Auswahl der wissenschaftlichen Literatur zum Thema „Fonctions hépatiques“
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Zeitschriftenartikel zum Thema "Fonctions hépatiques"
Bernard, Pauline, Ghita Benchekroun und Stéphane Blot. „Classification et diagnostic des insuffisances hépatiques congénitales chez le chien : les shunts porto-systémiques mais pas que…“. Le Nouveau Praticien Vétérinaire canine & féline 20, Nr. 83 (Mai 2023): 44–51. http://dx.doi.org/10.1051/npvcafe/2023025.
Der volle Inhalt der QuelleSauvet, P., und L. Schouler. „Oméprazole et fonctions hépatiques“. La Revue de Médecine Interne 13, Nr. 5 (September 1992): 359–63. http://dx.doi.org/10.1016/s0248-8663(05)81200-7.
Der volle Inhalt der QuelleLuce, Eléanor, Antonietta Messina, Amandine Caillaud, Karim Si-Tayeb, Bertrand Cariou, Etienne Bur, Anne Dubart-Kupperschmitt und Jean-Charles Duclos-Vallée. „Les organoïdes hépatiques“. médecine/sciences 37, Nr. 10 (Oktober 2021): 902–9. http://dx.doi.org/10.1051/medsci/2021119.
Der volle Inhalt der QuelleBastin, Jean, und Fatima Djouadi. „Anomalies de la β-oxydation mitochondriale des acides gras“. médecine/sciences 35, Nr. 10 (Oktober 2019): 779–86. http://dx.doi.org/10.1051/medsci/2019156.
Der volle Inhalt der QuelleDharancy, S., M. Body-Malapel, A. Louvet, D. Berrebi, P. Gosset, J. Viala, D. Philpott et al. „CO.49 Le récepteur aux composés bactériens NOD1 régule les fonctions du neutrophile au cours des pathologies hépatiques“. Gastroentérologie Clinique et Biologique 33, Nr. 3 (März 2009): A121. http://dx.doi.org/10.1016/s0399-8320(09)72837-4.
Der volle Inhalt der QuelleFausther, Michel, und Jean Sévigny. „Les nucléosides et nucléotides extracellulaires régulent les fonctions hépatiques par le biais d’un système complexe de protéines membranaires“. Comptes Rendus Biologies 334, Nr. 2 (Februar 2011): 100–117. http://dx.doi.org/10.1016/j.crvi.2010.12.005.
Der volle Inhalt der QuelleAllaert, F. „P208 Évaluation des effets d’Han Hepa® sur les fonctions hépatiques : une étude contrôlée, randomisée et menée en double aveugle vs placebo“. Cahiers de Nutrition et de Diététique 48 (Dezember 2013): S159. http://dx.doi.org/10.1016/s0007-9960(13)70565-0.
Der volle Inhalt der QuelleAllaert, F. „P208 Évaluation des effets d’Han Hepa® sur les fonctions hépatiques : une étude contrôlée, randomisée et menée en double aveugle vs placebo“. Nutrition Clinique et Métabolisme 27 (Dezember 2013): S159. http://dx.doi.org/10.1016/s0985-0562(13)70539-9.
Der volle Inhalt der QuelleDonné, Romain, Maëva Saroul, Vanessa Maillet, Séverine Celton-Morizur und Chantal Desdouets. „La polyploïdie hépatique“. médecine/sciences 35, Nr. 6-7 (Juni 2019): 519–26. http://dx.doi.org/10.1051/medsci/2019094.
Der volle Inhalt der QuelleSuleman, Adam, Nigel Champion und Yuna Lee. „An Unusual Mimicker of Tumor Lysis Syndrome with Hepatic and Renal Failure“. Canadian Journal of General Internal Medicine 16, Nr. 4 (20.12.2021): 53–58. http://dx.doi.org/10.22374/cjgim.v16i4.518.
Der volle Inhalt der QuelleDissertationen zum Thema "Fonctions hépatiques"
Mion, François. „Exploration des fonctions métaboliques hépatiques : intérêts et limites des tests respiratoires utilisant le carbone 13“. Lyon 1, 1996. http://www.theses.fr/1996LYO1T054.
Der volle Inhalt der QuellePastor, Catherine M. „Modifications de la circulation et des fonctions hépatiques au cours du choc endotoxinique : rôle du monoxyde d'azote (NO)“. Paris 5, 1995. http://www.theses.fr/1995PA05CD05.
