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Biblio - Bibliographie IAL
Bibliographie IAL

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Recherche bibliographique scientifique

Moteur de recherche scientifique en Médecine, Biologie et Sciences

Accueil > Références bibliographiques

biblio

2008

  • Le Treut, YP, Gregoire, E, Belghiti, J, Boillot, O, Soubrane, O, Mantion, G, Cherqui, D, Castaing, D, Ruszniewski, P, Wolf, P, Paye, F, Salame, E, Muscari, F, Pruvot, FR & Baulieux, J 2008, « Predictors of long-term survival after liver transplantation for metastatic endocrine tumors: an 85-case French multicentric report », Am J Transplant, vol. 8, no. 6, p. 1205-13.
    Résumé : Liver transplantation (LTx) for metastatic endocrine tumors (MET) remains controversial due to the lack of clear selection criteria. From 1989 to 2005, 85 patients underwent LTx for MET. The primary tumor was located in the pancreas or duodenum in 40 cases, digestive tract in 26 and bronchial tree in five. In the remaining 14 cases, primary location was undetermined at the time of LTx. Hepatomegaly (explanted liver > or =120% of estimated standard liver volume) was observed in 53 patients (62%). Extrahepatic resection was performed concomitantly with LTx in 34 patients (40%), including upper abdominal exenteration (UAE) in seven. Postoperative in-hospital mortality was 14%. Overall 5-year survival was 47%. Independent factors of poor prognosis according to multivariate analysis included UAE (relative risk (RR): 3.72), primary tumor in duodenum or pancreas (RR: 2.94) and hepatomegaly (RR: 2.63). After exclusion of cases involving concomitant UAE, the other two factors were combined into a risk model. Five-year survival rate was 12% for the 23 patients presenting both unfavorable prognostic factors versus 68% for the 55 patients presenting one or neither factor (p < 10(-7)). LTx can benefit selected patients with nonresectable MET. Patients presenting duodeno-pancreatic MET in association with hepatomegaly are poor indications for LTx.
    Mots-clés : Adolescent, Adult, Aged, Analysis, Endocrine, Female, France, Gland, Humans, Liver, Male, Middle, Mortality, Neoplasms/secondary/, Neuroendocrine, Prognosis, Retrospective, Studies, surgery, Survival, Transplantation/, Tumors/secondary/.

  • Lefort, N, Feyeux, M, Bas, C, Féraud, O, Bennaceur-Griscelli, A, Tachdjian, G, Peschanski, M & Perrier, AL 2008, « Human embryonic stem cells reveal recurrent genomic instability at 20q11.21 », Nat Biotechnol, vol. 26, no. 12, p. 1364-6, viewed sans date, .
    Résumé : By analyzing five human embryonic stem (hES) cell lines over long-term culture, we identified a recurrent genomic instability in the human genome. An amplification of 2.5-4.6 Mb at 20q11.21, encompassing approximately 23 genes in common, was detected in four cell lines of different origins. This amplification, which has been associated with oncogenic transformation, may provide a selective advantage to hES cells in culture.
    Note Note
    <p>19029913</p>
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    <p>19029913</p>
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    <p>19029913</p>
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    <p>19029913</p>

  • Lévi, F 2008, « [The circadian-timing system: a determinant of drug activity and a target of anticancer treatments] », Ann Pharm Fr, vol. 66, no. 3, p. 175-84, viewed sans date, .
    Résumé : Cellular proliferation and drug detoxification are controlled over the 24h by the circadian-timing system, whose disruption can favor malignant processes. Thus, prolonged shift work appears to increase the risk of breast, colon or prostate cancer. Alterations in circadian physiology and/or molecular-clock genes accelerate cancer progression in experimental models and in cancer patients. In addition, anticancer treatments can also dampen or reinforce the circadian-timing system, as a function of dose and time of administration. The adjustment of anticancer-drug delivery to the circadian-timing system (chronotherapeutics) has allowed to reduce five-fold the incidence of severe adverse events as compared to constant rate infusion or wrongly-timed chronomodulated delivery in cancer patients. In experimental models, the best antitumor efficacy is usually obtained following treatment delivery near the least toxic time, a statement that also seems to apply to patients. Dedicated technologies include programmable in time pumps and rhythm monitors and are required for chronotherapeutics. Recent results have revealed that the optimal chronotherapeutic schedule could differ as a function of gender and circadian physiology. In conclusion, the circadian-timing system was shown to negatively control malignant proliferation via partly identified molecular mechanisms. The components of the circadian-timing system thus constitute new potential therapeutic targets in oncology. Mathematical models help toward a better understanding of the role of variability for the determination of the optimal chronotherapeutic schedule and constitute useful tools for the personalization of cancer chronotherapeutics.
    Note Note
    <p>18706346</p>
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    <p>18706346</p>
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    <p>18706346</p>
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    <p>18706346</p>

  • Lévi, FA 2008, « The circadian timing system: a coordinator of life processes: chronobiological investigations. Implications for the rhythmic delivery of cancer therapeutics », IEEE Eng Med Biol Mag, vol. 27, no. 1, p. 17-9, viewed sans date, .
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    <p>18270045</p>
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    <p>18270045</p>
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    <p>18270045</p>
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    <p>18270045</p>

  • Lévi, F, Altinok, A, Clairambault, J & Goldbeter, A 2008, « Implications of circadian clocks for the rhythmic delivery of cancer therapeutics », Philos Trans A Math Phys Eng Sci, vol. 366, no. 1880, p. 3575-98, viewed sans date, .
    Résumé : The circadian timing system (CTS) controls drug metabolism and cellular proliferation over the 24 hour day through molecular clocks in each cell. These cellular clocks are coordinated by a hypothalamic pacemaker, the suprachiasmatic nuclei, that generates or controls circadian physiology. The CTS plays a role in cancer processes and their treatments through the downregulation of malignant growth and the generation of large and predictable 24 hour changes in toxicity and efficacy of anti-cancer drugs. The tight interactions between circadian clocks, cell division cycle and pharmacology pathways have supported sinusoidal circadian-based delivery of cancer treatments. Such chronotherapeutics have been mostly implemented in patients with metastatic colorectal cancer, the second most common cause of death from cancer. Stochastic and deterministic models of the interactions between circadian clock, cell cycle and pharmacology confirmed the poor therapeutic value of both constant-rate and wrongly timed chronomodulated infusions. An automaton model for the cell cycle revealed the critical roles of variability in circadian entrainment and cell cycle phase durations in healthy tissues and tumours for the success of properly timed circadian delivery schedules. The models showed that additional therapeutic strategy further sets the constraints for the identification of the most effective chronomodulated schedules.
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    <p>18644767</p>
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    <p>18644767</p>
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    <p>18644767</p>
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    <p>18644767</p>

  • Martin, P, Simon, B, Lone, YC, Chatel, L, Barry, R, Inchauspe, G & Fournillier, A 2008, « A vector-based minigene vaccine approach results in strong induction of T-cell responses specific of hepatitis C virus », Vaccine, vol. 26, no. 20, p. 2471-81, viewed sans date, .
    Résumé : Multiepitope-based vaccines against hepatitis C virus (HCV) were designed in the form of three minigenes encompassing four domains of the NS3, NS4 and NS5B proteins that contain multiple class I/II restricted epitopes. The polyEp-WT minigene encodes all four domains in fusion, the polyEp-C minigene encodes the same fusion but optimised for mammalian translation and the polyEp-E3 minigene has an additional endoplasmic reticulum targeting sequence. Whereas the minigenes vectorised by DNA were poorly immunogenic, adenovirus vectorisation induced strong and broader IFNgamma-ELISpot and CTL responses in HLA-A2 transgenic mice. In addition, polyEp-WT and polyEp-E3 responses were found cross-reactive in a recombinant Listeria-NS3-based surrogate challenge. This study illustrates the potency of vectorised minigenes in the field of HCV vaccine development.
    Mots-clés : Adenoviridae/genetics Animals Colony Count, Cytotoxic/immunology Transduction, Genetic Vaccines, Microbial Epitopes/genetics/immunology Genetic Vectors Hepacivirus/genetics/*immunology Interferon-gamma/biosynthesis Listeria/genetics/growth & development Liver/immunology/microbiology Mice Mice, Synthetic/genetics/immunology Viral Hepatitis Vaccines/genetics/*immunology Viral Nonstructural Proteins/genetics/immunology, Transgenic Spleen/immunology/microbiology T-Lymphocytes.
  • Moniaux, N, Chakraborty, S, Yalniz, M, Gonzalez, J, Shostrom, VK, Standop, J, Lele, SM, Ouellette, M, Pour, PM, Sasson, AR, Brand, RE, Hollingsworth, MA, Jain, M & Batra, SK 2008, « Early diagnosis of pancreatic cancer: neutrophil gelatinase-associated lipocalin as a marker of pancreatic intraepithelial neoplasia », Br J Cancer, vol. 98, no. 9, p. 1540-7.
    Résumé : Pancreatic cancer is a highly lethal malignancy with a dismal 5-year survival of less than 5%. The scarcity of early biomarkers has considerably hindered our ability to launch preventive measures for this malignancy in a timely manner. Neutrophil gelatinase-associated lipocalin (NGAL), a 24-kDa glycoprotein, was reported to be upregulated nearly 27-fold in pancreatic cancer cells compared to normal ductal cells in a microarray analysis. Given the need for biomarkers in the early diagnosis of pancreatic cancer, we investigated the expression of NGAL in tissues with the objective of examining if NGAL immunostaining could be used to identify foci of pancreatic intraepithelial neoplasia, premalignant lesions preceding invasive cancer. To examine a possible correlation between NGAL expression and the degree of differentiation, we also analysed NGAL levels in pancreatic cancer cell lines with varying grades of differentiation. Although NGAL expression was strongly upregulated in pancreatic cancer, and moderately in pancreatitis, only a weak expression could be detected in the healthy pancreas. The average composite score for adenocarcinoma (4.26+/-2.44) was significantly higher than that for the normal pancreas (1.0) or pancreatitis (1.0) (P<0.0001). Further, although both well- and moderately differentiated pancreatic cancer were positive for NGAL, poorly differentiated adenocarcinoma was uniformly negative. Importantly, NGAL expression was detected as early as the PanIN-1 stage, suggesting that it could be a marker of the earliest premalignant changes in the pancreas. Further, we examined NGAL levels in serum samples. Serum NGAL levels were above the cutoff for healthy individuals in 94% of pancreatic cancer and 62.5% each of acute and chronic pancreatitis samples. However, the difference between NGAL levels in pancreatitis and pancreatic cancer was not significant. A ROC curve analysis revealed that ELISA for NGAL is fairly accurate in distinguishing pancreatic cancer from non-cancer cases (area under curve=0.75). In conclusion, NGAL is highly expressed in early dysplastic lesions in the pancreas, suggesting a possible role as an early diagnostic marker for pancreatic cancer. Further, serum NGAL measurement could be investigated as a possible biomarker in pancreatitis and pancreatic adenocarcinoma.
    Mots-clés : Acute-Phase Proteins/ analysis/genetics Adenocarcinoma/blood/chemistry/ diagnosis Adult Aged Blotting, Biological/ analysis/blood/genetics, Neoplasm/analysis ROC Curve Reverse Transcriptase Polymerase Chain Reaction Tumor Markers, Neoplastic Humans Immunohistochemistry Lipocalins/ analysis/blood/genetics Male Middle Aged Pancreatic Neoplasms/blood/chemistry/ diagnosis Proto-Oncogene Proteins/ analysis/blood/genetics RNA, Pancreatic Ductal/blood/chemistry/ diagnosis Cell Line, Tumor Early Diagnosis Enzyme-Linked Immunosorbent Assay Female Gene Expression Regulation, Western Carcinoma.
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    <p>2391106</p>
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    <p>2391106</p>
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    <p>2391106</p>

