Éditeur(s) : Cayenne : Imprimerie Emilio Gratien
Siècle(s) traité(s) : 20
Droits : Domaine public
Provenance : Ville de Pointe-à-Pitre. Réseau des bibliothèques
Permalien : http://www.manioc.org/patrimon/PAP11040
PAP11040

Éditeur(s) : Basse-Terre : Hôtel du Gouvernement
Siècle(s) traité(s) : 16
Droits : Domaine public
Provenance : Conseil départemental de la Guadeloupe. La Médiathèque Caraïbe
Permalien : http://www.manioc.org/patrimon/LAM17001
LAM17001

Éditeur(s) : HAL CCSD American Society of Nephrology
Résumé : International audience
Since the recent publication of data showing favorable outcomes for patients with HIV-1 and ESRD, kidney transplantation has become a therapeutic option in this population. However, reports have documented unexplained reduced allograft survival in these patients. We hypothesized that the unrecognized infection of the transplanted kidney by HIV-1 can compromise long-term allograft function. Using electron microscopy and molecular biology, we examined protocol renal transplant biopsies from 19 recipients with HIV-1 who did not have detectable levels of plasma HIV-1 RNA at transplantation. We found that HIV-1 infected the kidney allograft in 68% of these patients. Notably, HIV-1 infection was detected in either podocytes predominately (38% of recipients) or tubular cells only (62% of recipients). Podocyte infection associated with podocyte apoptosis and loss of differentiation markers as well as a faster decline in allograft function compared with tubular cell infection. In allografts with tubular cell infection, epithelial cells of the proximal convoluted tubules frequently contained abnormal mitochondria, and both patients who developed features of subclinical acute cellular rejection had allografts with tubular cell infection. Finally, we provide a novel noninvasive test for determining HIV-1 infection of the kidney allograft by measuring HIV-1 DNA and RNA levels in patients' urine. In conclusion, HIV-1 can infect kidney allografts after transplantation despite undetectable viremia, and this infection might influence graft outcome.
ISSN: 1046-6673

hal-01121764
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01121764
DOI : 10.1681/ASN.2013050564
PUBMED : 24309185
PUBMEDCENTRAL : PMC3904571

Éditeur(s) : Basse-Terre : Imp. du Gouvernement

Droits : Domaine public
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/ADG17092
ADG17092

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) : HAL CCSD
Résumé : International audience
o abstract
1st International Conference of the Marine Fungal Natural Products Consortium (MaFNaP2015), joint with the 14th International Marine and Freshwater Mycology Symposium
Nantes, France

hal-01444924
http://hal.univ-reunion.fr/hal-01444924

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
BACKGROUND AND AIMS: Infection by hepatitis C virus is a worldwide health problem. An inadequate Th2 cytokine response promotes the fibrosis-cirrhosis fate. Immune-modulating molecules favoring a Th2 profile, such as HLA-G molecules of the HLA class Ib family, may play a role in chronic hepatitis. HLA-G contributes to the escape of tumors, and their involvement in viral infections has been increasingly described. The aim of this work was to study the expression of HLA-G in the liver, its cellular source and its regulation in cases of chronic C hepatitis. METHODS: HLA-G cells in blocks of liver derived from patients infected with HCV were labeled by immunohistochemistry and enumerated. Double immunofluorescence allowed the identification of the cellular source. HLA-G secretion by a human mast cell line was quantified by ELISA after various stimulations. After treatment with IFN-α real-time PCR was performed to determine the kinetics of cytokine expression profiles, followed by heat map clustering analysis. RESULTS: The number of HLA-G + cells was significantly associated with the area of fibrosis. For the first time, we identify the HLA-G+ cells as being mast cells. HLA-G secretion was significantly induced in human mast cells stimulated by IL-10 or interferons of class I. The transcriptome of the secretome of this cell line stimulated by IFN-α revealed that i) the HLA-G gene is upregulated late, ii) T lymphocytes and NK cells are recruited. CONCLUSIONS: These findings suggest an autocrine loop in the genesis of HCV liver fibrosis, based on mast cells expressing HLA-G.
ISSN: 0168-8278

hal-00874106
https://hal.archives-ouvertes.fr/hal-00874106
https://hal.archives-ouvertes.fr/hal-00874106/document
https://hal.archives-ouvertes.fr/hal-00874106/file/Amiot-Expression-HLA-G-revised.pdf
DOI : 10.1016/j.jhep.2013.09.006

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

Éditeur(s) : Lyon : chez l'éditeur des annales
Extrait de : Collection faisant suite aux lettres édifiantes
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Archives territoriales de Guyane
Permalien : http://www.manioc.org/patrimon/GAD11046
GAD11046

Éditeur(s) : Basse-Terre : Imprimerie catholique
Résumé : Publié à l'occasion du Tricentenaire des Antilles
Siècle(s) traité(s) : 20
Droits : Domaine public
Provenance : Ville de Pointe-à-Pitre. Réseau des bibliothèques
Permalien : http://www.manioc.org/patrimon/PAP11061
PAP11061

Éditeur(s) : Paris : Victor Retaux et fils
Siècle(s) traité(s) : 19
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/ADG18115
ADG18115

Éditeur(s) : Paris : Armand Colin
Résumé : In-18, VII-375 p.
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/ADG17007
ADG17007

Éditeur(s) : Paris : A. Faivre
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Ville de Pointe-à-Pitre. Réseau des bibliothèques
Permalien : http://www.manioc.org/patrimon/PAP11045
PAP11045

Date de création : 1895-01-01

Éditeur(s) : Strasbourg : F.-X. Le Roux
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Collectivité territoriale de Guyane. Bibliothèque Alexandre-Franconie
Permalien : http://www.manioc.org/patrimon/FRA11034
FRA11034

Éditeur(s) : Lyon : chez l'éditeur des annales
Extrait de : Collection faisant suite aux lettres édifiantes
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Archives territoriales de Guyane
Permalien : http://www.manioc.org/patrimon/GAD11042
GAD11042

Éditeur(s) : Paris : Didier et Cie
Siècle(s) traité(s) : 18
Droits : Domaine public
Provenance : Collectivité territoriale de Martinique. Bibliothèque Schoelcher
Permalien : http://www.manioc.org/patrimon/SCH13237
SCH13237

Éditeur(s) : Paris : Imprimerie d' E. Duverger
Résumé : 2 Vol.
Siècle(s) traité(s) : 19
Droits : Domaine public
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/ADG17117
ADG17117

Éditeur(s) : Paris : Librairie Victor Lecoffre Paris : Librairie catholique internationale
Siècle(s) traité(s) : 18
Droits : Domaine public
Provenance : Conseil départemental de la Guadeloupe. La Médiathèque Caraïbe
Permalien : http://www.manioc.org/patrimon/LAM17012
LAM17012

Éditeur(s) : Paris : Colnet
Résumé : 3 vol. in-8° , cartes et plans
Siècle(s) traité(s) : 18
Droits : Domaine public
Provenance : Archives départementales de Guadeloupe
Permalien : http://www.manioc.org/patrimon/ADG17006
ADG17006

Éditeur(s) : HAL CCSD BioMed Central
Résumé : International audience
ISSN: 1742-4690

inserm-00868818
http://www.hal.inserm.fr/inserm-00868818
http://www.hal.inserm.fr/inserm-00868818/document
http://www.hal.inserm.fr/inserm-00868818/file/1742-4690-10-S1-P26.pdf
DOI : 10.1186/1742-4690-10-S1-P26