Der volle Inhalt der QuelleNG-Bonaventure, Kim Heng. „Clonage d'une séquence d'ADN de foie humain qui rétablit l'expression des fonctions hépatiques dans une cellule dédifférenciée d'hépatome de rat“. Paris 7, 1990. http://www.theses.fr/1990PA077071.
Der volle Inhalt der QuelleBosquier, Hélène. „Maintien de fonctions hépatospécifiques du métabolisme des xénobiotiques dans une lignée hépatocytaire (mhPKT) issue d'une souris transgénique exprimant L-PK/TAg“. Paris 5, 1997. http://www.theses.fr/1997PA05P003.
Der volle Inhalt der QuelleSafwan, Zaiter Hasan. „Le marqueur de sénescence p16Ink4a dans le développement, l'âge adulte et le vieillissement“. Electronic Thesis or Diss., Université Côte d'Azur, 2023. http://www.theses.fr/2023COAZ6029.
Der volle Inhalt der QuelleAging is a biological feature that is characterized by gradual degeneration of function of cells, tissues, organs, or an intact organism due to accumulation of environmental factors and stresses with time. Several factors have been attributed to aging such as oxidative stress, telomere shortening, DNA damage and most importantly, the deposit of senescent cells (SnCs). These are irreversibly mitotically inactive, yet metabolically active cells. The reason underlying their senescence lies within the extrinsic and the intrinsic arms. The extrinsic arm is mainly characterized by the expression and the secretory profile known as the senescence associated secretory phenotype (SASP). The intrinsic arm results from the impact of several genes meant to regulate the cell cycle, such as the tumor suppressor genes p16Ink4a (p16), p19ARF (p19) and p21. P16 is a tumor suppressor and cell cycle regulator that has been linked to aging and senescence. Extensive research has revealed that p16 expression is significantly increased in SnCs, as well as during natural aging or age-related pathologies. Based on this fact, p16 is considered as a specific biomarker for identifying SnCs and aging. Whilst a potential role of p19 and p21 has been demonstrated in embryonic development, yet p16 has been less well documented. To investigate p16's potential role in development, we conducted a developmental expression study of p16, beside the tumor suppressors p19 and p21, and examined their RNA expression in the brain, heart, liver, and kidney of mice at embryonic, postnatal, adult, and old ages. Moreover, immunohistochemistry (IHC) was used to examine p16 expression at the protein level. We found that p16 expression was highly dynamic in all organs during embryonic and postnatal stages, and it was significantly more upregulated in old mice compared to p19 and p21. Furthermore, we found that p16 mRNA and protein were more prevalent in liver endothelial cells (ECs) than parenchymal cells in old mice. These findings point to a possible role for p16 in embryonic development, as well as a potential selective role for p16 in liver ECs.Therefore, we aimed at better understanding the role of p16 in biological processes of liver ECs Hence, we used small hairpin (shRNA) constructs and a p16 cDNA-GFP vector transduced via a lentivirus, to knock-down and over-express p16 in-vitro, in order to assess the loss and gain of function in two types of liver ECs, CD31+ vascular ECs and CD146+ sinusoidal endothelial cells (LSECs). Cells were isolated from the liver through magnetic activated cells sorting (MACS) assay using a magnetic bead-attached monoclonal antibodies against CD31 and CD146 surface markers. Non-coding sequence and an empty-GFP vector transduced cells were used as a control for shRNA and p16-GFP transduced cells, respectively
Margall, Ducos Germain. „La ploïdie hépatique : mécanismes et fonctions“. Paris 6, 2008. http://www.theses.fr/2008PA066068.
Der volle Inhalt der QuelleAdler, Michael. „Contribution à l'étude de la fonction hépatique: application pour l'indication d'une transplantation hépatique“. Doctoral thesis, Universite Libre de Bruxelles, 1990. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213099.
Der volle Inhalt der QuelleHajdari, Shefqet. „Fonctions des protéines HP1 dans l'homéostasie du foie“. Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT079.