  • Monnet, X, Vidal-Petiot, E, Osman, D, Hamzaoui, O, Durrbach, A, Goujard, C, Miceli, C, Bouree, P & Richard, C 2008, « Critical care management and outcome of severe Pneumocystis pneumonia in patients with and without HIV infection », Crit Care, vol. 12, no. 1, p. R28, viewed sans date, .
    Résumé : BACKGROUND: Little is known about the most severe forms of Pneumocystis jiroveci pneumonia (PCP) in HIV-negative as compared with HIV-positive patients. Improved knowledge about the differential characteristics and management modalities could guide treatment based on HIV status. METHODS: We retrospectively compared 72 patients (73 cases, 46 HIV-positive) admitted for PCP from 1993 to 2006 in the intensive care unit (ICU) of a university hospital. RESULTS: The yearly incidence of ICU admissions for PCP in HIV-negative patients increased from 1993 (0%) to 2006 (6.5%). At admission, all but one non-HIV patient were receiving corticosteroids. Twenty-three (85%) HIV-negative patients were receiving an additional immunosuppressive treatment. At admission, HIV-negative patients were significantly older than HIV-positive patients (64 [18 to 82] versus 37 [28 to 56] years old) and had a significantly higher Simplified Acute Physiology Score (SAPS) II (38 [13 to 90] versus 27 [11 to 112]) but had a similar PaO2/FiO2 (arterial partial pressure of oxygen/fraction of inspired oxygen) ratio (160 [61 to 322] versus 183 [38 to 380] mm Hg). Ventilatory support was required in a similar proportion of HIV-negative and HIV-positive cases (78% versus 61%), with a similar proportion of first-line non-invasive ventilation (NIV) (67% versus 54%). NIV failed in 71% of HIV-negative and in 13% of HIV-positive patients (p < 0.01). Mortality was significantly higher in HIV-negative than HIV-positive cases (48% versus 17%). The HIV-negative status (odds ratio 3.73, 95% confidence interval 1.10 to 12.60) and SAPS II (odds ratio 1.07, 95% confidence interval 1.02 to 1.12) were independently associated with mortality at multivariate analysis. CONCLUSION: The yearly incidence of ICU admissions for PCP in HIV-negative patients in our unit increased from 1993 to 2006. The course of the disease and the outcome were worse in HIV-negative patients. NIV often failed in HIV-negative cases, suggesting that NIV must be watched closely in this population.
    Mots-clés : Artificial Retrospective Studies, Pneumocystis/complications/*drug therapy/epidemiology Pneumonia, Ventilator-Associated/*microbiology Respiration.
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    <p>2374632</p>
  • Moucari, R, Asselah, T, Cazals-Hatem, D, Voitot, H, Boyer, N, Ripault, MP, Sobesky, R, Martinot-Peignoux, M, Maylin, S, Nicolas-Chanoine, MH, Paradis, V, Vidaud, M, Valla, D, Bedossa, P & Marcellin, P 2008, « Insulin resistance in chronic hepatitis C: association with genotypes 1 and 4, serum HCV RNA level, and liver fibrosis », Gastroenterology, vol. 134, no. 2, p. 416-23.
    Résumé : BACKGROUND & AIMS: Our study was designed to test the association between insulin resistance (IR) and hepatitis C virus (HCV) genotypes, serum HCV RNA level and liver fibrosis stage in a large prospective cohort of chronic hepatitis C (CHC) patients. METHODS: Six hundred consecutive patients (CHC, n = 500; chronic hepatitis B (CHB), n = 100) were evaluated on the day of liver biopsy. IR (Homeostasis Model for Assessment of Insulin Resistance) and all components of the metabolic syndrome were assessed. By logistic regression, independent factors associated with IR and those associated with significant fibrosis were assessed in nondiabetic and noncirrhotic CHC, respectively. Parameters of IR were compared between hepatitis B and 240 CHC matched by epidemiologic, metabolic, and histologic features. RESULTS: IR was present in 32.4% of the 462 nondiabetic CHC and associated with the metabolic syndrome, genotypes 1 and 4, significant fibrosis, and severe steatosis. IR was diagnosed in 15% of 145 CHC without metabolic syndrome or significant fibrosis, and associated with genotypes 1 and 4, high serum HCV RNA level, and moderate-severe necroinflammation. Significant fibrosis was present in 51.1% of the 454 noncirrhotic CHC patients and associated with male sex, age >40 years, IR, moderate-severe necroinflammation, and severe steatosis. IR was less frequent in CHB than in matched CHC (5% vs 35%, respectively, P < .001). CONCLUSIONS: IR is a specific feature of CHC, associated with genotypes 1 and 4 and high serum HCV RNA level. Significant fibrosis is associated with IR independent from steatosis.
    Mots-clés : Adult Aged Biopsy Cohort Studies Disease Progression Fatty Liver/physiopathology Female Genotype Hepacivirus/ genetics/pathogenicity Hepatitis C, Chronic/ physiopathology Humans Insulin Resistance/ physiology Liver/pathology Liver Cirrhosis/physiopathology/ virology Logistic Models Male Metabolic Syndrome X/physiopathology Middle Aged Prevalence Prospective Studies RNA, Viral/ blood Severity of Illness Index.
  • Mourra, N, Hoeffel, C, Duvillard, P, Guettier, C, Flejou, JF & Tiret, E 2008, « Adrenalectomy for clinically isolated metastasis from colorectal carcinoma: report of eight cases », Dis Colon Rectum, vol. 51, no. 12, p. 1846-9.
    Résumé : PURPOSE: Metastasis to the adrenal glands is a relatively frequent finding at autopsy. Adrenal metastasis of colorectal carcinoma is rare (14 percent). Isolated adrenal metastasis is even rarer, and presents a therapeutic dilemma. METHODS: Between 1997 and 2006, eight patients (5 men; mean age, 62 years) underwent adrenalectomy for metastasis of colorectal carcinoma. The tumors were Stage D in four cases, Stage B in two cases, and Stage C in the remaining two. Adjuvant chemotherapy was instituted. RESULTS: All patients were asymptomatic, and adrenal metastasis was suspected from an elevated serum level of carcinoembryogenic antigen or discovered by computed tomography. Adrenal metastases were metachronous in seven patients, with median disease-free interval of 3.75 years. At the time of follow-up, one patient remained alive and free of disease 12 months after adrenalectomy, one patient was lost to follow-up after 22 months, and 6 patients have died from malignancy. The mean survival for the patients who died was 32 months. CONCLUSIONS: The rarity of isolated adrenal metastasis of colorectal carcinoma makes a randomized, prospective trial comparing surgery vs. nonsurgical management highly unlikely. Our results provide further support for surgical resection of solitary adrenal metastasis, which may translate into survival benefit.
    Mots-clés : Adrenal, Adrenalectomy, Aged, Carcinoma/, Colorectal, Disease-Free, Gland, Humans, Male, Middle, Neoplasms/, Outcome, pathology, secondary/, surgery, Survival, Treatment.

  • Paradiso Galatioto, G, Gravina, GL, Angelozzi, G, Sacchetti, A, Innominato, PF, Pace, G, Ranieri, G & Vicentini, C 2008, « May antioxidant therapy improve sperm parameters of men with persistent oligospermia after retrograde embolization for varicocele? », World J Urol, vol. 26, no. 1, p. 97-102, viewed sans date, .
    Résumé : We performed a randomized, prospective, controlled, intention to treat study in order to determine the effectiveness of an antioxidant therapy in improve the quality of seminal fluid parameters and the natural pregnancies in men with persistent oligospermia (5-20 million/ml) 6 months after retrograde embolization. Forty-two subjects were enrolled and randomized in the study. Treated group (20 subjects) was assigned to receive antioxidant therapy (NAC 600 mg and vitamins-minerals). Untreated group (22 subjects) received no adjunctive medical therapy and was used as controls. Our data were analyzed with an intention to treat strategy. A statistically significant increase in sperm count after antioxidant therapy was recorded (P=0.009). After this therapy, no statistical differences in percentage of WHO class A motile sperm (P=0.752) and typical forms (P=0.926) were found. The univariate logistic regression analysis showed that a man treated with antioxidant therapy presented a probability to have a normal sperm count 20-fold (OR=20.1; CI 95%=1.05-43.2; P=0.014) higher than a man who was untreated. No significant impact on spontaneous pregnancies was found after antioxidant therapy. Despite this preliminary data, we show that antioxidant therapy based on a combination of NAC and micronutrient supplementation can be helpful in improve the sperm count at least in a subset of oligospermic males. However, this improving in sperm count is not associated with a significant increase in spontaneous pregnancies after 12 months.
    Note Note
    <p>17982752</p>
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    <p>17982752</p>
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    <p>17982752</p>
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    <p>17982752</p>

  • Picone, O, Brisset, S, Senat, M-V, Maurin, M-L, Frydman, R & Tachdjian, G 2008, « [Risk of missed diagnosis of 22q11.2 deletion in a fetal cardiac conotruncal malformation when another chromosomal abnormality is detected] », J Gynecol Obstet Biol Reprod (Paris), vol. 37, no. 3, p. 299-301, viewed sans date, .
    Résumé : We present a rare case of prenatal diagnosis of two de novo chromosome structural rearrangements including a translocation (1;3) associated with a 22q11.2 deletion. The amniocentesis was performed because the systematic ultrasound examination revealed: right aortic cross with double aortic arch, with normal size of aorta and pulmonary artery. Our report emphasises that 22q11.2 deletion must be looked for when a fetal cardiac conotruncal malformation is diagnosed, even in the presence of another chromosomal abnormality. In prenatal diagnosis, this can have implication for patient management and genetic counselling.
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    <p>18160230</p>
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    <p>18160230</p>
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    <p>18160230</p>

