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253 results on '"Wu, Chang-Yi"'

1. Application Research of New Remote Sensing Technology in Tree Obstruction Detection of Power Patrol Line

Author

Liu, Lan Lan, Luo, Mei Qiu, Huang, Jie, Wu, Chang Yi, Luo, Wen, Liu, Xin Chao, Cao, Ming Yu, Liu, Pan, Angrisani, Leopoldo, Series Editor, Arteaga, Marco, Series Editor, Chakraborty, Samarjit, Series Editor, Chen, Jiming, Series Editor, Chen, Shanben, Series Editor, Chen, Tan Kay, Series Editor, Dillmann, Rüdiger, Series Editor, Duan, Haibin, Series Editor, Ferrari, Gianluigi, Series Editor, Ferre, Manuel, Series Editor, Jabbari, Faryar, Series Editor, Jia, Limin, Series Editor, Kacprzyk, Janusz, Series Editor, Khamis, Alaa, Series Editor, Kroeger, Torsten, Series Editor, Li, Yong, Series Editor, Liang, Qilian, Series Editor, Martín, Ferran, Series Editor, Ming, Tan Cher, Series Editor, Minker, Wolfgang, Series Editor, Misra, Pradeep, Series Editor, Mukhopadhyay, Subhas, Series Editor, Ning, Cun-Zheng, Series Editor, Nishida, Toyoaki, Series Editor, Oneto, Luca, Series Editor, Panigrahi, Bijaya Ketan, Series Editor, Pascucci, Federica, Series Editor, Qin, Yong, Series Editor, Seng, Gan Woon, Series Editor, Speidel, Joachim, Series Editor, Veiga, Germano, Series Editor, Wu, Haitao, Series Editor, Zamboni, Walter, Series Editor, Zhang, Junjie James, Series Editor, Tan, Kay Chen, Series Editor, Yadav, Sanjay, editor, Arya, Yogendra, editor, Muhamad, Nor Asiah, editor, and Sebaa, Karim, editor

Published
2024
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9. Research progress on the role and mechanism of visfatin in sepsis-related organ injury

Author

KUANG Zhong-shen, CONG Zhu-kai, WU Chang-yi, YANG Ning, ZONG Ya-nan, GUO Xiang-yang

Subjects
visfatin, sepsis, mods, Medicine
Abstract

Sepsis is a common acute and critical disease in clinic. Systemic inflammatory response (SIRS) is one of the key mechanisms for the occurrence of sepsis. Visfatin, as an important cytokine, is involved in the occurrence and development of “cytokines storm” caused by sepsis. Recent clinical and basic research have shown that visfatin plays an important role in the occurrence and development of sepsis, and inhibition of visfatin expression can improve the systemic inflammatory response and the damage of lung, heart, liver and other important organs caused by sepsis. Based on the analysis of current clinical and basic research results, visfatin are expected to become an indicator of the severity of sepsis and a potential target for clinical intervention.

Published
2022
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13. Diphenyl disulfide potentiates the apoptosis of breast cancer cells through Bax proteolytic activation with accompanying autophagy.

Author

Chen, Sheng‐Yuan, Chiu, Chien‐Chih, Hung, Chun‐Tzu, Pan, Wen‐Hsiung, Chen, Yen‐Chun, Bow, Yung‐Ding, Li, Wan‐Ju, Hsu, Sheng‐Kai, Lin, I‐Ling, Wen, Zhi‐Hong, and Wu, Chang‐Yi

Subjects
BREAST cancer, DIPHENYL, AUTOPHAGY, CELL proliferation, APOPTOSIS, WESTERN immunoblotting, BREAST, CANCER cells
Abstract

Breast cancer is a leading cause of cancer‐related death worldwide, and chemoresistance often leads to poor patient outcomes. In this study, we investigated the anticancer activity of synthetic diphenyl disulfide (DPDS) in breast cancer cell lines. DPDS inhibited cellular proliferation and viability in a dose‐dependent manner and reduced colony formation, an index of clonogenicity. Annexin‐V and 7‐AAD double staining showed that DPDS could induce the apoptosis of breast cancer cells. Western blotting of the expression of Bax p21 and its cleaved form p18 suggested the activation of p18 Bax‐induced apoptosis. Furthermore, the increased expression of the autophagy marker LC3B‐II indicated autophagic lysosome accumulation induced by DPDS. Our findings suggest that DPDS has potential as a candidate for treating breast cancer, and further modifications and optimizations are warranted. [ABSTRACT FROM AUTHOR]

Published
2023
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19. diTFPP, a Phenoxyphenol, Sensitizes Hepatocellular Carcinoma Cells to C2-Ceramide-Induced Autophagic Stress by Increasing Oxidative Stress and ER Stress Accompanied by LAMP2 Hypoglycosylation

Author

Chiu, Chien-Chih, primary, Chen, Yen-Chun, additional, Bow, Yung-Ding, additional, Chen, Jeff Yi-Fu, additional, Liu, Wangta, additional, Huang, Jau-Ling, additional, Shu, En-De, additional, Teng, Yen-Ni, additional, Wu, Chang-Yi, additional, and Chang, Wen-Tsan, additional

