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Biblio - Bibliographie IAL
Bibliographie IAL

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Recherche bibliographique scientifique

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Accueil > Références bibliographiques

biblio

2014


  • Laverdet, B, Micallef, L, Lebreton, C, Mollard, J, Lataillade, J-J, Coulomb, B & Desmoulière, A 2014, « Use of mesenchymal stem cells for cutaneous repair and skin substitute elaboration », Pathologie-biologie, vol. 62, no. 2, p. 108-117.
    Résumé : Human mesenchymal stem cells (MSCs) are a heterogeneous population of fibroblast-like cells, which are present in different locations, including bone marrow, adipose tissue, extra-foetal tissues, gingiva and dermis. MSCs, which present multipotency capacities, important expansive potential and immunotolerance properties, remain an attractive tool for tissue repair and regenerative medicine. Currently, several studies and clinical trials highlight the use of MSCs in cutaneous repair underlining that their effects are essentially due to the numerous factors that they release. MSCs are also used in skin substitute development. In this study, we will first discuss the different sources of MSCs actually available. We will then present results showing that bone marrow-derived MSCs prepared according to Good Manufacturing Practices and included in a dermal equivalent are able to promote appropriate epidermis growth and differentiation. These data demonstrate that bone marrow-derived MSCs represent a satisfactory alternative to dermal fibroblasts in order to develop skin substitute. In addition, MSCs could provide a useful alternative to sustain epidermis development and to promote wound healing.

  • Levesque, E, Hoti, E, Azoulay, D, Ichai, P, Samuel, D & Saliba, F 2014, « The implementation of an Intensive Care Information System allows shortening the ICU length of stay », Journal of Clinical Monitoring and Computing.
    Résumé : Intensive care information systems (ICIS) implemented in intensive care unit (ICU) were shown to improve patient safety, reduce medical errors and increase the time devolved by medical/nursing staff to patients care. Data on the real impact of ICIS on patient outcome are scarce. This study aimed to evaluate the effects of ICIS on the outcome of critically-ill patients. From January 2004 to August 2006, 1,397 patients admitted to our ICU were enrolled in this observational study. This period was divided in two phases: before the implementation of ICIS (BEFORE) and after implementation of ICIS (AFTER). We compared standard ICU patient's outcomes: mortality, length of stay in ICU, hospital stay, and the re-admission rate depending upon BEFORE and AFTER. Although patients admitted AFTER were more severely ill than those of BEFORE (SAPS II: 32.1 ± 17.5 vs. 30.5 ± 18.5, p = 0.014, respectively), their ICU length of stay was significantly shorter (8.4 ± 15.2 vs. 6.8 ± 12.9 days; p = 0.048) while the re-admission rate and mortality rate were similar (4.4 vs. 4.2 %; p = 0.86, and 9.6 vs 11.2 % p = 0.35, respectively) in patients admitted AFTER. We observed that the implementation of ICIS allowed shortening of ICU length of stay without altering other patient outcomes.

  • Levesque, E, Saliba, F, Ichaï, P & Samuel, D 2014, « Outcome of patients with cirrhosis requiring mechanical ventilation in ICU », Journal of Hepatology, vol. 60, no. 3, p. 570-578.
    Résumé : INTRODUCTION: Mortality rate of patients with cirrhosis admitted to the intensive care unit (ICU) and requiring mechanical ventilation varies between 60 and 91%. The aim of our study is to assess the prognosis of these patients, their 1-year outcome and to analyze predictive factors of long-term mortality. METHODS: From May 2005 to May 2011, we studied 246 consecutive patients with cirrhosis requiring mechanical ventilation either at admission or during their ICU stay. RESULTS: Alcohol was the most common etiology of the cirrhosis (69%). Bleeding related to portal hypertension (30%) and severe sepsis (33%) were the most common reasons for admission. ICU and hospital mortality were respectively 65.9% and 70.3%. Prognostic severity scores, the need for other organ support therapy, infection, and total bilirubin value at ICU admission were significantly associated with ICU mortality. Eighty-four patients (34.1%) were discharged from the ICU. Among these patients, the one-year survival was only of 32%. Logistic regression analysis, using survival at one year as the endpoint, identified two independent risk factors: the length of ventilation (odds ratio [OR] = 1.1; 95% CI, 1.0-1.2; p = 0.02) and total bilirubin at ICU discharge (OR = 1.3; 95% CI, 1.1-1.5; p = 0.006). CONCLUSION: Patients with cirrhosis admitted to the liver ICU and who required mechanical ventilation have a poor prognosis with a 1-year mortality of 89%. At ICU discharge, a total bilirubin level higher than 64.5 μmol/L and length of ventilation higher than 9 days could help the hepatologists to identify patients at risk of death in the year following the ICU discharge.

  • Negroni, E, Henault, E, Chevalier, F, Gilbert-Sirieix, M, Van Kuppevelt, TH, Papy-Garcia, D, Uzan, G & Albanese, P 2014, « Glycosaminoglycan modifications in duchenne muscular dystrophy: specific remodeling of chondroitin sulfate/dermatan sulfate », Journal of Neuropathology and Experimental Neurology, vol. 73, no. 8, p. 789-797.
    Résumé : Widespread skeletal muscle degeneration and impaired regeneration lead to progressive muscle weakness and premature death in patients with Duchenne muscular dystrophy (DMD). Dystrophic muscles are progressively replaced by nonfunctional tissue because of exhaustion of muscle precursor cells and excessive accumulation of extracellular matrix (ECM). Sulfated glycosaminoglycans (GAGs) are components of the ECM and are increasingly implicated in the regulation of biologic processes, but their possible role in the progression of DMD pathology is not understood. In the present study, we performed immunohistochemical and biochemical analyses of endogenous GAGs in skeletal muscle biopsies of 10 DMD patients and 11 healthy individuals (controls). Immunostaining targeted to specific GAG species showed greater deposition of chondroitin sulfate (CS)/dermatan (DS) sulfate in DMD patient biopsies versus control biopsies. The selective accumulation of CS/DS in DMD biopsies was confirmed by biochemical quantification assay. In addition, high-performance liquid chromatography analysis demonstrated a modification of the sulfation pattern of CS/DS disaccharide units in DMD muscles. In conclusion, our data open up a new path of investigation and suggest that GAGs could represent a new and original therapeutic target for improving the success of gene or cell therapy for the treatment of muscular dystrophies.

  • Pourcelot, M & Arnoult, D 2014, « Mitochondrial Dynamics and The Innate Anti-Viral Immune Response », The FEBS journal.
    Résumé : The innate immune system has a key role in the mammalian immune response. In the cytosol, RNA viruses are sensed by the RIG-I-like receptors (RLRs) that trigger a complex signaling cascade where the mitochondrial antiviral signaling (MAVS) protein plays a central role in mediating the innate host response through the induction of antiviral and inflammatory responses. Hence, mitochondria are now emerging as a fundamental hub for innate anti-viral immunity beyond their known roles in the metabolic processes and the control of programmed cell death. This review summarizes the findings related to the MAVS protein, mitochondria and their dynamics, in the innate immune response to RNA viruses. This article is protected by copyright. All rights reserved.

  • Proust, R, Crouin, C, Gandji, LY, Bertoglio, J & Gesbert, F 2014, « The adaptor protein SAP directly associates with PECAM-1 and regulates PECAM-1-mediated-cell adhesion in T-like cell lines », Molecular Immunology, vol. 58, no. 2, p. 206-213.
    Résumé : SAP is a small cytosolic adaptor protein expressed in hematopoietic lineages whose main function is to regulate intracellular signaling pathways induced by the triggering of members of the SLAM receptor family. In this paper, we have identified the adhesion molecule PECAM-1 as a new partner for SAP in a conditional yeast two-hybrid screen. PECAM-1 is an immunoglobulin-like molecule expressed by endothelial cells and leukocytes, which possesses both pro- and anti-inflammatory properties. However, little is known about PECAM-1 functions in T cells. We show that SAP directly and specifically interacts with the cytosolic tyrosine 686 of PECAM-1. We generated different T-like cell lines in which SAP or PECAM-1 are expressed or down modulated and we demonstrate that a diminished SAP expression correlates with a diminished PECAM-1-mediated adhesion. Although SAP has mainly been shown to associate with SLAM receptors, we evidence here that SAP is a new actor downstream of PECAM-1.
    Mots-clés : Amino Acid Sequence, Antigens, CD31, Base Sequence, Cell Adhesion, Cell Line, HeLa Cells, Humans, Intracellular Signaling Peptides and Proteins, Jurkat Cells, Molecular Sequence Data, Protein Binding, Protein Interaction Domains and Motifs, T-Lymphocytes.

  • Roche, B & Samuel, D 2014, « Prevention of hepatitis B virus reinfection in liver transplant recipients », Intervirology, vol. 57, no. 3-4, p. 196-201.
    Résumé : Antiviral therapy using newer nucleos(t)ide analogues with lower resistance rates such as entecavir or tenofovir could suppress hepatitis B virus (HBV) replication, improve liver function, delay or obviate the need for liver transplantation in some patients, and reduce the risk of HBV recurrence. The combination of long-term antiviral and low-dose hepatitis B immune globulin (HBIG) can effectively prevent HBV recurrence in more than 90% of transplant recipients. Some form of HBV prophylaxis needs be continued indefinitely after transplantation. However, in patients with a low risk of HBV recurrence (i.e. HBV DNA levels undetectable before transplantation), it is possible to discontinue HBIG and maintain long-term antiviral therapy. A more cautious approach to prophylaxis regimen is necessary for those patients with high pretransplant HBV DNA levels, those with limited antiviral options if HBV recurrence occurs (i.e. HIV or HDV coinfection, preexisting drug resistance), those with a high risk of hepatocellular carcinoma recurrence, and those with a risk of noncompliance to antiviral therapy. © 2014 S. Karger AG, Basel.

