Browsing by Author "Hsu, Chih-Hung"

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40-Gb/s Time-Division-Multiplexed Passive Optical Networks Using Downstream OOK and Upstream OFDM Modulations
(2010-01-15)
Yeh, Chien-Hung
;
Chow, Chi-Wai
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Hsu, Chih-Hung
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光電工程學系
;
Department of Photonics
In this investigation, we first propose and investigate a 40-Gb/s time-division-multiplexed passive optical network (TDM-PON) using four wavelength-multiplexed signals in both downstream and upstream traffic. Here, each downstream signal uses 10-Gb/s on-off keying (OOK) format encoded by a Mach-Zehnder modulator (MZM) in 1.5-mu m band. And each upstream channel utilizes the highly spectral efficient 10-Gb/s orthogonal frequency-division-multiplexing quadrature amplitude modulation (OFDM-QAM) generated by directly modulating a 1.3-mu m laser. Based on the proposed scheme, 40-Gb/s data traffic in a TDM-PON can be obtained easily by using four wavelength-multiplexed channels. In addition, the performance of the proposed PON architecture has also been discussed.
A 40-Gb/s OFDM PON System Based on 10-GHz EAM and 10-GHz Direct-Detection PIN
(2012-01-01)
Chen, Hsing-Yu
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Wei, Chia Chien
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Hsu, Dar-Zu
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Yuang, Maria C.
;
Chen, Jyehong
This letter demonstrates a 40-Gb/s optical double-sideband (ODSB) orthogonal frequency-division multiplexing passive optical network (OFDM-PON) system using a cost-effective 10-GHz-bandwidth electroabsorption modulator (EAM). By employing a subcarrier-adaptive modulation format and pre-emphasis, we successfully achieve 20-km EAM-based single-mode-fiber (SMF) transmission.
A Novel Passive Optical Network Architecture Supporting Seamless Integration of RoF and OFDMA Signals
(2010-03-15)
Lin, Yu-Min
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Tien, Po-Lung
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Yuang, Maria C.
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Lee, Steven S. W.
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Chen, Jason (Jyehong)
In this letter, we propose a novel passive optical network (PON) architecture supporting radio-over-fiber signals and orthogonal frequency-division multiple access (OFDMA) PON signals. The architecture transports upstream multiple remote antenna's wireless signals using only one upstream wavelength. In addition, the windowed-orthogonal frequency-division-multiplexing technique is employed to mitigate interference during the integration process. Experimental results shows that 10-Gb/s OFDMA and three radio-frequency signals at 2.1 GHz are successfully transmitted over 20-km single-mode fiber in a 32-optical-network-unit PON.
Ash2l interacts with Oct4-stemness circuitry to promote super-enhancer-driven pluripotency network
(2019-11-04)
Tsai, Ping-Hsing
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Chien, Yueh
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Wang, Mong-Lien
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Hsu, Chih-Hung
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Laurent, Benoit
Pluripotency and cell fates can be modulated through the regulation of super-enhancers; however, the underlying mechanisms are unclear. Here, we showed a novel mechanism in which Ash2l directly binds to super-enhancers of several stemness genes to regulate pluripotency and self-renewal in pluripotent stem cells. Ash2l recruits Oct4/Sox2/Nanog (OSN) to form Ash2l/OSN complex at the super-enhancers of Jarid2, Nanog, Sox2 and Oct4, and further drives enhancer activation, upregulation of stemness genes, and maintains the pluripotent circuitry. Ash2l knockdown abrogates the OSN recruitment to all super-enhancers and further hinders the enhancer activation. In addition, CRISPRi/dCas9-mediated blocking of Ash2l-binding motifs at these super-enhancers also prevents OSN recruitment and enhancer activation, validating that Ash2l directly binds to super-enhancers and initiates the pluripotency network. Transfection of Ash2l with W118A mutation to disrupt Ash2l-Oct4 interaction fails to rescue Ash2l-driven enhancer activation and pluripotent gene upregulation in Ash2l-depleted pluripotent stem cells. Together, our data demonstrated Ash2l formed an enhancer-bound Ash2l/OSN complex that can drive enhancer activation, govern pluripotency network and stemness circuitry.
Demonstration of a Novel PON System with Distributed Real-Time Bandwidth Allocation
(2009)
Yuang, Maria C.
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Lin, Shih-Hsuan
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Lee, Steven S. W.
