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M. J. Kao,F. C. Hsu,J. B. Guo,K. D. Huang,D. X. Peng 대한금속·재료학회 2013 ELECTRONIC MATERIALS LETTERS Vol.9 No.6
This project investigated the tribological properties of Cu-benzotriazole (BTA) composite nanoparticles as lubricant additives. BTA functions as a stabilizer for the Cu nanoparticles and as a protector from oxidation of the Cu nanoparticles in various test circumstances. Tribological experiments were conducted using a pin-on-disk (ASTM G99) test for the wear scar diameter, friction coefficient, and morphology of worn surfaces. Furthermore,the dispersivity of these Cu-BTA nanoparticles in liquid paraffin oil was measured using a UV/VIS spectrophotometer. The experiment results revealed the dispersion capability of the benzotriazole-capped Cu nanoparticles and indicated the dispersing stability in liquid paraffin oil for the BTA-capped surface of Cu nanoparticles. The testing results demonstrate that the Cu-BTA nanoparticle used as an additive in liquid paraffin oil at an appropriate concentration exhibits better tribological properties than those of pure paraffin oil. Moreover,Cu-BTA functioning as an additive has different anti-wear abilities due to its small size effect. Finally, the repair ability of Cu-BTA nanoparticles on the worn surfaces was observed using SEM and EDS.
Focal amplification and oncogene dependency of GAB2 in breast cancer
Bocanegra, M,Bergamaschi, A,Kim, Y H,Miller, M A,Rajput, A B,Kao, J,Langerød, A,Han, W,Noh, D -Y,Jeffrey, S S,Huntsman, D G,Børresen-Dale, A -L,Pollack, J R Macmillan Publishers Limited 2010 Oncogene Vol.29 No.5
DNA amplifications in breast cancer are frequent on chromosome 11q, in which multiple driver oncogenes likely reside in addition to cyclin D1 (CCND1). One such candidate, the scaffolding adapter protein, GRB2-associated binding protein 2 (GAB2), functions in ErbB signaling and was recently shown to enhance mammary epithelial cell proliferation, and metastasis of ERBB2 (HER2/neu)-driven murine breast cancer. However, the amplification status and function of GAB2 in the context of amplification remain undefined. In this study, by genomic profiling of 172 breast tumors, and fluorescence in situ hybridization validation in an independent set of 210 scorable cases, we observed focal amplification spanning GAB2 (11q14.1) independent of CCND1 (11q13.2) amplification, consistent with a driver role. Further, small interfering RNA (siRNA)-mediated knockdown of GAB2 in breast cancer lines (SUM52, SUM44PE and MDA468) with GAB2 amplification revealed a dependency on GAB2 for cell proliferation, cell-cycle progression, survival and invasion, likely mediated through altered phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling. GAB2 knockdown also reduced proliferation and survival in a cell line (BT474) with ERBB2 amplification, consistent with the possibility that GAB2 can function downstream of ERBB2. Our studies implicate focal amplification of GAB2 in breast carcinogenesis, and underscore an oncogenic role of scaffolding adapter proteins, and a potential new point of therapeutic intervention.
( Mark Sulkowski ),( Kwang-hyub Han ),( Jia-horng Kao ),( Jenny C. Yang ),( Bing Gao ),( Diana M. Brainard ),( Wan-long Chuang ),( Edward J. Gane ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: HBV reactivation during HCV treatment with direct-acting antiviralregimens has been reported in HCV infected patients who areHB surface antigen (HBsAg) negative, HB core antibody (HBcAb) positive,and HBV DNA undetectable. To evaluate the risk of HBV reactivationin these HCV infected patients, we analyzed samples froma Phase 3b study, GS-US-337-0131, of ledipasvir/sofosbuvir (LDV/SOF)for 12 weeks conducted in Korea and Taiwan where HBV is endemic.All enrolled subjects were HBsAg negative at screening per protocol.The SVR12 rate was 98% in this trial.Methods: A serum sample per patient, collected during post-treatmentfollow up was analyzed for HBcAb. Samples positive for HBcAb wereanalyzed for HBV DNA and retested for HBsAg if HBV DNA wasdetectable.Results: 173 of 178 patients had one post-treatment sample withinthe 1 year stability limit. Of the 173 patients, 60% (n=103) wereHBcAb positive and HBsAg negative; no subject was HBsAg positive.Two of 103 patients had HBV DNA <20 IU/mL, detected and theremaining patients were <20 IU/mL, target not detected. MedianALT during treatment and post-treatment follow-up were similar betweenHBcAb positive and negative patients; all patients had ALTdeclined from baseline. No patients had clinical signs of HBV reactivationduring treatment or post-treatment follow up. No differencesin overall adverse events or laboratory abnormality observedin patients who were HBcAb positive or negative.Conclusions: Among 103 HCV-infected patients with reactive HB coreantibody and absent HB surface antigen, there was no evidence ofHBV reactivation following successful HCV treatment with LDV/SOF.These data suggest HBV reactivation in patients with HCV and reactiveHB core antibody is uncommon. A Phase 3b study evaluating 12weeks of LDV/SOF in patients with chronic HCV and overt HBV (HBsAgpositive) co-infection is ongoing in Taiwan and can provide furthersafety information.
( Mark Sulkowski ),( Kwang-hyub Han ),( Jia-horng Kao ),( Jenny C. Yang ),( Bing Gao ),( Diana M. Brainard ),( Wan-long Chuang ),( Edward J. Gane ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: HBV reactivation during HCV treatment with direct-acting antiviralregimens has been reported in HCV infected patients who areHB surface antigen (HBsAg) negative, HB core antibody (HBcAb) positive,and HBV DNA undetectable. To evaluate the risk of HBV reactivationin these HCV infected patients, we analyzed samples froma Phase 3b study, GS-US-337-0131, of ledipasvir/sofosbuvir (LDV/SOF)for 12 weeks conducted in Korea and Taiwan where HBV is endemic.All enrolled subjects were HBsAg negative at screening per protocol.The SVR12 rate was 98% in this trial.Methods: A serum sample per patient, collected during post-treatmentfollow up was analyzed for HBcAb. Samples positive for HBcAb wereanalyzed for HBV DNA and retested for HBsAg if HBV DNA wasdetectable.Results: 173 of 178 patients had one post-treatment sample withinthe 1 year stability limit. Of the 173 patients, 60% (n=103) wereHBcAb positive and HBsAg negative; no subject was HBsAg positive.Two of 103 patients had HBV DNA <20 IU/mL, detected and theremaining patients were <20 IU/mL, target not detected. MedianALT during treatment and post-treatment follow-up were similar betweenHBcAb positive and negative patients; all patients had ALTdeclined from baseline. No patients had clinical signs of HBV reactivationduring treatment or post-treatment follow up. No differencesin overall adverse events or laboratory abnormality observedin patients who were HBcAb positive or negative.Conclusions: Among 103 HCV-infected patients with reactive HB coreantibody and absent HB surface antigen, there was no evidence ofHBV reactivation following successful HCV treatment with LDV/SOF.These data suggest HBV reactivation in patients with HCV and reactiveHB core antibody is uncommon. A Phase 3b study evaluating 12weeks of LDV/SOF in patients with chronic HCV and overt HBV (HBsAgpositive) co-infection is ongoing in Taiwan and can provide furthersafety information.