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| 1 | Fibrinolytic and in flammatorg processes in pleural effusions显示文摘 | Philip JF Slessi MC Philip JC | 1995 | EurRespir J1995，8，： | 1 |
| 2 | The use of the simple genetic algorithm in finding the critical factor of safety in slope stability analysis显示文摘 | Paul Mc Combie Philip Wilkinson | 2002 | Computers and Geotechnics2002，29，8： | 1 |
| 3 | Fibrinolgtil and in flammatorg processes in pleural effusions显示文摘 | Philip JF Alessi MC Philip JC | 1995 | Eur Respir J1995，8，： | 1 |
| 4 | Logistics Costs and the Location of the Fim:A One-Dimensional Comparative Satic Approach显示文摘 | PHILIP Mc CANN | 1996 | Location Science1996，4，： | 1 |
| 5 | Barriers to successful treatment completion in child sexual abuse survivors显示文摘 | Paul Mc Pherson Philip Scribano Jack Stevens | 2012 | Journal of Interpersonal Violence2012，27，1： | 1 |
| 6 | Primary mediastinal synovial sarcoma with trans- diaphragmatic extension presentingasa pericardial effusion 显示文摘 | Korula A Shah A Philip MA Kuruvila K Pradhip J Pal MC eta1 | 2009 | Singapore Med J2009，50，： | 1 |
| 7 | Amyloid-beta-dependent phosphorylation of collapsin response mediator protein-2 dissociates kinesin in Alzheimer's disease显示文摘Alzheimer’s disease(AD)is a neurodegenerative disorder characterized by accumulation of amyloid plaques and neurofibrillary tangles.Prior to the development of these characteristic pathological hallmarks of AD,anterograde axonal transport is impaired.However,the key proteins that initiate these intracellular impairments remain elusive.The collapsin response mediator protein-2(CRMP-2)plays an integral role in kinesin-1-dependent axonal transport and there is evidence that phosphorylation of CRMP-2releases kinesin-1.Here,we tested the hypothesis that amyloid-beta(Aβ)-dependent phosphorylation of CRMP-2 disrupts its association with the kinesin-1(an anterograde axonal motor transport protein)in AD.We found that brain sections and lysates from AD patients demonstrated elevated phosphorylation of CRMP-2 at the T555 site.Additionally,in the transgenic Tg2576 mouse model of familial AD(FAD)that exhibits Aβaccumulation in the brain with age,we found substantial co-localization of p T555CRMP-2and dystrophic neurites.In SH-SY5Y differentiated neuronal cultures,Aβ-dependent phosphorylation of CRMP-2 at the T555 site was also elevated and this reduced the CRMP-2 association with kinesin-1.The overexpression of an unphosphorylatable form of CRMP-2 in neurons promoted the re-establishment of CRMP-2-kinesin association and axon elongation.These data suggest that Aβ-dependent phosphorylation of CRMP-2 at the T555 site may directly impair anterograde axonal transport protein function,leading to neuronal defects. | Sara H.Mokhtar Min Joung Kim Kylie A.Magee Pei Mun Aui Speros Thomas Maha M.Bakhuraysah Amani A.Alrehaili Jae Young Lee David L.Steer Rachel Kenny Catriona Mc Lean Michael F.Azari Antonis Birpanagos Ewlina Lipiec Philip Heraud Bayden Wood Steven Petratos | 2018 | Neural Regeneration Research2018，13，6： | 1 |
| 8 | Industrial clusters:Complexes,agglorneration and/or social networks?显示文摘 | Ian R Gordon Philip Mc Cann | 2000 | Urban Studies2000，37，3： | 1 |
| 9 | Barriers to Successful Treatment Completion in Child Sexual Abuse Survivors显示文摘 | Paul Mc Pherson Philip Scribano Jack Stevens | 2012 | Journal of Interpersonal Violence2012，27，1： | 1 |
| 10 | High-dise methotrexate and HELP(holoxan,eldesine,platinum)-doxorubicin in non-metastatic osteosarcoma of the extremity:A French multicentre pilot study显示文摘 | Iliescu C Demaille MC | 1999 | Ann Oncol1999，10，： | 1 |
| 11 | The structure and evolution of industrial clusters: Transactions, technology and knowledge spillovers显示文摘 | Simona L Philip MC | 2006 | Research Policy2006，，35： | 1 |
| 12 | Roles of apolipoprotein E in Alzheimer's disease and other neurological disorders 显示文摘 | Philip BV Joseph MC David MH | 2011 | Lancet Neu- ro12011，10，3： | 1 |
| 13 | The Structure and Evolution of Industrial Clusters:Transactions,Technology and Knowledge Spillovers显示文摘 | Iammarino S Philip Mc Cann | 2006 | Research Policy2006，35，7： | 1 |