  • Picone, O, Fuchs, F, Sénat, M-V, Brisset, S, Tachdjian, G, Audibert, F, Fernandez, H & Frydman, R 2008, « [Evaluation of the third trimester amniocentesis for fetal karyotyping in women with fear of pregnancy loss] », J Gynecol Obstet Biol Reprod (Paris), vol. 37, no. 4, p. 385-91, viewed sans date, .
    Résumé : OBJECTIVES: The aim of this study is to determine the complications of third trimester amniocentesis for fetal karyotyping among women unwilling to accept the fetal loss risks of second trimester amniocentesis. MATERIALS AND METHODS: A retrospective study was carried out from January 1998 to December 2006 of 182 singleton pregnancies that underwent a late amniocentesis (after 32 weeks) for fetal karyotyping. The indications were integrated risk (maternal age, first trimester nuchal translucency, second trimester maternal serum markers) over 1/250 (n=68), isolated maternal age over 38 years (n=51), isolated abnormal second trimester biochemical markers (n=34), history of personal or familial a chromosomal abnormality (n=21) or maternal choice (n=8). Presence of fetal abnormalities at ultrasound or context of viral or parasitologic seroconversion as well as multiple pregnancies were considered as non-inclusion criteria. RESULTS: Median maternal age and gestational age at sampling were 39 years (range 23-48) and 32.4 weeks (29.5-37.6). Median interval between amniocentesis and definitive results of amniocentesis on the one hand, and delivery on the on the hand were 15 days (7-42) and 47 days (8-69), respectively. There were no chromosomal abnormality and non-termination of pregnancy. Nine patients out of 182(5%) had a spontaneous labour followed by premature delivery before 37 weeks and six women (3.3%) among those nine displayed preterm premature rupture of membranes (PPROM). Four patients out of 182 (2%) gave birth before definitive karyotyping result but all of them had a direct fluorescence in situ hybridisation analysis with a normal karyotyping result known well before delivery. CONCLUSIONS: The risk of preterm premature rupture of membrane is 3.3%, with a 5% risk of premature delivery before 37 weeks. This late procedure provides a safe reassurance to women who are unwilling to accept the risks of earlier amniocentesis. However, it should only be used in particular situation and in countries were legislation allows late termination of pregnancy.
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    <p>18191913</p>
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  • Picone, O, Senat, M-V, Rosenblatt, J, Audibert, F, Tachdjian, G & Frydman, R 2008, « Fear of pregnancy loss and fetal karyotyping: a place for third-trimester amniocentesis? », Fetal Diagn Ther, vol. 23, no. 1, p. 30-5, viewed sans date, .
    Résumé : OBJECTIVE: To assess the complications of third-trimester amniocentesis for fetal karyotyping in women unwilling to accept the fetal loss risks of second-trimester amniocentesis. METHODS: Retrospective study of singleton pregnancies that underwent a third-trimester amniocentesis for karyotyping. 150 complete charts between 1998 and 2005 were reviewed. RESULTS: The indications were: isolated abnormal second-trimester biochemical markers (n = 57), isolated maternal age >38 years (n = 46), integrated risk (maternal age, first-trimester nuchal translucency, second-trimester maternal serum markers) >1/250 (n = 22), history of chromosomal abnormality (n = 17) or maternal choice (n = 8). The median maternal age and gestational age at sampling were: 40 years (23-48), 32.4 weeks (29.7-37.1). Median interval between amniocentesis, definitive result of amniocentesis, and delivery were 14 days (7-42), and 49 days (10-67) respectively. There were no abnormal karyotypes and no termination of pregnancy. Six women out of 150 (4%) had spontaneous labor before 36 weeks (2% after 36 weeks). CONCLUSION: The risk of spontaneous labor before 37 weeks after late amniocentesis is 4% (2% before 36 weeks). This technique provides a late but safe reassurance to women who are unwilling to accept the risks of earlier fetal karyotyping. This is of interest to countries such as France where legislation permits late termination of pregnancy.
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    <p>17934295</p>
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  • Plancoulaine, S, Mohamed, MK, Arafa, N, Bakr, I, Rekacewicz, C, Tregouet, DA, Obach, D, El Daly, M, Thiers, V, Feray, C, Abdel-Hamid, M, Abel, L & Fontanet, A 2008, « Dissection of familial correlations in hepatitis C virus (HCV) seroprevalence suggests intrafamilial viral transmission and genetic predisposition to infection », Gut, vol. 57, no. 9, p. 1268-74.
    Résumé : OBJECTIVE: Unsafe injections and transfusions used during treatments are considered to be responsible for many cases of transmission of hepatitis C virus (HCV) in developing countries, but cannot account for a substantial proportion of present infections. The aim of the present work was to investigate familial clustering of HCV infection in a population living in a highly endemic area. DESIGN, SETTING AND PARTICIPANTS: A large seroepidemiological survey was conducted on 3994 subjects (age range, 2-88 years) from 475 familial clusters in an Egyptian rural area. Epidemiological methods appropriate for the analysis of correlated data were used to estimate risk factors and familial dependences for HCV infection. A phylogenetic analysis was conducted to investigate HCV strain similarities within and among families. MAIN OUTCOME MEASURES: HCV familial correlations adjusted for known risk factors, similarities between viral strains. RESULTS: Overall HCV seroprevalence was 12.3%, increasing with age. After adjustment for relevant risk factors, highly significant intrafamilial resemblances in HCV seroprevalence were obtained between father-offspring (odds ratio (OR) = 3.4 (95% confidence interval (CI), 1.8 to 6.2)), mother-offspring (OR = 3.8 (95% CI, 2.5 to 5.8)), and sibling-sibling (OR = 9.3 (95% CI, 4.9 to 17.6)), while a weaker dependence between spouses (OR = 2.2 (95% CI, 1.3 to 3.7)) was observed. Phylogenetic analysis showed greater HCV strain similarity between family members than between unrelated subjects, indicating that correlations can be explained, in part, by familial sources of virus transmission. In addition, refined dissection of correlations between first-degree relatives supported the role of host genes predisposing to HCV infection. CONCLUSIONS: Current HCV infection in endemic countries has a strong familial component explained, at least partly, by specific modes of intrafamilial viral transmission and by genetic predisposition to infection.
    Mots-clés : 80 and over Child Child, Adolescent Adult Age Distribution Aged Aged, Preschool Egypt/epidemiology Female Genetic Predisposition to Disease Hepacivirus/classification Hepatitis C/epidemiology/ genetics/ transmission/virology Humans Infectious Disease Transmission, Vertical Male Middle Aged Phylogeny Reverse Transcriptase Polymerase Chain Reaction/methods Risk Factors Seroepidemiologic Studies Sex Distribution.
  • Ponnusamy, MP, Singh, AP, Jain, M, Chakraborty, S, Moniaux, N & Batra, SK 2008, « MUC4 activates HER2 signalling and enhances the motility of human ovarian cancer cells », Br J Cancer, vol. 99, no. 3, p. 520-6.
    Résumé : The mucin MUC4 is a high molecular weight transmembrane glycoprotein. It consists of a mucin-type subunit (MUC4alpha) and a transmembrane growth factor-like subunit (MUC4beta). The mucin MUC4 is overexpressed in many epithelial malignancies including ovarian cancer, suggesting a possible role in the pathogenesis of these cancers. In this study, we investigated the functional role of MUC4 in the human ovarian cancer cell line SKOV3. The mucin MUC4 was ectopically expressed by stable transfection, and its expression was examined by western blot and confocal microscopy analyses. The in vitro studies demonstrated an enhanced motility of MUC4-expressing SKOV3 cells compared with the vector-transfected cells. The mucin MUC4 expression was associated with apparent changes in actin organisation, leading to the formation of microspike, lammelopodia and filopodia-like cellular projections. An enhanced protein expression and activation of HER2, a receptor tyrosine kinase, was also seen, although no significant change was observed in HER-2 transcript levels in the MUC4-transfected SKOV3 cells. Reciprocal co-immunoprecipitation revealed an interaction of MUC4 with HER2. Further, the MUC4-overexpressing SKOV3 cells exhibited an increase in the phosphorylation of focal adhesion kinase (FAK), Akt and ERK, downstream effectors of HER2. Taken together, our findings demonstrate that MUC4 plays a role in ovarian cancer cell motility, in part, by altering actin arrangement and potentiating HER2 downstream signalling in these cells.
    Mots-clés : Base Sequence Cell Line, erbB-2/genetics/ metabolism Reverse Transcriptase Polymerase Chain Reaction Signal Transduction, Fluorescence Mucin-4 Mucins/ physiology Neoplasm Metastasis Ovarian Neoplasms/metabolism/ pathology RNA, Messenger/genetics Receptor, Tumor DNA Primers Female Humans Microscopy.
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    <p>2527793</p>
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    <p>2527793</p>
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    <p>2527793</p>
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    <p>2527793</p>
  • Pozdzik, AA, Salmon, IJ, Husson, CP, Decaestecker, C, Rogier, E, Bourgeade, MF, Deschodt-Lanckman, MM, Vanherweghem, JL & Nortier, JL 2008, « Patterns of interstitial inflammation during the evolution of renal injury in experimental aristolochic acid nephropathy », Nephrol Dial Transplant, vol. 23, no. 8, p. 2480-91.
    Résumé : BACKGROUND: Interstitial inflammation is a prominent feature associated with the severity of renal injury and progressive kidney failure. We utilized an animal model of aristolochic acid (AA)-induced nephropathy (AAN) to assess patterns of infiltration and inflammation during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis. METHODS: Male Wistar rats receiving sc daily AA or vehicle were sacrificed between Days 1 and 35. Infiltrating mononuclear cells were characterized by immunohistochemistry. The kidney infiltrating T lymphocytes were phenotyped by flow cytometry. Urinary levels of Th-1/ Th-2 cytokines, of monocyte chemoattractant protein-1 and of active transforming growth factor-beta (TGF-beta) were measured. Tissue expression of phosphorylated smad 2/3 protein was used to examine the TGF-beta signalling pathway. RESULTS: In AA rats, monocytes/macrophages and T lymphocytes predominantly infiltrated areas of necrotic proximal tubular cells. The coexpressions of ED1 and/or Ki-67/MHCII by infiltrating cells reflected monocyte/macrophage proliferation and their activation, respectively. The accumulation of cytotoxic T lymphocytes was attested by severe signs of CD8+ cell tubulitis. The CD8/E-cadherin costaining confirmed intrarenal homing of CD8+CD103+ cells. Urinary levels of proinflammatory cytokines and of active TGF-beta significantly increased at Days 10 and 35. An early and persistent nuclear overexpression of phosphorylated smad 2/3 protein was detected in tubular and interstitial compartments. CONCLUSION: An early and massive interstitial inflammation characterized by activated monocytes/macrophages and cytotoxic CD8+CD103+ T lymphocytes is demonstrated for the first time during the progression of experimental AAN. The involvement in an interstitial fibrosis onset of active TGF-beta is highly suggested, at least via the psmad 2/3 intracellular signalling pathway.
    Mots-clés : Animal Fibrosis Kidney/ drug effects/ pathology/physiopathology Kidney Failure, Animals Aristolochic Acids/ toxicity Disease Models, Chronic/chemically induced/pathology/physiopathology Macrophages/immunology/pathology Male Monocytes/immunology/pathology Rats Rats, Wistar Signal Transduction Smad2 Protein/metabolism Smad3 Protein/metabolism T-Lymphocytes/immunology/pathology Transforming Growth Factor beta/metabolism.