  • Sebagh, M, Allard, M-A, Cunha, AS, Ruiz, A, Araujo, R, Lemoine, A, Paule, B, Delvart, V, Cherqui, D, Vibert, E & Adam, R 2014, « A proposed new method for assessing the pathological response to chemotherapy in resected colorectal liver metastases », British Journal of Cancer, vol. 111, no. 3, p. 470-476.
    Résumé : Background:Pathological response (PR) to preoperative chemotherapy for colorectal liver metastases (CLM) is recognised as a prognostic factor of outcome. However, the optimal system to assess this parameter is still debated. This study focuses on current methods and proposes a possibly better method for assessing PR.Methods:Among 223 patients resected for CLM between 2004 and 2011, after more than three cycles of chemotherapy, the percentage of tumour cells, necrosis and fibrosis, and the tumour regression grade were assessed for each of 802 nodules. Pathological response was evaluated according to validated methods and their combinations. A new method combined the percentage of tumour cells and the size of all nodules as follows: , where n is each separate nodule, % is the percentage of remaining tumour cells within nodule n (%) and s is the size of nodule n (cm).The prognostic value of each method was calculated.Results:After a median follow-up of 47 months (3-106), the cumulative 5-year overall survival rate after liver resection was 59%. The proposed method categorised as follows: 0 residual tumour; 0.1-6-cm residual tumour; >6-cm residual tumour, and necrosis rate >50% stratified prognosis (P=0.0027; P=0.02), while the other methods did not. At multivariate analysis, our method remained an independent predictor of outcome (P=0.001).Conclusions:Combining the percentage of tumour cells multiplied by the size of each separate tumour seems to be a better method for assessing PR. External validation is required.

  • Siffroi-Fernandez, S, Dulong, S, Li, X-M, Filipski, E, Gréchez-Cassiau, A, Peteri-Brünback, B, Meijer, L, Lévi, F, Teboul, M & Delaunay, F 2014, « Functional genomics identify Birc5/survivin as a candidate gene involved in the chronotoxicity of cyclin-dependent kinase inhibitors », Cell Cycle (Georgetown, Tex.), vol. 13, no. 6, p. 984-991.
    Résumé : The circadian timing system orchestrates most of mammalian physiology and behavior in synchrony with the external light/dark cycle. This regulation is achieved through endogenous clocks present in virtually all body cells, where they control key cellular processes, including metabolism, transport, and the cell cycle. Consistently, it has been observed in preclinical cancer models that both the efficacy and toxicity of most chemotherapeutic drugs depend on their time of administration. To further explore the molecular basis underlying the link between the circadian timing system and the cellular response to anticancer drugs, we investigated the circadian transcriptome and CDK inhibitor toxicity in colon mucosa cells. We first show here that among 181 circadian transcripts, approximately 30% of them drive the cell cycle in the healthy mouse colon mucosa, with a majority peaking during the early resting phase. The identification of 26 mitotic genes within this cluster further indicated that the transcriptional coordination of mitosis by the circadian clock participates in the gating of cell division in this tissue. Subsequent selective siRNA-mediated silencing of these 26 targets revealed that low expression levels of the mitotic and anti-apoptotic gene Birc5/survivin significantly and specifically increased the sensitivity of colon epithelial cells to CDK inhibitors. By identifying Birc5/survivin as a potential determinant for the circadian modulation of CDK inhibitor toxicity, these data provide a mechanistic basis for the preclinical development of future CDK inhibitor-based chronotherapeutic strategies.

  • Sloma, I, Vincent, H, Addebbous, A, Rivoisy, C, Turhan, AG & Michot, J-M 2014, « Haemophagocytic histiocyte in a peripheral blood film », British Journal of Haematology, vol. 165, no. 2, p. 163.
    Résumé : PMID: 24372340
    Mots-clés : Aged, Fatal Outcome, Female, Histiocytes, Humans, Lymphohistiocytosis, Hemophagocytic, Phagocytosis.

  • Steichen, C, Luce, E, Maluenda, J, Tosca, L, Moreno-Gimeno, I, Desterke, C, Dianat, N, Goulinet-Mainot, S, Awan-Toor, S, Burks, D, Marie, J, Weber, A, Tachdjian, G, Melki, J & Dubart-Kupperschmitt, A 2014, « Messenger RNA- versus retrovirus-based induced pluripotent stem cell reprogramming strategies: analysis of genomic integrity », Stem Cells Translational Medicine, vol. 3, no. 6, p. 686-691.
    Résumé : The use of synthetic messenger RNAs to generate human induced pluripotent stem cells (iPSCs) is particularly appealing for potential regenerative medicine applications, because it overcomes the common drawbacks of DNA-based or virus-based reprogramming strategies, including transgene integration in particular. We compared the genomic integrity of mRNA-derived iPSCs with that of retrovirus-derived iPSCs generated in strictly comparable conditions, by single-nucleotide polymorphism (SNP) and copy number variation (CNV) analyses. We showed that mRNA-derived iPSCs do not differ significantly from the parental fibroblasts in SNP analysis, whereas retrovirus-derived iPSCs do. We found that the number of CNVs seemed independent of the reprogramming method, instead appearing to be clone-dependent. Furthermore, differentiation studies indicated that mRNA-derived iPSCs differentiated efficiently into hepatoblasts and that these cells did not load additional CNVs during differentiation. The integration-free hepatoblasts that were generated constitute a new tool for the study of diseased hepatocytes derived from patients' iPSCs and their use in the context of stem cell-derived hepatocyte transplantation. Our findings also highlight the need to conduct careful studies on genome integrity for the selection of iPSC lines before using them for further applications.
    Mots-clés : Cell Differentiation, Cells, Cultured, Cellular Reprogramming, DNA Copy Number Variations, Fibroblasts, Gene Expression Profiling, Gene Expression Regulation, Developmental, Genetic Vectors, Genotype, Hepatocytes, Humans, Induced Pluripotent Stem Cells, Oligonucleotide Array Sequence Analysis, Phenotype, Polymorphism, Single Nucleotide, Retroviridae, RNA, Messenger, Transcription Factors, Transfection.

  • Torossian, F, Anginot, A, Chabanon, A, Clay, D, Guerton, B, Desterke, C, Boutin, L, Marullo, S, Scott, MGH, Lataillade, J-J & Le Bousse-Kerdilès, M-C 2014, « CXCR7 participates in CXCL12-induced CD34+ cell cycling through β-arrestin-dependent Akt activation », Blood, vol. 123, no. 2, p. 191-202.
    Résumé : In addition to its well-known effect on migration and homing of hematopoietic stem/progenitor cells (HSPCs), CXCL12 chemokine also exhibits a cell cycle and survival-promoting factor for human CD34(+) HSPCs. CXCR4 was suggested to be responsible for CXCL12-induced biological effects until the recent discovery of its second receptor, CXCR7. Until now, the participation of CXCR7 in CXCL12-induced HSPC cycling and survival is unknown. We show here that CXCL12 was capable of binding CXCR7 despite its scarce expression at CD34(+) cell surface. Blocking CXCR7 inhibited CXCL12-induced Akt activation as well as the percentage of CD34(+) cells in cycle, colony formation, and survival, demonstrating its participation in CXCL12-induced functional effects in HSPCs. At steady state, CXCR7 and β-arrestin2 co-localized near the plasma membrane of CD34(+) cells. After CXCL12 treatment, β-arrestin2 translocated to the nucleus, and this required both CXCR7 and CXCR4. Silencing β-arrestin expression decreased CXCL12-induced Akt activation in CD34(+) cells. Our results demonstrate for the first time the role of CXCR7, complementary to that played by CXCR4, in the control of HSPC cycling, survival, and colony formation induced by CXCL12. We also provide evidence for the involvement of β-arrestins as signaling hubs downstream of both CXCL12 receptors in primary human HSPCs.
    Mots-clés : Antigens, CD34, Arrestins, Cell Cycle, Cell Survival, Chemokine CXCL12, Colony-Forming Units Assay, Enzyme Activation, Hematopoietic Stem Cells, Humans, Intracellular Space, Phosphorylation, Protein Binding, Protein Transport, Proto-Oncogene Proteins c-akt, Receptors, CXCR.

  • Tran, HV, Piro, B, Reisberg, S, Huy Nguyen, L, Dung Nguyen, T, Duc, HT & Pham, MC 2014, « An electrochemical ELISA-like immunosensor for miRNAs detection based on screen-printed gold electrodes modified with reduced graphene oxide and carbon nanotubes », Biosensors & Bioelectronics, vol. 62, p. 25-30.
    Résumé : We design an electrochemical immunosensor for miRNA detection, based on screen-printed gold electrodes modified with reduced graphene oxide and carbon nanotubes. An original immunological approach is followed, using antibodies directed to DNA.RNA hybrids. An electrochemical ELISA-like amplification strategy was set up using a secondary antibody conjugated to horseradish peroxidase (HRP). Hydroquinone is oxidized into benzoquinone by the HRP/H2O2 catalytic system. In turn, benzoquinone is electroreduced into hydroquinone at the electrode. The catalytic reduction current is related to HRP amount immobilized on the surface, which itself is related to miRNA.DNA surface density on the electrode. This architecture, compared to classical optical detection, lowers the detection limit down to 10fM. Two miRNAs were studied: miR-141 (a prostate biomarker) and miR-29b-1 (a lung cancer biomarker).

