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Overexpression of Ornithine Decarboxylase Suppresses Thapsigargin-Induced Apoptosis
Wei-Chung Hsieh,Pei-Chen Hsu,Ya-Fan Liao,Shu-Ting Young,Zeng-Wei Wang,Chih-Li Lin,Gregory J. Tsay,Huei Lee,Hui-Chih Hung,Guang-Yaw Liu 한국분자세포생물학회 2010 Molecules and cells Vol.30 No.4
Ornithine decarboxylase (ODC), the key enzyme of poly-amine biosynthesis, has paradoxical roles in apoptosis. Our published papers show overexpression of ODC pre-vents the apoptosis induced by many cytotoxic drugs. Thapsigargin (TG) is an inhibitor of the sarcoplasmic/en-doplasmic reticulum (ER) Ca2+ ATPase (SERCA) pumps and causes ER stress-induced apoptosis. We used ODC overexpressing cell lines to examine whether overexpres-sion of ODC inhibits TG-induced apoptosis. Our results indicated overexpression of ODC attenuated TG-induced apoptosis. Overexpression of ODC blocked procaspse-4 cleavage and phosphorylation of protein kinase-like ER-resident kinase (PERK), triggered by TG. It also attenuated the increase in CAAT/enhancer binding protein homolo-gous protein (CHOP). Cells with overexpressed ODC had greater Bcl-2 expression. Overexpression of ODC pre-served the expression of Bcl-2, inhibited the increase in Bak and stabilized mitochondrial membrane potential without the influences of TG. Cytochrome c release and downstream caspase activation were blocked. That is, overexpression of ODC inhibits the mitochondria-medi-ated apoptotic pathway, induced by TG. Finally, overex-pression of ODC maintains the protein and mRNA expres-sion of SERCA. In conclusion, overexpression of ODC suppresses TG-induced apoptosis by blocking caspase-4 activation and PERK phosphorylation, attenuating CHOP expression and inhibiting the mitochondria-mediated apoptotic pathway.
An Efficient If Routing Lookup by Using Routing Interval
Wang, Pi-Chung,Chan, Chia-Tai,Chen, Yaw-Chung The Korean Institute of Communications and Informa 2001 Journal of communications and networks Vol.3 No.4
Nowadays, the commonly used table lookup scheme for IP routing is based on the sc-called classless interdomain routing (CIDR). With CIDR, routers must find out the best matching prefix (BMP) for IP packets forwarding, this complicates the IP lookup. Currently, this process is mainly performed in software and several schemes hale been proposed for hardware implementation. Since the IP lookup performance is a major design issue for the new generation routers, in this article we investigate the properties of the routing table and present a new approach for IP lookups, our approach is not based Gn BMP and significantly reduces the complexity, thus the computation cast of existing schemes can be significantly reduced. We also propose an efficient IP lookup algorithm, with which we improve the binary search on prefixes to 30 millions of packets per second (MPPS) and 5,000 route updates/s under the same experiment setup with an even larger routing table.
Overexpression of Ornithine Decarboxylase Suppresses Thapsigargin-Induced Apoptosis
Hsieh, Wei-Chung,Hsu, Pei-Chen,Liao, Ya-Fan,Young, Shu-Ting,Wang, Zeng-Wei,Lin, Chih-Li,Tsay, Gregory J.,Lee, Huei,Hung, Hui-Chih,Liu, Guang-Yaw Korean Society for Molecular and Cellular Biology 2010 Molecules and cells Vol.30 No.4
Ornithine decarboxylase (ODC), the key enzyme of polyamine biosynthesis, has paradoxical roles in apoptosis. Our published papers show overexpression of ODC prevents the apoptosis induced by many cytotoxic drugs. Thapsigargin (TG) is an inhibitor of the sarcoplasmic/endoplasmic reticulum (ER) $Ca^{2+}$ ATPase (SERCA) pumps and causes ER stress-induced apoptosis. We used ODC overexpressing cell lines to examine whether overexpression of ODC inhibits TG-induced apoptosis. Our results indicated overexpression of ODC attenuated TG-induced apoptosis. Overexpression of ODC blocked procaspse-4 cleavage and phosphorylation of protein kinase-like ER-resident kinase (PERK), triggered by TG. It also attenuated the increase in CAAT/enhancer binding protein homologous protein (CHOP). Cells with overexpressed ODC had greater Bcl-2 expression. Overexpression of ODC preserved the expression of Bcl-2, inhibited the increase in Bak and stabilized mitochondrial membrane potential without the influences of TG. Cytochrome c release and downstream caspase activation were blocked. That is, overexpression of ODC inhibits the mitochondria-mediated apoptotic pathway, induced by TG. Finally, overexpression of ODC maintains the protein and mRNA expression of SERCA. In conclusion, overexpression of ODC suppresses TG-induced apoptosis by blocking caspase-4 activation and PERK phosphorylation, attenuating CHOP expression and inhibiting the mitochondria-mediated apoptotic pathway.
Performance Evaluation of Ethernet Frame Burst Mode in EPON Downstream Link
Wen-Kang Jia,Yaw-Chung Chen 한국전자통신연구원 2008 ETRI Journal Vol.30 No.2
We apply IEEE 802.3 frame burst mode (FBM) to the Ethernet passive optical network (EPON) downstream link and compare its performance with non-frame burst mode for various traffic patterns. Although in light traffic loads (ρ<0.5) the efficiency of the FBM mechanism is not significant, it does feature high throughput, small jitter, low queue occupancy, and short queuing delay in optical line terminals under various traffic loads with various numbers of optical network units (ONUs). The FBM performance always approaches that of full-duplex mode, especially under heavy traffic loads (ρ>0.5). Moreover, an increase in number of ONUs will decrease the burst performance. Our work shows that FBM scheme is very useful for EPON transmission and has low design complexity.
Gallop-Vegas: An Enhanced Slow-Start Mechanism for TCP Vegas
Ho Cheng-Yuan,Chan Yi-Cheng,Chen Yaw-Chung The Korea Institute of Information and Commucation 2006 Journal of communications and networks Vol.8 No.3
In this article, we present a new slow-start variant, which improves the throughput of transmission control protocol (TCP) Vegas. We call this new mechanism Gallop-Vegas because it quickly ramps up to the available bandwidth and reduces the burstiness during the slow-start phase. TCP is known to send bursts of packets during its slow-start phase due to the fast window increase and the ACK-clock based transmission. This phenomenon causes TCP Vegas to change from slow-start phase to congestion-avoidance phase too early in the large bandwidth-delay product (BDP) links. Therefore, in Gallop-Vegas, we increase the congestion window size with a rate between exponential growth and linear growth during slow-start phase. Our analysis, simulation results, and measurements on the Internet show that Gallop-Vegas significantly improves the performance of a connection, especially during the slow-start phase. Furthermore, it is implementation feasible because only sending part needs to be modified.