  • Quteineh, L, Verstuyft, C, Durrbach, A, Letierce, A, Ferlicot, S, Charpentier, B & Becquemont, L 2008, « Impact of VKORC1 haplotypes on long-term graft function in kidney transplantation », Transplantation, vol. 86, no. 6, p. 779-83, viewed sans date, .
    Résumé : BACKGROUND: Chronic allograft injury is the major cause of renal allograft loss after the first year of transplantation. Vitamin K epoxide reductase complex subunit 1 (VKORC1) haplotype combinations were found to be associated with the risk of developing vascular diseases. We aimed to study the effect of VKORC1 haplotypes on long-term graft function in a cohort of kidney transplant recipients. METHOD: A total of 288 renal allograft recipients participated in the study. Long-term renal graft function was measured by the estimation of the glomerular filtration rate. VKORC1 C+1173T single nucleotide polymorphism (rs9934438) was used as a tagging single nucleotide polymorphism for VKORC1*2 haplotype. RESULTS: Patients homozygous for VKORC1*2 haplotype showed less deterioration of renal graft function compared with the other patients (hazard ratio: 0.34, 95% confidence interval: 0.26-0.87, P=0.02). The same results were obtained in a multivariate analysis, where VKORC1 haplotypes showed to be an independent predictor of long-term graft function when adjusted to other variables contributing to long-term renal graft outcome. CONCLUSION: Our results suggest that VKORC1 haplotypes may play a role in the long-term renal allograft function. These findings need to be replicated in prospective clinical studies.
    Mots-clés : Single Nucleotide Proportional Hazards Models Proteinuria Recurrence Retrospective Studies Survival Rate Treatment Outcome.

  • Quteineh, L, Verstuyft, C, Furlan, V, Durrbach, A, Letierce, A, Ferlicot, S, Taburet, AM, Charpentier, B & Becquemont, L 2008, « Influence of CYP3A5 genetic polymorphism on tacrolimus daily dose requirements and acute rejection in renal graft recipients », Basic Clin Pharmacol Toxicol, vol. 103, no. 6, p. 546-52, viewed sans date, .
    Résumé : Tacrolimus is a widely used immunosuppressive drug in organ transplantation. Its oral bioavailability varies greatly between individuals, and it is a substrate of cytochrome P450 3A (CYP3A) and P-glycoprotein. Our objective was to determine the influence of CYP3A5 and ABCB1 genetic polymorphisms on tacrolimus daily requirements and on transplantation outcome. One hundred and thirty-six renal graft recipients treated with tacrolimus were genotyped for CYP3A5 (6986A>G), ABCB1 exon26 (3435C>T) and exon21 (2677G>T/A) single nucleotide polymorphisms. Genotypes were correlated to tacrolimus daily dose at 1-week, 1-, 6- and 12-month post-transplantation and with transplantation outcome. At 1-month post-transplantation, tacrolimus daily dose was higher for patients with CYP3A5*1/*1 genotype compared to CYP3A5*3/*3 genotype (0.26 +/- 0.03 versus 0.16 +/- 0.01 mg/kg/day, respectively, P < 0.0001). Similar results were obtained at 6- and 12-month post-transplantation. Furthermore, CYP3A5*1 homozygotes were associated with increased risk of acute rejection episodes compared to patients with CYP3A5*1/*3 and CYP3A5*3/*3 genotypes (38% versus 10% and 9%, respectively, P = 0.01). CYP3A5 genetic polymorphism was not associated with tacrolimus-related nephrotoxicity. ABCB1 polymorphisms were not related with transplantation outcome. CYP3A5 genetic polymorphism appeared in our study to affect tacrolimus daily dose requirements and transplantation outcome. Screening for this single nucleotide polymorphism before the transplantation might be helpful for the selection of adequate initial daily dose and to achieve the desired immunosuppression.
    Mots-clés : Acute Disease Cohort Studies Cytochrome P-450 CYP3A/*genetics Dose-Response Relationship, Drug Female Genotype Graft Rejection/enzymology/*prevention & control Hospitals, Genetic Retrospective Studies Risk Factors Tacrolimus/administration & dosage/adverse effects/*pharmacokinetics, University Humans Immunosuppressive Agents/administration & dosage/adverse effects/*pharmacokinetics *Kidney Transplantation Male Middle Aged Outpatients P-Glycoprotein/genetics *Polymorphism.

  • Rad, FH, Ulusakarya, A, Gad, S, Sibony, M, Juin, F, Richard, S, Machover, D & Uzan, G 2008, « Novel somatic mutations of the VHL gene in an erythropoietin-producing renal carcinoma associated with secondary polycythemia and elevated circulating endothelial progenitor cells », Am J Hematol, vol. 83, no. 2, p. 155-8, viewed sans date, .
    Résumé : Mutation of the VHL tumor suppressor gene is a frequent genetic event in the carcinogenesis of renal-cell carcinoma (RCC). Circulating endothelial progenitor cells (EPCs) have important role in neoangiogenesis, and mobilization of these cells is induced by various growth factors including erythropoietin (EPO). With this regard, we analyzed a patient with EPO-producing clear-cell RCC and polycythemia. DNA extraction and sequencing analysis of the VHL gene were performed from the tumor and the adjacent normal renal tissue. Isolated and cultured circulating EPCs from the blood taken with phlebotomy were characterized by flow cytometry and immunofluorescence analysis. This RCC had two novel somatic mutations of the VHL gene, p.Leu128Pro and p.Asn131Lys. Culture of blood mononuclear cells revealed a strikingly high number of endothelial cell colonies derived from EPCs (nearly 10-fold more than in controls). Elevated number of circulating EPCs seems to be related to high EPO production from RCC with novel double somatic mutation of the VHL gene in this patient.
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  • Raimondo, G, Allain, JP, Brunetto, MR, Buendia, MA, Chen, DS, Colombo, M, Craxi, A, Donato, F, Ferrari, C, Gaeta, GB, Gerlich, WH, Levrero, M, Locarnini, S, Michalak, T, Mondelli, MU, Pawlotsky, JM, Pollicino, T, Prati, D, Puoti, M, Samuel, D, Shouval, D, Smedile, A, Squadrito, G, Trepo, C, Villa, E, Will, H, Zanetti, AR & Zoulim, F 2008, « Statements from the Taormina expert meeting on occult hepatitis B virus infection », J Hepatol, vol. 49, no. 4, p. 652-7.
    Résumé : Raimondo, Giovanni; Allain, Jean-Pierre; Brunetto, Maurizia R; Buendia, Marie-Annick; Chen, Ding-Shinn; Colombo, Massimo; Craxi, Antonio; Donato, Francesco; Ferrari, Carlo; Gaeta, Giovanni B; Gerlich, Wolfram H; Levrero, Massimo; Locarnini, Stephen; Michalak, Thomas; Mondelli, Mario U; Pawlotsky, Jean-Michel; Pollicino, Teresa; Prati, Daniele; Puoti, Massimo; Samuel, Didier; Shouval, Daniel; Smedile, Antonina; Squadrito, Giovanni; Trepo, Christian; Villa, Erica; Will, Hans; Zanetti, Alessandro R; Zoulim, Fabien; Congresses; England; J Hepatol. 2008 Oct;49(4):652-7. doi: 10.1016/j.jhep.2008.07.014. Epub 2008 Jul 31.
    Mots-clés : Carcinoma, Hepatocellular/etiology DNA, Viral/genetics Hepatitis B/complications/ epidemiology/ transmission Hepatitis B virus/genetics/immunology Humans Italy Liver Neoplasms/etiology Risk Factors.


  • Reman, O, Pigneux, A, Huguet, F, Vey, N, Delannoy, A, Fegueux, N, de Botton, S, Stamatoullas, A, Tournilhac, O, Buzyn, A, Charrin, C, Boucheix, C, Gabert, J, Lhéritier, V, Vernant, J-P, Fière, D, Dombret, H, Thomas, X & group, GET-LALA 2008, « Central nervous system involvement in adult acute lymphoblastic leukemia at diagnosis and/or at first relapse: results from the GET-LALA group », Leuk Res, vol. 32, no. 11, p. 1741-50, viewed sans date, .
    Résumé : Outcome of adult acute lymphoblastic leukemia (ALL) with central nervous system (CNS) involvement is not clearly defined. We studied 104 patients presenting with CNS involvement at diagnosis among 1493 patients (7%) included into the LALA trials, and 109 patients presenting CNS disease at the time of first relapse among the 709 relapsing patients (15%). Eighty-seven patients (84%) with CNS leukemia at diagnosis achieved complete remission (CR). Fifty-three patients underwent stem cell transplantation (SCT): 25 allogeneic SCT, 28 autologous SCT, while 34 continued with chemotherapy alone. Seven-year overall survival (OS) and disease-free survival (DFS) were 34% and 35%, respectively. There were no significant differences in terms of CR, OS and DFS among patients with CNS involvement at diagnosis and those without CNS disease. There were also no differences among the two groups regarding T lineage ALL, B lineage ALL, and among those who underwent SCT. After a first relapse, 38 patients with CNS recurrence (35%) achieved a second CR. The median OS was 6.3 months. Outcome was similar to that of relapsing patients without CNS disease. CNS leukemia in adult ALL is uncommon at diagnosis as well as at the time of first relapse. With intensification therapy, patients with CNS leukemia at diagnosis have a similar outcome than those who did not present with CNS involvement. CNS leukemia at first relapse remains of similar poor prognosis than all other adult ALL in first relapse.
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    <p>18508120</p>
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  • Rocha-Perugini, V, Montpellier, C, Delgrange, D, Wychowski, C, Helle, F, Pillez, A, Drobecq, H, Le Naour, F, Charrin, S, Levy, S, Rubinstein, E, Dubuisson, J & Cocquerel, L 2008, « The CD81 partner EWI-2wint inhibits hepatitis C virus entry », PLoS One, vol. 3, no. 4, p. e1866, viewed sans date, .
    Résumé : Two to three percent of the world's population is chronically infected with hepatitis C virus (HCV) and thus at risk of developing liver cancer. Although precise mechanisms regulating HCV entry into hepatic cells are still unknown, several cell surface proteins have been identified as entry factors for this virus. Among these molecules, the tetraspanin CD81 is essential for HCV entry. Here, we have identified a partner of CD81, EWI-2wint, which is expressed in several cell lines but not in hepatocytes. Ectopic expression of EWI-2wint in a hepatoma cell line susceptible to HCV infection blocked viral entry by inhibiting the interaction between the HCV envelope glycoproteins and CD81. This finding suggests that, in addition to the presence of specific entry factors in the hepatocytes, the lack of a specific inhibitor can contribute to the hepatotropism of HCV. This is the first example of a pathogen gaining entry into host cells that lack a specific inhibitory factor.
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    <p>18382656</p>
  • Roche, B & Samuel, D 2008, « Liver transplantation in viral hepatitis: prevention of recurrence », Best Pract Res Clin Gastroenterol, vol. 22, no. 6, p. 1153-69.
    Résumé : End-stage liver disease caused by the hepatitis B and C viruses (HBV and HCV) are major indications for liver transplantation. Outcome depends largely on the prevention of allograft reinfection. The advent of long-term hepatitis B immune globulin administration and the introduction of new antiviral agents were a major breakthrough in the management of these patients. Today, survival after orthotopic liver transplantation (OLT) is similar to that of patients transplanted for HBsAg-negative liver disease, and the risk of recurrence is below 10%. In contrast, HCV reinfection is almost constant and significantly impairs patient and graft survival. Factors that may influence disease severity and consequently progression of HCV graft injury remain unclear. Pre-transplantation and prophylactic post-transplantation antiviral treatments are limited by low applicability and poor tolerance. Treatment of established graft lesions with combination therapy gave promising results, with sustained virological response in 25-45% of patients, but indications, modality and duration of treatment should be assessed.
    Mots-clés : Antiviral Agents/therapeutic use Clinical Trials as Topic Drug Therapy, Combination Hepatitis B/drug therapy/ surgery Hepatitis C/drug therapy/ surgery Humans Immunization, Passive Immunoglobulins/therapeutic use Immunologic Factors/therapeutic use Liver Transplantation Postoperative Care/methods Preoperative Care/methods Recurrence/prevention & control Treatment Outcome.
  • Roche, B, Sebagh, M, Canfora, ML, Antonini, T, Roque-Afonso, AM, Delvart, V, Saliba, F, Duclos-Vallee, JC, Castaing, D & Samuel, D 2008, « Hepatitis C virus therapy in liver transplant recipients: response predictors, effect on fibrosis progression, and importance of the initial stage of fibrosis », Liver Transpl, vol. 14, no. 12, p. 1766-77.
    Résumé : Antiviral therapy after liver transplantation (LT) using interferon (IFN) and ribavirin (RBV) can achieve a sustained virological response (SVR) rate ranging from 20% to 45%. The aims of our study were to assess efficacy and tolerability of therapy, effect on fibrosis progression and the importance of the initial fibrosis stage to outcome. A total of 113 hepatitis C virus (HCV)-infected LT patients received 133 courses of IFN (standard, n = 29, pegylated IFN [pegIFN], n = 104) and RBV (75% genotype 1). Early virological response (EVR), end-of-treatment (EOT), and SVR were obtained in 74%, 55%, and 38%, respectively. EVR, completion of treatment, viral load before therapy, genotype non-1, and use of pegIFN were predictive of SVR, but only EVR remained in the multivariate analysis. SVR was obtained in 45% patients who received a second course of therapy. Paired biopsies at baseline, at EOT and at long-term were available in 42 patients. The mean fibrosis stage remained stable in patients with SVR and increased in patients without response. Rejection episodes were observed in 6% of patients. Tolerability of therapy decrease in patients with fibrosis stage > or =3 on baseline liver biopsy. A total of 20% of them died or were retransplanted due to liver failure as opposed to 1% of patients who had fibrosis stage <3. In conclusion, IFN and RBV achieved SVR in 38% of patients. EVR is independently associated with SVR. Fibrosis stage remained stable in patients with SVR and increased in nonresponders. Fibrosis stage > or =3 was associated with a high rate of liver failure, arguing for an early introduction of antiviral therapy.
    Mots-clés : Adult Aged Antiviral Agents/ therapeutic use Disease Progression Drug Therapy, Combination Female Follow-Up Studies Hepatitis C.
  • Roque-Afonso, AM, Bralet, MP, Ichai, P, Desbois, D, Vaghefi, P, Castaing, D, Samuel, D & Dussaix, E 2008, « Chickenpox-associated fulminant hepatitis that led to liver transplantation in a 63-year-old woman », Liver Transpl, vol. 14, no. 9, p. 1309-12.
    Résumé : A 63-year-old woman treated with prednisone for sinusitis developed fulminant liver failure due to a clinically unsuspected primary varicella zoster virus infection. The diagnosis of herpetic hepatitis was made from a liver biopsy, and varicella zoster virus viremia was detected by polymerase chain reaction. She was treated successfully with transplantation and perioperative administration of acyclovir.
    Mots-clés : Acute/ complications/ therapy Liver Transplantation/ methods Middle Aged Polymerase Chain Reaction Prednisone/adverse effects Treatment Outcome, Acyclovir/therapeutic use Antiviral Agents/therapeutic use Biopsy Chickenpox/ complications/therapy Female Herpesvirus 3, Human/ metabolism Humans Liver/virology Liver Failure.