  • Vibert, E, Pittau, G, Gelli, M, Cunha, AS, Jamot, L, Faivre, J, Castro Benitez, C, Castaing, D & Adam, R 2014, « Actual incidence and long-term consequences of posthepatectomy liver failure after hepatectomy for colorectal liver metastases », Surgery, vol. 155, no. 1, p. 94-105.
    Résumé : INTRODUCTION: Posthepatectomy liver failure (PHLF) is a severe complication after hepatectomy for colorectal liver metastases. This study evaluated its actual incidence and its effects on short- and long-term overall survival (OS) in a specialized center. MATERIALS AND METHODS: Between 2006 and 2008, 193 patients who underwent 232 hepatectomies (147 minor and 85 major) for colorectal liver metastasis were studied prospectively. Hepatectomy was performed if the remnant liver volume was >0.5% of body weight. Uni- and multivariate analyses on OS after all hepatectomies (n = 232) or major resection only (n = 85) were then performed on pre-, intra-, and postoperative (including pathological) data to determine the consequences of PHLF by comparison with those of other intra- and postoperative events. RESULTS: The 3-month postoperative mortality rate was 0.8%. PHLF was observed in six patients (7%) after major hepatectomy and in one (0.6%) after minor hepatectomy. With a 25-month follow-up, the 2-year OS rate was 84%. Preoperatively, pulmonary metastasis was the only determinant of OS. Intra- and postoperatively, four factors were determinant of OS: PHLF (risk ratio [RR] = 3.84, P = .04), mental confusion (RR = 3.11, P = .006), fluid collection (RR = 2.9, P = .01) and transfusion (RR = 2.27, P = .009). After major hepatectomy, only PHLF (RR = 4.14, P = .01) and confusion (RR = 3.6, P = .02) were identified. CONCLUSION: With improvements in postoperative management, PHLF was found to be less responsible for 3-month mortality but remains an event that exerts a major impact on 2-year survival.
    Mots-clés : Aged, Colorectal Neoplasms, Female, Follow-Up Studies, France, Hepatectomy, Humans, Incidence, Liver, Liver Failure, Liver Neoplasms, Male, Middle Aged, Postoperative Complications, Retrospective Studies.

  • Von den Hoff, JW, Agren, MS, Coulomb, B, Eming, SA & Lataillade, J-J 2014, « The 23rd Annual Meeting of the European Tissue Repair Society (ETRS) in Reims, France », Fibrogenesis & tissue repair, vol. 7, no. 1, p. 3.
    Résumé : The 23rd Annual Meeting of the European Tissue Repair Society, Reims, France, October 23 to 25, 2013 focused on tissue repair and regenerative medicine covering topics such as stem cells, biomaterials, tissue engineering, and burns.

  • Zemirli, N, Pourcelot, M, Ambroise, G, Hatchi, E, Vazquez, A & Arnoult, D 2014, « Mitochondrial hyperfusion promotes NF-κB activation via the mitochondrial E3 ligase MULAN », The FEBS journal, vol. 281, no. 14, p. 3095-3112.
    Résumé : Mitochondria are dynamic organelles with a morphology resulting from the balance between two opposing processes: fusion and fission. Little is known about the function of mitochondrial fusion, beside its role in the maintenance of mitochondrial DNA. We report here that enforced mitochondrial hyperfusion, due to the expression of a dominant-negative mutant of Drp1 or of MARCH5, promotes NF-κB activation in a TAK1- and IKK-dependent manner, through the mitochondrial E3 ubiquitin ligase MULAN. The capability of MULAN to activate NF-κB depends on its RING domain and on the E3 ubiquitin ligase TRAF2. Under physiological conditions, stress-induced mitochondrial hyperfusion (SIMH) is also accompanied by NF-κB activation, and the prevention of SIMH or the knockdown of MULAN impairs NF-κB activation. During SIMH, MULAN forms a complex with TRAF2 and modulates its ubiquitylation, signifying that TRAF2 may serve as an ubiquitylated transmitter of NF-κB signaling in this pathway. Our results suggest that mitochondria, through their dynamics, convert stress signals into a cell response leading to NF-κB activation. STRUCTURED DIGITAL ABSTRACT: TRAF2 physically interacts with MULAN by anti bait coip (View interaction).

  • Zemirli, N, Pourcelot, M, Dogan, N, Vazquez, A & Arnoult, D 2014, « The E3 ubiquitin ligase RNF121 is a positive regulator of NF-κB activation », Cell communication and signaling: CCS, vol. 12, p. 72.
    Résumé : BACKGROUND: The nuclear factor κB (NF-κB) family members regulate several biological processes as cell proliferation and differentiation, inflammation, immunity and tumor progression. Ubiquitination plays a key role in NF-κB activation and the ubiquitylated transmitters of the NF-κB signaling cascade accumulate in close proximity to endomembranes. FINDINGS: We performed an unbiased siRNA library screen targeting the 46 E3 ubiquitin ligases bearing transmembrane domains to uncover new modulators of NF-κB activation, using tumor necrosis factor-α (TNF-α) receptor (TNFR) stimulation as a model. We report here the identification of a new Golgi Apparatus-resident protein, RNF121, as an enhancer of NF-κB promoter activity through the catalytic function of its RING domain. From a molecular standpoint, while knocking down RNF121 did not alter RIP1 ubiquitination and IKK activation, the proteasomal degradation of IκBα was impaired suggesting that this E3 ubiquitin ligase regulates this process. However, RNF121 did not directly ubiquitinate IκBα While they were found in the same complex. Finally, we discovered that RNF121 acts as a broad regulator of NF-κB signaling since its silencing also dampens NF-κB activation following stimulation of Toll-Like Receptors (TLRs), Nod-Like Receptors (NLRs), RIG-I-Like Receptors (RLRs) or after DNA damages. CONCLUSIONS: These results unveil an unexpected role of Golgi Apparatus and reveal RNF121 as a new player involved in the signaling leading to NF-κB activation.

2013


  • Ackermann, O, Gonzales, E, Keller, M, Guettier, C, Gissen, P & Jacquemin, E 2013, « ARC Syndrome Due to VIPAR Mutation is Another Cause of Neonatal Cholestasis with Normal Serum Gammaglutamyl Transferase Activity », J Pediatr Gastroenterol Nutr.
    Résumé : Ackermann, Oanez; Gonzales, Emmanuel; Keller, Marion; Guettier, Catherine; Gissen, Paul; Jacquemin, Emmanuel; J Pediatr Gastroenterol Nutr. 2013 May 1.

  • Addeo, P, Delpero, JR, Paye, F, Oussoultzoglou, E, Fuchshuber, PR, Sauvanet, A, Sa Cunha, A, Le Treut, YP, Adham, M, Mabrut, JY, Chiche, L & Bachellier, P 2013, « Pancreatic fistula after a pancreaticoduodenectomy for ductal adenocarcinoma and its association with morbidity: a multicentre study of the French Surgical Association », HPB (Oxford).
    Résumé : BACKGROUNDS: A pancreatic fistula (PF) is the most relevant complication after a pancreaticoduodenectomy (PD). This retrospective multicentric study attempts to elucidate the risk factors and complications of a PF in a large cohort of patients undergoing a PD for ductal adenocarcinoma. METHODS: Using a survey tool, clinical data of 1325 patients undergoing a PD for ductal adenocarcinoma at 37 institutions, between January 2004 and December 2009, were collected. Peri-operative risk factors associated with PF and its association with morbidity and mortality were assessed. Morbidity and PF were graded according to the ISGPF (International Study group for pancreatic fistula) definition and the Dindo-Clavien classification. RESULTS: Overall PF, mortality, morbidity and relaparotomy rates were 14.3%, 3.8%, 54.4% and 11.7%, respectively. PF occurred more frequently after a pancreaticojejunostomy (PJ) compared with a pancreaticogastrostomy (PG) (16.8% vs. 10.4%; P = 0.0012). Independent risk factors for PF by multivariate analysis were absence of pre-operative diabetes (P = 0.0014), PJ reconstruction (P = 0.0035), soft pancreatic parenchyma (P < 0.0001) and low-volume centre (P = 0.0286). Clinically relevant PF (grade B and C) and severe complications (Dindo-Clavien grade IIIB, IV, V) were significantly more frequent after PJ than PG (71.6% vs. 28.3%; P = 0.030 and 24.8% vs. 19.1%; P = 0.015, respectively). Overall mortality and relaparotomy rates were similar after PG and PJ. CONCLUSIONS: A soft pancreatic parenchyma, the absence of pre-operative diabetes, PJ and low-volume centre are independent risk factors for PF after PD for ductal adenocarcinoma. A significantly higher incidence and clinical severity of PF are associated with PJ.