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Shih, Julin
;
Lin, Yu-Min
This paper demonstrates a novel distributed control PON system (DCPON). Equipped with a distributed adaptable DBA algorithm that enables real-time precise bandwidth allocation, DCPON achieves high utilization, fairness, low request/response time, and superior service differentiation. (C)2009 Optical Society of America
Histone Demethylase RBP2 Promotes Lung Tumorigenesis and Cancer Metastasis
(2013-08-01)
Teng, Yu-Ching
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Lee, Cheng-Feng
;
Li, Ying-Shiuan
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Chen, Yi-Ren
;
Hsiao, Pei-Wen
The retinoblastoma binding protein RBP2 (KDM5A) is a histone demethylase that promotes gastric cancer cell growth and is enriched in drug-resistant lung cancer cells. In tumor-prone mice lacking the tumor suppressor gene RB or MEN1, genetic ablation of RBP2 can suppress tumor initiation, but the pathogenic breadth and mechanistic aspects of this effect relative to human tumors have not been defined. Here, we approached this question in the context of lung cancer. RBP2 was overexpressed in human lung cancer tissues where its depletion impaired cell proliferation, motility, migration, invasion, and metastasis. RBP2 oncogenicity relied on its demethylase and DNA-binding activities. RBP2 upregulated expression of cyclins D1 and E1 while suppressing the expression of cyclin-dependent kinase inhibitor p27 (CDKN1B), each contributing to RBP2-mediated cell proliferation. Expression microarray analyses revealed that RBP2 promoted expression of integrin-beta 1 (ITGB1), which is implicated in lung cancer metastasis. Mechanistic investigations established that RBP2 bound directly to the p27, cyclin D1, and ITGB1 promoters and that exogenous expression of cyclin D1, cyclin E1, or ITGB1 was sufficient to rescue proliferation or migration/invasion, respectively. Taken together, our results establish an oncogenic role for RBP2 in lung tumorigenesis and progression and uncover novel RBP2 targets mediating this role. (C)2013 AACR.
Musashi-1 Enhances Glioblastoma Cell Migration and Cytoskeletal Dynamics through Translational Inhibition of Tensin3
(2017-08-18)
Chen, Hsiao-Yun
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Lin, Liang-Ting
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Wang, Mong-Lien
;
Laurent, Benoit
;
Hsu, Chih-Hung
The RNA-binding protein Musashi-1 (MSI1) exerts essential roles in multiple cellular functions, such as maintenance of self-renewal and pluripotency of stem cells. MSI1 overexpression has been observed in several tumor tissues, including glioblastoma (GBM), and is considered as a well-established marker for tumor metastasis and recurrence. However, the molecular mechanisms by which MSI1 regulates cell migration are still undetermined. Here we reported that MSI1 alters cell morphology, promotes cell migration, and increases viscoelasticity of GBM cells. We also found that MSI1 directly binds to the 3'UTR of Tensin 3 (TNS3) mRNA, a negative regulator of cell migration, to inhibit its translation. Additionally, we identified that RhoA-GTP could be a potential regulator in MSI1/TNS3-mediated cell migration and morphological changes. In a xenograft animal model, high expression ratio of MSI1 to TNS3 enhanced GBM tumor migration. We also confirmed that MSI1 and TNS3 expressions are mutually exclusive in migratory tumor lesions, and GBM patients with MSI1(high)/TNS3(low) pattern tend to have poor clinical outcome. Taken together, our findings suggested a critical role of MSI1-TNS3 axis in regulating GBM migration and highlighted that the ratio of MSI1/TNS3 could predict metastatic and survival outcome of GBM patients.
TET1 Suppresses Cancer Invasion by Activating the Tissue Inhibitors of Metalloproteinases
(2012-09-01)
Hsu, Chih-Hung
;
Peng, Kai-Lin
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Kang, Ming-Lun
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Chen, Yi-Ren
;
Yang, Yu-Chih
Tumor suppressor gene silencing through cytosine methylation contributes to cancer formation. Whether DNA demethylation enzymes counteract this oncogenic effect is unknown. Here, we show that TET1, a dioxygenase involved in cytosine demethylation, is downregulated in prostate and breast cancer tissues. TET1 depletion facilitates cell invasion, tumor growth, and cancer metastasis in prostate xenograft models and correlates with poor survival rates in breast cancer patients. Consistently, enforced expression of TET1 reduces cell invasion and breast xenograft tumor formation. Mechanistically, TET1 suppresses cell invasion through its dioxygenase and DNA binding activities. Furthermore, TET1 maintains the expression of tissue inhibitors of metalloproteinase (TIMP) family proteins 2 and 3 by inhibiting their DNA methylation. Concurrent low expression of TET1 and TIMP2 or TIMP3 correlates with advanced node status in clinical samples. Together, these results illustrate a mechanism by which TET1 suppresses tumor development and invasion partly through downregulation of critical gene methylation.