  • Saffroy, R, Benyamina, A, Pham, P, Marill, C, Karila, L, Reffas, M, Debuire, B, Reynaud, M & Lemoine, A 2008, « Protective effect against alcohol dependence of the thermolabile variant of MTHFR », Drug Alcohol Depend, vol. 96, no. 1-2, p. 30-6, viewed sans date, .
    Résumé : BACKGROUND: Hyperhomocysteinemia is frequently observed in alcohol-dependent subjects, in particularly in those with marked withdrawal symptoms. The common C677T transition on the methylenetetrahydrofolate reductase (MTHFR) gene influences homocysteinemia. Our objective was to study the prevalence of the MTHFR C677T polymorphism in alcohol-dependent subjects and the influence of this polymorphism on symptoms associated with alcoholism. METHODS: MTHFR C677T polymorphism was determined in 93 control subjects and 242 alcohol-dependent subjects. Serum homocysteine, folate and vitamin B12 levels together with hepatic biological parameters were determined in the control and alcohol-dependent subjects. RESULTS: Hyperhomocysteinemia is frequently observed in alcohol-dependent subjects, particularly in those with marked withdrawal symptoms. Alcohol-dependent subjects showed a significant decrease in MTHFR 677TT prevalence (9%, 21/242) compared to controls (18%, 17/93) (p<0.02). The relative risk estimated as an odds ratio for alcoholism in subjects with the TT genotype is 0.42 (odd ratio 95% confidence interval, 0.21-0.83). Moreover, drinkers with TT genotype presented lower values for markers of alcohol misuse (p<0.05), better liver function tests, a lower frequency of relapses and no marked withdrawal symptoms as assessed by the Lesch typology. CONCLUSION: MTHFR 677TT genotype could play a protective role against alcohol dependence. Moreover, when subjects with MTHFR 677TT genotype become dependent to alcohol, they seem to constitute a subgroup of alcoholic patients with a decreased risk for developing neurotoxic withdrawal symptoms and hepatic toxicity.
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  • Saliba, F & Dupont, B 2008, « Renal impairment and amphotericin B formulations in patients with invasive fungal infections », Med Mycol, vol. 46, no. 2, p. 97-112.
    Résumé : A systematic review was performed to examine renal function in patients with invasive fungal infections, comparing the nephrotoxicity caused by conventional amphotericin B deoxycholate (c-AmB) with that induced by the use of lipid-based amphotericin B formulations. The analysis considered all comparative studies published in the literature between January 1996 and May 2007. The outcome data reviewed herein focused on renal toxicity as measured by serum creatinine (S-Cr) and the doubling or the mean difference in S-Cr levels from baseline to the end of therapy or the need for dialysis. We found that AmB lipid complex (ABLC), liposomal AmB (L-AmB) and AmB colloidal dispersion (ABCD) were significantly less nephrotoxic than c-AmB in all reported studies. ABLC and L-AmB caused low and comparable nephrotoxicity in nine studies. In one randomized study, L-AmB was significantly less nephrotoxic than ABLC. No studies compared ABCD nephrotoxicity to the other lipid formulations. Based on our review we conclude that lipid formulations of amphotericin B are an important strategy to preserve renal function and improve survival in critically ill patients who require treatment for systemic fungal infections.
    Mots-clés : Agents/therapeutic, Amphotericin, Antifungal, B/therapeutic, chemically, Dialysis, drug, Humans, induced, Insufficiency/, Mycoses/, Outcome, Renal, Therapy, toxicity, Treatment, use/.
  • Salloum, C & Castaing, D 2008, « [Surgical margin status in hepatectomy for liver tumors] », Bull Cancer, vol. 95, no. 12, p. 1183-91.
    Résumé : It is admitted that only complete tumor clearance with negative surgical margins provides benefit for patients undergoing surgery for hepatobiliary malignancies. For hepatocellular carcinoma, since micrometastases disseminate via portal venous branches, anatomic resection is preferred over non-anatomic resection in liver resection carried out with curative intent. Thus, an anatomic liver resection with a wider resection margin theoretically gives a higher potential for cure. However, preserving non-tumorous liver parenchyma is an important consideration, especially in cirrhotic liver resection to decrease the incidence of postoperative liver failure. The optimal liver resection margin is still controversial. It seems that a resection margin of 2 cm is associated with a decreased postoperative recurrence rate and improved survival outcomes especially for hepatocellular carcinoma <or= 2 cm. Due to the unsatisfying alternatives in the medical and interventional treatment of intrahepatic cholangiocarcinoma, hepatic resection, whenever technically possible, should be enforced. Expected narrow hepatic resection margins should not exclude patients from potentially curative surgery, and should not be used as a reason to establish palliative treatment instead since R1 resection is compatible with long-term survival. Aggressive hepatic surgery could and should therefore be performed if the peri-operative mortality is low. For hilar cholangiocarcinoma, surgical radicality has been shown in multivariate analyses of multiples studies to be the only parameter with a significant impact on survival. Extended right-side hepatectomies seems to give the best oncologic results. A predicted margin of < 1 cm after resection of hepatic colorectal metastases should not be used as an exclusion criterion for resection and will not impair patients' prognosis. Resection should be performed whatever the width of the surgical margin, rather than not performing the resection at all.
    Mots-clés : Bile Duct Neoplasms/mortality/pathology/surgery Bile Ducts, Hepatocellular/mortality/pathology/surgery Cholangiocarcinoma/mortality/pathology/surgery Colorectal Neoplasms/pathology Hepatectomy/ methods/mortality Humans Liver Cirrhosis/complications Liver Neoplasms/mortality/ pathology/secondary/surgery Neoplasm, Intrahepatic Carcinoma, Residual.
  • Samuel, D 2008, « [Liver transplantation for chronic hepatitis B] », Gastroenterol Clin Biol, vol. 32, no. 1 Pt 2, p. S25-33.
    Résumé : Liver transplantation for hepatitis B represents 5-10 % of all liver transplantations performed in Europe. The prognosis after liver transplantation is related to the efficacy of prophylaxis of HBV graft reinfection. The risk of HBV reinfection is directly related to the HBV viral load at transplantation. HBV prophylaxis after transplantation with long-term administration of anti-HBS immune globulins (HBIG) or with monoprophylaxis with lamivudine can reduce significantly the risk of HBV recurrence mainly in patients without active HBV replication. Antivirals such as lamivudine, adefovir, entecavir or tenofovir can control HBV replication in patients with decompensated HBV cirrhosis waiting for transplantation. However, there is a risk of HBV viral breakthrough during nucleo (t) side antiviral treatment. The use of an antiviral alone or in combination should take into account the antiviral efficacy and the risk of viral resistance. The post-transplant combination of antiviral therapy and HBIG prophylaxis is very effective in reducing the rate of HBV reinfection to less than 10 % even in patients with HBV replication at transplantation. In the absence of active viral replication at transplantation, the possibilty to discontinue HBIG prophylaxis at long-term after transplantation with maintenance of antiviral treatment or HBV vaccination is in evaluation. The use of new antiviral therapies (nucleos(t)ide analogues) has dramatically improved the prognosis of patients with HBV reinfection of the graft. The current 5-year survival after liver transplantation for HBV related liver disease is 85 %. In conclusion, the prophylaxis of HBV reinfection combining antiviral therapy prior to transplantation, and combination of HBIG and antiviral therapy post-transplantation is effective in reducing the rate of HBV reinfection to less than 10 %.
    Mots-clés : Chronic/ surgery Humans Immunoglobulins/therapeutic use Liver Transplantation Postoperative Complications/prevention & control/virology Prognosis Recurrence/prevention & control Viral Load, Hepatitis B/prevention & control Hepatitis B.
  • Samuel, D, Weber, R, Stock, P, Duclos-Vallee, JC & Terrault, N 2008, « Are HIV-infected patients candidates for liver transplantation? », J Hepatol, vol. 48, no. 5, p. 697-707.
    Résumé : Samuel, Didier; Weber, Rainer; Stock, Peter; Duclos-Vallee, Jean-Charles; Terrault, Norah; Review; England; J Hepatol. 2008 May;48(5):697-707. doi: 10.1016/j.jhep.2008.02.009. Epub 2008 Feb 27.
    Mots-clés : Antiretroviral Therapy, Highly Active CD4 Lymphocyte Count HIV Infections/ complications/immunology Hepatitis B/complications/drug therapy/immunology Hepatitis C/complications/drug therapy/immunology Humans Immunosuppression Liver Transplantation.


