561 results on '"Tang, Jen"'
Search Results
202. Flow Injection Amperometric Detection of Hydrazine by Electrocatalytic Oxidation at a Perfluorosulfonated Ionomer/Ruthenium Oxide Pyrochlore Chemically Modified Electrode
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Zen, Jyh-Myng., primary and Tang, Jen-Sen., additional
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- 1995
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203. Design of Screening Procedures: A Review
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Tang, Kwei, primary and Tang, Jen, additional
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- 1994
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204. Statistical equivalency and optimality of simple step-stress accelerated test plans for the exponential distribution.
- Author
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Hu, ChENg ‐ Hung, Plante, Robert D., and Tang, JEN
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ACCELERATED life testing ,NAVAL research ,EXPONENTS ,EXPONENTIATION ,PSYCHOLOGICAL stress - Abstract
Accelerated life testing (ALT) is commonly used to obtain reliability information about a product in a timely manner. Several stress loading designs have been proposed and recent research interests have emerged concerning the development of equivalent ALT plans. Step-stress ALT (SSALT) is one of the most commonly used stress loadings because it usually shortens the test duration and reduces the number of required test units. This article considers two fundamental questions when designing a SSALT and provides formal proofs in answer to each. Namely: (1) can a simple SSALT be designed so that it is equivalent to other stress loading designs? (2) when optimizing a multilevel SSALT, does it degenerate to a simple SSALT plan? The answers to both queries, under certain reasonable model assumptions, are shown to be a qualified YES. In addition, we provide an argument to support the rationale of a common practice in designing a SSALT, that is, setting the higher stress level as high as possible in a SSALT plan. © 2012 Wiley Periodicals, Inc. Naval Research Logistics, 2013 [ABSTRACT FROM AUTHOR]
- Published
- 2013
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205. A note on parallel machine replacement
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Tang, Jen, primary and Tang, Kwei, additional
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- 1993
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206. Malignant thymoma: Long-term outcomes with radiotherapy.
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Huang, Ming-Yii, Huang, Chih-Jen, Tang, Jen-Yang, Huang, Chun-Ming, Yang, Sheau-Fang, and Chou, Shah-Hwa
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THYMOMA ,HEALTH outcome assessment ,CANCER radiotherapy ,BIOPSY ,SURGICAL excision ,UNIVARIATE analysis ,MULTIVARIATE analysis ,RADIATION doses - Abstract
Abstract: We analyzed the clinical outcome of stage II to IV malignant thymoma. This study focused on the treatment of 60 cases that combined surgery (biopsy or resection) and radiation therapy (with or without chemotherapy). Univariate and multivariate analyses of prognostic factors predicting survival were carried out. There is a statistically significant relationship between the extent of surgery and the local control (19.4% of relapse after complete resection vs. 41.2% of relapse after partial resection or biopsy, p =0.0001). Mediastinal radiation dose (≥50Gy) had a significant effect in decreasing recurrence (p =0.0001) and distant metastasis (p =0.011). The rates of local recurrence (30%) and distant metastasis (25%) justify recommending a higher dose of mediastinal radiation (≥50Gy) for patients with malignant thymoma. [Copyright &y& Elsevier]
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- 2012
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207. High-dose-rate brachytherapy for the treatment of nonmelanoma skin cancer.
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Huang, Ya-Yun, Lan, Cheng-Che, and Tang, Jen-Yang
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- 2019
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208. Testing independence of several groups of variables
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Tang, Jen, primary and Gupta, Rrjun K., additional
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- 1990
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209. Univariate X control charts for individual characteristics in a multinormal model.
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Serel, Dogan A., Moskowitz, Herbert, and Tang, Jen
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QUALITY control charts ,EXPERIMENTAL design ,ALGORITHMS ,RISK ,METHODOLOGY ,STATISTICAL process control ,STATISTICAL sampling - Abstract
The early work on multivariate statistical process control was built upon Hotelling's T[SUP2] control chart which was developed to simultaneously monitor the means of correlated quality variables. This chart, however, has a drawback, namely, the problem of identifying the responsible variable(s) when an out-of-control signal occurs. One alternative is to use a separate &Xbar; control chart for each individual characteristic with equal risks, based on Bonferroni inequality. In this study, we show that, from an economic perspective, it may be desirable to have unequal type I risks for the individual charts, because of different inspection and restoration costs associated with each variable. We obtain their risk ratios, which are measures of relative importance of the variables monitored. Then, based on these risk ratios, we develop computer algorithms for finding the exact control limits for individual variables from a multinormal distribution, in the sense that the overall type I risk of the charts is equal to the desired value. Numerical studies show that the proposed methods give optimal or near-optimal results from an economic as well as statistical point of view. [ABSTRACT FROM AUTHOR]
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- 2000
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210. Nepenthes Extract Induces Selective Killing, Necrosis, and Apoptosis in Oral Cancer Cells.
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Yang, Kun-Han, Tang, Jen-Yang, Chen, Yan-Ning, Chuang, Ya-Ting, Tsai, I-Hsuan, Chiu, Chien-Chih, Li, Li-Jie, Chien, Tsu-Ming, Cheng, Yuan-Bin, Chang, Fang-Rong, Yen, Ching-Yu, and Chang, Hsueh-Wei
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CELL death , *ORAL cancer , *CANCER cells , *DNA adducts , *NECROSIS , *APOPTOSIS , *BREAST cancer , *HEME oxygenase - Abstract
Ethyl acetate Nepenthes extract (EANT) from Nepenthes thorellii × (ventricosa × maxima) shows antiproliferation and apoptosis but not necrosis in breast cancer cells, but this has not been investigated in oral cancer cells. In the present study, EANT shows no cytotoxicity to normal oral cells but exhibits selective killing to six oral cancer cell lines. They were suppressed by pretreatment of the antioxidant inhibitor N-acetylcysteine (NAC), demonstrating that EANT-induced cell death was mediated by oxidative stress. Concerning high sensitivity to EANT, Ca9-22 and CAL 27 oral cancer cells were chosen for exploring detailed selective killing mechanisms. EANT triggers a mixture of necrosis and apoptosis as determined by annexin V/7-aminoactinmycin D analysis. Still, they show differential switches from necrosis at a low (10 μg/mL) concentration to apoptosis at high (25 μg/mL) concentration of EANT in oral cancer cells. NAC induces necrosis but suppresses annexin V-detected apoptosis in oral cancer cells. Necrostatin 1 (NEC1), a necroptosis inhibitor, moderately suppresses necrosis but induces apoptosis at 10 μg/mL EANT. In contrast, Z-VAD-FMK, a pancaspase inhibitor, slightly causes necrosis but suppresses apoptosis at 10 μg/mL EANT. Furthermore, the flow cytometry-detected pancaspase activity is dose-responsively increased but is suppressed by NAC and ZVAD, although not for NEC1 in oral cancer cells. EANT causes several oxidative stress events such as reactive oxygen species, mitochondrial superoxide, and mitochondrial membrane depolarization. In response to oxidative stresses, the mRNA for antioxidant signaling, such as nuclear factor erythroid 2-like 2 (NFE2L2), catalase (CAT), heme oxygenase 1 (HMOX1), and thioredoxin (TXN), are overexpressed in oral cancer cells. Moreover, EANT also triggers DNA damage, as detected by γH2AX and 8-oxo-2′-deoxyguanosine adducts. The dependence of oxidative stress is validated by the evidence that NAC pretreatment reverts the changes of cellular and mitochondrial stress and DNA damage. Therefore, EANT exhibits antiproliferation involving an oxidative stress-dependent necrosis/apoptosis switch and DNA damage in oral cancer cells. [ABSTRACT FROM AUTHOR]
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- 2021
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211. Comparison of Antioxidant and Anticancer Properties of Soft Coral-Derived Sinularin and Dihydrosinularin.
