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- Zhang, Lin, et al.
(författare)
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Proactive Cross-Channel Gain Estimation for Spectrum Sharing in Cognitive Radio
- 2016
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Ingår i: IEEE Journal on Selected Areas in Communications. - : Institute of Electrical and Electronics Engineers (IEEE). - 0733-8716 .- 1558-0008. ; 34:10, s. 2776-2790
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Tidskriftsartikel (refereegranskat)abstract
- In an underlay cognitive radio network, the cross-channel gain from a cognitive transmitter (CT) to a primary receiver (PR) is crucial for spectrum sharing. By exploiting the relaying capability of the CT, we propose a proactive estimation scheme for the cross-channel gain. Specifically, the CT proactively acts as a full-duplex amplify-and-forward (AF) relay for primary transceivers to trigger the power adaption of a primary transmitter (PT). By carefully designing the relay signal, the CT is able to obtain an estimation of the cross-channel gain by observing the power adaption. To demonstrate the accuracy of the estimation, we analytically characterize both an upper bound and a lower bound of the estimation performance. Furthermore, we study the impact of CT's relaying on the primary transmission and observe that the impact is related to the CT's location. By introducing a factor phi (0 <= phi <= 1) to denote the probability that the CT's relaying improves the primary transmission instead of causes interference, we design the CT location as a function of f. Numerical results show that the estimation error of the proactive estimation scheme can be as small as 1.7% with success estimation probability around 91%. By comparing with the state of the art, we show the advantages of the proposed estimator.
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| 3. |
- Zhu, Wuyang, et al.
(författare)
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Interaction of E2 glycoprotein with heparan sulfate is crucial for cellular infection of Sindbis virus
- 2010
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 5:3, s. e9656-
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Tidskriftsartikel (refereegranskat)abstract
- Cell culture-adapted strains of Sindbis virus (SINV) initially attach to cells by the ability to interact with heparan sulfate (HS) through selective mutation for positively charged amino acid (aa) scattered in E2 glycoprotein (W. B. Klimstra, K. D. Ryman, and R. E. Johnston, J. Virol. 72: 7357-7366, 1998). Here we have further confirmed that interaction of E2 protein with HS is crucial for cellular infection of SINV based on the reverse genetic system of XJ-160 virus, a Sindbis-like virus (SINLV). Both SINV YN87448 and SINLV XJ-160 displayed similar infectivity on BHK-21, Vero, or C6/36 cells, but XJ-160 failed to infect mouse embryonic fibroblast (MEF) cells. The molecular mechanisms underlying the selective infectivity of XJ-160 were approached by substituting the E1, E2, or both genes of XJ-160 with that of YN87448, and the chimeric virus was denominated as XJ-160/E1, XJ-160/E2, or XJ-160/E1E2, respectively. In contrast to the parental XJ-160, all chimeric viruses became infectious to wild-type MEF cells (MEF-wt). While MEF-Ext(-/-) cells, producing shortened HS chains, were resistant not only to XJ-160, but also to YN87448 as well as the chimeric viruses, indicating that the inability of XJ-160 to infect MEF-wt cells likely due to its incompetent discrimination of cellular HS. Treatment with heparin or HS-degrading enzyme resulted in a substantial decrease in plaque formation by YN87448, XJ-160/E2, and XJ-160/E1E2, but had marginal effect on XJ-160 and XJ-160/E1, suggesting that E2 glycoprotein from YN87448 plays a more important role than does E1 in mediating cellular HS-related cell infection. In addition, the peptide containing 145-150 aa from E2 gene of YN87448 specifically bound to heparin, while the corresponding peptide from the E2 gene of XJ-160 essentially showed no binding to heparin. As a new dataset, these results clearly confirm an essential role of E2 glycoprotein, especially the domain of 145-150 aa, in SINV cellular infection through the interaction with HS.
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