  • Allard, MA, Adam, R, Ruiz, A, Vibert, E, Paule, B, Levi, F, Sebagh, M, Guettier, C, Azoulay, D & Castaing, D 2013, « Is unexpected peritoneal carcinomatosis still a contraindication for resection of colorectal liver metastases?: Combined resection of colorectal liver metastases with peritoneal deposits discovered intra-operatively », Eur J Surg Oncol.
    Résumé : AIMS: The discovery of unexpected peritoneal carcinomatosis (PC) at the time of hepatectomy for colorectal liver metastases (CLM) is usually considered a contraindication for continuing resection. The first aim of this study was to assess the long-term outcome of patients operated for CLM, and who presented unexpected PC during laparotomy. The second aim was to identify preoperative predictors of PC. METHODS: All patients at a single center between 1985 and 2010 who had unexpected PC, discovered during planed resection of CLM, and negative preoperative imaging for PC were selected. Clinicopathological data were retrospectively analyzed to assess survival outcomes and to identify predictors of unexpected PC. RESULTS: Out of the 1340 operated patients for CLM, 42 (3%) had unexpected PC. Only patients (n = 30; 71%) who had PC limited to two abdominal regions (Median peritoneal cancer index (PCI): 2 (1-6)) were resected. Twelve patients were not resected due to the extent of peritoneal disease. The overall survival of the 30 patients resected for CLM who had limited PC was 18% at 5 years (median: 42 months). On multivariate analysis, a previous history of PC, a pT4 stage and bilobar CLM were independent predictors of unexpected PC. CONCLUSION: Unexpected PC should not be a contraindication for resection provided that the PCI is low and complete resection of all peritoneal and hepatic lesions can be achieved. Previous history of PC, a pT4 primary tumor and bilobar CLM are associated with increased risk of unexpected PC.
  • Andreou, A, Vauthey, JN, Cherqui, D, Zimmitti, G, Ribero, D, Truty, MJ, Wei, SH, Curley, SA, Laurent, A, Poon, RT, Belghiti, J, Nagorney, DM & Aloia, TA 2013, « Improved long-term survival after major resection for hepatocellular carcinoma: a multicenter analysis based on a new definition of major hepatectomy », J Gastrointest Surg, vol. 17, no. 1, p. 66-77; discussion p 77.
    Résumé : BACKGROUND: Advances in the surgical management of hepatocellular carcinoma (HCC) have expanded the indications for curative hepatectomy, including more extensive liver resections. The purpose of this study was to examine long-term survival trends for patients treated with major hepatectomy for HCC. PATIENTS AND METHODS: Clinicopathologic data for 1,115 patients with HCC who underwent hepatectomy between 1981 and 2008 at five hepatobiliary centers in France, China, and the USA were assessed. In addition to other performance metrics, outcomes were evaluated using resection of >/=4 liver segments as a novel definition of major hepatectomy. RESULTS: Major hepatectomy was performed in 539 patients. In the major hepatectomy group, median tumor size was 10 cm (range: 1-27 cm) and 22 % of the patients had bilateral lesions. The TNM Stage distribution included 29 % Stage I, 31 % Stage II, 38 % Stage III, and 2 % Stage IV. The postoperative histologic examination indicated that chronic liver disease was present in 35 % of the patients and tumor microvascular invasion was identified in 60 % of the patients. The 90-day postoperative mortality rate was 4 %. After a median follow-up time of 63 months, the 5-year overall survival rate was 40 %. Patients treated with right hepatectomy (n = 332) and those requiring extended hepatectomy (n = 207) had similar 90-day postoperative mortality rates (4 % and 4 %, respectively, p = 0.976) and 5-year overall survival rates (42 % and 36 %, respectively, p = 0.523). Postoperative mortality and overall survival rates after major hepatectomy were similar among the participating countries (p > 0.1) and improved over time with 5-year survival rates of 30 %, 40 %, and 51 % for the years 1981-1989, 1990-1999, and the most recent era of 2000-2008, respectively (p = 0.004). In multivariate analysis, factors that were significantly associated with worse survivals included AFP level >1,000 ng/mL, tumor size >5 cm, presence of major vascular invasion, presence of extrahepatic metastases, positive surgical margins, and earlier time period in which the major hepatectomy was performed. CONCLUSIONS: This multinational, long-term HCC survival analysis indicates that expansion of surgical indications to include major hepatectomy is justified by the significant improvement in outcomes over the past three decades observed in both the East and the West.
    Mots-clés : 80 and over Carcinoma, Adolescent Adult Aged Aged.


  • Antonini, TM, Lozeron, P, Lacroix, C, Mincheva, Z, Durrbach, A, Slama, M, Vibert, E, Samuel, D & Adams, D 2013, « Reversibility of Acquired Amyloid Polyneuropathy After Liver Retransplantation », Am J Transplant, viewed sans date, .
    Résumé : Domino liver transplantation (DLT) has become an accepted procedure designed to address problems with organ limited supply. However, cases of acquired amyloid neuropathy are increasingly being recognized following this procedure. Until now, only one patient had undergone liver retransplantation and follow-up findings were not reported. We describe the case of a 72-year-old patient with partial recovery from acquired amyloid neuropathy following retransplantation with a deceased donor 7 years after DLT performed for end-stage liver disease. His clinical and paraclinical improvement is described, and the impact of this case on the indication for a domino procedure and the challenges linked to retransplantation are discussed.

  • Aoubid Iaaza, L, Bessede, T, Eschwege, P, Hammoudi, Y, Durrbach, A & Benoit, G 2013, « [Arterial anastomotic aneurysms after kidney and pancreas transplantation: diagnosis and management] », Prog Urol, vol. 23, no. 5, p. 329-35, viewed sans date, .
    Résumé : OBJECTIVE: The objective of our study was to assess the frequency, circumstances of diagnosis and treatment of anastomotic arterial aneurysms and compare them to the literature. MATERIAL AND METHOD: A single-center series of 3000 kidney transplants and 126 pancreas transplants between 1974 and 2010 was studied retrospectively. Ten patients had anastomotic arterial aneurysms: eight after kidney transplantation and two after pancreas-kidney transplantation. Diagnosis was based on the association Doppler ultrasonography-angioscanner. RESULTS: Ten arterial anastomotic aneurysms were identified. The circumstances of discovery were clinical in eight cases, half of them by hemodynamic collapsus. A majority of our patients (60%) were diagnosed in the year following the transplantation and two cases were discovered after transplantectomy. Pancreas-kidney transplantation had a high risk for arterial anastomotic aneurysm. Candida albicans was isolated in preoperative samples in four cases. The management consisted to transplantectomy in seven patients, revascularization of the lower limb in six patients and one renal transplant preservation. We found two lower limb ischemia and two deaths by a fatal intraoperative haemorrhage and vascular cerebral haemorrhage. No recurrence was identified after in the follow-up ranged from 20 months to 12 years. CONCLUSION: Arterial anastomotic aneurysm was in our study a serious complication that requires emergency surgery. The transplantectomy followed by revascularization of the limb is the treatment of choice associated to an appropriate antifungal or antibiotic treatment.
  • Awad, A, Sar, S, Barre, R, Cariven, C, Marin, M, Salles, JP, Erneux, C, Samuel, D & Gassama-Diagne, A 2013, « FSHIP2 regulates epithelial cell polarity through its lipid product, which binds to Dlg1, a pathway subverted by hepatitis C virus core protein », Mol Biol Cell, vol. 24, no. 14, p. 2171-85.
    Résumé : The main targets of hepatitis C virus (HCV) are hepatocytes, the highly polarized cells of the liver, and all the steps of its life cycle are tightly dependent on host lipid metabolism. The interplay between polarity and lipid metabolism in HCV infection has been poorly investigated. Signaling lipids, such as phosphoinositides (PIs), play a vital role in polarity, which depends on the distribution and expression of PI kinases and PI phosphatases. In this study, we report that HCV core protein, expressed in Huh7 and Madin-Darby canine kidney (MDCK) cells, disrupts apicobasal polarity. This is associated with decreased expression of the polarity protein Dlg1 and the PI phosphatase SHIP2, which converts phosphatidylinositol 3,4,5-trisphosphate into phosphatidylinositol 4,5-bisphosphate (PtdIns(3,4)P2). SHIP2 is mainly localized at the basolateral membrane of polarized MDCK cells. In addition, PtdIns(3,4)P2 is able to bind to Dlg1. SHIP2 small interfering RNA or its catalytically dead mutant disrupts apicobasal polarity, similar to HCV core. In core-expressing cells, RhoA activity is inhibited, whereas Rac1 is activated. Of interest, SHIP2 expression rescues polarity, RhoA activation, and restricted core level in MDCK cells. We conclude that SHIP2 is an important regulator of polarity, which is subverted by HCV in epithelial cells. It is suggested that SHIP2 could be a promising target for anti-HCV treatment.
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  • Ballesta, A & Clairambault, J 2013, « Physiologically Based Mathematical Models to Optimize Therapies Against Metastatic Colorectal Cancer: a Mini-Review », Curr Pharm Des, viewed sans date, .
    Résumé : Understanding and improving the effects of combined drug treatments in metastatic colorectal Cancer (mCRC) is a multidisciplinary and multiscale problem, that can benefit from a systems biology approach. Although a quite limited number of active drugs have been approved for clinical applications, a variety of combined delivery regimen options are actually used in the clinic, so that choosing between them, or designing new ones, is not an obvious task, which calls for some rationalization based on physiological principles. We propose some physiologically based molecular pharmacokinetics-pharmacodynamics models for the main cytotoxic drugs used in the clinic and call for others describing more recently used agents, such as associated with monoclonal antibodies. We also advocate simultaneously designing models of the proliferating cell populations under therapeutic control, for cancer is primarily a disruption of physiological control on tissue proliferation. These two types of models are based on differential equations to continuously describe both the fate of drugs in the organism, from infusion until pharmacological effects, and their impact on the proliferation of cell populations, healthy and tumor. The multiscale nature of colorectal cancer, from the disruption of intracellular pathways to tumor growth observed at the macroscopic level, together with its frequent multilocal extension by simultaneous metastases in various healthy tissues of the organism at the time of diagnosis, and later, call for multiscale mathematical models. We thus propose a multi-level vision of cytotoxic drug use in the clinic, in which the weapon in the hands of clinicians, a drug combination regimen, the targets -wanted and unwanted - on which it exerts its effects, molecular pathways in proliferating cell populations, and the environment of the latter in a whole organism, are all considered in order to design a rationale for appropriate shooting, i.e., treatment optimization under patient-tailored constraints.
  • Banares, R, Nevens, F, Larsen, FS, Jalan, R, Albillos, A, Dollinger, M, Saliba, F, Sauerbruch, T, Klammt, S, Ockenga, J, Pares, A, Wendon, J, Brunnler, T, Kramer, L, Mathurin, P, de la Mata, M, Gasbarrini, A, Mullhaupt, B, Wilmer, A, Laleman, W, Eefsen, M, Sen, S, Zipprich, A, Tenorio, T, Pavesi, M, Schmidt, HH, Mitzner, S, Williams, R & Arroyo, V 2013, « Extracorporeal albumin dialysis with the molecular adsorbent recirculating system in acute-on-chronic liver failure: the RELIEF trial », Hepatology, vol. 57, no. 3, p. 1153-62.
    Résumé : Acute-on-chronic liver failure (ACLF) is a frequent cause of death in cirrhosis. Albumin dialysis with the molecular adsorbent recirculating system (MARS) decreases retained substances and improves hemodynamics and hepatic encephalopathy (HE). However, its survival impact is unknown. In all, 189 patients with ACLF were randomized either to MARS (n=95) or to standard therapy (SMT) (n=94). Ten patients (five per group) were excluded due to protocol violations. In addition, 23 patients (MARS: 19; SMT: 4) were excluded from per-protocol (PP) analysis (PP population n=156). Up to 10 6-8-hour MARS sessions were scheduled. The main endpoint was 28-day ITT and PP survival. There were no significant differences at inclusion, although the proportion of patients with Model for Endstage Liver Disease (MELD) score over 20 points and with spontaneous bacterial peritonitis (SBP) as a precipitating event was almost significantly greater in the MARS group. The 28-day survival was similar in the two groups in the ITT and PP populations (60.7% versus 58.9%; 60% versus 59.2% respectively). After adjusting for confounders, a significant beneficial effect of MARS on survival was not observed (odds ratio [OR]: 0.87, 95% confidence interval [CI] 0.44-1.72). MELD score and HE at admission and the increase in serum bilirubin at day 4 were independent predictors of death. At day 4, a greater decrease in serum creatinine (P=0.02) and bilirubin (P=0.001) and a more frequent improvement in HE (from grade II-IV to grade 0-I; 62.5% versus 38.2%; P=0.07) was observed in the MARS group. Severe adverse events were similar. CONCLUSION: At scheduled doses, a beneficial effect on survival of MARS therapy in patients with ACLF could not be demonstrated. However, MARS has an acceptable safety profile, has significant dialysis effect, and nonsignificantly improves severe HE.
    Mots-clés : Adult End Stage Liver Disease/mortality/ therapy Female Hospitalization/statistics & numerical data Humans Liver Cirrhosis/mortality/therapy Liver Failure.