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Wang, Sheng-Chieh, Li, Ruei-Nian, Lin, Li-Ching, Tang, Jen-Yang, Su, Jui-Hsin, Sheu, Jyh-Horng, and Chang, Hsueh-Wei
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MARINE natural products ,ANTIOXIDANTS ,LUNGS ,LIVER cells ,LIVER cancer ,CANCER cells - Abstract
Marine natural products are abundant resources for antioxidants, but the antioxidant property of the soft corals-derived sinularin and dihydrosinularin were unknown. This study aimed to assess antioxidant potential and antiproliferation effects of above compounds on cancer cells, and to investigate the possible relationships between them. Results show that sinularin and dihydrosinularin promptly reacted with 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2-azinobis (3-ethyl-benzothiazoline-6-sulfonic acid) (ABTS), and hydroxyl (
• OH), demonstrating a general radical scavenger activity. Sinularin and dihydrosinularin also show an induction for Fe+3 -reduction and Fe+2 -chelating capacity which both strengthen their antioxidant activities. Importantly, sinularin shows higher antioxidant properties than dihydrosinularin. Moreover, 24 h ATP assays show that sinularin leads to higher antiproliferation of breast, lung, and liver cancer cells than dihydrosinularin. Therefore, the differential antioxidant properties of sinularin and dihydrosinularin may contribute to their differential anti-proliferation of different cancer cells. [ABSTRACT FROM AUTHOR]- Published
- 2021
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212. Pomegranate Extract (POMx) Induces Mitochondrial Dysfunction and Apoptosis of Oral Cancer Cells.
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Peng, Sheng-Yao, Lin, Li-Ching, Chen, Shu-Rong, Farooqi, Ammad A., Cheng, Yuan-Bin, Tang, Jen-Yang, and Chang, Hsueh-Wei
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ORAL cancer ,POMEGRANATE ,MITOCHONDRIAL DNA ,MITOCHONDRIA ,NUCLEAR DNA ,CANCER cells ,MITOCHONDRIAL membranes - Abstract
The anticancer effect of pomegranate polyphenolic extract POMx in oral cancer cells has rarely been explored, especially where its impact on mitochondrial functioning is concerned. Here, we attempt to evaluate the proliferation modulating function and mechanism of POMx against human oral cancer (Ca9-22, HSC-3, and OC-2) cells. POMx induced ATP depletion, subG1 accumulation, and annexin V/Western blotting-detected apoptosis in these three oral cancer cell lines but showed no toxicity to normal oral cell lines (HGF-1). POMx triggered mitochondrial membrane potential (MitoMP) disruption and mitochondrial superoxide (MitoSOX) generation associated with the differential downregulation of several antioxidant gene mRNA/protein expressions in oral cancer cells. POMx downregulated mitochondrial mass, mitochondrial DNA copy number, and mitochondrial biogenesis gene mRNA/protein expression in oral cancer cells. Moreover, POMx induced both PCR-based mitochondrial DNA damage and γH2AX-detected nuclear DNA damage in oral cancer cells. In conclusion, POMx provides antiproliferation and apoptosis of oral cancer cells through mechanisms of mitochondrial impairment. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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213. Marine Sponge Aaptos suberitoides Extract Improves Antiproliferation and Apoptosis of Breast Cancer Cells without Cytotoxicity to Normal Cells In Vitro.
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Shiau, Jun-Ping, Lee, Min-Yu, Tang, Jen-Yang, Huang, Hsin, Lin, Zheng-Yu, Su, Jui-Hsin, Hou, Ming-Feng, Cheng, Yuan-Bin, and Chang, Hsueh-Wei
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SPONGES (Invertebrates) , *BREAST cancer , *CANCER cells , *APOPTOSIS , *MITOCHONDRIAL membranes , *MEMBRANE potential - Abstract
The anticancer effects and mechanisms of marine sponge Aaptos suberitoides were rarely assessed, especially for methanol extract of A. suberitoides (MEAS) to breast cancer cells. This study evaluated the differential suppression effects of proliferation by MEAS between breast cancer and normal cells. MEAS demonstrated more antiproliferation impact on breast cancer cells than normal cells, indicating oxidative stress-dependent preferential antiproliferation effects on breast cancer cells but not for normal cells. Several oxidative stress-associated responses were highly induced by MEAS in breast cancer cells but not normal cells, including the generations of cellular and mitochondrial oxidative stress as well as the depletion of mitochondrial membrane potential. MEAS downregulated cellular antioxidants such as glutathione, partly contributing to the upregulation of oxidative stress in breast cancer cells. This preferential oxidative stress generation is accompanied by more DNA damage (γH2AX and 8-hydroxy-2-deoxyguanosine) in breast cancer cells than in normal cells. N-acetylcysteine reverted these MEAS-triggered responses. In conclusion, MEAS is a potential natural product for treating breast cancer cells with the characteristics of preferential antiproliferation function without cytotoxicity to normal cells in vitro. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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214. Marine anticancer drugs in modulating miRNAs and antioxidant signaling.
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Chuang, Ya-Ting, Yen, Ching-Yu, Tang, Jen-Yang, Wu, Kuo-Chuan, Chang, Fang-Rong, Tsai, Yi-Hong, Chien, Tsu-Ming, and Chang, Hsueh-Wei
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ANTINEOPLASTIC agents , *MICRORNA , *OXIDATIVE stress , *ANTIOXIDANTS , *MARINE natural products , *MARINE toxins - Abstract
Several marine drugs exert anticancer effects by inducing oxidative stress, which becomes overloaded and kills cancer cells when redox homeostasis is imbalanced. The downregulation of antioxidant signaling induces oxidative stress, while its upregulation attenuates oxidative stress. Marine drugs have miRNA-modulating effects against cancer cells. However, the potential antioxidant targets of such drugs have been rarely explored. This review aims to categorize the marine-drug-modulated miRNAs that downregulate their antioxidant targets, causing oxidative stress in anticancer treatments. We also categorize the downregulation of oxidative-stress-inducing miRNAs in antioxidant protection among non-cancer cells. We summarize the putative antioxidant targets of miRNA-modulating marine drugs by introducing a bioinformatics tool (miRDB). Finally, the marine drugs affecting antioxidant targets are surveyed. In this way, the connections between marine drugs and their modulating miRNA and antioxidant targets are innovatively categorized to provide a precise network for exploring their potential anticancer functions and protective effects on non-cancer cells. • The downregulation of antioxidant signaling induces oxidative stress. • The upregulation of antioxidant signaling attenuates oxidative stress. • This review categorizes marine-drugs, miRNAs, antioxidant targets, and ROS in anticancer treatments. • Antioxidant targets of miRNA-modulating marine drugs are retrieved bioinformatically. • Marine drugs, miRNA, and antioxidant targets are innovatively connected. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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215. Oxidative Stress-Dependent Synergistic Antiproliferation, Apoptosis, and DNA Damage of Ultraviolet-C and Coral-Derived Sinularin Combined Treatment for Oral Cancer Cells.
