In this paper, we propose a clustered multihop cellular network （cMCN） architecture and study its performance using fixed channel assignment （FCA） scheme for uplink transmission. The proposed cMCN using FCA can be...In this paper, we propose a clustered multihop cellular network （cMCN） architecture and study its performance using fixed channel assignment （FCA） scheme for uplink transmission. The proposed cMCN using FCA can be applied with some reuse factors. An analytical model based on Markov chain is developed to analyze its performance and validated through computer simulation. And then, we implement direct peer-to-peer communication （DC） in cMCN by considering more reasonable conditions in practice. DC means that two calls communicate directly instead of going through base stations. The results show that cMCN with FCA can reduce the call blocking probability significantly as compared with the traditional single-hop cellular networks with FCA and can be further reduced by using DC.展开更多
Human ether-a-go-go-related gene （HERG1） K^＋ channels are overexpressed in leukemia, which contributes to neoangiogene- sis. The purpose of this study was to investigate the role of HERG1 K^＋ channels on leukemia ...Human ether-a-go-go-related gene （HERG1） K^＋ channels are overexpressed in leukemia, which contributes to neoangiogene- sis. The purpose of this study was to investigate the role of HERG1 K^＋ channels on leukemia angiogenesis. We cultured human umbili- cal vein endothelial cells （HUVECs） in conditioned media, which were derived from leukemic cells with or without E-4031, a HERG1 K^＋ channel special inhibitor. The HUVECs proliferation was mea- sured using CCK-8 assay and migration by a Trans-well. Endothelial tube formation was investigated using Matrigel. Vascular endothelial growth factor （VEGF） levels were tested by ELISA and VEGF mRNA expression using RT-PCR. Our results revealed that blocking HERG1 K^＋ channels could inhibit leukemia-induced HUVECs pro- liferation, migration, and tube formation in vitro. The results sug- gested that HERG1 K~ channels could increase leukemia angio- genesis. Furthermore, blockage of HERG1 K^＋ channels could also decrease leukemic cells secreting VEGF and expressing VEGF mRNA. HERG1 K^＋ channels have a promoting effect on leukemia angiogenesis, and the possible mechanism may be that HERG1 K^＋ channels enhance VEGF expression. Thus, HERG1 K4 channel is a potential target of antiangiogenesis in leukemia.展开更多
文摘In this paper, we propose a clustered multihop cellular network （cMCN） architecture and study its performance using fixed channel assignment （FCA） scheme for uplink transmission. The proposed cMCN using FCA can be applied with some reuse factors. An analytical model based on Markov chain is developed to analyze its performance and validated through computer simulation. And then, we implement direct peer-to-peer communication （DC） in cMCN by considering more reasonable conditions in practice. DC means that two calls communicate directly instead of going through base stations. The results show that cMCN with FCA can reduce the call blocking probability significantly as compared with the traditional single-hop cellular networks with FCA and can be further reduced by using DC.
基金Supported by the National Natural Science Foundation of China(30971112)
文摘Human ether-a-go-go-related gene （HERG1） K^＋ channels are overexpressed in leukemia, which contributes to neoangiogene- sis. The purpose of this study was to investigate the role of HERG1 K^＋ channels on leukemia angiogenesis. We cultured human umbili- cal vein endothelial cells （HUVECs） in conditioned media, which were derived from leukemic cells with or without E-4031, a HERG1 K^＋ channel special inhibitor. The HUVECs proliferation was mea- sured using CCK-8 assay and migration by a Trans-well. Endothelial tube formation was investigated using Matrigel. Vascular endothelial growth factor （VEGF） levels were tested by ELISA and VEGF mRNA expression using RT-PCR. Our results revealed that blocking HERG1 K^＋ channels could inhibit leukemia-induced HUVECs pro- liferation, migration, and tube formation in vitro. The results sug- gested that HERG1 K~ channels could increase leukemia angio- genesis. Furthermore, blockage of HERG1 K^＋ channels could also decrease leukemic cells secreting VEGF and expressing VEGF mRNA. HERG1 K^＋ channels have a promoting effect on leukemia angiogenesis, and the possible mechanism may be that HERG1 K^＋ channels enhance VEGF expression. Thus, HERG1 K4 channel is a potential target of antiangiogenesis in leukemia.