  • Scatton, O, Chiappini, F, Liu, X-H, Riou, P, Marconi, A, Debuire, B, Azoulay, D & Lemoine, A 2008, « Generation and modulation of hepatocellular carcinoma circulating cells: a new experimental model », J Surg Res, vol. 150, no. 2, p. 183-9, viewed sans date, .
    Résumé : BACKGROUND: To establish a new experimental model of human hepatocellular carcinoma by orthotopic implantation of tumoral cells with its subsequent removal, to generate and modulate circulating tumoral cells. MATERIALS AND METHODS: Three human hepatoma cell lines (HepG2, PLC/PRF, and Mahlavu) were orthotopically implanted under the Glisson's capsule of the left lateral lobe of the liver in a total of 56 non-obese diabetic/severe combined immunodeficiency mice. Tumor removal was performed 30 d after injection, and a laparotomy without tumor removal was done in control mice. Generation of circulating cells was monitored by flow cytometry using fluorescein isothiocyanate-conjugated anti-HLA antibody. RESULTS: In 26 mice implanted with Mahlavu cells, 20 developed a unique tumor allowing a resection (77%), which was technically feasible in 80% of cases. The overall perioperative mortality was 30% (3/10) after resection; no mortality was observed in the control group. The circulating tumoral cells decreased dramatically after resection of the tumor as compared with control mice. CONCLUSION: This new model is feasible and may be an interesting useful tool to study the hepatocellular carcinoma metastatic process and is consistent with the human clinical practice.
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  • Schwarz, NG, Revillion, M, Roque-Afonso, AM, Dussaix, E, Giraud, M, Liberpre, C, Couturier, E & Delarocque Astagneau, E 2008, « A food-borne outbreak of hepatitis A virus (HAV) infection in a secondary school in Upper Normandy, France, in November 2006 », Euro Surveill, vol. 13, no. 22.
    Résumé : In November 2006, six symptomatic cases of hepatitis A in pupils of a secondary school in Upper Normandy, France, were reported to the district health service. This paper describes the outbreak investigation undertaken with the aim to identify the vehicle and source of infection, implement control measures and estimate the size of the outbreak. A primary case at the secondary school was defined as a pupil or a member of the staff with IgM anti-HAV detected in the serum and with onset of symptoms between 12 and 21 November 2006; a secondary case was defined as a contact to a primary case and who developed symptoms and had IgM anti-HAV two to seven weeks later. We performed a case control study of primary cases, controls being pupils visiting the same school (cases/controls 1:4) and inspected the canteen facilities. All 13 canteen employees were examined for anti-HAV IgM antibodies. A phylogenetic analysis of HAV of cases was performed. We identified 10 primary and 5 secondary cases. Among primary cases 90% reported eating liver pate at the canteen compared to 62% among controls (OR 5.5, 95% CI 0.62-256.9). One liver pate sample contained markers of faecal contamination. HAV genotypes were of one identical type. All 13 canteen employees were negative for IgM anti-HAV while four had anti-HAV total antibodies. We found deficiencies regarding food preparing procedures and insufficient hand washing facilities. The vehicle of the outbreak was believed to be the liver pate but the source of HAV could not be identified. Insufficient facilities in the canteen hindered staff from maintaining a high hygiene standard and were subsequently improved.
    Mots-clés : &, A/, Adolescent, Adult, Assessment/, Contamination/, data, disease, epidemiology, Factors, Female, Food, France/epidemiology, Hepatitis, Humans, Incidence, Male, methods, numerical, Outbreaks/, Population, Risk, Schools/, statistics, Surveillance.

  • Shah, A, Alberts, S & Adam, R 2008, « Accomplishments in 2007 in the management of curable metastatic colorectal cancer », Gastrointest Cancer Res, vol. 2, no. 3 Suppl, p. S13-8, viewed sans date, .
    Résumé : Overview of the Disease IncidencePrognosisCurrent Therapy Standards Colorectal Liver Metastases (CRLM) Resectable TumorsStrategies To Convert Nonresectable Liver Metastases to Resectable StatusSynchronous Colorectal Liver MetastasesPredictors of Survival After Resection of CRLMPeritoneal Carcinomatosis (PC) From Colorectal CancerColorectal Pulmonary Metastases (CRPM)Colorectal Liver Metastases With Extrahepatic DiseaseAccomplishments (or Lack of Accomplishments) During the Year Therapy New Staging SystemPreventive Measures for CRLMSystemic ChemotherapySelective Internal Radiation Therapy (SIRT)Proposed Definition of Cure From CRLMBasic ScienceWhat Needs To Be Done? Optimizing Patient CareControversies and DisagreementsFuture Directions Comments on ResearchObstacles to Progress.
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  • Sobesky, R, Lebray, P, Nalpas, B, Vallet-Pichard, A, Fontaine, H, Lagneau, JL & Pol, S 2008, « Pathological evolution of hepatitis C virus-"Healthy carriers" », World J Gastroenterol, vol. 14, no. 24, p. 3861-5.
    Résumé : AIM: To determine factors associated with fibrosis progression in hepatitis C virus (HCV)-infected patients without significant initial pathological lesions. METHODS: Seventy six untreated HCV-infected patients with initially normal liver as defined by a Knodell score < or = 3, with 2 liver biopsies and detectable HCV-RNA were included. Markers of fibrosis progression were assessed. RESULTS: Median duration of infection and time between paired biopsies was 13 (95% CI: 1-28) and 4 (95% CI: 2-16) years respectively. Alanine-transaminase (ALT) activity was normal in 43.4% of cases. 50% demonstrated progression of the necro-inflammation and 34% of fibrosis after a median time evolution of 4 years (95% CI: 2-16). The median difference in the necro-inflammation and fibrosis score between biopsies was low, 1.5 and 0.0 respectively. Univariate analysis showed there was no difference between fibrosis activity or evolution according to genotype or viral load. A higher fibrosis progression (P = 0.03) was observed in patients with body mass index (BMI) > 25. Fibrosis progression correlated with the time interval between biopsies (P = 0.01). A significant progression of activity (1.7 vs 0.4, P < 0.05) or fibrosis (0.9 vs 0.0, P < 0.01) was observed in patients with elevated ALT. There was a significant correlation between activity progression and fibrosis progression (P = 0.003). Multivariate analysis demonstrated that fibrosis progression was associated with elevated ALT, BMI > 25 and the time interval between 2 biopsies. CONCLUSION: There is no fibrosis progression in 66% of patients without significant initial histopathological lesion. Fibrosis progression is associated with elevated ALT and BMI > 25.
    Mots-clés : Viral/blood Severity of Illness Index Viral Load.
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    <p>2721443</p>
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  • Tabone-Eglinger, S, Bahleda, R, Cote, JF, Terrier, P, Vidaud, D, Cayre, A, Beauchet, A, Theou-Anton, N, Terrier-Lacombe, MJ, Lemoine, A, Penault-Llorca, F, Le Cesne, A & Emile, JF 2008, « Frequent EGFR Positivity and Overexpression in High-Grade Areas of Human MPNSTs », Sarcoma, vol. 2008, p. 849156, viewed sans date, .
    Résumé : Malignant peripheral nerve sheath tumours (MPNSTs) are highly malignant and resistant. Transformation might implicate up regulation of epidermal growth factor receptor (EGFR). Fifty-two MPNST samples were studied for EGFR, Ki-67, p53, and survivin expression by immunohistochemistry and for EGFR amplification by in situ hybridization. Results were correlated with clinical data. EGFR RNA was also quantified by RT-PCR in 20 other MPNSTs and 14 dermal neurofibromas. Half of the patients had a neurofibromatosis type 1 (NF1). EGFR expression, detected in 86% of MPNSTs, was more frequent in NF1 specimens and closely associated with high-grade and p53-positive areas. MPNSTs expressed more EGFR transcripts than neurofibromas. No amplification of EGFR locus was observed. NF1 status was the only prognostic factor in multivariate analysis, with median survivals of 18 and 43 months for patients with or without NF1. Finally, EGFR might become a new target for MPNSTs treatment, especially in NF1-associated MPNSTs.
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    <p>2526168</p>
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  • Tabone-Eglinger, S, Subra, F, El Sayadi, H, Alberti, L, Tabone, E, Michot, JP, Theou-Anton, N, Lemoine, A, Blay, JY & Emile, JF 2008, « KIT mutations induce intracellular retention and activation of an immature form of the KIT protein in gastrointestinal stromal tumors », Clin Cancer Res, vol. 14, no. 8, p. 2285-94, viewed sans date, .
    Résumé : PURPOSE: Gastrointestinal stromal tumors (GIST) are frequently associated with gain-of-function mutations of KIT, which can be inhibited by imatinib both in vitro and in vivo. The survival of patients with GIST, following imatinib therapy, has been correlated with the nature of mutations but not with KIT expression. EXPERIMENTAL DESIGN: Subcellular localization, activation, and trafficking of the mature and the immature forms of KIT were investigated in GIST samples and in NIH3T3 cells infected with two different GIST-type exon 11-mutated human KIT cDNA. RESULTS: Paranuclear dot expression of KIT was more frequent in GISTs with homozygous KIT mutations than in those with heterozygous (P = 0.01) or no mutations (P < 0.01). Activation of the immature 125 kDa form of KIT was detected in most GISTs with KIT mutations but not in GISTs without KIT mutations. In NIH3T3 cells, mutant KIT was mainly retained within endoplasmic reticulum and Golgi compartments in an immature constitutively phosphorylated form, whereas the wild-type KIT was expressed at the plasma membrane, in a mature nonphosphorylated form. Imatinib-induced inhibition of the phosphorylation of immature and mature mutant KIT proteins resulted in the restoration of KIT expression at the cell surface. CONCLUSIONS: These results show that GIST-type KIT mutations induce an activation-dependent alteration of normal maturation and trafficking, resulting in the intracellular retention of the activated kinase within the cell. These observations likely account for the absence of correlation between response to imatinib and KIT expression using immunohistochemistry and may deserve to be investigated in other tyrosine kinase-activated tumors.
    Mots-clés : *Mutation, 3T3, Animals, c-kit/*genetics/*metabolism, Cell, Cells, Factor/pharmacology, Gastrointestinal, Humans, Mice, NIH, Phosphorylation, Proteins, Proto-Oncogene, Stem, Stromal, Tumors/genetics/*metabolism.