  • Barkholt, L, Flory, E, Jekerle, V, Lucas-Samuel, S, Ahnert, P, Bisset, L, Büscher, D, Fibbe, W, Foussat, A, Kwa, M, Lantz, O, Mačiulaitis, R, Palomäki, T, Schneider, CK, Sensebé, L, Tachdjian, G, Tarte, K, Tosca, L & Salmikangas, P 2013, « Risk of tumorigenicity in mesenchymal stromal cell-based therapies–bridging scientific observations and regulatory viewpoints », Cytotherapy, vol. 15, no. 7, p. 753-9, viewed sans date, .
    Résumé : In the past decade, the therapeutic value of mesenchymal stromal cells (MSCs) has been studied in various indications, thereby taking advantage of their immunosuppressive properties. Easy procurement from bone marrow, adipose tissue or other sources and conventional in vitro expansion culture have made their clinical use attractive. Bridging the gap between current scientific knowledge and regulatory prospects on the transformation potential and possible tumorigenicity of MSCs, the Cell Products Working Party and the Committee for Advanced Therapies organized a meeting with leading European experts in the field of MSCs. This meeting elucidated the risk of potential tumorigenicity related to MSC-based therapies from two angles: the scientific perspective and the regulatory point of view. The conclusions of this meeting, including the current regulatory thinking on quality, nonclinical and clinical aspects for MSCs, are presented in this review, leading to a clearer way forward for the development of such products.
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  • Barrault, C, Roudot-Thoraval, F, Tran Van Nhieu, J, Atanasiu, C, Kluger, MD, Medkour, F, Douvin, C, Mallat, A, Zafrani, ES, Cherqui, D & Duvoux, C 2013, « Non-invasive assessment of liver graft fibrosis by transient elastography after liver transplantation », Clin Res Hepatol Gastroenterol.
    Résumé : BACKGROUND: Liver stiffness measurement (LSM) by transient elastography (TE) (FibroScan((R))) is a validated method of quantifying liver fibrosis in non-transplanted patients with hepatitis C virus (HCV). It could be useful in follow-up after liver transplantation (LT). The aim of this study was to assess the diagnostic accuracy of LSM in evaluating liver fibrosis after LT in patients with and without recurrent HCV. PATIENTS AND METHODS: Forty-three patients (mean age 57.6+/-9.9 years), 28 (65.1%) HCV-positive patients and 15 (34.9%) HCV-negative patients underwent gold standard liver biopsy and TE 55.8+/-4.9 months after transplantation. Liver fibrosis was scored on biopsy specimens according to METAVIR (F0-F4). Accuracy of TE and optimal stiffness cut-off values for fibrosis staging were determined by a receiver-operating characteristics (ROC) curve analysis. RESULTS: Median stiffness values were significantly different for METAVIR score less than 2 (5.8kPa) vs. METAVIR score greater to equal to 2 (9.6kPa) (P<0.001). The area under the ROC curve was 0.83 for METAVIR score greater to equal to 2 (95%CI: 0.71-0.95). The optimal stiffness cut-off value was 7kPa for METAVIR scores greater to equal to 2. The results were similar whether the patients had recurrent HCV infection or not. CONCLUSIONS: These results indicate that transient elastography accurately identifies LT recipients with significant fibrosis, irrespective of HCV status. It is a promising non-invasive tool to assess graft fibrosis progression after LT in patients with HCV recurrence, as well as for screening of late graft fibrosis of other etiologies. Transient elastography could reduce the use of invasive protocol biopsies.
  • Beleoken, E, Sobesky, R, Le Caer, JP, Le Naour, F, Sebagh, M, Moniaux, N, Roche, B, Mustafa, MZ, Guettier, C, Johanet, C, Samuel, D, Bouhris, JH, Duclos-Vallee, JC & Ballot, E 2013, « Immunoproteomic analysis of potentially severe non-graft-versus-host disease hepatitis after allogenic bone marrow transplantation », Hepatology, vol. 57, no. 2, p. 689-99.
    Résumé : The development of potentially severe non-graft-versus-host disease (GVHD) hepatitis resembling autoimmune hepatitis (AIH) has been reported after bone marrow transplantation (BMT). The aim of this study was to better characterize this form of hepatitis, particularly through the identification of autoantigens recognized by patient sera. Five patients who received an allogeneic BMT for the treatment of hematological diseases developed liver dysfunction with histological features suggestive of AIH. Before and during the onset of hepatic dysfunction, sera were tested on immunoblottings performed with cytosolic, microsomal, mitochondrial, and nuclear proteins from rat liver homogenate and resolved by two-dimensional electrophoresis. Antigenic targets were identified by mass spectrometry. During the year that followed BMT, all patients presented with GVHD. Acute hepatitis then occurred after the withdrawal, or during the tapering, of immunosuppressive therapy. At that time, no patients had a history of liver toxic drug absorption, patent viral infection, or any histopathological findings consistent with GVHD. Immunoreactive spots stained by sera collected at the time of hepatic dysfunction were more numerous and more intensely expressed than those stained by sera collected before. Considerable patient-dependent pattern heterogeneity was observed. Among the 259 spots stained exclusively by sera collected at the time of hepatitis, a total of 240 spots were identified, corresponding to 103 different proteins. Twelve of them were recognized by sera from 3 patients. CONCLUSIONS: This is the first immunological description of potentially severe non-GVHD hepatitis occurring after BMT, determined using a proteomic approach and enabling a discussion of the mechanisms that transform an alloimmune reaction into an autoimmune response. Any decision to withdraw immunosuppression after allogeneic BMT should be made with caution.
    Mots-clés : Adult Animals Bone Marrow Transplantation/ adverse effects Female Graft vs Host Disease/ etiology/immunology Hepatitis, Autoimmune/ etiology/immunology Humans Male Middle Aged Proteomics Rats Transplantation, Homologous/ immunology.
  • Benhenda, S, Ducroux, A, Riviere, L, Sobhian, B, Ward, MD, Dion, S, Hantz, O, Protzer, U, Michel, ML, Benkirane, M, Semmes, OJ, Buendia, MA & Neuveut, C 2013, « Methyltransferase PRMT1 is a binding partner of HBx and a negative regulator of hepatitis B virus transcription », J Virol, vol. 87, no. 8, p. 4360-71.
    Résumé : The hepatitis B virus X protein (HBx) is essential for virus replication and has been implicated in the development of liver cancer. HBx is recruited to viral and cellular promoters and activates transcription by interacting with transcription factors and coactivators. Here, we purified HBx-associated factors in nuclear extracts from HepG2 hepatoma cells and identified protein arginine methyltransferase 1 (PRMT1) as a novel HBx-interacting protein. We showed that PRMT1 overexpression reduced the transcription of hepatitis B virus (HBV), and this inhibition was dependent on the methyltransferase function of PRMT1. Conversely, depletion of PRMT1 correlated with increased HBV transcription. Using a quantitative chromatin immunoprecipitation assay, we found that PRMT1 is recruited to HBV DNA, suggesting a direct effect of PRMT1 on the regulation of HBV transcription. Finally, we showed that HBx expression inhibited PRMT1-mediated protein methylation. Downregulation of PRMT1 activity was further observed in HBV-replicating cells in an in vivo animal model. Altogether, our results support the notion that the binding of HBx to PRMT1 might benefit viral replication by relieving the inhibitory activity of PRMT1 on HBV transcription.
    Mots-clés : Genetic Virus Replication.
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  • Benkabbou, A, Castaing, D, Salloum, C, Adam, R, Azoulay, D & Vibert, E 2013, « Treatment of failed Roux-en-Y hepaticojejunostomy after post-cholecystectomy bile ducts injuries », Surgery, vol. 153, no. 1, p. 95-102, viewed sans date, .
    Résumé : BACKGROUND: Roux-en-Y hepaticojejunostomy (RYHJ) is the most well-accepted treatment for most post-cholecystectomy bile duct injuries (BDI). RYHJ failure is a complex situation that requires expert planning and the possibility of using a combination of operative, radiologic, and endoscopic techniques. The aim of this study was to report our experience with a multidisciplinary approach to failed RYHJ after post-cholecystectomy BDI. METHODS: Between January 1996 and March 2008, 44 consecutive patients were managed for RYHJ failure in our department. They presented with recurrent cholangitis in 40 patients (91%) and/or jaundice in 9 (20%). First-line treatment consisted of primary revisionary surgery in 26 cases (59%; repeat RYHJ in 22 and hepatectomy in 4) and a percutaneous approach in 18 cases (41%; biliary interventions in 16 and portal vein embolization in 2). RESULTS: Postoperative mortality was nil. Postoperative morbidity was 11% after repeat RYHJ without hepatectomy, 80% (bile leaks) after hepatectomy, and 10% (mild cholangitis and hemobilia) after a percutaneous approach. Delayed revisionary surgery with the intent to wait for bile duct dilation failed in all 5 patients. With a mean follow-up of 49 ± 40 months, second- or third-line treatment was attempted in 7 patients (16%). One patient (2%) died because of suicide. Overall clinical success defined by the absence of incapacitating biliary symptoms after treatment was achieved in 39 patients (89%). CONCLUSION: An immediate, multidisciplinary approach including repeat biliary surgery and/or a percutaneous approach in a tertiary hepatobiliary center is required to obtain good, long-term results when treating the failure of RYHJ post-cholecystectomy BDI.
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  • Berenguer, M, Roche, B, Aguilera, V, Duclos-Vallee, JC, Navarro, L, Rubin, A, Pons, JA, de la Mata, M, Prieto, M & Samuel, D 2013, « Efficacy of the retreatment of hepatitis C virus infections after liver transplantation: role of an aggressive approach », Liver Transpl, vol. 19, no. 1, p. 69-77.
    Résumé : A sustained virological response (SVR) is achieved by 30% of naive liver transplantation (LT) recipients treated with pegylated interferon (PEG-IFN) and ribavirin (RBV). Almost no data are available about retreatment. The aim of this study was to assess the efficacy, tolerability, and SVR predictors of retreatment. Data were collected from 4 centers on the retreatment of prior nonresponders to standard therapy or PEG-IFN (with or without RBV) and relapsers. Seventy-nine of 301 treatment-experienced LT patients (26%), who had a median age of 59 years (range = 35-77 years) and were mostly male (72%) and infected with genotype 1 (87%), were retreated with PEG-IFN and RBV at a median of 6.9 years after LT. During the first course of therapy, 35% were treated with interferon, 49% received tacrolimus, 52% received steroids, and 49.5% were relapsers. Retreatment was started at a median of 1.9 years (range = 45 days to 8.2 years) after the end of the first course. The proportion of patients with cirrhosis increased from 10% to 37% (P < 0.001). In addition, in retreated patients, full initial RBV doses (P = 0.03), growth factors [erythropoietin (P < 0.001) and granulocyte colony-stimulating factor (P = 0.048)], and transfusions (P = 0.03) were used more frequently, and the treatment duration was longer (P = 0.03). An end-of-treatment response was achieved in 61%, whereas SVR, which was associated with improved survival, occurred in 28 (35%). The variables predicting SVR were age (P = 0.04), disease severity [fibrosis (50% with F0-F2 versus 26% with F3-4), P = 0.03; bilirubin, P = 0.006; platelet count, P = 0.03], adherence, and viral kinetics. None of the patients without an early virological response achieved SVR. There was a trend of prior relapsers achieving higher SVR rates than prior nonresponders. In conclusion, SVR, which was achieved by approximately one-third of the retreated patients, can be predicted with the same variables used for naive LT recipients (age, disease severity, adherence, and viral kinetics) and is associated with enhanced survival.