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Peng, Sheng-Yao, Tang, Jen-Yang, Li, Ruei-Nian, Huang, Hurng-Wern, Wu, Chang-Yi, Chiu, Chien-Chih, Chang, Fang-Rong, Zhang, Hong-Wei, Lee, Yun-Jou, Sheu, Jyh-Horng, Chang, Hsueh-Wei, Arenas, Meritxell, and Franco, Pierfrancesco
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MOUTH tumors , *CELL lines - Abstract
Simple Summary: Combined treatments with low side effects enhance anticancer applications. This study focusses on validating the potential synergistic antiproliferation of the combined treatment of ultraviolet-C and the coral-derived compound sinularin (UVC/sinularin) in oral cancer cells. This study confirms that UVC/sinularin synergistically and selectively inhibits oral cancer cell proliferation with low cytotoxicity on normal oral cells. The mechanisms involve the enhanced cellular and mitochondrial oxidative stress that cause apoptosis, DNA damage, and mitochondrial dysfunction in oral cancer cells. Combined treatment is increasingly used to improve cancer therapy. Non-ionizing radiation ultraviolet-C (UVC) and sinularin, a coral Sinularia flexibilis-derived cembranolide, were separately reported to provide an antiproliferation function to some kinds of cancer cells. However, an antiproliferation function using the combined treatment of UVC/sinularin has not been investigated as yet. This study aimed to examine the combined antiproliferation function and explore the combination of UVC/sinularin in oral cancer cells compared to normal oral cells. Regarding cell viability, UVC/sinularin displays the synergistic and selective killing of two oral cancer cell lines, but remains non-effective for normal oral cell lines compared to treatments in terms of MTS and ATP assays. In tests using the flow cytometry, luminescence, and Western blotting methods, UVC/sinularin-treated oral cancer cells exhibited higher reactive oxygen species production, mitochondrial superoxide generation, mitochondrial membrane potential destruction, annexin V, pan-caspase, caspase 3/7, and cleaved-poly (ADP-ribose) polymerase expressions than that in normal oral cells. Accordingly, oxidative stress and apoptosis are highly induced in a combined UVC/sinularin treatment. Moreover, UVC/sinularin treatment provides higher G2/M arrest and γH2AX/8-hydroxyl-2′deoxyguanosine-detected DNA damages in oral cancer cells than in the separate treatments. A pretreatment can revert all of these changes of UVC/sinularin treatment with the antioxidant N-acetylcysteine. Taken together, UVC/sinularin acting upon oral cancer cells exhibits a synergistic and selective antiproliferation ability involving oxidative stress-dependent apoptosis and cellular DNA damage with low toxic side effects on normal oral cells. [ABSTRACT FROM AUTHOR]
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- 2021
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216. Isocitrate dehydrogenase mutation hot spots in acute lymphoblastic leukemia and oral cancer
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Tang, Jen‐Yang, Chang, Chun‐Chi, Lin, Pei‐Chin, and Chang, Jan‐Gowth
- Abstract
Isocitrate dehydrogenase (IDH) encodes a nicotinamide adenine dinucleotide phosphate+‐dependent enzyme for oxidative decarboxylation of isocitrate and has an essential role in the tricarboxylic acid cycle. Mutations of IDH1 and IDH2 have been identified in patients with glioma, leukemia, and other cancers. However, the incidence of IDH mutations in acute myeloid leukemia in Taiwan is much lower than that reported in Western countries. The reason for the difference is unknown and its clinical implications remain unclear. Acute lymphoblastic leukemia (ALL) is a heterogenous hematopoietic malignancy. Oral squamous cell carcinoma (OSCC) results from chronic carcinogen exposures and is highly prevalent in trucking workers, especially in southern Taiwan. Subtypes of both diseases require specific treatments, and molecular markers for developing tailored treatments are limited. High‐resolution melting (HRM) analysis is now a widely used methodology for rapid, accurate, and low‐cost mutation scanning. In this study, 90 adults with OSC and 31 children with ALL were scanned by HRM analysis for IDH1 and IDH2 mutation hot spots. In ALL, the allele frequency was 3.23% in both IDH1 and IDH2. In OSCC, the allele frequency was 2.22% in IDH2. A synonymous mutation over pG313 (c.939A > G) of IDH2 was found in both pediatric ALL and adult OSCC. Therefore, we concluded that mutations of IDH are uncommon in ALL and OSCC and are apparently not a major consideration when selecting treatment modalities.
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- 2012
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217. Square-wave voltammetric determination of uric acid by catalytic oxidation at a...
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Zen, Jyh-Myng and Tang, Jen-Sen
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URIC acid , *VOLTAMMETRY , *ELECTRODES , *OXIDATION - Abstract
Describes a Nafion/ruthenium oxide pyrochlore chemically modified electrode for the determination of uric acid by Osteryoung square-wave voltammetry. Effect of pH on the voltammetric oxidation of uric acid; Effect of square-wave parameters and calibration curve; Interference effect; Sample analysis.
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- 1995
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218. Control Charts for Dependent and Independent Measurements Based on Bootstrap Methods.
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Liu, Regina Y. and Tang, Jen
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GRAPHIC methods , *STATISTICAL bootstrapping , *DISTRIBUTION (Probability theory) , *NONPARAMETRIC statistics , *MANUFACTURING processes - Abstract
Shewhart charts are widely accepted as standard tools for monitoring manufacturing processes of univariate, independent, and "nearly" normal measurements. They are not as well developed beyond these types of data. We generalize the idea of Shewhart charts to cover other types of data commonly encountered in practice. More specifically, we develop some valid control charts for dependent data and for independent data that are not necessarily "nearly" normal. We derive the proposed charts from the moving blocks bootstrap and the standard bootstrap methods. Their constructions are completely nonparametric, and no distributional assumptions are required. Some simulated as well as real data examples are included, and they are very supportive of the proposed methods. [ABSTRACT FROM AUTHOR]
- Published
- 1996
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219. DESIGN OF PRODUCT SPECIFICATIONS FOR MULTI-CHARACTERISTIC INSPECTION.
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Tang, Kwei and Tang, Jen
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TAGUCHI methods ,STOCHASTIC systems ,QUALITY control ,INFORMATION storage & retrieval systems ,ECONOMIC models ,MATHEMATICAL models ,ECONOMETRICS ,INFORMATION science ,TECHNICAL specifications - Abstract
A product often requires inspection on more than one characteristic. The traditional method determines inspection specifications for each characteristic independently. This practice ignores the interactions among characteristics in determining the disposition of an item, and prohibits tradeoffs among the quality of characteristics. In this paper, two multi-characteristic screening (complete inspection) models are proposed with different information processing requirements. In both models, screening specifications are jointly determined by considering all the economic and stochastic factors associated with the characteristics of interest. However, in Model 1, each characteristic has separate screening specifications and the inspection results of conformance (acceptance or rejections) of all the characteristics are used to determine the disposition of an item. In the second model, a joint screening rule based on an aggregation of characteristics is used to allow direct tradeoffs among the quality of characteristics. To implement the second model, the exact measured values of all characteristics of an item have to be recorded and used for a decision on that item. These two models are formulated and the solution procedures are developed. A numerical study is used to compare the cost performance and other plan characteristics of the independently-determined single characteristic models and the two multi-characteristic models. [ABSTRACT FROM AUTHOR]
- Published
- 1989
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220. A one-sided single screening procedure based on individual unit misclassification error.
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Hsien-Tang Tsai, Moskowitz, Herbert, and Tang, Jen
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QUALITY control ,PRODUCT quality ,FACTORY management ,CONSUMER protection - Abstract
A procedure is proposed for screening applications in quality control that eliminates overselection (namely, the condition where the proportion of accepted screened items is greater than the proportion of conforming items in the original population) and controls for individual unit misclassification error (IME), namely, the probability of an accepted/selected item being below specification. Screening involves selecting items whose performance is within specifications based on observing one or more correlated screening variables in lieu of observing the performance variable directly. Overselection and an uncontrollably high IME can occur when (1) there is a high correlation between the performance and screening variables and (2) the proportion of conforming items among accepted items (or its complement, average outgoing quality (AOQ)), is prespecified as in, for example, Owen et al. (1975). We instead propose a procedure that prespecifies a maximum tolerable IME (emaxa) for accepted items, which eliminates overselection and assures that the IME of each outgoing item as well as the AOQ are both equal to or less than emaxa. The quality of each individual item as well as AOQ is thereby explicitly controlled. Only the use of standard normal tables is required to implement our proposed procedure. [ABSTRACT FROM AUTHOR]
- Published
- 1995
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221. A Two-Sided Screening Procedure Using Several Correlated Variables.
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Tang, Jen and Kwei Tang
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MATHEMATICAL variables ,STATISTICAL correlation ,ECONOMIC models ,COST control ,MATHEMATICS - Abstract
When inspection on the performance variable of interest is destructive or costly, it is attractive to use other variables which are correlated with the performance variable and which are inexpensive to inspect as the screening variables. The idea of using a single correlated variable in a complete screening procedure has drawn much attention recently. In this paper, we extend a previously defined economic model for a screening procedure using more than one correlated variable. The screening specifications are based on a linear combination of the correlated variables, and if an item fails to conform to the screening specifications, it is rejected and excluded from shipment. The screening specifications are determined so that the total cost, the sum of three components, is minimized. [ABSTRACT FROM AUTHOR]
- Published
- 1989
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222. Constructing And Maintaining A Beta Process Distribution For Bayesian Quality Audit Systems.
- Author
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Tang, Kwei, Peters, Michael, and Tang, Jen
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MANUFACTURED products ,BAYESIAN analysis ,MANUFACTURING processes ,MANUFACTURING execution systems ,PRODUCTION methods ,RAPID prototyping - Abstract
The process distribution of a manufacturing process which reflects past experience with the quality levels of outgoing lots is an indispensible input of the Bayesian quality audit systems. A distance-method estimator for the process distribution is developed and shown to be superior to the commonly used method-of-moments estimator. En a continuous manufacturing process, the process distribution needs to be updated after each new lot is inspected. Several updating procedures including the posterior distribution, the exponential smoothing method, the moving window method and the all periods method are proposed and compared by a simulation study. [ABSTRACT FROM AUTHOR]
- Published
- 1987
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223. On the type-B integral equation and the distribution of wilks statist for testing independence of several groups of variables.
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Tang, Jen and Gupta, A.K.