| 14 | Daclatasvir vs telaprevir plus peginterferon alfa/ribavirin for hepatitis C virus genotype 1显示文摘AIM: To evaluate daclatasvir vs telaprevir, each combined with peginterferon alfa-2a/ribavirin(peg IFN/RBV), in treatment-naive hepatitis C virus(HCV) genotype(GT) 1-infected patients.METHODS: In this phase 3, randomized, open-label, noninferiority study, 602 patients were randomly assigned(2:1) to daclatasvir vs telaprevir, stratified by IL28 B rs12979860 host genotype(CC vs non-CC), cirrhosis status(compensated cirrhosis vs no cirrhosis), and HCV GT1 subtype(GT1a vs GT1b). Patients were selected by study inclusion criteria from a total of 793 enrolled patients. Patients received daclatasvir 60 mg once daily or telaprevir 750 mg 3 times daily plus peg IFN/RBV. Daclatasvir recipients received 24 wk of daclatasvir plus peg IFN/RBV; those without an extended rapid virologic response(e RVR; undetectable HCV-RNA at weeks 4 and 12) received an additional 24 wk of peg IFN/RBV. Telaprevir-treated patients received 12 wk of telaprevir plus peg IFN/RBV followed by 12(with e RVR) or 36(no e RVR) wk of peg IFN/RBV. The primary objective was to compare for noninferiority of sustained virologic response rates at posttreatment week 12(SVR12) in GT1b-infected patients. Key secondary objectives were to demonstrate that the rates of anemia(hemoglobin < 10 g/d L) and rashrelated events, through week 12, were lower with daclatasvir + peg IFN/RBV than with telaprevir + peg IFN/RBV among GT1b-infected patients. Resistance testing was performed using population-based sequencing of the NS5 A region for all patients at baseline, and for patients with virologic failure or relapse and HCV-RNA ≥ 1000 IU/m L, to investigate any link between NS5 A polymorphisms associated with daclatasvir resistance and virologic outcome. RESULTS: Patient demographics and disease characteristics were generally balanced across treatment arms; however, there was a higher proportion of black/African Americans in the daclatasvir groups(6.0% and 8.2% in the GT1 b and GT1 a groups, respectively) than in the telaprevir groups(2.2% and 3.0%). Among GT1 binfected patients, daclatasvir plus peg IFN/RBV was noninferior to telaprevir plus peg IFN/RBV for SVR12 [85%(228/268) vs 81%(109/134); difference, 4.3%(95%CI:-3.3% to 11.9%)]. Anemia(hemoglobin < 10 g/d L) was significantly less frequent with daclatasvir than with telaprevir [difference,-29.1%(95%CI:-38.8% to-19.4%)]. Rash-related events were also less common with daclatasvir than with telaprevir, but the difference was not statistically significant. In GT1 ainfected patients, SVR12 was 64.9% with daclatasvir and 69.7% with telaprevir. Among both daclatasvir and telaprevir treatment groups, across GT1b- or GT1a-infected patients, lower response rates were observed in patients with IL28 B non-CC and cirrhosis- factors known to affect response to peg IFN/RBV. Consistent with these observations, a multivariate logistic regression analysis in GT1b-infected patients d e m o n s t ra t e d t h a t S V R 1 2 wa s a s s o c i a t e d w i t h IL28 B host genotype(CC vs non-CC, P = 0.011) and cirrhosis status(absent vs present, P = 0.031). NS5 A polymorphisms associated with daclatasvir resistance(at L28, R30, L31, or Y93) were observed in 17.3% of GT1b-infected patients at baseline; such variants did not appear to be absolute predictors of failure since 72.1% of these patients achieved SVR12 compared with 86.9% without these polymorphisms. Among GT1b-infected patients, treatment was completed by 85.4%(229/268) in the daclatasvir group, and by 85.1%(114/134) in the telaprevir group, and among GT1a-infected patients, by 67.2%(90/134) and 69.7%(46/66), respectively. Discontinuations(of all 3 agents) due to an AE were more frequent with telaprevir than with daclatasvir, whereas discontinuations due to lack of efficacy were more frequent with daclatasvir, due, in part, to differences in futility criteria. CONCLUSION: Daclatasvir plus peg IFN/RBV demonstrated noninferiority to telaprevir plus peg IFN/RBV for SVR12 and was well-tolerated in treatment-naive GT1 binfected patients, supporting the use of daclatasvir with other direct-acting antivirals. | Ira Jacobson Stefan Zeuzem Robert Flisiak Brygida Knysz Stefan Lueth Dorota Zarebska-Michaluk Ewa Janczewska Peter Ferenci Moises Diago Anna Linda Zignego Rifaat Safadi Yaacov Baruch Dzhamal Abdurakhmanov Stephen Shafran Dominique Thabut Rafael Bruck Adrian Gadano Alexander James Thompson Justin Kopit Fiona Mc Phee Tracy Michener Eric A Hughes Philip D Yin Stephanie Noviello | 2016 | World Journal of Gastroenterology2016，22，12： | 1 |
| 15 | Adrenal myelolipoma显示文摘 | Katherine MC Philip JK David SM | 1996 | AJR1996，166，3： | 1 |
| 16 | Fibrinolytic and inflammatory processes in pleural effusions显示文摘 | Phlilip JE Aless MC Philip JC | 1995 | Eur Respir J1995，8，： | 1 |
| 17 | Fibrinogen and inflammatory processes in pleural effusions显示文摘 | Philip JF Alessi MC Philip JC | 1995 | Eur Respir J1995，8，1： | 1 |
| 18 | Corneal shape in hyperopia显示文摘 | Julia CM Leo GC Philip MC | 1998 | Clin Exp Opt1998，3，： | 1 |
| 19 | Fibrinogen and inflammatory processes in pleural effusions显示文摘 | Philip JF Alessi MC Philip JC | 1995 | Eur Respir J1995，8，8： | 1 |
| 20 | Peritoneal dialysis-first policy made successful: perspectives and actions显示文摘 | Philip KL Kai MC | 2013 | Am J Kidney Dis2013，62，5： | 1 |
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