  • Tachdjian, G, Aboura, A, Portnoï, M-F, Pasquier, M, Bourcigaux, N, Simon, T, Rousseau, G, Finkel, L, Benkhalifa, M & Christin-Maitre, S 2008, « Cryptic Xp duplication including the SHOX gene in a woman with 46,X, del(X)(q21.31) and premature ovarian failure », Hum Reprod, vol. 23, no. 1, p. 222-6, viewed sans date, .
    Résumé : BACKGROUND: Premature ovarian failure (POF) is defined as amenorrhoea for >6 months, occurring before the age of 40, with an FSH serum level in the menopausal range. Although Xq deletions have been known for a long time to be associated with POF, the mechanisms involved in X deletions in order to explain ovarian failure remain unknown. In order to look for potentially cryptic chromosomal imbalance, we used high-resolution genomic analysis to characterize X chromosome deletions associated with POF. METHODS: Three patients with POF presenting terminal Xq deletions detected by conventional cytogenetics were included in the study. Genome wide microarray comparative genomic hybridization (CGH) at a resolution of 1 Mb and fluorescence in situ hybridization (FISH) was performed. RESULTS: Microarray CGH and FISH studies characterized the three deletions as del(X)(q21.2), del(X)(q21.31) and del(X)(q22.33). Microarray CGH showed that the del(X)(q21.31) was also associated with a Xpter duplication including the SHOX gene. In these patients with POF, deletions or duplications of autosomes have been excluded. CONCLUSION: This study is the first one using microarray in patients with POF. It demonstrates that putative X chromosome deletions can be associated with other chromosomal imbalances such as duplications, and therefore illustrates the use of microarray CGH to screen chromosomal abnormalities in patients with POF.
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  • Tahiri, F, Le Naour, F, Huguet, S, Lai-Kuen, R, Samuel, D, Johanet, C, Saubamea, B, Tricottet, V, Duclos-Vallee, JC & Ballot, E 2008, « Identification of plasma membrane autoantigens in autoimmune hepatitis type 1 using a proteomics tool », Hepatology, vol. 47, no. 3, p. 937-48.
    Résumé : Autoimmune hepatitis (AIH) is a liver disease with circulating autoantibodies predominantly directed against widely held cellular components. Because AIH is a liver-specific disease, autoantibodies against plasma membrane antigens may be involved in its pathogenesis and have been reported; however, no definite identification has been described. We thus investigated the fine specificity of anti-hepatocyte plasma membrane autoantibodies in type 1 AIH (AIH-1) using a proteomic tool. A plasma membrane-enriched fraction was validated using enzymatic activity and western blot analysis experiments. Sera from AIH-1 patients (n = 65) and from 90 controls, that is, healthy blood donors (n = 40) and patients with systemic diseases (n = 20) or other liver diseases (n = 30), were studied by immunoblot performed with plasma membrane proteins resolved by either sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) or 2-dimensional (2D) electrophoresis. Proteins contained in the immunoreactive spots were identified by sequences provided by ion-trap mass spectrometry. Hepatocytes probed with sera were also studied using confocal immunofluorescence and immunoelectron microscopy. The more prominent bands stained by patient sera were located at 38 kDa, 48, 50, 52 kDa, 62 kDa, 70 kDa, and a 95-kDa double band. Six proteins with known potential plasma membrane expression were identified: liver arginase (38 kDa), cytokeratins (CK) 8 and 18 (48-52 kDa), heat shock proteins (HSP) of 60, 70, 90 kDa, and valosin-containing protein (VCP) of 92 kDa. The presence of anti-membrane antibodies was confirmed by immunofluorescence and immunoelectron microscopy. CONCLUSION: Overall, our data demonstrate that liver arginase, CK 8/18, HSP 60, HSP 70, HSP 90, and VCP represent potential candidate targets on liver membrane for autoantibodies in AIH-1.
    Mots-clés : Adolescent Adult Aged Autoantibodies/blood/ immunology Autoantigens/immunology/ isolation & purification Cell Membrane/ immunology Child Female Hepatitis, Autoimmune/diagnosis/ immunology Hepatocytes/immunology Humans Immunoblotting Male Membrane Proteins/immunology/ isolation & purification Middle Aged Proteomics.


  • Tamgüney, G, Giles, K, Glidden, DV, Lessard, P, Wille, H, Tremblay, P, Groth, DF, Yehiely, F, Korth, C, Moore, RC, Tatzelt, J, Rubinstein, E, Boucheix, C, Yang, X, Stanley, P, Lisanti, MP, Dwek, RA, Rudd, PM, Moskovitz, J, Epstein, CJ, Cruz, TD, Kuziel, WA, Maeda, N, Sap, J, Ashe, KH, Carlson, GA, Tesseur, I, Wyss-Coray, T, Mucke, L, Weisgraber, KH, Mahley, RW, Cohen, FE & Prusiner, SB 2008, « Genes contributing to prion pathogenesis », J Gen Virol, vol. 89, no. Pt 7, p. 1777-88, viewed sans date, .
    Résumé : Prion diseases are caused by conversion of a normally folded, non-pathogenic isoform of the prion protein (PrP(C)) to a misfolded, pathogenic isoform (PrP(Sc)). Prion inoculation experiments in mice expressing homologous PrP(C) molecules on different genetic backgrounds displayed different incubation times, indicating that the conversion reaction may be influenced by other gene products. To identify genes that contribute to prion pathogenesis, we analysed incubation times of prions in mice in which the gene product was inactivated, knocked out or overexpressed. We tested 20 candidate genes, because their products either colocalize with PrP, are associated with Alzheimer's disease, are elevated during prion disease, or function in PrP-mediated signalling, PrP glycosylation, or protein maintenance. Whereas some of the candidates tested may have a role in the normal function of PrP(C), our data show that many genes previously implicated in prion replication have no discernible effect on the pathogenesis of prion disease. While most genes tested did not significantly affect survival times, ablation of the amyloid beta (A4) precursor protein (App) or interleukin-1 receptor, type I (Il1r1), and transgenic overexpression of human superoxide dismutase 1 (SOD1) prolonged incubation times by 13, 16 and 19 %, respectively.
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  • Tanabe, KK, Lemoine, A, Finkelstein, DM, Kawasaki, H, Fujii, T, Chung, RT, Lauwers, GY, Kulu, Y, Muzikansky, A, Kuruppu, D, Lanuti, M, Goodwin, JM, Azoulay, D & Fuchs, BC 2008, « Epidermal growth factor gene functional polymorphism and the risk of hepatocellular carcinoma in patients with cirrhosis », JAMA, vol. 299, no. 1, p. 53-60, viewed sans date, .
    Résumé : CONTEXT: Overexpression of epidermal growth factor (EGF) in the liver induces transformation to hepatocellular carcinoma in animal models. Polymorphisms in the EGF gene modulate EGF levels. OBJECTIVE: To assess the relationship among human EGF gene single-nucleotide polymorphism, EGF expression, and risk of hepatocellular carcinoma. DESIGN, SETTING, AND PARTICIPANTS: Molecular mechanisms linking the 61*G allele polymorphism to EGF expression were examined in human hepatocellular carcinoma cell lines and human liver tissue. A case-control study involving 207 patients with cirrhosis was conducted at the Massachusetts General Hospital (1999-2006) and a validation case-control study involving 121 patients with cirrhosis was conducted at Hopital Paul Brousse (1993-2006). Restriction fragment-length polymorphism was used to determine the EGF gene polymorphism genotype. Logistic regression analysis was used to assess the association between the EGF polymorphism and hepatocellular carcinoma risk. MAIN OUTCOME MEASURES: Mechanisms by which the EGF gene polymorphism modulates EGF levels and associations among EGF gene polymorphism, EGF levels, and hepatocellular carcinoma. RESULTS: Transcripts from the EGF 61*G allele exhibited more than a 2-fold longer half-life than those from the 61*A allele, and EGF secretion was 2.3-fold higher in G/G hepatocellular carcinoma cell lines than A/A cell lines. Serum EGF levels were 1.8-fold higher in G/G patients than A/A patients, and liver EGF levels were 2.4-fold higher in G/G patients than A/A patients. Among the 207 patients with cirrhosis in the Massachusetts study population, 59 also had hepatocellular carcinoma. Analysis of the distribution of allelic frequencies revealed that there was a 4-fold odds of hepatocellular carcinoma in G/G patients compared with A/A patients in the Massachusetts study population (odds ratio, 4.0; 95% confidence interval [CI], 1.6-9.6; P = .002). Logistic regression analysis demonstrated that the number of copies of G was significantly associated with hepatocellular carcinoma after adjusting for age, sex, race, etiology, and severity of cirrhosis (G/G or A/G vs A/A; hazard ratio, 3.49; 95% CI, 1.29-9.44; P = .01). The significant association was validated in the French patients with alcoholic cirrhosis and hepatocellular carcinoma. CONCLUSION: The EGF gene polymorphism genotype is associated with risk for development of hepatocellular carcinoma in liver cirrhosis through modulation of EGF levels.
    Mots-clés : Carcinoma, Cultured Enzyme-Linked Immunosorbent Assay Epidermal Growth Factor/*genetics/metabolism Female Gene Expression Regulation, Hepatocellular/etiology/*genetics/metabolism Case-Control Studies Cell Line, Neoplastic Genotype Humans Liver Cirrhosis/*complications/genetics/metabolism Liver Neoplasms/etiology/*genetics/metabolism Male Middle Aged Polymerase Chain Reaction *Polymorphism, Single Nucleotide Risk Factors, Tumor Cells.


  • Tateo, M, Sebagh, M, Bralet, M-P, Teicher, E, Azoulay, D, Mallet, V, Pol, S, Castaing, D, Samuel, D & Duclos-Vallée, J-C 2008, « A new indication for liver transplantation: nodular regenerative hyperplasia in human immunodeficiency virus-infected patients », Liver Transpl, vol. 14, no. 8, p. 1194-8, viewed sans date, .
    Résumé : Nodular regenerative hyperplasia is one of the causes of noncirrhotic portal hypertension and has recently been described in human immunodeficiency virus-infected patients, and the potential role of a prothrombotic state and hepatotoxic antiretroviral medication has been suggested. Moreover, it is now established that liver transplantation is feasible in HIV-infected patients. We describe here our experience concerning 3 HIV-infected patients with severe complications of nodular regenerative hyperplasia treated with liver transplantation.
    Mots-clés : Adult, complications, Diseases/etiology/, Female, HIV, Humans, Hyperplasia/etiology/surgery, Infections/, Liver, Liver/, Male, pathology, surgery, Transplantation.
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    <p>18668652</p>