Der volle Inhalt der QuelleChromatin is known for its essential role in establishment and maintenance of cellular identity. Accordingly, disturbances in chromatin’s dynamics are common events in cancers. Chromatin structure and dynamics is highly dependent upon HP1, small non-histone chromosomal proteins that are known to be involved in heterochromatin silencing but also in gene expression regulation, DNA replication and DNA damage repair. To better characterize HP1 functions in mammals, we have studied the consequences of the inactivation of the corresponding genes in mice. Unexpectedly, we demonstrated that inactivation of either HP1a or HP1g lead to a high predisposition of mice to develop tumors specifically within liver. Hence, we established mice models allowing simultaneous inactivation of HP1a/HP1b and HP1a/HP1g specifically within hepatocytes. These models (HP1abliverKO and HP1agliverKO) displayed a significant increased incidence of tumor development within liver, demonstrating that HP1 are liver specific tumor suppressors. Histological analysis of HP1abliverKO livers showed defects that resembled those observed in a human liver pathology known as nonalcoholic steatohepatitis (NASH) characterized by an increase of steatosis, followed by an increased inflammation and the development of fibrosis that finally leads to tumors in old animals. In the case of HP1agliverKO mice, even though inflammation and tumor development were observed, this was not linked with steatosis, strongly suggesting that the underlying mechanisms are specific of each HP1 isoform. In order to reveal molecular mechanisms, we did expression analysis in the liver of 5 weeks old mice, which revealed a strong enrichment of genes encoding for members of the KRAB-ZFP of transcriptional repressors family within genes regulated by HP1ag or HP1ab. This result is of particular interest since it is known that these repressors are regulated by the corepressor TRIM28 which has been shown to require its interaction with HP1 to fulfill its functions suggesting a loop of auto-regulation between HP1, TRIM28 and KRAB-ZFP. Using mice expressing a TRIM28 protein unable to interact with HP1 specifically within hepatocytes, we demonstrated here that the disruption of the interaction between TRIM28 and HP1 lead to spontaneous development of tumors within liver and to over-expression of the same KRAB-ZFP as those deregulated in HP1abliverKO and HP1agliverKO mice. Chromatin immunoprecipitation (ChIP) pinpointed that TRIM28 and HP1 are inter-dependently recruited to the 5’ and/or 3’ ends of KRAB-ZFP genes to regulate their expression. We also observed deregulation of some cancer related genes, such as Tert (Telomerase reverse transcriptase), Nox4 (NADPH oxidase 4), AR (Androgen receptor), GPC3 (Glypican3), Arid1a (AT-Rich Interaction Domain 1A), and interestingly these alterations are depended upon the inactivated HP1 isotype, reflecting distinct molecular oncogenesis. In order to elucidate the possible impact of HP1 on global organization of the nucleus, I performed immunofluorescence analysis in the liver cryosections of 5 weeks old mice. Our data suggest that constitutive heterochromatic features (H3K9me3) are replaced by facultative heterochromatic features (H3K27me3) in absence of HP1ag and that heterochromatic pericentric foci tend to slightly be delocalized. Finally, to better understand the chromosomal rearrangements profile in HP1-dependent liver tumor, we performed Comparative genomic hybridization (CGH) in old tumoral liver. As anticipated, multiple events of gain and loss in copy number variations (CNV) in subchromosomal regions were observed, especially for chromosomes 4, where some KRAB-ZFP members are affected. Altogether, our data demonstrated that HP1 are liver-specific tumor suppressor. They also suggest that HP1 main function within liver is to regulate TRIM28 activity and thereby regulate the expression and repression activity of KRAB-ZFP and ultimately liver homeostasis
Comte, Blandine. „Néoglucogénèse à partir du glycérol dans les cellules hépatiques isolées de rat : utilisation des isotopes stables“. Lyon 1, 1990. http://www.theses.fr/1990LYO1T059.
Der volle Inhalt der QuelleFirrincieli, Delphine. „Le récepteur nucléaire de la vitamine D en physiopathologie hépatique : fonctions protectrices dans l'épithélium biliaire“. Paris 6, 2012. http://www.theses.fr/2012PA066186.
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Bertrand, A. M., L. Theuriet, M. Colle, C. Pienkowski, S. Soskin, O. Richard, F. Huet et al. „Syndrome de Turner et fonction hépatique chez l’enfant et l’adolescente“. In Le syndrome de Turner, 123–34. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-87855-8_12.
Der volle Inhalt der QuelleRoy, P. „Conséquences de l'altération de la fonction hépatique“. In Pharmacie Clinique Pratique en Oncologie, 115–18. Elsevier, 2020. http://dx.doi.org/10.1016/b978-2-294-76375-5.00014-2.
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