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- 저자 : Zuo Xiaolin (검색결과 2 건)
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A Medium Access Control Mechanism for Distributed In-band Full-Duplex Wireless Networks
( Haiwei Zuo ),( Yanjing Sun ),( Song Li ),( Qiang Ni ),( Xiaolin Wang ),( Xiaoguang Zhang ) 한국인터넷정보학회 2017 KSII Transactions on Internet and Information Syst Vol.11 No.11
In-band full-duplex (IBFD) wireless communication supports symmetric dual transmission between two nodes and asymmetric dual transmission among three nodes, which allows improved throughput for distributed IBFD wireless networks. However, inter-node interference (INI) can affect desired packet reception in the downlink of three-node topology. The current Half-duplex (HD) medium access control (MAC) mechanism RTS/CTS is unable to establish an asymmetric dual link and consequently to suppress INI. In this paper, we propose a medium access control mechanism for use in distributed IBFD wireless networks, FD-DMAC (Full-Duplex Distributed MAC). In this approach, communication nodes only require single channel access to establish symmetric or asymmetric dual link, and we fully consider the two transmission modes of asymmetric dual link. Through FD-DMAC medium access, the neighbors of communication nodes can clearly know network transmission status, which will provide other opportunities of asymmetric IBFD dual communication and solve hidden node problem. Additionally, we leverage FD-DMAC to transmit received power information. This approach can assist communication nodes to adjust transmit powers and suppress INI. Finally, we give a theoretical analysis of network performance using a discrete-time Markov model. The numerical results show that FD-DMAC achieves a significant improvement over RTS/CTS in terms of throughput and delay.
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Identification a novel de novo RUNX2 frameshift mutation associated with cleidocranial dysplasia
Gong Lei,Odilov Bekzod,Han Feng,Liu Fuqiang,Sun Yujing,Zhang Ningxin,Zuo Xiaolin,Yang Jiaojiao,Wang Shouyu,Hou Xinguo,Ren Jianmin 한국유전학회 2022 Genes & Genomics Vol.44 No.6
Background: Cleidocranial dysplasia (CCD) is a rare genetic disorder affecting bone and cartilage development. Clinical features of CCD comprise short stature, delayed ossification of craniofacial structures with numerous Wormian bones, underdeveloped or aplastic clavicles and multiple dental anomalies. Several studies have revealed that CCD development is strongly linked with different mutations in runt-related transcription factor 2 (RUNX2) gene. Objective: Identification and functional characterization of RUNX2 mutation associated with CCD. Methods: We performed genetic testing of a patient with CCD using whole exome sequencing and found a novel RUNX2 frameshift mutation: c.1550delT in a sporadic case. We also compared the functional activity of the mutant and wild-type RUNX2 through immunofluorescence microscopy and osteocalcin promoter luciferase assay. Results: We found a novel RUNX2 frameshift mutation, c.1550delT (p.Trp518Glyfs*60). Both mutant RUNX2 and wild-type RUNX2 protein were similarly confined in the nuclei. The novel mutation caused abrogative transactivation activity of RUNX2 on osteocalcin promoter. Conclusions: We explored a novel RUNX2 deletion/frameshift mutation in a sporadic CCD patient. This finding suggests that the VWRPY domain may play a key role in RUNX2 transactivation ability.
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