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Wei Zhou,Zhi-yuan Wei,Guang-fei Wang,Kang-ning Han,Ran Liu,Lian-Hua Ma 한국섬유공학회 2021 Fibers and polymers Vol.22 No.4
Accurate characterisation of transverse tensile deformation and damage evolution is of importance for evaluatingthe failure behaviors of three-dimensional (3D) braided composites. In the present study, a finite element method (FEM) andseveral non-destructive testing methods including acoustic emission, digital image correlation, and infrared thermography aredeveloped to investigate the transverse tensile deformation and damage evolution of 3D five-directional braided composites. In the finite element approach, a matrix-impregnated fiber bundles (MIFB) model and a representative volume cell (RVC)model, which take into account the fiber bundles and matrix, are respectively established to predict the effective mechanicalproperties of fiber bundles and simulate the deformation and progressive damage of such composites. The damaged locationsand the failure modes including matrix crack, fiber debonding and shear fracture of fiber are predicted and verified byexperimental tests. The non-destructive tests show that the transverse tensile fracture process can be divided into four stageswhich correspond to acoustic emission signals severally. The combination of the FEM based numerical modeling andmultiple non-destructive characterisation methods can accurately monitor the deformation and damage behaviors of 3Dbraided composites under transverse tensile loads and thus provide a reference for structural health monitoring of compositesin practical application.
Liu, Yi-Qing,Zhang, Guo-An,Zhang, Bing-Chang,Wang, Yong,Liu, Zheng,Jiao, Yu-Lian,Liu, Ning,Zhao, Yue-Ran Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.3
Background: Prostate cancer is one of the main causes of cancer death, and drug resistance is the leading reason for therapy failure. However, how this occurs is largely unknown. We therrfore aimed to study the response of DU145 cells to cisplatin. Materials and Methods: Du145 prostate cancer cells were treated with a low dose of cisplatin for 24 h and cell viability and number were determined by MTT assay and trypan blue exclusion assay, respectively. The real time polymerase chain reaction (PCR) was used to assess responses to cisplatin treatment. Results: After 24h $2{\mu}g/ml$ treatment did not result in significant reduction in cell viability or number. However, it led to enhanced cancer cell invasiveness. E-cadherin mRNA was reduced, and vimentin, Snail, Slug, metalloproteinase 9 (MMP9) mRNA expression increased significantly, a feature of epithelial-mesenchymal transition (EMT). Conclusions: Short time low concentration cisplatin treatment leads to elevated invasiveness of DU145 cancer cells and this is possibly due to EMT.
Zhou Meng-jiao,Yang Jia-jie,Ma Ting-yao,Feng Ge-xuan,Wang Xue-lian,Wang Li-Yong,Ge Yu-ze,Gao Ran,Hong-liang Liu,Shan Lin,Kong Lu,Chen Xiao-hong 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
MYB-NFIB fusion and NOTCH1 mutation are common hallmark genetic events in salivary gland adenoid cystic carcinoma (SACC). However, abnormal expression of MYB and NOTCH1 is also observed in patients without MYB-NFIB fusion and NOTCH1 mutation. Here, we explore in-depth the molecular mechanisms of lung metastasis through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation. Twenty-five types of cells in primary and metastatic tissues were identified via Seurat clustering and categorized into four main stages ranging from near-normal to cancer-based on the abundance of each cell cluster in normal tissue. In this context, we identified the Notch signaling pathway enrichment in almost all cancer cells; RNA velocity, trajectory, and sub-clustering analyses were performed to deeply investigate cancer progenitor-like cell clusters in primary tumor-associated lung metastases, and signature genes of progenitor-like cells were enriched in the “MYC_TARGETS_V2” gene set. In vitro, we detected the NICD1-MYB-MYC complex by co-immunoprecipitation (Co-IP) and incidentally identified retinoic acid (RA) as an endogenous antagonist of genes in the “MYC_TARGETS_V2” gene set. Following this, we confirmed that all-trans retinoic acid (ATRA) suppresses the lung metastasis of SACC by correcting erroneous cell differentiation mainly caused by aberrant NOTCH1 or MYB expression. Bioinformatic, RNA-seq, and immunohistochemical (IHC) analyses of primary tissues and metastatic lung tissues from patients with SACC suggested that RA system insufficiency partially promotes lung metastasis. These findings imply the value of the RA system in diagnosis and treatment.