  • Bidard, F-C, Belin, L, Delaloge, S, Lerebours, F, Ngo, C, Reyal, F, Alran, S, Giacchetti, S, Marty, M, Lebofsky, R & Pierga, J-Y 2013, « Time-Dependent Prognostic Impact of Circulating Tumor Cells Detection in Non-Metastatic Breast Cancer: 70-Month Analysis of the REMAGUS02 Study », Int J Breast Cancer, vol. 2013, p. 130470, viewed sans date, .
    Résumé : Introduction. In non-metastatic breast cancer patients, the REMAGUS02 neoadjuvant study was the first to report a significant impact of circulating tumor cells (CTCs) detection by the CellSearch system on the distant metastasis-free survival (DMFS) and overall survival (OS) endpoints. However, these results were only reported after a short follow-up. Here, we present the updated data, with a longer follow-up. Material and Methods. CTC count was performed before and after neoadjuvant chemotherapy in 118 patients and correlated to survival. Results. CTC count results were available before and/or after neoadjuvant chemotherapy in 115 patients. After a median follow-up of 70 months, detection of ≥1 CTC/7.5 mL before chemotherapy (N = 95) was significantly associated with DMFS (P = 0.04) and OS (P = 0.03), whereas postchemotherapy CTC detection (N = 85) had no significant impact. In multivariable analysis, prechemotherapy CTC and triple negative phenotype were the two independent prognostic factors for survival. We observed that the CTC impact is most significant during the first three years of follow-up. Discussion. We confirm that the detection of CTC is independently associated with a significantly worse outcome, but mainly during the first 3-4 years of follow-up. No prognostic impact is seen in patients who are still relapse-free at this moment.
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  • Billy, F, Clairambault, J, Delaunay, F, Feillet, C & Robert, N 2013, « Age-structured cell population model to study the influence of growth factors on cell cycle dynamics », Math Biosci Eng, vol. 10, no. 1, p. 1-17, viewed sans date, .
    Résumé : Cell proliferation is controlled by many complex regulatory networks. Our purpose is to analyse, through mathematical modeling, the effects of growth factors on the dynamics of the division cycle in cell populations. Our work is based on an age-structured PDE model of the cell division cycle within a population of cells in a common tissue. Cell proliferation is at its first stages exponential and is thus characterised by its growth exponent, the first eigenvalue of the linear system we consider here, a growth exponent that we will explicitly evaluate from biological data. Moreover, this study relies on recent and innovative imaging data (fluorescence microscopy) that make us able to experimentally determine the parameters of the model and to validate numerical results. This model has allowed us to study the degree of simultaneity of phase transitions within a proliferating cell population and to analyse the role of an increased growth factor concentration in this process. This study thus aims at helping biologists to elicit the impact of growth factor concentration on cell cycle regulation, at making more precise the dynamics of key mechanisms controlling the division cycle in proliferating cell populations, and eventually at establishing theoretical bases for optimised combined anticancer treatments.
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  • Boleslawski, E, Bouras, AF, Truant, S, Liddo, G, Herrero, A, Badic, B, Audet, M, Altieri, M, Laurent, A, Declerck, N, Navarro, F, Letoublon, C, Wolf, P, Chiche, L, Cherqui, D & Pruvot, FR 2013, « Hepatic artery ligation for arterial rupture following liver transplantation: a reasonable option », Am J Transplant, vol. 13, no. 4, p. 1055-62.
    Résumé : Hepatic artery (HA) rupture after liver transplantation is a rare complication with high mortality. This study aimed to review the different managements of HA rupture and their results. From 1997 to 2007, data from six transplant centers were reviewed. Of 2649 recipients, 17 (0.64%) presented with HA rupture 29 days (2-92) after transplantation. Initial management was HA ligation in 10 patients, reanastomosis in three, aorto-hepatic grafting in two and percutaneous arterial embolization in one. One patient died before any treatment could be initiated. Concomitant biliary leak was present in seven patients and could be subsequently treated by percutaneous and/or endoscopic approaches in four patients. Early mortality was not observed in patients with HA ligation and occurred in 83% of patients receiving any other treatment. After a median follow-up of 70 months, 10 patients died (4 after retransplantation), and 7 patients were alive without retransplantation (including 6 with HA ligation). HA ligation was associated with better 3-year survival (80% vs. 14%; p=0.002). Despite its potential consequences on the biliary tract, HA ligation should be considered as a reasonable option in the initial management for HA rupture after liver transplantation. Unexpectedly, retransplantation was not always necessary after HA ligation in this series.
  • Burra, P, Germani, G, Adam, R, Karam, V, Marzano, A, Lampertico, P, Salizzoni, M, Filipponi, F, Klempnauer, JL, Castaing, D, Kilic, M, Carlis, LD, Neuhaus, P, Yilmaz, S, Paul, A, Pinna, AD, Burroughs, AK & Russo, FP 2013, « Liver transplantation for HBV-related cirrhosis in Europe: an ELTR study on evolution and outcomes », J Hepatol, vol. 58, no. 2, p. 287-96.
    Résumé : BACKGROUND & AIMS: HBV-related chronic liver disease is one of the most common indications for liver transplantation (LT) in Europe. The ELTR database was used to evaluate outcomes and evolution over 20 years (01/1988 and 12/2010). METHODS: HBV transplanted patients were analysed according to indication for LT: decompensated cirrhosis (HBVdec) or hepatocellular carcinoma (HBV/HCC). These groups were compared with co-infected patients HBV/HDV (HBDV), HBV/HCV (HBCV), HBV/HDV/HCV (HBDCV); n = 16,664 and with HCV patients (n = 2452) according to LT indication. RESULTS: 5912 patients were transplanted for HBV (78% HBVdec, 22% HBV/HCC), with HBV/HCC patients who increased from 15.8% in 1988-1995 to 29.6% in 2006-2010 (p < 0.001). In HBVdec patients, 1, 3, 5, and 10 year patient and graft survival was 83%, 78%, 75%, 68%, and 80%, 74%, 71%, 64%, respectively, significantly better than HBV/HCC (84%, 73%, 68%, 61%, and 81%, 70%, 65%, 58% respectively; p = 0.001 and p = 0.026). In 2006-2010 patient and graft survival significantly improved compared to 1988-1995, both for HBVdec and HBV/HCC (each p < 0.001). A better patient and graft survival was seen in HBV/HCC patients with HBV-DNA(-) compared to HBV-DNA(+) at the time of LT (p < 0.001). Disease recurrence, as cause of death/graft loss, was significantly reduced in recent years compared to the past: currently <1% for HBVdec and 3% for HBV/HCC. CONCLUSIONS: Outcomes of LT for HBV have improved in recent years, with disease recurrence being no longer a significant cause of death/graft loss. HBV-DNA at the time of LT seems to influence survival only in HBV/HCC patients.
  • Cabau, M, Luc, G, Terrebonne, E, Belleanne, G, Vendrely, V, Sa Cunha, A & Collet, D 2013, « Lymph node invasion might have more prognostic impact than R status in advanced esophageal adenocarcinoma », Am J Surg, vol. 205, no. 6, p. 711-7.
    Résumé : BACKGROUND: Advanced esophageal adenocarcinomas are associated with 5-year survival rates ranging from 14% to 35%. Nodal status and tumor clearance are the main prognostic factors. However, their respective prognostic values have not been compared to date. METHODS: Seventy consecutive patients with stage T3 adenocarcinomas of the esophagus or gastric cardia were retrospectively assessed. Neoadjuvant therapy was indicated in all cases. Prognostic values of R0 resection and nodal status were evaluated using univariate and multivariate analyses. RESULTS: Neoadjuvant therapy was achieved in 62 patients, 41 with radiochemotherapy and 21 with perioperative chemotherapy. Transthoracic esophagectomy and transhiatal esophagectomy were performed in 54 and 15 patients, respectively. Clavien-Dindo grade III or IV complications occurred in 16 patients (23%). Two patients died in the hospital (3%). In univariate and multivariate analyses, nodal status was the main independent factor predicting overall survival; tumor clearance (R0 or R1) had less prognostic impact and was not statistically significant. Furthermore, R1 resection was a prognostic indicator for metastatic recurrence. CONCLUSIONS: These results indicate that nodal status has more prognostic impact than R status in stage T3 adenocarcinomas of the esophagus or gastric cardia. Thus, local control in R1 patients by postoperative radiotherapy is not justified.
    Mots-clés : 80 and over Antineoplastic Combined Chemotherapy Protocols/therapeutic use Cardia/pathology Chemoradiotherapy Chemotherapy, Adenocarcinoma/ mortality/ pathology/therapy Adult Aged Aged.

