstrated that ER is not required per se for the establishment and/or maintenance of chromatin modifications at the majority of its BSs. This is presumably a consequence of a strong overlap between ER and hepatocyte nuclear factor 4 alpha BSs. In contrast, 40% of the BSs of the pioneer factor forkhead box protein a (Foxa2) were dependent upon ER expression, and ER expression also affected the distribution of nucleosomes harboring dimethylated lysine 4 of Histone H3 around Foxa2 BSs. We finally show that, in addition to a network of liver-specific transcription factors including CCAAT/enhancer-binding protein and hepatocyte nuclear factor 4 alpha, ER might be required for proper Foxa2 function in this tissue.
ISSN: 0888-8809

hal-01357623
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01357623
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01357623/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01357623/file/Changes%20in%20gene%20expression%201%20and%20Estrogen%20Receptor_accepted.pdf
DOI : 10.1210/me.2015-1311

Éditeur(s) : Paris : Recueil Sirey
Résumé : 6e édition, entièrement revue et condensée par Maurice Besson. Introduction générale par René Maunier.
Siècle(s) traité(s) : 16
Droits : Domaine public
Provenance : Communauté d'agglomération de La Rochelle. Médiathèque Michel-Crépeau
Permalien : http://www.manioc.org/patrimon/MMC16029
MMC16029

Éditeur(s) : Amsterdam : Jean Evertsz Cloppenburch
Siècle(s) traité(s) : 17
Droits : Domaine public
Provenance : Communauté d'agglomération de La Rochelle. Médiathèque Michel-Crépeau
Permalien : http://www.manioc.org/patrimon/MMC16127-3
MMC16127-3

Éditeur(s) : Paris : Michel Sonnius
Résumé : 5e édition

Provenance : Ville de Bordeaux. Bibliothèque municipale
Permalien : http://www.manioc.org/patrimon/BBX19009
BBX19009

Siècle(s) traité(s) : 17
Droits : Domaine public
Provenance : Archives territoriales de Guyane
Permalien : http://www.manioc.org/patrimon/GAD11008
GAD11008

Éditeur(s) : HAL CCSD Nature Publishing Group
Résumé : International audience
Most tumors undergo metabolic reprogramming towards glycolysis, the so-called Warburg effect, to support growth and survival. Overexpression of IF1, the physiological inhibitor of the F0F1ATPase, has been related to this phenomenon and appears to be a relevant marker in cancer. Environmental contributions to cancer development are now widely accepted but little is known about the underlying intracellular mechanisms. Among the environmental pollutants humans are commonly exposed to, benzo[a]pyrene (B[a]P), the prototype molecule of polycyclic aromatic hydrocarbons (PAHs), is a well-known human carcinogen. Besides apoptotic signals, B[a]P can also induce survival signals in liver cells, both likely involved in cancer promotion. Our previous works showed that B[a]P elicited a Warburg-like effect, thus favoring cell survival. The present study aimed at further elucidating the molecular mechanisms involved in the B[a]P-induced metabolic reprogramming, by testing the possible involvement of IF1. We presently demonstrate, both in vitro and in vivo, that PAHs, especially B[a]P, strongly increase IF1 expression. Such an increase, which might rely on β2-adrenergic receptor activation, notably participates to the B[a]P-induced glycolytic shift and cell survival in liver cells. By identifying IF1 as a target of PAHs, this study provides new insights about how environmental factors may contribute to related carcinogenesis.
ISSN: 2045-2322

hal-01518808
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01518808
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01518808/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01518808/file/Hardonni%C3%A8re%20et%20al%202017.pdf
DOI : 10.1038/s41598-017-00269-7

Éditeur(s) : Rouen : Bonaventure Le Brun

Droits : Domaine public
Provenance : Communauté d'agglomération de La Rochelle. Médiathèque Michel-Crépeau
Permalien : http://www.manioc.org/patrimon/MMC16028
MMC16028

Éditeur(s) : Paris : Librairie Larousse
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Communauté d'agglomération de La Rochelle. Médiathèque Michel-Crépeau
Permalien : http://www.manioc.org/patrimon/MMC16023-1
MMC16023-1

Éditeur(s) : Paris : Arthus Bertrand
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Martinique. Bibliothèque Schoelcher
Permalien : http://www.manioc.org/patrimon/SCH13079
SCH13079

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Experimental studies have demonstrated that the antileukemic trivalent inorganic arsenic prevents the development of severe pro-inflammatory diseases mediated by excessive Th1 and Th17 cell responses. Differentiation of Th1 and Th17 subsets is mainly regulated by interleukins (ILs) secreted from dendritic cells (DCs) and the ability of inorganic arsenic to impair interferon-γ and IL-17 secretion by interfering with the physiology of DCs is unknown. In the present study, we demonstrate that high concentrations of sodium arsenite (As(III), 1-2 μM) clinically achievable in plasma of arsenic-treated patients, block differentiation of human peripheral blood monocytes into immature DCs (iDCs) by inducing their necrosis. Differentiation of monocytes in the presence of non-cytotoxic concentrations of As(III) (0.1 to 0.5 μM) only slightly impacts endocytotic activity of iDCs or expression of co-stimulatory molecules in cells activated with lipopolysaccharide. However, this differentiation in the presence of As(III) strongly represses secretion of IL-12p70 and IL-23, two major regulators of Th1 and Th17 activities, from iDCs stimulated with different toll-like receptor (TLR) agonists in metalloid-free medium. Such As(III)-exposed DCs also exhibit reduced mRNA levels of IL12A and/or IL12B genes when activated with TLR agonists. Finally, differentiation of monocytes with non-cytotoxic concentrations of As(III) subsequently reduces the ability of activated DCs to stimulate the release of interferon-γ and IL-17 from Th cells. In conclusion, our results demonstrate that clinically relevant concentrations of inorganic arsenic markedly impair in vitro differentiation and functions of DCs, which may contribute to the putative beneficial effects of the metalloid towards inflammatory autoimmune diseases.
ISSN: 0041-008X

