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RISS 인기검색어
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- 저자 : ( F Poordad ) (검색결과 3 건)
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( Jp Bronowicki ),( M Davis ),( S Flamm ),( S Gordon ),( E Lawitz ),( E Yoshida ),( J Galati ),( V Luketic ),( J Mccone ),( I Jacobson ),( P Marcellin ),( A Muir1 ),( F Poordad ),( Ld Pedicone ),( W D 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.-
Background: Patients in the PR control arms of BOC Phase 2/3 studies who did not achieve SVR could enroll in PROVIDE and receive BOC+PR. This interim analysis examines the preliminary efficacy and safety of BOC+PR in patients who failed prior treatment with PR. Methods: BOC (800 mg TID with food) was given with P 1.5 mcg/kg/week and weight-based R (600-1400 mg/day) BID for up to 44 weeks. If >2 weeks had elapsed since end of treatment in the previous study, PR was given for 4 weeks before adding BOC. Protocol specified analyses include patients who received at least one dose of BOC. Denominators for on-treatment response include patients who reached the specific time point or discontinued. The denominators for SVR include all patients who reached end of follow-up, discontinued, or were treatment failures. Results: Characteristics of 168 enrolled patients were: 67% male, 84% Caucasian, mean age 52 years, mean BMI 27.9 kg/m2, 77% high viral load (>800,000 IU/mL; mean log10 6.26); 10% cirrhotic; 61% subtype 1a. Table shows the proportion of BOC treated patients with undetectable HCV RNA at tested time points. SVR was achieved in 40% of prior null responders (<2 log10 decline in HCV RNA at TW12 in prior study) and 68% of prior partial responders/relapsers; 78% (38/49) of prior null responders and 24% (26/107) of prior partial responders/ relapsers had <1 log10 decline in HCV RNA after the PR lead in. Overall SVR was 47% in patients with <1 log10 decline with lower SVR rates in prior null responders (36%) vs. prior partial responders/relapsers (65%). 68% of patients with >1 log decline achieved SVR (55% prior null responders; 70% prior partial responders/relapsers). Seven percent of patients discontinued due to AEs, while 48% experienced anemia, 34% dysgeusia and 22% neutropenia. Conclusions: BOC+PR achieved high SVR rates regardless of prior response to PR. The degree of interferon responsiveness after PR lead in correlates with prior response and can help predict SVR for prior null responders. The safety profile is comparable to that previously reported for BOC+PR.
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( Jp Bronowicki ),( M Davis ),( S Flamm ),( S Gordon ),( E Lawitz ),( E Yoshida ),( J Galati ),( V Luketic ),( J Mccone ),( Jacobson ),( P Marcellin ),( A Muir ),( F Poordad ),( Ld Pedicone ),( W Deng 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.1
Background: Patients in the PR control arms of BOC Phase 2/3 studies who did not achieve SVR could enroll in PROVIDE and receive BOC+PR. This interim analysis examines the preliminary efficacy and safety of BOC+PR in patients who failed prior treatment with PR. Methods: BOC (800 mg TID with food) was given with P 1.5 mcg/kg/week and weight-based R (600-1400 mg/day) BID for up to 44 weeks. If >2 weeks had elapsed since end of treatment in the previous study, PR was given for 4 weeks before adding BOC. Protocol specified analyses include patients who received at least one dose of BOC. Denominators for on-treatment response include patients who reached the specific time point or discontinued. The denominators for SVR include all patients who reached end of follow-up, discontinued, or were treatment failures. Results: Characteristics of 168 enrolled patients were: 67% male, 84% Caucasian, mean age 52 years, mean BMI 27.9 kg/m2, 77% high viral load (>800,000 IU/mL; mean log10 6.26); 10% cirrhotic; 61% subtype 1a. Table shows the proportion of BOC treated patients with undetectable HCV RNA at tested time points. SVR was achieved in 40% of prior null responders (<2 log10 decline in HCV RNA at TW12 in prior study) and 68% of prior partial responders/relapsers; 78% (38/49) of prior null responders and 24% (26/107) of prior partial responders/ relapsers had <1 log10 decline in HCV RNA after the PR lead in. Overall SVR was 47% in patients with <1 log10 decline with lower SVR rates in prior null responders (36%) vs. prior partial responders/relapsers (65%). 68% of patients with >1 log decline achieved SVR (55% prior null responders; 70% prior partial responders/relapsers). Seven percent of patients discontinued due to AEs, while 48% experienced anemia, 34% dysgeusia and 22% neutropenia. Conclusions: BOC+PR achieved high SVR rates regardless of prior response to PR. The degree of interferon responsiveness after PR lead in correlates with prior response and can help predict SVR for prior null responders. The safety profile is comparable to that previously reported for BOC+PR.
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Colin M. Dinney,Lu-Dong Zhao,Charles D. Conrad,Jay M. Duker,Richard O. Karas,Zhibin Hu,Michele A. Hamilton,Thomas R. Gillis,Thomas M. Parker,Bing Fan,Andrew H. Advani,Fred B. Poordad,Paulette L. Fauce 한국미생물학회 2015 The journal of microbiology Vol.53 No.10
Chronic HBV infection is the leading cause of liver cirrhosis and hepatic cancer, but the individual responses toward HBV infection are highly variable, ranging from asymptomatic to chronic active hepatitis B inflammation. In this study, we hypothesized that the different individual responses to HBV infection was associated with differences in HBV-specific CD8+ T cell-mediated inflammation and cytotoxicity. Blood samples were collected from subjects with asymptomatic HBV-infection, subjects undergoing active chronic HBV flares (active CHB), and subjects with HBV-infected hepatocellular carcinoma (HBV-HCC). By tetramer staining, we found that all three groups had similar frequencies of HBVspecific CD8+ T cells. However, after HBV peptide stimulation, the HBV-specific CD8+ T cells in asymptomatic subjects had significantly stronger interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), and CD107a expression than those in active CHB and HBV-HCC patients. Examination of surface marker expression revealed that the PD-1-Tim-3- double-negative cell population was the main contributor to HBV-specific inflammation. In active CHB patients and HBV-HCC patients, however, the frequencies of activated PD-1-Tim-3- cells were significantly reduced. Moreover, the serum HBV DNA titer was not correlated with the frequencies of HBV-specific CD8+ T cells but was inversely correlated with the frequencies of IFN-g-expressing and CD107a-express cells in response to HBV stimulation. Together, our data demonstrated that the status of HBVspecific CD8+ T cell exhaustion was associated with different clinical outcomes of chronic HBV infection.
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