Published
2022
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28. Molecular design of near-infrared fluorescent Pdots for tumor targeting: aggregation-induced emission versus anti-aggregation-caused quenching† †Electronic supplementary information (ESI) available: Experimental section, NMR spectra, and additional information as noted in the text. See DOI: 10.1039/c8sc03510e

Author

Tsai, Wei-Kai, Wang, Chun-I., Liao, Chia-Hsien, Yao, Chun-Nien, Kuo, Tsai-Jhen, Liu, Ming-Ho, Hsu, Chao-Ping, Lin, Shu-Yi, Wu, Chang-Yi, Pyle, Joseph R., Chen, Jixin, and Chan, Yang-Hsiang

Subjects
Chemistry
Abstract

This article presents the first work to fundamentally study the effect of steric hindrance in Pdot systems., Semiconducting polymer dots (Pdots) have recently emerged as a new type of ultrabright fluorescent probe that has been proved to be very useful for biomedical imaging. However, Pdots often suffer from serious fluorescence aggregation-caused quenching (ACQ) especially for near-infrared (NIR) fluorescent Pdots. This article compared two strategies to overcome the ACQ effect in near-infrared emissive Pdot systems: aggregation-induced emission (AIE) and anti-aggregation-caused quenching (anti-ACQ). The results show that the anti-ACQ platform outperforms the AIE system. The fluorescence quantum yield of anti-ACQ-based Pdots can be over 50% and the average per-particle brightness of the Pdots is about 5 times higher than that of the commercially available quantum dots. To help understand why the monomer conformations could greatly affect the optical properties of Pdots, molecular dynamics simulations were performed for the first time in such complicated Pdot systems. To demonstrate applications for in vivo fluorescence imaging, both microangiography imaging on living zebrafish embryos and specific tumor targeting on mice were performed. We anticipate that these studies will pave the way for the design of new highly fluorescent Pdot systems.

Published
2018

29. Oxidative Stress-Dependent Synergistic Antiproliferation, Apoptosis, and DNA Damage of Ultraviolet-C and Coral-Derived Sinularin Combined Treatment for Oral Cancer Cells

Author

Peng, Sheng-Yao, primary, Tang, Jen-Yang, additional, Li, Ruei-Nian, additional, Huang, Hurng-Wern, additional, Wu, Chang-Yi, additional, Chiu, Chien-Chih, additional, Chang, Fang-Rong, additional, Zhang, Hong-Wei, additional, Lee, Yun-Jou, additional, Sheu, Jyh-Horng, additional, and Chang, Hsueh-Wei, additional

Published
2021
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30. diTFPP, a Phenoxyphenol, Sensitizes Hepatocellular Carcinoma Cells to C 2 -Ceramide-Induced Autophagic Stress by Increasing Oxidative Stress and ER Stress Accompanied by LAMP2 Hypoglycosylation.

Author

Chiu, Chien-Chih, Chen, Yen-Chun, Bow, Yung-Ding, Chen, Jeff Yi-Fu, Liu, Wangta, Huang, Jau-Ling, Shu, En-De, Teng, Yen-Ni, Wu, Chang-Yi, and Chang, Wen-Tsan

Subjects
PHENOLS, AUTOPHAGY, ENDOPLASMIC reticulum, GLYCOSYLATION, CERAMIDES, OXIDATIVE stress, GENE expression, CELL lines, HEPATOCELLULAR carcinoma, SPHINGOLIPIDS, DRUG resistance in cancer cells
Abstract

Simple Summary: Chemotherapy is the major treatment modality for advanced or unresectable hepatocellular carcinoma (HCC). Unfortunately, chemoresistance carries a poor prognosis in HCC patients. Exogenous ceramide, a sphingolipid, has been well documented to exert anticancer effects; however, recent reports showed ceramide resistance, which limits the development of the ceramide-based cancer treatment diTFPP, a novel phenoxyphenol compound that has been shown to sensitize HCC cells to ceramide treatment. Here, we further clarified the mechanism underlying diTFPP-mediated sensitization of HCC to C2-ceramide-induced stresses, including oxidative stress, ER stress, and autophagic stress, especially the modulation of LAMP2 glycosylation, the lysosomal membrane protein that is crucial for autophagic fusion. This study may shed light on the mechanism of ceramide resistance and help in the development of adjuvants for ceramide-based cancer therapeutics. Hepatocellular carcinoma (HCC), the most common type of liver cancer, is the leading cause of cancer-related mortality worldwide. Chemotherapy is the major treatment modality for advanced or unresectable HCC; unfortunately, chemoresistance results in a poor prognosis for HCC patients. Exogenous ceramide, a sphingolipid, has been well documented to exert anticancer effects. However, recent reports suggest that sphingolipid metabolism in ceramide-resistant cancer cells favors the conversion of exogenous ceramides to prosurvival sphingolipids, conferring ceramide resistance to cancer cells. However, the mechanism underlying ceramide resistance remains unclear. We previously demonstrated that diTFPP, a novel phenoxyphenol compound, enhances the anti-HCC effect of C2-ceramide. Here, we further clarified that treatment with C2-ceramide alone increases the protein level of CERS2, which modulates sphingolipid metabolism to favor the conversion of C2-ceramide to prosurvival sphingolipids in HCC cells, thus activating the unfolded protein response (UPR), which further initiates autophagy and the reversible senescence-like phenotype (SLP), ultimately contributing to C2-ceramide resistance in these cells. However, cotreatment with diTFPP and ceramide downregulated the protein level of CERS2 and increased oxidative and endoplasmic reticulum (ER) stress. Furthermore, insufficient LAMP2 glycosylation induced by diTFPP/ceramide cotreatment may cause the failure of autophagosome–lysosome fusion, eventually lowering the threshold for triggering cell death in response to C2-ceramide. Our study may shed light on the mechanism of ceramide resistance and help in the development of adjuvants for ceramide-based cancer therapeutics. [ABSTRACT FROM AUTHOR]

