Browsing by Author "Lee, Yi-Chen"

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An EEG-based Approach for Evaluating Graphic Icons from the Perspective of Semantic Distance
(2015)
Cherng, Fu-Yin
;
Lin, Wen-Chieh
;
King, Jung-Tai
;
Lee, Yi-Chen
;
資訊工程學系
Graphic icons play an increasingly important role in interface design due to the proliferation of digital devices in recent years. Their ability to express information in a universal fashion allows us to immediately interact with new applications, systems, and devices. Icons can, however, cause user confusion and frustration if designed poorly. Several studies have evaluated icons using behavioral-performance metrics such as reaction time as well as self-report methods. However, determining the usability of icons based on behavioral measures alone is not straightforward, because users\' interpretations of the meaning of icons involve various cognitive processes and perceptual mechanisms. Moreover, these perceptual mechanisms are affected not only by the icons themselves, but by usage scenarios. Thus, we need a means of sensitively and continuously measuring users\' different cognitive processes when they are interacting with icons. In this study, we propose an EEG-based approach to icon evaluation, in which users\' EEG signals are measured in multiple usage scenarios. Based on a combination of EEG and behavioral results, we provide a novel interpretation of the participants\' perception during these tasks, and identify some important implications for icon design.
An EEG-based Approach for Evaluating Graphic Icons from the Perspective of Semantic Distance
(2016)
Cherng, Fu-Yin
;
Lin, Wen-Chieh
;
King, Jung-Tai
;
Lee, Yi-Chen
;
資訊工程學系
Graphic icons play an increasingly important role in interface design due to the proliferation of digital devices in recent years. Their ability to express information in a universal fashion allows us to immediately interact with new applications, systems, and devices. Icons can, however, cause user confusion and frustration if designed poorly. Several studies have evaluated icons using behavioral-performance metrics such as reaction time as well as self-report methods. However, determining the usability of icons based on behavioral measures alone is not straightforward, because users\' interpretations of the meaning of icons involve various cognitive processes and perceptual mechanisms. Moreover, these perceptual mechanisms are affected not only by the icons themselves, but by usage scenarios. Thus, we need a means of sensitively and continuously measuring users\' different cognitive processes when they are interacting with icons. In this study, we propose an EEG-based approach to icon evaluation, in which users\' EEG signals are measured in multiple usage scenarios. Based on a combination of EEG and behavioral results, we provide a novel interpretation of the participants\' perception during these tasks, and identify some important implications for icon design.
DNA Repair Protein Rad51 Induces Tumor Growth and Metastasis in Esophageal Squamous Cell Carcinoma via a p38/Akt-Dependent Pathway
(2020-06-01)
Chiu, Wen-Chin
;
Fang, Pen-Tzu
;
Lee, Yi-Chen
;
Wang, Yen-Yun
;
Su, Yu-Han
Background Rad51 is a protein which plays a vital role in DNA double-strand break repair and maintenance of telomeres. However, the underlying mechanism for its action in esophageal squamous cell carcinoma (ESCC) remains unclear. Patients and Methods Eighty-seven patients with ESCC were enrolled in this study. Expression of Rad51 in ESCC was determined by immunohistochemistry and correlated with clinicopathological variables by Chi square test. The role of Rad51 in patient survival was determined by Kaplan-Meier estimates. The effects of Rad51 knockdown and overexpression on esophageal cancer growth, migration, and invasion were examined using TE8, CE81T, and KYSE70 cells. The mechanisms involved were also analyzed. Nude mice models were used for assessment of tumor growth. Results Rad51 staining was predominantly observed in ESCC patients. ESCC patients with high Rad51 expression had significantly decreased survival (P < 0.001) combined with increased tumor size (P = 0.034) and lymph node metastasis (P = 0.039). Rad51 overexpression promoted, while its knockdown attenuated, esophageal cancer cell viability through cell cycle entry and migration/invasion via epithelial-mesenchymal transition. Moreover, Rad51 overexpression increased colony formation in vitro and tumor growth in vivo. In addition, high Rad51 expression increased cancer progression through the p38/Akt/Snail signaling pathway. Conclusions This study indicates a new biological role for Rad51 in ESCC progression. Rad51 may serve as a potential prognostic biomarker and therapeutic target for ESCC patients.
Essential Role of Visfatin in Lipopolysaccharide and Colon Ascendens Stent Peritonitis-Induced Acute Lung Injury
(2019-04-04)
Lee, Yi-Chen
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Lin, Chun-Yu
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Chen, Yen-Hsu
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Chiu, Wen-Chin
;
Wang, Yen-Yun
Acute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NF kappa B pathway, and increased the expression of pro-inflammatory cytokines, including IL1-beta, IL-6, and TNF-alpha in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NF kappa B pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.
Extracellular Visfatin-Promoted Malignant Behavior in Breast Cancer Is Mediated Through c-Abl and STAT3 Activation
(2016-09-01)
Hung, Amos C.