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- 1987
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224. Effects of Zinc Compound on Body Weight and Recovery of Bone Marrow in Mice Treated with Total Body Irradiation
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Huang, Ming‐Yii, Lian, Shi‐Long, Wu, Hsin‐Lung, Chai, Chee‐Yin, Chang, Shun‐Jen, Huang, Chih‐Jen, and Tang, Jen‐Yang
- Abstract
This study aimed to investigate if zinc compound would have effects on body weight loss and bone marrow suppression induced by total body irradiation (TBI). ICR mice were divided randomly into two groups and treated with test or control compounds. The test compound contained zinc (amino acid chelated with bovine prostate extract), and the control was reverse osmosis pure water (RO water). One week after receiving the treatment, mice were unirradiated, or irradiated with 6 or 3 Gy by 6MV photon beams to the total body. Body weight changes were examined at regular intervals. Three and 5 weeks after the radiation, animals were sacrificed to examine the histologic changes in the bone marrow. Lower body weight in the period of 1‐5 weeks after radiation and poor survival rate were found after the 6 Gy TBI, as compared with the 3 Gy groups. The median survival time after 6 Gy and 3 Gy TBI for mice given the test compound were 26 and 76 days, respectively, and the corresponding figures were 14 and 70 days, respectively, for mice given the control compound (p < 0.00001). With zinc supplement, the mean body weight in mice which received the same dose of radiation was 7‐8 g heavier than in the water‐supplement groups during the second and third weeks (p < 0.05). Hence, there was no statistically significant difference in survival rate between zinc and water supplement in mice given the same dose of irradiation. Histopathologically there was less recovery of bone marrow cells in the 6Gy groups compared with the 3Gy groups. In the 3 Gy water‐supplement group, the nucleated cells and megakaryocytes were recovered in the fifth week when recovery was still not seen in the 6Gy group. With zinc supplement, these cells were recovered in the third week. In this study, we found that zinc is beneficial to body weight in mice treated with TBI. Histologic examination of bone marrow showed better recovery of bone marrow cells in groups of mice fed with zinc. This study suggests that zinc can be used as supplements in cancer patients receiving radiotherapy to reduce radiation‐induced complications.
- Published
- 2007
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225. On testing homogeneity of variances for gaussian models
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Tang Jen and Arjun K. Gupta
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Condensed Matter::Quantum Gases ,Statistics and Probability ,Applied Mathematics ,Gaussian ,Brown–Forsythe test ,Bartlett's test ,symbols.namesake ,Levene's test ,Modeling and Simulation ,Likelihood-ratio test ,Statistics ,Test statistic ,symbols ,F-test of equality of variances ,Statistics, Probability and Uncertainty ,Statistic ,Mathematics - Abstract
In this paper exact distribution of Bartlett's statistic for testing equality of variances for Gaussian models is derived for equal as well as unequal sample sizes. Percentage points have also been tabulated for an equivalent test statistic.
- Published
- 1987
226. Physalis peruviana -Derived Physapruin A (PHA) Inhibits Breast Cancer Cell Proliferation and Induces Oxidative-Stress-Mediated Apoptosis and DNA Damage.
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Yu, Tzu-Jung, Cheng, Yuan-Bin, Lin, Li-Ching, Tsai, Yi-Hong, Yao, Bo-Yi, Tang, Jen-Yang, Chang, Fang-Rong, Yen, Chia-Hung, Ou-Yang, Fu, Chang, Hsueh-Wei, Stagos, Dimitrios, and Kourti, Maria
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CANCER cell proliferation ,CAPE gooseberry ,DNA damage ,BREAST cancer ,EPIDERMAL growth factor receptors ,PURINERGIC receptors ,ANNEXINS ,EPIDERMAL growth factor - Abstract
Breast cancer expresses clinically heterogeneous characteristics and requires multipurpose drug development for curing the different tumor subtypes. Many withanolides have been isolated from Physalis species showing anticancer effects, but the anticancer function of physapruin A (PHA) has rarely been investigated. In this study, the anticancer properties of PHA in breast cancer cells were examined by concentration and time-course experiments. In terms of cellular ATP content, PHA inhibited the proliferation of three kinds of breast cancer cells: MCF7 (estrogen receptor (ER)+, progesterone receptor (PR)+/−, human epidermal growth factor receptor 2 (HER2)−), SKBR3 (ER−/PR−/HER2+), and MDA-MB-231 (triple-negative). Moreover, PHA induced G2/M arrest in MCF7 and MDA-MB-231 cells. In terms of flow cytometry, PHA induced the generation of reactive oxygen species (ROS), the generation of mitochondrial superoxide, mitochondrial membrane potential depletion, and γH2AX-detected DNA damage in breast cancer MCF7 and MDA-MB-231 cells, which were suppressed by the ROS inhibitor N-acetylcysteine (NAC). In terms of flow cytometry and Western blotting, PHA induced apoptotic expression (annexin V, and intrinsic and extrinsic apoptotic signaling), which was suppressed by NAC and an apoptosis inhibitor (Z-VAD-FMK), in breast cancer cells. Therefore, PHA is a potential anti-breast-cancer natural product that modulates the oxidative-stress response, cell-cycle disturbance, apoptosis, and γH2AX-detected DNA damage. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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227. Correction: Ou-Yang, F. et al. Antiproliferation for Breast Cancer Cells by Ethyl Acetate Extract of Nepenthes thorellii x (ventricosa x maxima). Int. J. Mol. Sci. 2019, 20 , 3238.
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Ou-Yang, Fu, Tsai, I-Hsuan, Tang, Jen-Yang, Yen, Ching-Yu, Cheng, Yuan-Bin, Farooqi, Ammad Ahmad, Chen, Shu-Rong, Yu, Szu-Yin, Kao, Jun-Kai, and Chang, Hsueh-Wei
- Subjects
CANCER cells ,BREAST cancer - Abstract
Antiproliferation for Breast Cancer Cells by Ethyl Acetate Extract of Nepenthes thorellii x (ventricosa x maxima). We found that the SP 1 sp H and SP 13 sp C spectra data (Figure 1 and Figure 2) of the main compound of EANT is plumbagin because our compound shows a I J i value of 1.5. EANT Induces Oxidative Stress on Breast Cancer Cells (Page 8: line 1 of the Third Paragraph of 3.2) Plumbagin is a common naphthoquinone in Nepenthes. [Extracted from the article]
- Published
- 2021
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228. A BATTERY-LESS (PASSIVE) IRID TAG IMPLEMENTED WITH AN ENERGY-HARVESTING SCHEME.
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TANG-JEN LIU and KUO-HSIEN HSIA
- Subjects
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ENERGY harvesting , *RADIO waves , *WIRELESS communications , *KNOWLEDGE transfer , *SOLAR cells , *INFRARED technology - Published