  • Tattoli, I, Carneiro, LA, Jehanno, M, Magalhaes, JG, Shu, Y, Philpott, DJ, Arnoult, D & Girardin, SE 2008, « NLRX1 is a mitochondrial NOD-like receptor that amplifies NF-kappaB and JNK pathways by inducing reactive oxygen species production », EMBO Rep, vol. 9, no. 3, p. 293-300, viewed sans date, .
    Résumé : NOD-like receptors (NLRs) are a family of intracellular sensors of microbial- or danger-associated molecular patterns. Here, we report the identification of NLRX1, which is a new member of the NLR family that localizes to the mitochondria. NLRX1 alone failed to trigger most of the common signalling pathways, including nuclear factor-kappaB (NF)-kappaB- and type I interferon-dependent cascades, but could potently trigger the generation of reactive oxygen species (ROS). Importantly, NLRX1 synergistically potentiated ROS production induced by tumour necrosis factor alpha, Shigella infection and double-stranded RNA, resulting in amplified NF-kappaB-dependent and JUN amino-terminal kinases-dependent signalling. Together, these results identify NLRX1 as a NLR that contributes to the link between ROS generation at the mitochondria and innate immune responses.
    Mots-clés : Acid, Amino, B/*metabolism, Cells, data, effects, effects/*enzymology, effects/physiology, Factor-alpha/pharmacology, HeLa, Humans, JNK, Kinases/*metabolism, Mitochondria/drug, Mitochondrial, Mitogen-Activated, Molecular, Necrosis, NF-kappa, Oxygen, Phylogeny, Protein, Proteins/chemistry/*metabolism, Reactive, Sequence, Shigella/drug, Signal, Species/*metabolism, Transduction/drug, Tumor.
    Note Note
    <p>2267388</p>
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    <p>2267388</p>
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    <p>2267388</p>
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    <p>2267388</p>
  • Vibert, E & Castaing, D 2008, « Surgical treatment of liver metastases of gynecological cancer: local treatment of a systemic disease », Onkologie, vol. 31, no. 8-9, p. 425-6.
    Résumé : Vibert, Eric; Castaing, Denis; Editorial; Switzerland; Onkologie. 2008 Sep;31(8-9):425-6. doi: 10.1159/000143274. Epub 2008 Jul 31.
    Mots-clés : Female Genital Neoplasms, Female/surgery Hepatectomy/ methods Humans Liver Neoplasms/ secondary/ surgery.
  • Vibert, E & Samuel, D 2008, « Molecular tools and hepatocellular carcinoma: Adding help or confusion in liver transplantation? », J Hepatol, vol. 49, no. 4, p. 498-501.
    Résumé : Vibert, Eric; Samuel, Didier; Comment; Editorial; England; J Hepatol. 2008 Oct;49(4):498-501. doi: 10.1016/j.jhep.2008.07.004. Epub 2008 Jul 18.
    Mots-clés : Biological/ genetics, Carcinoma, Hepatocellular/blood supply/ genetics/ surgery Gene Frequency/genetics Humans Liver Neoplasms/blood supply/ genetics/ surgery Liver Transplantation Loss of Heterozygosity/genetics Neoplasm Recurrence, Local/ diagnosis/epidemiology Neovascularization, Pathologic/complications Prognosis Risk Factors Treatment Outcome Tumor Markers.

  • Villalva, C, Sorel, N, Bonnet, M-L, Guilhot, J, Mayeur-Rousse, C, Guilhot, F, Chomel, J-C & Turhan, AG 2008, « Neutrophil gelatinase-associated lipocalin expression in chronic myeloid leukemia », Leuk Lymphoma, vol. 49, no. 5, p. 984-8, viewed sans date, .
    Résumé : The murine equivalent of neutrophil gelatinase-associated lipocalin (NGAL) was previously found to be increased by BCR-ABL expression in murine models of chronic myeloid leukemia (CML). Our study evaluates, in CML patients at various clinical stages, the levels of NGAL mRNA in blood samples and protein in sera. A highly significant increase of mRNA expression and protein secretion was shown in patients at diagnosis. The parallel expression of NGAL and BCR-ABL at the early stage of CML process allows us to suggest that NGAL could play an important role in the physiopathology of CML.
    Note Note
    <p>18464118</p>
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    <p>18464118</p>
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    <p>18464118</p>
    Note Note
    <p>18464118</p>


  • Wicherts, DA, Miller, R, de Haas, RJ, Bitsakou, G, Vibert, E, Veilhan, L-A, Azoulay, D, Bismuth, H, Castaing, D & Adam, R 2008, « Long-term results of two-stage hepatectomy for irresectable colorectal cancer liver metastases », Ann Surg, vol. 248, no. 6, p. 994-1005, viewed sans date, .
    Résumé : OBJECTIVE: To assess feasibility, risks, and long-term outcome of 2-stage hepatectomy as a means to improve resectability of colorectal liver metastases (CLM). SUMMARY BACKGROUND DATA: Two-stage hepatectomy uses compensatory liver regeneration after a first noncurative hepatectomy to enable a second curative resection. METHODS: Between October 1992 and January 2007, among 262 patients with initially irresectable CLM, 59 patients (23%) were planned for 2-stage hepatectomy. Patients were eligible when single resection could not achieve complete treatment, even in combination with chemotherapy, portal embolization, or radiofrequency, but tumors could be totally removed by 2 sequential resections. Feasibility and outcomes were prospectively evaluated. RESULTS: Two-stage hepatectomy was feasible in 41 of 59 patients (69%). Eighteen patients failed to complete the second hepatectomy because of disease progression (n = 17) or bad performance status (n = 1). The 41 successfully treated patients had a mean number of 9.1 metastases (mean diameter, 48.5 mm at diagnosis). Chemotherapy was delivered before (95%), in between (78%), and after (78%) the 2 hepatectomies. Mean delay between the 2 liver resections was 4.2 months. Postoperative mortality was 0% and 7% (3/41) after the first and second hepatectomy, respectively. Morbidity rates were also higher after the second procedure (59% vs. 20%) (P < 0.001). Five-year survival was 31% on an intention to treat basis, and all but 2 patients who did not complete the 2-stage strategy died within 19 months. After a median follow-up of 24.4 months (range, 3.7-130.3), overall 3- and 5-year survivals for patients that completed both hepatectomies were 60% and 42%, respectively, after the first hepatectomy (median survival, 42 months from first hepatectomy and 57 months from metastases diagnosis). Disease-free survivals were 26% and 13% at 3 and 5 years, respectively. CONCLUSIONS: Two-stage hepatectomy provides a 5-year survival of 42% and a hope of long-term survival for selected patients with extensive bilobar CLM, irresectable by any other means.
    Mots-clés : 80 and over Chemotherapy, Adjuvant Colorectal Neoplasms/pathology Combined Modality Therapy Cryotherapy Disease-Free Survival Embolization, Adult Aged Aged.
    Note Note
    <p>19092344</p>
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    <p>19092344</p>
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    <p>19092344</p>
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    <p>19092344</p>
  • Wyplosz, B, Carlotti, A, Escaut, L, Vignier, N, Guettier, C, Agbalika, F, Vittecoq, D & Dupin, N 2008, « Initial human herpesvirus-8 rash and multicentric Castleman disease », Clin Infect Dis, vol. 47, no. 5, p. 684-8.
    Résumé : We describe a human immunodeficiency virus-infected man with relapsing rashes and reactivation of human herpesvirus-8 (HHV-8) infection, which evolved into multicentric Castleman disease. Initial skin biopsy revealed infiltrating HHV-8-positive plasmablasts, a subset of which supported lytic infection. We document the first case, to our knowledge, of HHV-8-induced rash and suggest that circulating plasmablasts drive HHV-8 to target tissues.
    Mots-clés : Aged Exanthema/ etiology Giant Lymph Node Hyperplasia/ etiology Herpesviridae Infections/ complications/ virology Herpesvirus 8, Human/ isolation & purification Humans Male Plasma Cells/virology Skin/pathology.


  • Yalaoui, S, Zougbédé, S, Charrin, S, Silvie, O, Arduise, C, Farhati, K, Boucheix, C, Mazier, D, Rubinstein, E & Froissard, P 2008, « Hepatocyte permissiveness to Plasmodium infection is conveyed by a short and structurally conserved region of the CD81 large extracellular domain », PLoS Pathog, vol. 4, no. 2, p. e1000010, viewed sans date, .
    Résumé : Invasion of hepatocytes by Plasmodium sporozoites is a prerequisite for establishment of a malaria infection, and thus represents an attractive target for anti-malarial interventions. Still, the molecular mechanisms underlying sporozoite invasion are largely unknown. We have previously reported that the tetraspanin CD81, a known receptor for the hepatitis C virus (HCV), is required on hepatocytes for infection by sporozoites of several Plasmodium species. Here we have characterized CD81 molecular determinants required for infection of hepatocytic cells by P. yoelii sporozoites. Using CD9/CD81 chimeras, we have identified in CD81 a 21 amino acid stretch located in a domain structurally conserved in the large extracellular loop of tetraspanins, which is sufficient in an otherwise CD9 background to confer susceptibility to P. yoelii infection. By site-directed mutagenesis, we have demonstrated the key role of a solvent-exposed region around residue D137 within this domain. A mAb that requires this region for optimal binding did not block infection, in contrast to other CD81 mAbs. This study has uncovered a new functionally important region of CD81, independent of HCV E2 envelope protein binding domain, and further suggests that CD81 may not interact directly with a parasite ligand during Plasmodium infection, but instead may regulate the function of a yet unknown partner protein.
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    <p>18389082</p>
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    <p>18389082</p>
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    <p>18389082</p>
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    <p>18389082</p>
  • Yan, XB, Mei, L, Feng, X, Wan, MR, Chen, Z, Pavio, N & Brechot, C 2008, « Hepatitis C virus core proteins derived from different quasispecies of genotype 1b inhibit the growth of Chang liver cells », World J Gastroenterol, vol. 14, no. 18, p. 2877-81.
    Résumé : AIM: To investigate the influence of different quasispecies of hepatitis C virus (HCV) genotype 1b core protein on growth of Chang liver cells. METHODS: Three eukaryotic expression plasmids (pEGFP-N1/core) that contained different quasispecies truncated core proteins of HCV genotype 1b were constructed. These were derived from tumor (T) and non-tumor (NT) tissues of a patient infected with HCV and C191 (HCV-J6). The core protein expression plasmids were transiently transfected into Chang liver cells. At different times, the cell cycle and apoptosis was assayed by flow cytometry, and cell proliferation was assayed by methyl thiazolyl tetrazolium (MTT) assay. RESULTS: The proportion of S-phase Chang liver cells transfected with pEGFP-N1/core was significantly lower than that of cells transfected with blank plasmid at three different times after transfection (all P < 0.05). The proliferation ratio of cells transfected with pEGFP-N1/core was significantly lower than that of cells transfected with blank plasmid. Among three different quasispecies, T, NT and C191 core expression cells, there was no significant difference in the proportion of S- and G0/G1-phase cells. The percentage of apoptotic cells was highest for T (T > NT > C191), and apoptosis was increased in cells transfected with pEGFP-N1/core as the transfection time increased (72 h > 48 h > 24 h). CONCLUSION: These results suggest that HCV genotype 1b core protein induces apoptosis, and inhibits cell-cycle progression and proliferation of Chang liver cells. Different quasispecies core proteins of HCV genotype 1b might have some differences in the pathogenesis of HCV persistent infection and hepatocellular carcinoma.
    Mots-clés : Apoptosis/drug, Cell, chemistry/genetics, Core, Cycle/drug, cytology/drug, drug, effects, Genotype, Hepacivirus/, Humans, Liver/, pharmacology, Plasmids, Proliferation/, Proteins/, Transfection, Viral.
    Note Note
    <p>2710731</p>
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    <p>2710731</p>
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    <p>2710731</p>
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    <p>2710731</p>

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