Published
2022
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31. A Marine Terpenoid, Heteronemin, Induces Both the Apoptosis and Ferroptosis of Hepatocellular Carcinoma Cells and Involves the ROS and MAPK Pathways

Author

Chang, Wen-Tsan, primary, Bow, Yung-Ding, additional, Fu, Pei-Jung, additional, Li, Chia-Yang, additional, Wu, Chang-Yi, additional, Chang, Yi-Hua, additional, Teng, Yen-Ni, additional, Li, Ruei-Nian, additional, Lu, Mei-Chin, additional, Liu, Yi-Chang, additional, and Chiu, Chien-Chih, additional

Published
2021
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33. The Phenoxyphenol Compound 4-HPPP Selectively Induces Antiproliferation Effects and Apoptosis in Human Lung Cancer Cells through Aneupolyploidization and ATR DNA Repair Signaling

Author

Liu, Wangta, primary, Wu, Chang-Yi, additional, Lu, Mei-Jei, additional, Chuang, Yung-Jen, additional, Tsai, Eing-Mei, additional, Leu, Steve, additional, Lin, I-Ling, additional, Ko, Chih-Jan, additional, Chiu, Chien-Chih, additional, and Chang, Wen-Tsan, additional

Published
2020
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44. Phytochemical naphtho[1,2-b] furan-4,5‑dione induced topoisomerase II-mediated DNA damage response in human non-small-cell lung cancer

Author

Chien, Ching-Ming, primary, Yang, Juan-Cheng, additional, Wu, Pin-Hsuan, additional, Wu, Chang-Yi, additional, Chen, Guan-Yu, additional, Wu, Yang-Chang, additional, Chou, Chon-Kit, additional, Tseng, Chih-Hua, additional, Chen, Yeh-Long, additional, Wang, Li-Fang, additional, and Chiu, Chien-Chih, additional

Published
2019
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45. Molecular design of near-infrared fluorescent Pdots for tumor targeting: aggregation-induced emissionversusanti-aggregation-caused quenching

Author

Tsai, Wei-Kai, primary, Wang, Chun-I., additional, Liao, Chia-Hsien, additional, Yao, Chun-Nien, additional, Kuo, Tsai-Jhen, additional, Liu, Ming-Ho, additional, Hsu, Chao-Ping, additional, Lin, Shu-Yi, additional, Wu, Chang-Yi, additional, Pyle, Joseph R., additional, Chen, Jixin, additional, and Chan, Yang-Hsiang, additional

Published
2019
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49. Differential control of Zap1-regulated genes in response to zinc deficiency in Saccharomyces cerevisiae

Author

Wu Chang-Yi, Bird Amanda J, Chung Lisa M, Newton Michael A, Winge Dennis R, and Eide David J

Subjects
Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background The Zap1 transcription factor is a central player in the response of yeast to changes in zinc status. We previously used transcriptome profiling with DNA microarrays to identify 46 potential Zap1 target genes in the yeast genome. In this new study, we used complementary methods to identify additional Zap1 target genes. Results With alternative growth conditions for the microarray experiments and a more sensitive motif identification algorithm, we identified 31 new potential targets of Zap1 activation. Moreover, an analysis of the response of Zap1 target genes to a range of zinc concentrations and to zinc withdrawal over time demonstrated that these genes respond differently to zinc deficiency. Some genes are induced under mild zinc deficiency and act as a first line of defense against this stress. First-line defense genes serve to maintain zinc homeostasis by increasing zinc uptake, and by mobilizing and conserving intracellular zinc pools. Other genes respond only to severe zinc limitation and act as a second line of defense. These second-line defense genes allow cells to adapt to conditions of zinc deficiency and include genes involved in maintaining secretory pathway and cell wall function, and stress responses. Conclusion We have identified several new targets of Zap1-mediated regulation. Furthermore, our results indicate that through the differential regulation of its target genes, Zap1 prioritizes mechanisms of zinc homeostasis and adaptive responses to zinc deficiency.

Published
2008
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