- 2017
229. Low Dose Combined Treatment with Ultraviolet-C and Withaferin a Enhances Selective Killing of Oral Cancer Cells.
- Author
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Peng, Sheng-Yao, Wang, Yen-Yun, Lan, Ting-Hsun, Lin, Li-Ching, Yuan, Shyng-Shiou F., Tang, Jen-Yang, and Chang, Hsueh-Wei
- Subjects
ORAL cancer ,REACTIVE oxygen species ,CANCER cells ,POLY ADP ribose ,LUCIFERASES ,CANCER cell proliferation ,NONIONIZING radiation - Abstract
Withaferin A (WFA), a Withania somnifera-derived triterpenoid, is an anticancer natural product. The anticancer effect of nonionizing radiation such as ultraviolet-C (UVC) as well as the combined treatment of UVC and WFA is rarely investigated. Low dose UVC and/or WFA treatments (12 J/m
2 and/or 1 μM) were chosen to evaluate antioral cancer cell line effects by examining cytotoxicity, cell cycle disruption, apoptosis induction, and DNA damage. For two cancer cell lines (Ca9-22 and HSC-3), single treatment (UVC or WFA) showed about 80% viability, while a combined treatment of UVC/WFA showed about 40% viability. In contrast, there was noncytotoxicity to normal oral cell lines (HGF-1). Compared to single treatment and control, low dose UVC/WFA shows high inductions of apoptosis in terms of flow cytometric detections for subG1, annexin V, pancaspase changes as well as Western blotting for detecting cleaved poly (ADP-ribose) polymerase (c-PARP) and caspase 3 (c-Cas 3) and luciferase assay for detecting Cas 3/7 activity. Low dose UVC/WFA also showed high inductions of oxidative stress and DNA damage in terms of flow cytometric detections of reactive oxygen species (ROS), mitochondrial superoxide (MitoSOX) generation, and membrane potential (MitoMP) destruction, γH2AX and 8-oxo-2'deoxyguanosine (8-oxodG) types of DNA damages. For comparison, low dose UVC/WFA show rare inductions of annexin V, Cas 3/7 activity, ROS, MitoSOX, and MitoMP changes to normal oral HGF-1 cells. Therefore, low dose UVC/WFA provides a novel selectively killing mechanism to oral cancer cells, suggesting that WFA is a UVC sensitizer to inhibit the proliferation of oral cancer cells. [ABSTRACT FROM AUTHOR]- Published
- 2020
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230. The Forgotten Women of Pre-Code: An Annotated Filmography and Bibliography
- Author
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Tang, Jennifer
- Published
- 2011
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231. Granulocyte colony-stimulating factor in the cord blood of premature neonates born to mothers with pregnancy-induced hypertension
- Author
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Tsao, Po-Nien, Teng, Ru-Jeng, Tang, Jen-Ruey, and Yau, Kuo-Inn Tsou
- Abstract
Objectives:To estimate the cord blood levels of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in preterm infants and to study the relationship of these levels to pregnancy-induced hypertension (PIH) and absolute neutrophil counts. Study design:G-CSF and GM-CSF levels in the cord blood of preterm neonates (n = 74) either with or without maternal PIH were estimated by enzyme-linked immunosorbent assay. Results:Infants in the PIH group had lower white blood cell, absolute neutrophil, absolute lymphocyte, and monocyte counts. The levels of G-CSF in cord blood were significantly lower in infants whose mothers had PIH (P= .04) and in infants with neutropenia (P= .01). G-CSF levels were positively correlated with both absolute neutrophil count (P= .02) and total white blood cell count (P= .01). GM-CSF was undetectable in all subjects. According to logistic regression with neutropenia as the dependent variable, only maternal PIH (P< .001), gestational age (P< .001), and G-CSF (P= .01) were independently related. Conclusion:In this study maternal PIH and low gestational age were significantly associated with neutropenia in premature infants. Low G-CSF levels may contribute to the neutropenia that is commonly seen in infants born to mothers with PIH. (J Pediatr 1999;135:56-9)
- Published
- 1999
- Full Text
- View/download PDF
232. Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells.
- Author
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Wang, Sheng-Chieh, Wang, Yen-Yun, Lin, Li-Ching, Chang, Meng-Yang, Yuan, Shyng-Shiou F., Tang, Jen-Yang, and Chang, Hsueh-Wei
- Subjects
DNA damage ,ORAL cancer ,CANCER cells ,REACTIVE oxygen species ,OXIDATIVE stress ,POLY ADP ribose - Abstract
The sensitizing effect of chromone-derived compounds on UVC-induced proliferation inhibition has not been comprehensively investigated so far. The subject of this study was to examine the proliferation change of oral cancer cells while using the combined treatment of UVC (254 nm) with our previously developed sulfonyl chromen-4-ones (CHW09), namely UVC/CHW09. Cell viability, apoptosis, oxidative stress, and DNA damage for the individual and combined treatments for UVC and/or CHW09 were examined in oral cancer Ca9-22 cells. In 24 h MTS assay, UVC (30 J/m
2 ; UVC30), or CHW09 (25 and 50 µg/mL; namely, CHW09-25 and CHW09-50) show 54%, 59%, and 45% viability. The combined treatment (UVC30/CHW09-25 and UVC30/CHW09-50) show lower cell viability (45% and 35%). Mechanistically, UVC/CHW09 induced higher apoptosis than individual treatments and untreated control, which were supported by the evidence of flow cytometry for subG1, annexin V/7-aminoactinomycin D, pancaspase and caspases 3/7 activity, and western blotting for cleaved poly(ADP-ribose) polymerase. Moreover, this cleaved PARP expression was downregulated by pancaspase inhibitor Z-VAD-FMK. UVC/CHW09 showed higher oxidative stress than individual treatments and untreated control in terms of flow cytometry for reactive oxygen species, mitochondrial membrane potential, and mitochondrial mass. Furthermore, UVC/CHW09 showed higher DNA damage than individual treatments and untreated control in terms of flow cytometry for H2A histone family member X and 8-oxo-2'-deoxyguanosine. In conclusion, combined treatment UVC/CHW09 suppresses proliferation, and promotes apoptosis, oxidative stress, and DNA damage against oral cancer cells, providing a novel application of sulfonyl chromen-4-ones in order to sensitize UVC induced proliferation inhibition for oral cancer therapy. [ABSTRACT FROM AUTHOR]- Published
- 2020
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233. Combined Treatment with Low Cytotoxic Ethyl Acetate Nepenthes Extract and Ultraviolet-C Improves Antiproliferation to Oral Cancer Cells via Oxidative Stress.
- Author
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Peng, Sheng-Yao, Lin, Li-Ching, Yang, Zhe-Wei, Chang, Fang-Rong, Cheng, Yuan-Bin, Tang, Jen-Yang, and Chang, Hsueh-Wei
- Subjects
ETHYL acetate ,ORAL cancer ,CANCER cells ,OXIDATIVE stress ,REACTIVE oxygen species ,CANCER cell proliferation - Abstract
Ultraviolet-C (UVC) irradiation provides an alternative radiotherapy to X-ray. UVC sensitizer from natural products may improve radiotherapy at low cytotoxic side effects. The aim of this study is to assess the regulation for oral cancer cell proliferation by a combined treatment of UVC and our previously reported anti-oral cancer natural product (ethyl acetate extract of Nepenthes adrianii × clipeata; EANA). The detailed possible UVC sensitizing mechanisms of EANA such as effects on cell proliferation, cell cycle, apoptosis, and DNA damage are investigated individually and in combination using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTS) assay, flow cytometry, and western blotting at low dose conditions. In a 24 h MTS assay, the low dose EANA (5 μg/mL) and low dose UVC (12 J/m
2 ) individually show 80% and combinedly 57% cell proliferation in oral cancer Ca9-22 cells; but no cytotoxicity to normal oral HGF-1 cells. Mechanistically, low dose EANA and low dose UVC individually induce apoptosis (subG1 accumulation, pancaspase activation, and caspases 3, 8, 9), oxidative stress (reactive oxygen species, mitochondrial superoxide, and mitochondrial membrane potential depletion), and DNA damage (γH2AX and 8-hydroxy-2′-deoxyguanosine). Moreover, the combined treatment (UVC/EANA) synergistically induces these changes. Combined low dose treatment-induced antiproliferation, apoptosis, oxidative stress, and DNA damage were suppressed by the ROS scavenger N-acetylcysteine. In conclusion, UVC/EANA shows synergistic antiproliferation, oxidative stress, apoptosis, and DNA damage to oral cancer cells in an oxidative stress-dependent manner. With the selective killing properties of low dose EANA and low dose UVC, EANA provides a novel UVC sensitizing agent to improve the anti-oral cancer therapy. [ABSTRACT FROM AUTHOR]- Published
- 2020
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- View/download PDF
234. Withanolide C Inhibits Proliferation of Breast Cancer Cells via Oxidative Stress-Mediated Apoptosis and DNA Damage.
- Author
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Yu, Tzu-Jung, Tang, Jen-Yang, Lin, Li-Ching, Lien, Wan-Ju, Cheng, Yuan-Bin, Chang, Fang-Rong, Ou-Yang, Fu, and Chang, Hsueh-Wei
- Subjects
CANCER cell proliferation ,DNA damage ,REACTIVE oxygen species ,POLY ADP ribose ,CANCER cells ,BREAST cancer ,ANNEXINS - Abstract
Some withanolides, particularly the family of steroidal lactones, show anticancer effects, but this is rarely reported for withanolide C (WHC)—especially anti-breast cancer effects. The subject of this study is to evaluate the ability of WHC to regulate the proliferation of breast cancer cells, using both time and concentration in treatment with WHC. In terms of ATP depletion, WHC induced more antiproliferation to three breast cancer cell lines, SKBR3, MCF7, and MDA-MB-231, than to normal breast M10 cell lines. SKBR3 and MCF7 cells showing higher sensitivity to WHC were used to explore the antiproliferation mechanism. Flow cytometric apoptosis analyses showed that subG1 phase and annexin V population were increased in breast cancer cells after WHC treatment. Western blotting showed that cleaved forms of the apoptotic proteins poly (ADP-ribose) polymerase (c-PARP) and cleaved caspase 3 (c-Cas 3) were increased in breast cancer cells. Flow cytometric oxidative stress analyses showed that WHC triggered reactive oxygen species (ROS) and mitochondrial superoxide (MitoSOX) production as well as glutathione depletion. In contrast, normal breast M10 cells showed lower levels of ROS and annexin V expression than breast cancer cells. Flow cytometric DNA damage analyses showed that WHC triggered γH2AX and 8-oxo-2′-deoxyguanosine (8-oxodG) expression in breast cancer cells. Moreover, N-acetylcysteine (NAC) pretreatment reverted oxidative stress-mediated ATP depletion, apoptosis, and DNA damage. Therefore, WHC kills breast cancer cells depending on oxidative stress-associated mechanisms. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
235. Methanol Extract of Usnea barbata Induces Cell Killing, Apoptosis, and DNA Damage against Oral Cancer Cells through Oxidative Stress.