  • Caillard, S, Porcher, R, Provot, F, Dantal, J, Choquet, S, Durrbach, A, Morelon, E, Moal, V, Janbon, B, Alamartine, E, Pouteil Noble, C, Morel, D, Kamar, N, Buchler, M, Mamzer, MF, Peraldi, MN, Hiesse, C, Renoult, E, Toupance, O, Rerolle, JP, Delmas, S, Lang, P, Lebranchu, Y, Heng, AE, Rebibou, JM, Mousson, C, Glotz, D, Rivalan, J, Thierry, A, Etienne, I, Moal, MC, Albano, L, Subra, JF, Ouali, N, Westeel, PF, Delahousse, M, Genin, R, Hurault de Ligny, B & Moulin, B 2013, « Post-transplantation lymphoproliferative disorder after kidney transplantation: report of a nationwide French registry and the development of a new prognostic score », J Clin Oncol, vol. 31, no. 10, p. 1302-9, viewed sans date, .
    Résumé : PURPOSE: Post-transplantation lymphoproliferative disorder (PTLD) is associated with significant mortality in kidney transplant recipients. We conducted a prospective survey of the occurrence of PTLD in a French nationwide population of adult kidney recipients over 10 years. PATIENTS AND METHODS: A French registry was established to cover a nationwide population of transplant recipients and prospectively enroll all adult kidney recipients who developed PTLD between January 1, 1998, and December 31, 2007. Five hundred patient cases of PTLD were referred to the French registry. The prognostic factors for PTLD were investigated using Kaplan-Meier and Cox analyses. RESULTS: Patients with PTLD had a 5-year survival rate of 53% and 10-year survival rate of 45%. Multivariable analyses revealed that age > 55 years, serum creatinine level > 133 mumol/L, elevated lactate dehydrogenase levels, disseminated lymphoma, brain localization, invasion of serous membranes, monomorphic PTLD, and T-cell PTLD were independent prognostic indicators of poor survival. Considering five variables at diagnosis (age, serum creatinine, lactate dehydrogenase, PTLD localization, and histology), we constructed a prognostic score that classified patients with PTLD as being at low, moderate, high, or very high risk for death. The 10-year survival rate was 85% for low-, 80% for moderate-, 56% for high-, and 0% for very high-risk recipients. CONCLUSION: This nationwide study highlights the prognostic factors for PTLD and enables the development of a new prognostic score. After validation in an independent cohort, the use of this score should allow treatment strategies to be better tailored to individual patients in the future.
    Mots-clés : &, Adolescent, Adult, Aged, Analysis, Complications/diagnosis/epidemiology/*etiology, data, Disorders/diagnosis/epidemiology/*etiology, effects, Factors, Female, Follow-Up, France/epidemiology, Humans, Kidney, Lymphoproliferative, Male, Middle, Multivariate, numerical, Postoperative, Prognosis, Prospective, Registries/statistics, Risk, Studies, Survival, Transplantation/*adverse, Young.

  • Cambot, M, Mazurier, C, Canoui-Poitrine, F, Hebert, N, Picot, J, Clay, D, Picard, V, Ripoche, P, Douay, L, Dubart-Kupperschmitt, A & Cartron, J-P 2013, « In vitro generated Rh(null) red cells recapitulate the in vivo deficiency: a model for rare blood group phenotypes and erythroid membrane disorders », Am J Hematol, vol. 88, no. 5, p. 343-9, viewed sans date, .
    Résumé : Lentiviral modification combined with ex vivo erythroid differentiation was used to stably inhibit RhAG expression, a critical component of the Rh(rhesus) membrane complex defective in the Rh(null) syndrome. The cultured red cells generated recapitulate the major alterations of native Rh(null) cells regarding antigen expression, membrane deformability, and gas transport function, providing the proof of principle for their use as model of Rh(null) syndrome and to investigate Rh complex biogenesis in human primary erythroid cells. Using this model, we were able to reveal for the first time that RhAG extinction alone is sufficient to explain ICAM-4 and CD47 loss observed on native Rh(null) RBCs. Together with the effects of RhAG forced expression in Rh(null) progenitors, this strongly strengthens the hypothesis that RhAG is critical to Rh complex formation. The strategy is also promising for diagnosis purpose in order to overcome the supply from rare blood donors and is applicable to other erythroid defects and rare phenotypes, providing models to dissect membrane biogenesis of multicomplex proteins in erythroid cells, with potential clinical applications in transfusion medicine.
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  • Candelier, J-J, Frappart, L, Diatta, AL, Yadaden, T, Cissé, M-L, Afoutou, J-M, Picard, J-Y, Mennesson, B, Slim, R, Si-Tayeb, K & Coullin, P 2013, « Differential expression of E-cadherin, β-catenin, and Lewis x between invasive hydatidiform moles and post-molar choriocarcinomas », Virchows Archiv: An International Journal of Pathology, vol. 462, no. 6, p. 653-663.
    Résumé : Trophoblast cell adhesion and migration are carefully coordinated during normal placental development. We have compared the expression of three adhesion molecules, E-cadherin, β-catenin, and Lewis x, by immunohistochemistry during normal trophoblast differentiation, and in hydatidiform moles and choriocarcinomas. Both E-cadherin and β-catenin were expressed in normal placenta cytotrophoblast, and this expression decreased with trophoblast maturation. E-cadherin was mainly localized along the contact between cytotrophoblast and syncytiotrophoblast, which indicates its role in the differentiation of the syncytial layer. Lewis x disappeared progressively during differentiation of normal villous vessels, and was expressed in molar pregnancies. Interestingly, whereas choriocarcinomas were not, or poorly, stained, invasive hydatidiform moles (invHMs) strongly expressed Lewis x in vascular structures. This observation correlated well with E-cadherin and β-catenin expression and suggests that these three markers are associated with the invasive transformation. The presence of robust endothelial structures in invHMs could also explain their ability to maintain organized villous architecture (contrary to metastatic choriocarcinomas) during their invasion of extrauterine tissues such as the lung or the brain after dissemination through the blood flow. In our hands, Lewis x appeared to be a new, reliable marker that can be used to clearly distinguish invHMs from choriocarcinomas.
    Mots-clés : Abnormal karyotype, Adult, Antigens, CD15, beta Catenin, Cadherins, choriocarcinoma, Diagnosis, Differential, Female, Gestational Age, Humans, Hydatidiform Mole, Invasive, In Situ Hybridization, Fluorescence, Pregnancy, Trophoblasts, Uterine Neoplasms.
  • Carrere, N, Mathonnet, M, Mirallie, E, Pattou, F & Sa-Cunha, A 2013, « Surgical treatment », Ann Endocrinol (Paris), vol. 74, no. 3, p. 191-5.
    Résumé : Carrere, Nicolas; Mathonnet, Muriel; Mirallie, Eric; Pattou, Francois; Sa-Cunha, Antonio; France; Ann Endocrinol (Paris). 2013 Jul;74(3):191-5. doi: 10.1016/j.ando.2013.05.004. Epub 2013 Jun 24.