inserm-00813758
http://www.hal.inserm.fr/inserm-00813758
DOI : 10.1016/j.taap.2012.11.008
PUBMED : 23164666

Éditeur(s) : Paris : Dufart père
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Martinique. Bibliothèque Schoelcher
Permalien : http://www.manioc.org/patrimon/SCH13037
SCH13037

Éditeur(s) : Paris : Lepetit jeune
Résumé : An X
Siècle(s) traité(s) : 18
Droits : Domaine public
Provenance : Communauté d'agglomération de La Rochelle. Médiathèque Michel-Crépeau
Permalien : http://www.manioc.org/patrimon/MMC16005
MMC16005

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Trivalent inorganic arsenic [As(III)] is an efficient anticancer agent used to treat patients suffering from acute promyelocytic leukemia. Recently, experimental studies have clearly demonstrated that this metalloid can also cure lymphoproliferative and/or pro-inflammatory syndromes in different murine models of chronic immune-mediated diseases. T helper (Th) 1 and Th17 lymphocytes play a central role in development of these diseases, in mice and humans, especially by secreting the potent pro-inflammatory cytokine interferon-γ and IL-17A, respectively. As(III) impairs basic functions of human T cells but its ability to modulate secretion of pro-inflammatory cytokines by differentiated Th lymphocytes is unknown. In the present study, we demonstrate that As(III), used at concentrations clinically achievable in plasma of patients, has no effect on the secretion of interferon-γ from Th1 cells but almost totally blocks the expression and the release of IL-17A from human Th17 lymphocytes co-stimulated for five days with anti-CD3 and anti-CD28 antibodies, in the presence of differentiating cytokines. In addition, As(III) specifically reduces mRNA levels of the retinoic-related orphan receptor (ROR)C gene which encodes RORγt, a key transcription factor controlling optimal IL-17 expression in fully differentiated Th17 cells. The metalloid also blocks initial expression of IL-17 gene induced by the co-stimulation, probably in part by impairing activation of the JNK/c-Jun pathway. In conclusion, our results demonstrate that As(III) represses expression of the major pro-inflammatory cytokine IL-17A produced by human Th17 lymphocytes, thus strengthening the idea that As(III) may be useful to treat inflammatory immune-mediated diseases in humans.
ISSN: 0041-008X

inserm-00872871
http://www.hal.inserm.fr/inserm-00872871
DOI : 10.1016/j.taap.2012.05.004
PUBMED : 22617429

Éditeur(s) : Paris : Marpon et Flammarion
Siècle(s) traité(s) : 19
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/ADG18176
ADG18176

Éditeur(s) : HAL CCSD
Résumé : International audience
Fucoxanthin is a carotenoid present in brown micro-and macro algae, that induces apoptosis or autophagy in cancer cells grown in vitro. In vivo studies confirmed its interest as a natural anticancer compound, as it exerts antitumoral, antimetastatic and antiangiogenic activities in animal models. Studies focused on the pharmacology of fucoxanthin in cancer cells and tumors have revealed that it affects a wide panel of cellular, molecular and tissular processes, suggesting that its biological activity may be related in part to a nonspecific integration in cell membranes, and possible interaction with lipid rafts. Thus, preliminary data confirming this interaction of fucoxanthin with lipid rafts were obtained in mast cells and hepatoma WIF-B9 cells. We here discuss this hypothesis, in view of the critical function of lipid rafts in cancer cell survival, invasivity and communication with the tumoral microenvironment.
ISSN: 2141-2294

hal-01391001
https://hal.archives-ouvertes.fr/hal-01391001
https://hal.archives-ouvertes.fr/hal-01391001/document
https://hal.archives-ouvertes.fr/hal-01391001/file/could-fucoxanthin-interaction-with-lipid-rafts-mediate-its-cytotoxicity-incancer-cells-.pdf
DOI : 10.4172/jomr.1000144

Éditeur(s) : Londres
Siècle(s) traité(s) : 15
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/ADG18250
ADG18250

Éditeur(s) : Paris : Julien, Lanier, Cosnard
Extrait de : Voyages et travaux des missionnaires de la Compagnie de Jésus pour servir de complément aux Lettres édifiantes, publiés par des pères de la même compagnie
Description : Tome 1 de "Voyages et travaux des missionnaires de la Compagnie de Jésus pour servir de complément aux Lettres édifiantes, publiés par des pères de la même compagnie"
Siècle(s) traité(s) : 17
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11074
FRA11074

Éditeur(s) : Paris : Librairie commerciale

Droits : Domaine public
Provenance : Université de Nantes. Service commun de la documentation
Permalien : http://www.manioc.org/patrimon/NAN13059-1
NAN13059-1