- Author
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Tang, Jen-Yang, Wu, Kuang-Han, Wang, Yen-Yun, Farooqi, Ammad Ahmad, Huang, Hurng-Wern, Yuan, Shyng-Shiou F., Jian, Ru-In, Tsao, Li-Yi, Chen, Po-An, Chang, Fang-Rong, Cheng, Yuan-Bin, Hu, Hao-Chun, and Chang, Hsueh-Wei
- Subjects
ORAL cancer ,CANCER cells ,DNA damage ,OXIDATIVE stress ,REACTIVE oxygen species - Abstract
Some lichens provide the resources of common traditional medicines and show anticancer effects. However, the anticancer effect of Usnproliea barbata (U. barbata) is rarely investigated, especially for oral cancer cells. The aim of this study was to investigate the cell killing function of methanol extracts of U. barbata (MEUB) against oral cancer cells. MEUB shows preferential killing against a number of oral cancer cell lines (Ca9-22, OECM-1, CAL 27, HSC3, and SCC9) but rarely affects normal oral cell lines (HGF-1). Ca9-22 and OECM-1 cells display the highest sensitivity to MEUB and were chosen for concentration effect and time course experiments to address its cytotoxic mechanisms. MEUB induces apoptosis of oral cancer cells in terms of the findings from flow cytometric assays and Western blotting, such as subG1 accumulation, annexin V detection, and pancaspase activation as well as poly (ADP-ribose) polymerase (PARP) cleavage. MEUB induces oxidative stress and DNA damage of oral cancer cells following flow cytometric assays, such as reactive oxygen species (ROS)/mitochondrial superoxide (MitoSOX) production, mitochondrial membrane potential (MMP) depletion as well as overexpression of γH2AX and 8-oxo-2′deoxyguanosine (8-oxodG). All MEUB-induced changes in oral cancer cells were triggered by oxidative stress which was validated by pretreatment with antioxidant N-acetylcysteine (NAC). In conclusion, MEUB causes preferential killing of oral cancer cells and is associated with oxidative stress, apoptosis, and DNA damage. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
236. Low Concentration of Withaferin a Inhibits Oxidative Stress-Mediated Migration and Invasion in Oral Cancer Cells.
- Author
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Yu, Tzu-Jung, Tang, Jen-Yang, Ou-Yang, Fu, Wang, Yen-Yun, Yuan, Shyng-Shiou F., Tseng, Kevin, Lin, Li-Ching, and Chang, Hsueh-Wei
- Subjects
- *
ORAL cancer , *CANCER cells , *MITOGEN-activated protein kinases , *CANCER cell migration , *HEME oxygenase , *ORAL mucosa , *FETAL hemoglobin , *EXTRACELLULAR signal-regulated kinases - Abstract
Withaferin A (WFA) has been reported to inhibit cancer cell proliferation based on high cytotoxic concentrations. However, the low cytotoxic effect of WFA in regulating cancer cell migration is rarely investigated. The purpose of this study is to investigate the changes in migration and mechanisms of oral cancer Ca9-22 cells after low concentrations of WFA treatment. WFA under 0.5 μM at 24 h treatment shows no cytotoxicity to oral cancer Ca9-22 cells (~95% viability). Under this condition, WFA triggers reactive oxygen species (ROS) production and inhibits 2D (wound healing) and 3D cell migration (transwell) and Matrigel invasion. Mechanically, WFA inhibits matrix metalloproteinase (MMP)-2 and MMP-9 activities but induces mRNA expression for a group of antioxidant genes, such as nuclear factor, erythroid 2-like 2 (NFE2L2), heme oxygenase 1 (HMOX1), glutathione-disulfide reductase (GSR), and NAD(P)H quinone dehydrogenase 1 (NQO1)) in Ca9-22 cells. Moreover, WFA induces mild phosphorylation of the mitogen-activated protein kinase (MAPK) family, including extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 expression. All WFA-induced changes were suppressed by the presence of ROS scavenger N-acetylcysteine (NAC). Therefore, these results suggest that low concentration of WFA retains potent ROS-mediated anti-migration and -invasion abilities for oral cancer cells. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
237. Combined Treatment with Cryptocaryone and Ultraviolet C Promotes Antiproliferation and Apoptosis of Oral Cancer Cells.
- Author
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Wang, Sheng-Chieh, Chang, Hsun-Shuo, Tang, Jen-Yang, Farooqi, Ammad Ahmad, Kuo, Yun-Tzu, Hsuuw, Yan-Der, Lee, Jai-Wei, and Chang, Hsueh-Wei
- Subjects
- *
POLY ADP ribose , *ORAL cancer , *DNA adducts , *CANCER cells , *CELL cycle , *REACTIVE oxygen species , *APOPTOSIS - Abstract
Cryptocaryone (CPC) was previously reported as preferential for killing natural products in oral cancer cells. However, its radiosensitizing potential combined with ultraviolet C (UVC) cell killing of oral cancer cells remains unclear. This study evaluates the combined anti-proliferation effect and clarifies the mechanism of combined UVC/CPC effects on oral cancer cells. UVC/CPC shows higher anti-proliferation than individual and control treatments in a low cytotoxic environment on normal oral cells. Mechanistically, combined UVC/CPC generates high levels of reactive oxygen species and induces mitochondrial dysfunction by generating mitochondrial superoxide, increasing mitochondrial mass and causing the potential destruction of the mitochondrial membrane compared to individual treatments. Moreover, combined UVC/CPC causes higher G2/M arrest and triggers apoptosis, with greater evidence of cell cycle disturbance, annexin V, pancaspase, caspases 3/7 expression or activity in oral cancer cells than individual treatments. Western blotting further indicates that UVC/CPC induces overexpression for cleaved types of poly (ADP-ribose) polymerase and caspase 3 more than individual treatments. Additionally, UVC/CPC highly induces γH2AX and 8-hydroxy-2'-deoxyguanosine adducts as DNA damage in oral cancer cells. Taken together, CPC shows a radiosensitizing anti-proliferation effect on UVC irradiated oral cancer cells with combined effects through oxidative stress, apoptosis and DNA damage. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
238. Ferroptosis-Regulated Natural Products and miRNAs and Their Potential Targeting to Ferroptosis and Exosome Biogenesis.
- Author
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Chuang, Ya-Ting, Yen, Ching-Yu, Chien, Tsu-Ming, Chang, Fang-Rong, Tsai, Yi-Hong, Wu, Kuo-Chuan, Tang, Jen-Yang, and Chang, Hsueh-Wei
- Subjects
- *
NATURAL products , *EXOSOMES , *MICRORNA , *EXTRACELLULAR vesicles , *TREATMENT effectiveness - Abstract
Ferroptosis, which comprises iron-dependent cell death, is crucial in cancer and non-cancer treatments. Exosomes, the extracellular vesicles, may deliver biomolecules to regulate disease progression. The interplay between ferroptosis and exosomes may modulate cancer development but is rarely investigated in natural product treatments and their modulating miRNAs. This review focuses on the ferroptosis-modulating effects of natural products and miRNAs concerning their participation in ferroptosis and exosome biogenesis (secretion and assembly)-related targets in cancer and non-cancer cells. Natural products and miRNAs with ferroptosis-modulating effects were retrieved and organized. Next, a literature search established the connection of a panel of ferroptosis-modulating genes to these ferroptosis-associated natural products. Moreover, ferroptosis-associated miRNAs were inputted into the miRNA database (miRDB) to bioinformatically search the potential targets for the modulation of ferroptosis and exosome biogenesis. Finally, the literature search provided a connection between ferroptosis-modulating miRNAs and natural products. Consequently, the connections from ferroptosis–miRNA–exosome biogenesis to natural product-based anticancer treatments are well-organized. This review sheds light on the research directions for integrating miRNAs and exosome biogenesis into the ferroptosis-modulating therapeutic effects of natural products on cancer and non-cancer diseases. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
239. Manoalide Preferentially Provides Antiproliferation of Oral Cancer Cells by Oxidative Stress-Mediated Apoptosis and DNA Damage.