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Lo, Steven
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Hou, Ming-Feng
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Lee, Yi-Chen
;
Tsai, Chun-Hao
Purpose: Visfatin is an adipocytokine involved in cellular metabolism, inflammation, and cancer. This study investigated the roles of extracellular visfatin in breast cancer, and explored underlying mechanisms in clinical and experimental settings. Experimental Design: Associations of serum visfatin with clinicopathologic characteristics and patient survival were assessed with Cox regression models and Kaplan-Meier analyses. Effects of extracellular visfatin on cultured breast cancer cells were examined, followed by in vivo investigation of tumor growth and metastasis in xenograft animal models. Imatinib and Stattic were used to inhibit c-Abl and STAT3 activation, respectively. Results: Breast cancer patients with high serum visfatin levels were associated with advanced tumor stage, increased tumor size and lymph node metastasis, and poor survival. Elevated phosphorylation of c-Abl and STAT3 in breast tumor tissues were correlated with high serum visfatin levels in patients. Visfatinpromoted in vitro cell viability and metastatic capability were suppressed by imatinib ( c-Abl inhibitor) and Stattic ( STAT3 inhibitor). Increased in vivo cell invasiveness was observed in zebrafish xenografted with visfatin-pretreated breast cancer cells. Tumor growth and lung metastasis occurred in visfatin-administered mice xenografted with breast cancer cells. Tail vein-injected mice with visfatin-pretreated breast cancer cells showed increased lung metastasis, which was suppressed by imatinib. Conclusions: Serum visfatin levels in breast cancer patients reveal potential prognostic values, and our findings that visfatin promoted breast cancer through activation of c-Abl and STAT3 may provide an important molecular basis for future design of targeted therapies that take into account different serum visfatin levels in breast cancer. (C) 2016 AACR.
Measuring the Influences of Musical Parameters on Cognitive and Behavioral Responses to Audio Notifications Using EEG and Large-scale Online Studies
(2019-01-01)
Cherng, Fu-Yin
;
Lee, Yi-Chen
;
King, Jung-Tai
;
Lin, Wen-Chieh
;
資訊工程學系
Prior studies have evaluated various designs for audio notifications. However, calls for more in-depth research on how such notifications work, especially at the level of users' cognitive states, have gone unanswered; and studies evaluating audio notifications with large numbers of participants in multiple environments have been rare. This study conducted an electroencephalography study (N=20) and an online study (N=967) to enhance understandings of how three musical parameters - melody (simple, complex), pitch (high, low), and tempo (fast, slow) - influenced users' cognition and behaviors. There are eight different notifications with different combinations of these parameters. The online study analyzed the effects of user-specific and environmental information on users' behaviors while they listened to these notifications. The results revealed that tempo and pitch have the main effect on the speed and strength (accuracy) of users' cognition and behaviors. The users' characteristics and environments influenced the effects of these musical parameters.
To Repeat or Not to Repeat? Redesigning Repeating Auditory Alarms Based on EEG Analysis
(2019-01-01)
Lee, Yi-Chen
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Cherng, Fu-Yin
;
King, Jung-Tai
;
Lin, Wen-Chieh
;
資訊工程學系
Auditory alarms that repeatedly interrupt users until they react are common, especially in the context of alarms. However, when an alarm repeats, our brains habituate to it and perceive it less and less, with reductions in both perception and attention-shifting: a phenomenon known as the repetition-suppression effect (RS). To retain users' perception and attention, this paper proposes and tests the use of pitch-and intensity-modulated alarms. Its experimental findings suggest that the proposed modulated alarms can reduce RS, albeit in different patterns, depending on whether pitch or intensity is the focus of the modulation. Specifically, pitch-modulated alarms were found to reduce RS more when the number of repetitions was small, while intensity-modulated alarms reduced it more as the number of repetitions increased. Based on these results, we make several recommendations for the design of improved repeating alarms, based on which modulation approach should be adopted in various situations.
Total Synthetic Protoapigenone WYC02 Inhibits Cervical Cancer Cell Proliferation and Tumour Growth through PIK3 Signalling Pathway
(2013-07-01)
Chen, Yun-Ju
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Kay, Nari
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Yang, Jinn-Moon
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Lin, Chih-Ta
;
Chang, Hsueh-Ling
Flavonoids have been intensively explored for their anticancer activity. In this study, a total synthetic flavonoid protoapigenone, known as WYC02, was analysed for its potential anticancer activity on human cervical cancer cells as well as the underlying mechanisms for these effects. The site-moiety maps are used to explore the binding site similarity, pharmacophore and docking pose similarity. The effect of WYC02 on cell viability, migration, invasion and apoptosis as well as the underlying mechanisms was analysed in vitro using human cervical cancer cells. The effect of WYC02 on in vivo tumour growth was assessed in a tumour xenograft study. WYC02 inhibited cell proliferation, MMPs activity, migration and invasion in cervical cancer cells. We speculated that WYC02 might inhibit the activities of PIK3 family proteins, including PIK3CA, PIK3CB, PIK3CD and PIK3CG. Indeed, WYC02 decreased the expression of PIK3 family proteins, especially PIK3CG, through ubiquitination and inhibited the activities of PIK3CG and PIK3 downstream molecules AKT1 and MTOR in cervical cancer cells. Furthermore, PIK3 signalling pathway was involved in the inhibitory effect of WYC02 on cervical cancer cell proliferation and tumour growth in vitro and in vivo. WYC02 inhibits cervical cancer cell proliferation and tumourigenesis via PIK3 signalling pathway and has the potential to be developed as a chemotherapeutic agent in cervical cancer.