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81篇 您的检索式:作者名="Pradat"
    题名 作者 年代 出处 被引量
1Rapid detection of genotypes and mutation in the pre - core promoyer and the pre - core region of hepatitis B virus genome: correlation with viral persistence and disease severity显示文摘Grandjecques C Pradat P Stuyer L 2000J Hepatol2000,33,3:1
2Efficacy and tolerance of a combination of tenofovir disoproxil fumarate plus emtricitabine in patients with chronic hepatitis B: a European multicenter study显示文摘Si-Ahmed SN Pradat P Zoutendijk R 2011Antiviral Res2011,92,1:1
3Rapid detection of genotypes and mutations in the pre-core and the pre-core region of hepatitis B virus genorne显示文摘Kidd-Ljunggren K Grandjacquesc P Pradat P 1997J Gen Virol1997,78,:1
4Causes of death in a post- mortem series of ALS patients 显示文摘Corcia P Pradat PF Salachas F 2008Amyotroph Lateral Scler2008,9,1:1
5Treatment of peripheral neuropathies with neutrotrophic factors: animal models and clinical trials 显示文摘Pradat PF 2003Rev Neurol (Paris)2003,159,2:1
6Abnormalities of satellite cells function in amyotrophic lateral sclerosis显示文摘Pradat PF Barani A Wanschitz J 0,,04:1
7Continuous delivery of neuortorphin 3 by gene therapy has a neuorportective effect in experimental models of diabetic and acrylarnide neu ropathies 显示文摘Pradat PF Kennel P N aimi-Sadaoui S 2001Hum Gene Ther2001,12,18:1
8The epidemiology of cardio- vascular defects part I : a study based on data from three large regis- tries of congenital malformations 显示文摘Pradat P Franeannet C Harris JA 2003Pediatr Cardol2003,24,3:1
9Viral and non-viral gene therapy partially prevents experimental cisplatin-induced neuropathy显示文摘Pradat PF Kennel P Naimi-Sadaoui S 2002Gene Ther2002,9,19:1
10Clinical relevance of total HCV core antigen testing for hepatitis C monitoring and for predicting patients response to therapy显示文摘Maynard M Pradat P Berthillon P 0,,:1
11Long-term follow-up of the hepati- tis C HENCORE cohort:response to therapy and occurrence of liver- related complications 显示文摘Pradat P Tillmann HL Sauleda S 2007J Viral Hepat2007,14,8:1
12Neuroflament light and heterogeneity of disease progression in amyotrophic lateral sclerosis:development and validation of a prediction model to improve interventional trials显示文摘Background:Interventional trials in amyotrophic lateral sclerosis(ALS)sufer from the heterogeneity of the disease as it considerably reduces statistical power.We asked if blood neuroflament light chains(NfL)could be used to antici‑pate disease progression and increase trial power.Methods:In 125 patients with ALS from three independent prospective studies-one observational study and two interventional trials-we developed and externally validated a multivariate linear model for predicting disease pro‑gression,measured by the monthly decrease of the ALS Functional Rating Scale Revised(ALSFRS-R)score.We trained the prediction model in the observational study and tested the predictive value of the following parameters assessed at diagnosis:NfL levels,sex,age,site of onset,body mass index,disease duration,ALSFRS-R score,and monthly ALSFRS-R score decrease since disease onset.We then applied the resulting model in the other two study cohorts to assess the actual utility for interventional trials.We analyzed the impact on trial power in mixed-efects models and compared the performance of the NfL model with two currently used predictive approaches,which anticipate disease progression using the ALSFRS-R decrease during a three-month observational period(lead-in)or since disease onset(ΔFRS).Results:Among the parameters provided,the NfL levels(P<0.001)and the interaction with site of onset(P<0.01)contributed signifcantly to the prediction,forming a robust NfL prediction model(R=0.67).Model application in the trial cohorts confrmed its applicability and revealed superiority over lead-in andΔFRS-based approaches.The NfL model improved statistical power by 61%and 22%(95%confdence intervals:54%-66%,7%-29%).Conclusion:The use of the NfL-based prediction model to compensate for clinical heterogeneity in ALS could signif‑cantly increase the trial power.NCT00868166,registered March23,2009;NCT02306590,registered December 2,2014.Simon Witzel Felix Frauhammer† Petra Steinacker David Devos Pierre‑François Pradat Vincent Meininger Stefen Halbgebauer Patrick Oeckl Joachim Schuster Simon Anders Johannes Dorst Markus Otto Albert C.Ludolph 2021Translational Neurodegeneration2021,10,3:1
13A rare disease but a classic ALS mimic syndrome显示文摘Pierre-Francois Pradat T 2014Sclerose lateraleamyotrophique2014,43,5:1
14Impact of lamivudine-resistance mutations on entecavir treatment outcome in hepatitis B显示文摘Koffi J Egounlety R Pradat P 2014Eur J Gastroenterol Hepatol2014,26,2:1
15Radiation-induced neuropathy in cancer survivors 显示文摘Delanian S Lefaix JL Pradat PF 2012Radiother Oncol2012,105,3:1
16Synthesis of Sulfones by phase-transfer alkylation of arenesulfinate salts显示文摘Jack K Crandall Chrostian Pradat 1985J Org Chem1985,50,8:1
17Predictive value of ALT levels for histologic findings in chronic hepatitis C:a European collaborative study显示文摘Pradat P Alberti A Poynard T 2002Hepatology2002,36,:1
18Late radiation injury to peripheral nerves 显示文摘Pradat PF Delanian S 2013Handb Clin Neural2013,115,:1
19Good practice in the management of amyotrophic lateral sclerosis: Clinical guidelines. An evidence‐based review with good practice points. EALSC Working Group显示文摘Peter Munch Andersen Gian Domenico Borasio Reinhard Dengler Orla Hardiman Katja Kollewe Peter Nigel Leigh Pierre‐Francois Pradat Vincenzo Silani Barbara Tomik 2007Amyotrophic Lateral Sclerosis2007,,4:1
20Rapid detection of genotypes and mutations in the pre-core promoter and the pre-core region of hepatitis B virus genome:correlation with viral persistence and disease severity显示文摘Grandjacques C Pradat P Stuyver L 0,,:1
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