- Author
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Wang, Hui-Ru, Tang, Jen-Yang, Wang, Yen-Yun, Farooqi, Ammad Ahmad, Yen, Ching-Yu, Yuan, Shyng-Shiou F., Huang, Hurng-Wern, and Chang, Hsueh-Wei
- Subjects
- *
ANTINEOPLASTIC agents , *CALCIUM antagonists , *CELL proliferation , *REACTIVE oxygen species , *APOPTOSIS , *BIOLOGICAL products , *CELL lines , *DNA , *FIBROBLASTS , *GENES , *MARINE animals , *MITOCHONDRIAL pathology , *MOUTH tumors , *SUPEROXIDE dismutase , *OXIDATIVE stress , *CASPASES , *ACETYLCYSTEINE , *PHARMACODYNAMICS - Abstract
Marine sponge-derived manoalide has a potent anti-inflammatory effect, but its potential application as an anti-cancer drug has not yet been extensively investigated. The purpose of this study is to evaluate the antiproliferative effects of manoalide on oral cancer cells. MTS assay at 24 h showed that manoalide inhibited the proliferation of six types of oral cancer cell lines (SCC9, HSC3, OC2, OECM-1, Ca9-22, and CAL 27) but did not affect the proliferation of normal oral cell line (human gingival fibroblasts (HGF-1)). Manoalide also inhibits the ATP production from 3D sphere formation of Ca9-22 and CAL 27 cells. Mechanically, manoalide induces subG1 accumulation in oral cancer cells. Manoalide also induces more annexin V expression in oral cancer Ca9-22 and CAL 27 cells than that of HGF-1 cells. Manoalide induces activation of caspase 3 (Cas 3), which is a hallmark of apoptosis in oral cancer cells, Ca9-22 and CAL 27. Inhibitors of Cas 8 and Cas 9 suppress manoalide-induced Cas 3 activation. Manoalide induces higher reactive oxygen species (ROS) productions in Ca9-22 and CAL 27 cells than in HGF-1 cells. This oxidative stress induction by manoalide is further supported by mitochondrial superoxide (MitoSOX) production and mitochondrial membrane potential (MitoMP) destruction in oral cancer cells. Subsequently, manoalide-induced oxidative stress leads to DNA damages, such as γH2AX and 8-oxo-2'-deoxyguanosine (8-oxodG), in oral cancer cells. Effects, such as enhanced antiproliferation, apoptosis, oxidative stress, and DNA damage, in manoalide-treated oral cancer cells were suppressed by inhibitors of oxidative stress or apoptosis, or both, such as N-acetylcysteine (NAC) and Z-VAD-FMK (Z-VAD). Moreover, mitochondria-targeted superoxide inhibitor MitoTEMPO suppresses manoalide-induced MitoSOX generation and γH2AX/8-oxodG DNA damages. This study validates the preferential antiproliferation effect of manoalide and explores the oxidative stress-dependent mechanisms in anti-oral cancer treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
240. Antiproliferation for Breast Cancer Cells by Ethyl Acetate Extract of Nepenthes thorellii x (ventricosa x maxima).
- Author
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Ou-Yang, Fu, Tsai, I-Hsuan, Tang, Jen-Yang, Yen, Ching-Yu, Cheng, Yuan-Bin, Farooqi, Ammad Ahmad, Chen, Shu-Rong, Yu, Szu-Yin, Kao, Jun-Kai, and Chang, Hsueh-Wei
- Abstract
Extracts from the Nepenthes plant have anti-microorganism and anti-inflammation effects. However, the anticancer effect of the Nepenthes plant is rarely reported, especially for breast cancer cells. Here, we evaluate the antitumor effects of the ethyl acetate extract of Nepenthesthorellii x (ventricosa x maxima) (EANT) against breast cancer cells. Cell viability and flow cytometric analyses were used to analyze apoptosis, oxidative stress, and DNA damage. EANT exhibits a higher antiproliferation ability to two breast cancer cell lines (MCF7 and SKBR3) as compared to normal breast cells (M10). A mechanistic study demonstrates that EANT induces apoptosis in breast cancer cells with evidence of subG1 accumulation and annexin V increment. EANT also induces glutathione (GSH) depletion, resulting in dramatic accumulations of reactive oxygen species (ROS) and mitochondrial superoxide (MitoSOX), as well as the depletion of mitochondrial membrane potential (MMP). These oxidative stresses attack DNA, respectively leading to DNA double strand breaks and oxidative DNA damage in γH2AX and 8-oxo-2′deoxyguanosine (8-oxodG) assays. Overall these findings clearly revealed that EANT induced changes were suppressed by the ROS inhibitor. In conclusion, our results have shown that the ROS-modulating natural product (EANT) has antiproliferation activity against breast cancer cells through apoptosis, oxidative stress, and DNA damage. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
241. Estimating low process average by inverse binomial sampling
- Author
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TANG, KWEI, primary, TANG, JEN, additional, and MOSKOWITZ, HERBERT, additional
- Published
- 1987
- Full Text
- View/download PDF
242. On the distribution of the product of independent beta random variables
- Author
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Tang, Jen, primary and Gupta, A.K, additional
- Published
- 1984
- Full Text
- View/download PDF
243. Effectiveness of a multidisciplinary antimicrobial stewardship program in reducing the rate of carbapenem-resistant Acinetobacter baumanniiin a university hospital of Taiwan
- Author
-
Hsu, Ti-Ying, Chen, Hsin-Pai, Yu, Hui-Chun, Lin, Yu-Ching, Weng, Yueh-Chun, Lee, Yuan-Ming, Lin, Chia-Wei, Tang, Jen-Jen, Li, Ya-Ping, Wang, Wei-Shu, and Lo, Su-Shun
- Published
- 2015
- Full Text
- View/download PDF
244. Ginger-Derived 3HDT Exerts Antiproliferative Effects on Breast Cancer Cells by Apoptosis and DNA Damage.
- Author
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Chen, Chung-Yi, Chen, Yan-Ning, Shiau, Jun-Ping, Tang, Jen-Yang, Hou, Ming-Feng, and Chang, Hsueh-Wei
- Subjects
- *
BREAST cancer , *CANCER cells , *TRIPLE-negative breast cancer , *DRUG efficacy , *REACTIVE oxygen species , *GLUTATHIONE - Abstract
Ginger-derived compounds are abundant sources of anticancer natural products. However, the anticancer effects of (E)-3-hydroxy-1-(4′-hydroxy-3′,5′-dimethoxyphenyl)-tetradecan-6-en-5-one (3HDT) have not been examined. This study aims to assess the antiproliferation ability of 3HDT on triple-negative breast cancer (TNBC) cells. 3HDT showed dose-responsive antiproliferation for TNBC cells (HCC1937 and Hs578T). Moreover, 3HDT exerted higher antiproliferation and apoptosis on TNBC cells than on normal cells (H184B5F5/M10). By examining reactive oxygen species, mitochondrial membrane potential, and glutathione, we found that 3HDT provided higher inductions for oxidative stress in TNBC cells compared with normal cells. Antiproliferation, oxidative stress, antioxidant signaling, and apoptosis were recovered by N-acetylcysteine, indicating that 3HDT preferentially induced oxidative-stress-mediated antiproliferation in TNBC cells but not in normal cells. Moreover, by examining γH2A histone family member X (γH2AX) and 8-hydroxy-2-deoxyguanosine, we found that 3HDT provided higher inductions for DNA damage, which was also reverted by N-acetylcysteine. In conclusion, 3HDT is an effective anticancer drug with preferential antiproliferation, oxidative stress, apoptosis, and DNA damage effects on TNBC cells. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