  • Casetti, L, Martin-Lannerée, S, Najjar, I, Plo, I, Augé, S, Roy, L, Chomel, J-C, Lauret, E, Turhan, AG & Dusanter-Fourt, I 2013, « Differential contributions of STAT5A and STAT5B to stress protection and tyrosine kinase inhibitor resistance of chronic myeloid leukemia stem/progenitor cells », Cancer Res, vol. 73, no. 7, p. 2052-8, viewed sans date, .
    Résumé : STAT5 fulfills essential roles in hematopoietic stem cell (HSC) self-renewal and chronic myeloid leukemia (CML), a prototypical stem cell malignancy. However, the specific contributions of the two related genes STAT5A and STAT5B have not been determined. In this study, we used a RNAi-based strategy to establish participation of these genes to CML disease and persistence following targeted therapy. We showed that STAT5A/STAT5B double-knockdown triggers CML cell apoptosis and suppresses both normal and CML HSC long-term clonogenic potential. STAT5A and STAT5B exhibited similar prosurvival activity, but STAT5A attenuation alone was ineffective at impairing growth of normal and CML CD34(+) cells isolated at diagnosis. In contrast, STAT5A attenuation was sufficient to enhance basal oxidative stress and DNA damage of normal CD34(+) and CML cells. Furthermore, it weakened the ability to manage exogenous oxidative stress, increased p53 (TRP53)/CHK-2 (CHEK2) stress pathway activation, and enhanced prolyl hydroxylase domain (PHD)-3 (EGLN3) mRNA expression. Only STAT5A and its transactivation domain-deficient mutant STAT5AΔ749 specifically rescued these activities. STAT5A attenuation was also active at inhibiting growth of CML CD34(+) cells from patients with acquired resistance to imatinib. Our findings show that STAT5A has a selective role in contributing to stress resistance through unconventional mechanisms, offering new opportunities to eradicate the most primitive and tyrosine kinase inhibitor-resistant CML cells with an additional potential to eradicate persistent stem cell populations.
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  • Cassinotto, C, Cortade, J, Belleannee, G, Lapuyade, B, Terrebonne, E, Vendrely, V, Laurent, C & Sa-Cunha, A 2013, « An evaluation of the accuracy of CT when determining resectability of pancreatic head adenocarcinoma after neoadjuvant treatment », Eur J Radiol, vol. 82, no. 4, p. 589-93.
    Résumé : BACKGROUND: To evaluate the accuracy of MDCT for determination of resectability R0 after neoadjuvant therapy in patients with pancreatic head adenocarcinoma locally advanced. METHODS: From January 2005 to December 2010, 80 patients with pancreatic head adenocarcinoma underwent multidetector CT before surgery. Of these, 38 patients received neoadjuvant therapy because tumor was considered locally advanced on baseline CT scan. We retrospectively correlated imaging interpretations with operative and histological data and compared results in patients without (control group) or with (neoadjuvant group) preoperative treatment. RESULTS: 41/42 patients in control group and 31/38 patients in neoadjuvant group finally had curative resection. While resection R0 is similar in both groups (83% and 81%), CT accuracy in determining resectability R0 was significantly decreased in neoadjuvant group (58% versus 83%; p=0.039). CT scan specificity was significantly lower after neoadjuvant therapy (52% versus 88% in control group) due to an overestimation of vascular invasion: 12/31 patients with complete resection in neoadjuvant group were evaluated at high risk of incomplete resection on CT scan. Tumor size tends to be underestimated in control group (-2mm) and overestimated in neoadjuvant group (+10mm). T-staging accuracy was decreased in neoadjuvant group (39% versus 78% in control group; p=0.002). CONCLUSION: Neoadjuvant therapy significantly decreases the accuracy of CT scan in determining operability, T-staging, and resectability R0 of pancreatic head carcinoma. Overestimation of tumor size and vascular invasion significantly reduces CT scan specificity after preoperative treatment.
  • Castillo-Rama, M, Sebagh, M, Sasatomi, E & Al., E 2013, « “Plasma cell hepatitis” in Liver Allografts: Identification and Characterization of an IgG4-rich Cohort », American Journal of Transplantation, vol. In Press, no. In Press a confirmer.

  • Chantran, Y, Ballot, E & Johanet, C 2013, « Autoantibodies in primary biliary cirrhosis: Antimitochondrial autoantibodies », Clin Res Hepatol Gastroenterol.
    Résumé : Chantran, Yannick; Ballot, Eric; Johanet, Catherine; Clin Res Hepatol Gastroenterol. 2013 Jun 14. pii: S2210-7401(13)00096-X. doi: .


  • Charrin, S, Latil, M, Soave, S, Polesskaya, A, Chrétien, F, Boucheix, C & Rubinstein, E 2013, « Normal muscle regeneration requires tight control of muscle cell fusion by tetraspanins CD9 and CD81 », Nat Commun, vol. 4, p. 1674, viewed sans date, .
    Résumé : Skeletal muscle regeneration after injury follows a remarkable sequence of synchronized events. However, the mechanisms regulating the typical organization of the regenerating muscle at different stages remain largely unknown. Here we show that muscle regeneration in mice lacking either CD9 or CD81 is abnormal and characterized by the formation of discrete giant dystrophic myofibres, which form more quickly in the absence of both tetraspanins. We also show that, in myoblasts, these two tetraspanins associate with the immunoglobulin domain molecule CD9P-1 (EWI-F/FPRP), and that grafting of CD9P-1-depleted myoblasts in regenerating muscles also leads to abnormal regeneration. In vitro myotubes lacking CD9P-1 or both CD9 and CD81 fuse with a higher frequency than normal myotubes. Our study unveils a mechanism preventing inappropriate fusion of myotubes that has an important role in the restitution of normal muscle architecture during muscle regeneration.
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  • Clairambault, J 2013, « Can theorems help treat cancer? », J Math Biol, vol. 66, no. 7, p. 1555-8, viewed sans date, .
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  • Clede, S, Lambert, F, Sandt, C, Kascakova, S, Unger, M, Harte, E, Plamont, MA, Saint-Fort, R, Deniset-Besseau, A, Gueroui, Z, Hirschmugl, C, Lecomte, S, Dazzi, A, Vessieres, A & Policar, C 2013, « Detection of an estrogen derivative in two breast cancer cell lines using a single core multimodal probe for imaging (SCoMPI) imaged by a panel of luminescent and vibrational techniques », Analyst, viewed sans date, .
    Résumé : 3-Methoxy-17alpha-ethynylestradiol or mestranol is a prodrug for ethynylestradiol and the estrogen component of some oral contraceptive formulations. We demonstrate here that a single core multimodal probe for imaging - SCoMPI - can be efficiently grafted onto mestranol allowing its tracking in two breast cancer cell lines, MDA-MB-231 and MCF-7 fixed cells. Correlative imaging studies based on luminescence (synchrotron UV spectromicroscopy, wide field and confocal fluorescence microscopies) and vibrational (AFMIR, synchrotron FTIR spectromicroscopy, synchrotron-based multiple beam FTIR imaging, confocal Raman microspectroscopy) spectroscopies were consistent with one another and showed a Golgi apparatus distribution of the SCoMPI-mestranol conjugate in both cell lines.
  • Coilly, A, Roche, B & Samuel, D 2013, « Current management and perspectives for HCV recurrence after liver transplantation », Liver Int, vol. 33 Suppl 1, p. 56-62.
    Résumé : Hepatitis C virus (HCV) infection is one of the leading causes of end-stage liver disease and the main indication for liver transplantation (LT) in most countries. All patients who undergo LT with detectable serum HCV RNA experience graft reinfection. Between 20 and 30% of patients develop cirrhosis within 5 years post-LT. The outcome of transplant patients with cirrhosis on the graft is severe, with a rate of decompensation at 1 year of around 40%. To date, retransplantation is the only option for patients who develop decompensation. Until 2011, standard antiviral therapy, using pegylated interferon (PEG-IFN) and ribavirin (RBV), was the only effective therapy. Obtaining a sustained virological response (SVR) in the setting of LT greatly improves overall and graft survival, but this only concerns 30% of transplanted patients. Direct-acting antivirals (DAA) such as protease inhibitors, polymerase or other non-structural proteins inhibitors represent a new era in HCV-associated liver disease. Although their use in the field of liver transplantation seems to be essential, there are some limitations due to safety and tolerance. One limitation is the potential interaction with calcineurin inhibitors. We describe the preliminary results of triple therapy with boceprevir or telaprevir in terms of efficacy and safety in liver transplant recipients.
    Mots-clés : Antiviral Agents/adverse effects/ therapeutic use Drug Therapy, Viral/blood Recombinant Proteins/therapeutic use Recurrence Ribavirin/therapeutic use Risk Factors Serine Proteinase Inhibitors/therapeutic use Time Factors Treatment Outcome Viral Load.

  • Coilly, A, Haïm-Boukobza, S, Roche, B, Antonini, TM, Pause, A, Mokhtari, C, Becq, A, Farahmand, H, Hauser, L, Duclos-Vallée, J-C, Samuel, D, Adam, R & Roque-Afonso, A-M 2013, « Posttransplantation hepatitis e: transfusion-transmitted hepatitis rising from the ashes », Transplantation, vol. 96, no. 2, p. e4-6, viewed sans date, .
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