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- 저자 : Zhihua Liang (검색결과 4 건)
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ABE based Access Control with Authenticated Dynamic Policy Updating in Clouds
Liang-Ao Zhang,Xingming Sun,Zhihua Xia,Qiuju Ji 보안공학연구지원센터 2015 International Journal of Security and Its Applicat Vol.9 No.8
Attribute-Based Encryption (ABE) is a promising cryptographic primitive to implement access control for secure data storage in the cloud. Since the data owner may frequently change the access policies defined in the ciphertext, it is significant to provide the capacity for dynamic policy updating. However the cloud should also authenticate the owner because the adversary may modify the access policies of the files in the cloud to prevent the legal users from accessing them. In this paper, we focus on the owner’s authentication in the ABE systems and propose a novel scheme which enables access control with authenticated dynamic policy updating in the cloud. We adapt the Pedersen commitment and Zero Knowledge Proof of Knowledge (ZKPK) to realize the anonymous authentication of the owner’s policy updating key without increasing any secret information to the owner side. The analysis shows that our scheme is authentic and efficient as well as adaptive to different types of access policies.
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Cloning and Functional Analysis of a cDNA Encoding Ginkgo biloba Farnesyl Diphosphate Synthase
Kexuan Tang,Peng Wang,Zhihua Liao,Liang Guo,Wenchao Li,Min Chen,Yan Pi,Yifu Gong,Xiaofen Sun 한국분자세포생물학회 2004 Molecules and cells Vol.18 No.2
Farnesyl diphosphate synthase (FPS; EC2.5.1.1/EC2. 5.1.10) catalyzes the synthesis of farnesyl diphosphate, and provides precursor for biosynthesis of sesquiterpene and isoprenoids containing more than 15 isoprene units in Ginkgo biloba. Here we report the cloning, characterization and functional analysis of a new cDNA encoding FPS from G. biloba. The full-length cDNA (designated GbFPS) had 1731 bp with an open reading frame of 1170 bp encoding a polypeptide of 390 amino acids. The deduced GbFPS was similar to other known FPSs and contained all the conserved regions of trans-prenyl chain-elongating enzymes. Structural modeling showed that GbFPS had the typical structure of FPS, the most prominent feature of which is the arrangement of 13 core helices around a large central cavity. Southern blot analysis revealed a small FPS gene family in G. biloba. Expression analysis indicated that GbFPS expression was high in roots and leaves, and low in stems. Functional complementation of GbFPS in an FPS-deficient strain confirmed that GbFPS mediates farnesyl diphosphate biosynthesis.
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Cell-in-Cell Death Is Not Restricted by Caspase-3 Deficiency in MCF-7 Cells
Shan Wang,Meifang He,Linmei Li,Zhihua Liang,Zehong Zou,Ailin Tao 한국유방암학회 2016 Journal of breast cancer Vol.19 No.3
Cell-in-cell structures are created by one living cell entering another homotypic or heterotypic living cell, which usually leads to the death of the internalized cell, specifically through caspase-dependent cell death (emperitosis) or lysosome-dependent cell death (entosis). Although entosis has attracted great attention, its occurrence is controversial, because one cell line used in its study (MCF-7) is deficient in caspase-3. Methods: We investigated this issue using MCF-7 and A431 cell lines, which often display cell-in-cell invasion, and have different levels of caspase-3 expression. Cell-in-cell death morphology, microstructures, and signaling pathways were compared in the two cell lines. Results: Our results confirmed that MCF-7 cells are caspase-3 deficient with a partial deletion in the CASP-3 gene. These cells underwent cell death that lacked typical apoptotic properties after staurosporine treatment, whereas caspase-3-sufficient A431 cells displayed typical apoptosis. The presence of caspase-3 was related neither to the lysosome-dependent nor to the caspase-dependent cell-in-cell death pathway. However, the existence of caspase-3 was associated with a switch from lysosome-dependent cell-in-cell death to the apoptotic cell-in-cell death pathway during entosis. Moreover, cellular hypoxia, mitochondrial swelling, release of cytochrome C, and autophagy were observed in internalized cells during entosis. Conclusion: The occurrence of caspase-independent entosis is not a cell-specific process. In addition, entosis actually represents a cellular self-repair system, functioning through autophagy, to degrade damaged mitochondria resulting from cellular hypoxia in cell-in-cell structures. However, sustained autophagy-associated signal activation, without reduction in cellular hypoxia, eventually leads to lysosome-dependent intracellular cell death.
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Weiguang Gu,Hua Zhang,Yiyu Lu,Minjing Li,Shuang Yang,Jianmiao Liang,Zhijian Ye,Zhihua Li,Minhong He,Xiaoliang Shi,Fei Wang,Dong You,Weiquan Gu,Weineng Feng 대한암학회 2023 Cancer Research and Treatment Vol.55 No.3
Purpose We aimed to evaluate whether the addition of pemetrexed is effective in improving progression-free survival (PFS) in epidermal growth factor receptor (EGFR)–mutated patients with or without concomitant alterations. Materials and Methods This multicenter clinical trial was conducted in China from June 15, 2018, to May 31, 2019. A total of 92 non–small cell lung cancer (NSCLC) patients harboring EGFR-sensitive mutations were included and divided into concomitant and non-concomitant groups. Patients in each group were randomly treated with EGFR–tyrosine kinase inhibitor (TKI) monotherapy or EGFR-TKI combined with pemetrexed in a ratio of 1:1. PFS was recorded as the primary endpoint. Results The overall median PFS of this cohort was 10.1 months. There were no significant differences in PFS between patients with and without concomitant and between patients received TKI monotherapy and TKI combined with pemetrexed (p=0.210 and p=0.085, respectively). Stratification analysis indicated that patients received TKI monotherapy had a significantly longer PFS in non-concomitant group than that in concomitant group (p=0.002). In concomitant group, patients received TKI combined with pemetrexed had a significantly longer PFS than patients received TKI monotherapy (p=0.013). Molecular dynamic analysis showed rapidly emerging EGFR T790M in patients received TKI monotherapy. EGFR mutation abundance decreased in patients received TKI combined chemotherapy, which supports better efficacy for a TKI combined chemotherapy as compared to TKI monotherapy. A good correlation between therapeutic efficacy and a change in circulating tumor DNA (ctDNA) status was found in 66% of patients, supporting the guiding role of ctDNA minimal residual disease (MRD) in NSCLC treatment. Conclusion EGFR-TKI monotherapy is applicable to EGFR-sensitive patients without concomitant alterations, while a TKI combined chemotherapy is applicable to EGFR-sensitive patients with concomitant alterations. CtDNA MRD may be a potential biomarker for predicting therapeutic efficacy.
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