Browsing by Author "Chen, Wen-Chuan"

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EM-Based Iterative Receivers for OFDM and BICM/OFDM Systems in Doubly Selective Channels
(2011-05-01)
Ku, Meng-Lin
;
Chen, Wen-Chuan
;
Huang, Chia-Chi
;
電機工程學系
;
Department of Electrical and Computer Engineering
In this paper, we resort to the expectation-maximization (EM) algorithm to tackle the inter-carrier interference (ICI) problem, caused by time-variant multipath channels, for both orthogonal frequency division multiplexing (OFDM) systems and bit-interleaved coded modulation (BICM)/OFDM systems. We first analyze the ICI in frequency domain with a reduced set of parameters, and following this analysis, we derive an EM algorithm for maximum likelihood (ML) data detection. An ML-EM receiver for OFDM systems and a TURBO-EM receiver for BICM/OFDM systems are then developed to reduce computational complexity of the EM algorithm and to exploit temporal diversity, the main idea of which is to integrate the proposed EM algorithm with a groupwise ICI cancellation method. Compared with the ML-EM receiver, the TURBO-EM receiver further employs a soft-output Viterbi algorithm (SOVA) decoder to exchange information with a maximum a posteriori (MAP) EM detector through the turbo principle. Computer simulation demonstrates that the two proposed receivers clearly outperform the conventional one-tap equalizer, and the performance of the TURBO-EM receiver is close to the matched-filter bound even at a normalized maximum Doppler frequency (MDF) up to 0.2.
Zebrafish WNK Lysine Deficient Protein Kinase 1 (wnk1) Affects Angiogenesis Associated with VEGF Signaling
(2014-08-29)
Lai, Ju-Geng
;
Tsai, Su-Mei
;
Tu, Hsiao-Chen
;
Chen, Wen-Chuan
;
Kou, Fong-Ji
The WNK1 (WNK lysine deficient protein kinase 1) protein is a serine/threonine protein kinase with emerging roles in cancer. WNK1 causes hypertension and hyperkalemia when overexpressed and cardiovascular defects when ablated in mice. In this study, the role of Wnk1 in angiogenesis was explored using the zebrafish model. There are two zebrafish wnk1 isoforms, wnk1a and wnk1b, and both contain all the functional domains found in the human WNK1 protein. Both isoforms are expressed in the embryo at the initiation of angiogenesis and in the posterior cardinal vein (PCV), similar to fms-related tyrosine kinase 4 (flt4). Using morpholino antisense oligonucleotides against wnk1a and wnk1b, we observed that wnk1 morphants have defects in angiogenesis in the head and trunk, similar to flk1/vegfr2 morphants. Furthermore, both wnk1a and wnk1b mRNA can partially rescue the defects in vascular formation caused by flk1/vegfr2 knockdown. Mutation of the kinase domain or the Akt/PI3K phosphorylation site within wnk1 destroys this rescue capability. The rescue experiments provide evidence that wnk1 is a downstream target for Vegfr2 (vascular endothelial growth factor receptor-2) and Akt/PI3K signaling and thereby affects angiogenesis in zebrafish embryos. Furthermore, we found that knockdown of vascular endothelial growth factor receptor-2 (flk1/vegfr2) or vascular endothelial growth factor receptor-3 (flt4/vegfr3) results in a decrease in wnk1a expression, as assessed by in situ hybridization and q-RT-PCR analysis. Thus, the Vegf/Vegfr signaling pathway controls angiogenesis in zebrafish via Akt kinase-mediated phosphorylation and activation of Wnk1 as well as transcriptional regulation of wnk1 expression.
Zebrafish WNK Lysine Deficient Protein Kinase 1 (wnk1) Affects Angiogenesis Associated with VEGF Signaling
(2014-08-29)
Lai, Ju-Geng
;
Tsai, Su-Mei
;
Tu, Hsiao-Chen
;
Chen, Wen-Chuan
;
Kou, Fong-Ji
The WNK1 (WNK lysine deficient protein kinase 1) protein is a serine/threonine protein kinase with emerging roles in cancer. WNK1 causes hypertension and hyperkalemia when overexpressed and cardiovascular defects when ablated in mice. In this study, the role of Wnk1 in angiogenesis was explored using the zebrafish model. There are two zebrafish wnk1 isoforms, wnk1a and wnk1b, and both contain all the functional domains found in the human WNK1 protein. Both isoforms are expressed in the embryo at the initiation of angiogenesis and in the posterior cardinal vein (PCV), similar to fms-related tyrosine kinase 4 (flt4). Using morpholino antisense oligonucleotides against wnk1a and wnk1b, we observed that wnk1 morphants have defects in angiogenesis in the head and trunk, similar to flk1/vegfr2 morphants. Furthermore, both wnk1a and wnk1b mRNA can partially rescue the defects in vascular formation caused by flk1/vegfr2 knockdown. Mutation of the kinase domain or the Akt/PI3K phosphorylation site within wnk1 destroys this rescue capability. The rescue experiments provide evidence that wnk1 is a downstream target for Vegfr2 (vascular endothelial growth factor receptor-2) and Akt/PI3K signaling and thereby affects angiogenesis in zebrafish embryos. Furthermore, we found that knockdown of vascular endothelial growth factor receptor-2 (flk1/vegfr2) or vascular endothelial growth factor receptor-3 (flt4/vegfr3) results in a decrease in wnk1a expression, as assessed by in situ hybridization and q-RT-PCR analysis. Thus, the Vegf/Vegfr signaling pathway controls angiogenesis in zebrafish via Akt kinase-mediated phosphorylation and activation of Wnk1 as well as transcriptional regulation of wnk1 expression.