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W. Li,H. J. Wang,M. Lin,B. Lai,D. Li,W. Pan 한국자기학회 2011 Journal of Magnetics Vol.16 No.3
The effect of the hot-compaction temperature on the microstructure and magnetic properties of anisotropic nanocrystalline magnets was investigated. The hot-compaction temperature was found to impact both the magnetic properties and the microstructure of die-upset magnets. The remanence of the isotropic precursor increases slightly with the improved hot-compaction temperature, and the grains start to grow on the flake boundary at higher hot-compaction temperatures. After hot deformation, it was found that the change in the magnetic properties was the inverse of that observed with the hot-compaction temperature. Microstructural investigation showed that die-upset magnets inherit the microstructural characteristics of their precursor. For the die-upset magnets, hot pressed at low temperature, scarcely any abnormal grain growth on the flake boundary can be seen. For those hot pressed at higher temperatures, however, layers with large equiaxed grains could be observed, which accounted for the poor alignment during the hot deformation, and thus the poor magnetic properties.
( L. Wei ),( F. Wang ),( M. Zhang ),( J. Jia ),( A.A. Yakovlev ),( W. Xie ),( E.Z. Burnevich ),( J. Niu ),( Y.J. Jung ),( X. Jiang ),( M. Xu ),( X. Chen ),( Q. Xie ),( J. Li ),( J. Hou ),( H. Tang ),( 대한간학회 2017 춘·추계 학술대회 (KASL) Vol.2017 No.1
Background/Aims: Treatment-naive GT 1b-infected patients from mainland China, South Korea and Russia were assessed for SVR at follow-up week 12 (SVR12) after receiving daclatasvir (60 mg, QD) and asunaprevir (100 mg, BID) (DCV+ASV). Methods: Patients were randomized 3:1 to receive DCV+ASV (24 weeks; immediate treatment [IM]) or 12 weeks of placebo followed by DCV+ASV (24 weeks; placebo-deferred treatment [PD]). The primary endpoint was to evaluate SVR12 in the IM arm to the historical rate for peginterferon/ribavirin (70%). Secondary endpoints included overall safety and safety comparisons between the treatment arms during the first 12 weeks. Results: 207 patients were randomized to IM (n=155) or PD (n=52); Asian (86%), female (59%), IL28B CC genotype (68%) and median age 49 (range 18-73) years; cirrhosis (13%), HCV RNA ≥6x106 IU/mL (53%). SVR12 in the IM arm was 92% and broadly unaffected by most baseline factors assessed (Figure); SVR12 was higher in patients without (96%) baseline NS5A-L31M/V or Y93H polymorphisms. There were 6 virologic breakthroughs, 6 relapses and 1 detectable HCV RNA at end-of-treatment in the IM arm. Safety was mostly comparable between the two arms during the first 12 weeks. The most frequent adverse events (AEs; ≥5%) during DCV+ASV (24 weeks) treatment in both arms were aminotransferase, bilirubin and INR elevations, hypertension, fatigue and respiratory tract infections; the most frequent treatment-emergent grade 3/4 laboratory abnormalities were aminotransferase (≤4.5%) and hematologic, lipase and total bilirubin abnormalities (≤2%); one patient (IM) discontinued DCV+ASV for aminotransferase elevations, nausea and jaundice (all reversible); one patient PD) discontinued DCV+ASV for a fatal AE unrelated to treatment. Conclusions: These data demonstrate that DCV+ASV is a highly efficacious and well tolerated treatment for treatment-naive HCV GT 1b-infected patients. Those treated immediately with DCV+ASV achieved a 92% SVR12 rate which was unaffected by factors known to attenuate response to interferon.