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Chang, Wen-Kui,Wang, Tzu-Po 한국품질경영학회 2001 The Asian Journal on Quality Vol.2 No.2
This paper illustrates a prototyping framework of the documentation-standards retrieval system via the data mining approach for enhancing software development quality. We first present an approach for designing a retrieval algorithm based on data mining, with the three basic technologies of machine learning, statistics and database management, applied to this system to speed up the searching time and increase the fitness. This approach derives from the observation that data mining can discover unsuspected relationships among elements in large databases. This observation suggests that data mining can be used to elicit new knowledge about the design of a subject system and that it can be applied to large legacy systems for efficiency. Finally, software development quality will be improved at the same time when the project managers retrieving for the documentation standards.
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Lei Chen,Kui-Po Yan,Xin-Can Liu,Wei Wang,Chao Li,Ming Li,Chun-Guang Qiu 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.1
This study investigated the interaction amongvalsartan (VAL), TGF-b pathways, and long non-codingRNA (lncRNA) cardiac hypertrophy-related factor (CHRF)in doxorubicin (DOX)-induced heart failure (HF), andexplored their roles in DOX-induced HF progression. HFmice models in vivo were constructed by DOX induction. The expression of CHRF and TGF-b1 in hearts wasdetected, along with cardiac function, caspase-3 activity,and cell apoptosis. Primary myocardial cells were pretreatedwith VAL, followed by DOX induction in vitro forfunctional studies, including the detection of cell apoptosiswith terminal deoxynucleotidyl transferase dUTP nick-endlabeling and the expression of proteins associated withTGF-b1 pathways. HF models were established in vivo andin vitro. Expression of CHRF and TGF-b1 was up-regulated,and cell apoptosis and caspase-3 activity wereincreased in the hearts and cells of the HF models. VALsupplementation alleviated the cardiac dysfunction andinjury in the HF process. Moreover, overexpressed CHRFup-regulated TGF-b1, promoted myocardial cell apoptosis,and reversed VAL’s cardiac protective effect, while interferenceof CHRF (si-CHRF) did the opposite. Down-regulationof CHRF reversed the increased expression of TGFb1and the downstream proteins induced by pcDNA-TGFb1in HL-1 cells, while overexpression of CHRF reversedthe VAL’s cardiac protective effect in vivo. In conclusion,VAL regulates TGF-b pathways through lncRNA CHRF toimprove DOX-induced HF.
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