245. Modulation of AKT Pathway-Targeting miRNAs for Cancer Cell Treatment with Natural Products.
- Author
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Shiau, Jun-Ping, Chuang, Ya-Ting, Yen, Ching-Yu, Chang, Fang-Rong, Yang, Kun-Han, Hou, Ming-Feng, Tang, Jen-Yang, and Chang, Hsueh-Wei
- Subjects
- *
NATURAL products , *MICRORNA , *CANCER treatment , *CELL physiology , *CANCER cells , *CARCINOGENESIS - Abstract
Many miRNAs are known to target the AKT serine-threonine kinase (AKT) pathway, which is critical for the regulation of several cell functions in cancer cell development. Many natural products exhibiting anticancer effects have been reported, but their connections to the AKT pathway (AKT and its effectors) and miRNAs have rarely been investigated. This review aimed to demarcate the relationship between miRNAs and the AKT pathway during the regulation of cancer cell functions by natural products. Identifying the connections between miRNAs and the AKT pathway and between miRNAs and natural products made it possible to establish an miRNA/AKT/natural product axis to facilitate a better understanding of their anticancer mechanisms. Moreover, the miRNA database (miRDB) was used to retrieve more AKT pathway-related target candidates for miRNAs. By evaluating the reported facts, the cell functions of these database-generated candidates were connected to natural products. Therefore, this review provides a comprehensive overview of the natural product/miRNA/AKT pathway in the modulation of cancer cell development. [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
246. Exact Distribution of Certain General Test Statistics in Multivariate Analysis
- Author
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Tang, Jen
- Subjects
- Mathematics, Statistics
- Published
- 1981
247. Physapruin A Enhances DNA Damage and Inhibits DNA Repair to Suppress Oral Cancer Cell Proliferation.
- Author
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Yu, Tzu-Jung, Yen, Ching-Yu, Cheng, Yuan-Bin, Yen, Chia-Hung, Jeng, Jiiang-Huei, Tang, Jen-Yang, and Chang, Hsueh-Wei
- Subjects
- *
CANCER cell proliferation , *ORAL cancer , *DNA damage , *CANCER cells , *GENE expression , *INHIBITION of cellular proliferation , *DNA repair - Abstract
The selective antiproliferation to oral cancer cells of Physalis peruviana-derived physapruin A (PHA) is rarely reported. Either drug-induced apoptosis and DNA damage or DNA repair suppression may effectively inhibit cancer cell proliferation. This study examined the selective antiproliferation ability of PHA and explored detailed mechanisms of apoptosis, DNA damage, and repair. During an ATP assay, PHA provided high cytotoxicity to two oral cancer cell lines (CAL 27 and Ca9-22) but no cytotoxicity to two non-malignant oral cells (HGF-1 and SG). This selective antiproliferation of PHA was associated with the selective generation of reactive oxygen species (ROS) in oral cancer cells rather than in non-malignant oral cells, as detected by flow cytometry. Moreover, PHA induced other oxidative stresses in oral cancer cells, such as mitochondrial superoxide generation and mitochondrial membrane potential depletion. PHA also demonstrated selective apoptosis in oral cancer cells rather than non-malignant cells in annexin V/7-aminoactinmycin D and caspase 3/7 activity assays. In flow cytometry and immunofluorescence assays, PHA induced γH2AX expressions and increased the γH2AX foci number of DNA damages in oral cancer cells. In contrast, the mRNA expressions for DNA repair signaling, including homologous recombination (HR) and non-homologous end joining (NHEJ)-associated genes, were inhibited by PHA in oral cancer cells. Moreover, the PHA-induced changes were alleviated by the oxidative stress inhibitor N-acetylcysteine. Therefore, PHA generates selective antiproliferation, oxidative stress, and apoptosis associated with DNA damage induction and DNA repair suppression in oral cancer cells. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
248. Regulatory effects of noncoding RNAs on the interplay of oxidative stress and autophagy in cancer malignancy and therapy.
- Author
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Liu, Pei-Feng, Farooqi, Ammad Ahmad, Peng, Sheng-Yao, Yu, Tzu-Jung, Dahms, Hans-Uwe, Lee, Cheng-Hsin, Tang, Jen-Yang, Wang, Sheng-Chieh, Shu, Chih-Wen, and Chang, Hsueh-Wei
- Subjects
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NON-coding RNA , *OXIDATIVE stress , *DRUG resistance in cancer cells , *AUTOPHAGY , *CANCER treatment - Abstract
Noncoding RNAs (ncRNAs) regulation of various diseases including cancer has been extensively studied. Reactive oxidative species (ROS) elevated by oxidative stress are associated with cancer progression and drug resistance, while autophagy serves as an ROS scavenger in cancer cells. However, the regulatory effects of ncRNAs on autophagy and ROS in various cancer cells remains complex. Here, we explore how currently investigated ncRNAs, mainly miRNAs and lncRNAs, are involved in ROS production through modulating antioxidant genes. The regulatory effects of miRNAs and lncRNAs on autophagy-related (ATG) proteins to control autophagy activity in cancer cells are discussed. Moreover, differential expression of ncRNAs in tumor and normal tissues of cancer patients are further analyzed using The Cancer Genome Atlas (TCGA) database. This review hypothesizes links between ATG genes- or antioxidant genes-modulated ncRNAs and ROS production, which might result in tumorigenesis, malignancy, and cancer recurrence. A better understanding of the regulation of ROS and autophagy by ncRNAs might advance the use of ncRNAs as diagnostic and prognostic markers as well as therapeutic targets in cancer therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
249. Philosophical Foundation of Enlightening by HsingI Chuan Education
- Author
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Lee, Chih-Ming and Tang, Jen-Ping
- Published
- 2002
250. Sequential Phosphorylation of Hepatitis C Virus NS5A Protein Requires the ATP-Binding Domain of NS3 Helicase.
- Author
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Chun-Chiao Yu, Pei-Chen Lin, Cho-Han Chiang, Shu-Tang Jen, Yen-Ling Lai, Shih-Chin Hsu, Lee-Chiang Lo, Jing-Jer Lin, Nei-Li Chan,a, and Ming-Jiun Yu
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HEPATITIS C virus , *VIRAL proteins , *DNA helicases , *CASEIN kinase , *NUCLEOSIDE triphosphatase , *CASEINS , *VIRAL nonstructural proteins , *PEPTIDES - Abstract
The propagation of the hepatitis C virus (HCV) is regulated in part by the phosphorylation of its nonstructural protein NS5A that undergoes sequential phosphorylation on several highly conserved serine residues and switches from a hypo- to a hyperphosphorylated state. Previous studies have shown that NS5A sequential phosphorylation requires NS3 encoded on the same NS3-NS4A-NS4B-NS5A polyprotein. Subtle mutations in NS3 without affecting its protease activity could affect NS5A phosphorylation. Given the ATPase domain in the NS3 COOH terminus, we tested whether NS3 participates in NS5A phosphorylation similarly to the nucleoside diphosphate kinase-like activity of the rotavirus NSP2 nucleoside triphosphatase (NTPase). Mutations in the NS3 ATP-binding motifs blunted NS5A hyperphosphorylation and phosphorylation at serines 225, 232, and 235, whereas a mutation in the RNA-binding domain did not. The phosphorylation events were not rescued with wild-type NS3 provided in trans. When provided with an NS3 ATPase-compatible ATP analog, N6-benzyl-ATP-g-S, thiophosphorylated NS5A was detected in the cells expressing the wild-type NS3-NS5B polyprotein. The thiophosphorylation level was lower in the cells expressing NS3-NS5B with a mutation in the NS3 ATP-binding domain. In vitro assays with a synthetic peptide and purified wild-type NS3 followed by dot blotting and mass spectrometry found weak NS5A phosphorylation at serines 222 and 225 that was sensitive to an inhibitor of casein kinase Ia but not helicase. When casein kinase Ia was included in the assay, much stronger phosphorylation was observed at serines 225, 232, and 235. We concluded that NS5A sequential phosphorylation requires the ATP-binding domain of the NS3 helicase and that casein kinase Ia is a potent NS5A kinase. IMPORTANCE For more than 20 years, NS3 was known to participate in NS5A sequential phosphorylation. In the present study, we show for the first time that the ATP-binding domain of NS3 is involved in NS5A phosphorylation. In vitro assays showed that casein kinase Ia is a very potent kinase responsible for NS5A phosphorylation at serines 225, 232, and 235. Our data suggest that ATP binding by NS3 probably results in conformational changes that recruit casein kinase Ia to phosphorylate NS5A, initially at S225 and subsequently at S232 and S235. Our discovery reveals intricate requirements of the structural integrity of NS3 for NS5A hyperphosphorylation and HCV replication. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
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