| 1. |
- Gezici, Sinan, et al.
(författare)
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Optimal Jammer Placement in Wireless Localization Systems
- 2016
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Ingår i: IEEE Transactions on Signal Processing. - 1053-587X .- 1941-0476. ; 64:17, s. 4534-4549
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Tidskriftsartikel (refereegranskat)abstract
- In this study, the optimal jammer placement problem is proposed and analyzed for wireless localization systems. In particular, the optimal location of a jammer node is obtained by maximizing the minimum of the Cramer-Rao lower bounds (CRLBs) for a number of target nodes under location related constraints for the jammer node. For scenarios with more than two target nodes, theoretical results are derived to specify conditions underwhich the jammer node is located as close to a certain target node as possible, or the optimal location of the jammer node is determined by two of the target nodes. Also, explicit expressions are provided for the optimal location of the jammer node in the presence of two target nodes. In addition, in the absence of distance constraints for the jammer node, it is proved, for scenarios with more than two target nodes, that the optimal jammer location lies on the convex hull formed by the locations of the target nodes and is determined by two or three of the target nodes, which have equalized CRLBs. Numerical examples are presented to provide illustrations of the theoretical results in different scenarios.
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| 2. |
- Gezici, Sinan, et al.
(författare)
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Optimal Jamming of Wireless Localization Systems
- 2015
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Ingår i: 2015 IEEE INTERNATIONAL CONFERENCE ON COMMUNICATION WORKSHOP. - : IEEE. - 9781467363051 ; , s. 877-882
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Konferensbidrag (refereegranskat)abstract
- In this study, optimal jamming of wireless localization systems is investigated. Two optimal power allocation schemes are proposed for jammer nodes in the presence of total and peak power constraints. In the first scheme, power is allocated to jammer nodes in order to maximize the average Cramer-Rao lower hound (CRLB) of target nodes whereas in the second scheme the power allocation is performed for the aim of maximizing the minimum CRLB of target nodes. Both schemes are formulated as linear programs, and a closed-form expression is obtained for the first scheme. Also, the full total power utilization property is specified for the second scheme. Simulation results are presented to investigate perlbrmance of the proposed schemes.
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| 3. |
- Keskin, Furkan, 1988, et al.
(författare)
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Jamming Strategies in Wireless Source Localization Systems
- 2019
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Ingår i: IEEE Wireless Communications Letters. - 2162-2345 .- 2162-2337. ; 8:4, s. 1141-1145
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Tidskriftsartikel (refereegranskat)abstract
- We consider optimal jamming strategies in wireless source localization systems, where anchor nodes estimate positions of target nodes in the presence of jammers that emit zero-mean Gaussian noise. The Cramér-Rao lower bound (CRLB) for target location estimation is derived and the problem of optimal power allocation for jammer nodes is formulated to maximize the average CRLB for target nodes under total and peak power constraints. Exploiting the special problem structure and successive convex approximation techniques, we develop an iterative algorithm that transforms the original non-convex problem into a sequence of convex geometric programs. In addition, we present a closed-form solution that is asymptotically optimal. Numerical results demonstrate the improved jamming performance of the proposed solutions over the uniform power allocation strategy.
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| 4. |
- Marazioti, Antonia, et al.
(författare)
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KRAS signaling in malignant pleural mesothelioma
- 2022
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Ingår i: EMBO Molecular Medicine. - : EMBO. - 1757-4684 .- 1757-4676. ; 14:2
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Tidskriftsartikel (refereegranskat)abstract
- Malignant pleural mesothelioma (MPM) arises from mesothelial cells lining the pleural cavity of asbestos-exposed individuals and rapidly leads to death. MPM harbors loss-of-function mutations in BAP1, NF2, CDKN2A, and TP53, but isolated deletion of these genes alone in mice does not cause MPM and mouse models of the disease are sparse. Here, we show that a proportion of human MPM harbor point mutations, copy number alterations, and overexpression of KRAS with or without TP53 changes. These are likely pathogenic, since ectopic expression of mutant KRASG12D in the pleural mesothelium of conditional mice causes epithelioid MPM and cooperates with TP53 deletion to drive a more aggressive disease form with biphasic features and pleural effusions. Murine MPM cell lines derived from these tumors carry the initiating KRASG12D lesions, secondary Bap1 alterations, and human MPM-like gene expression profiles. Moreover, they are transplantable and actionable by KRAS inhibition. Our results indicate that KRAS alterations alone or in accomplice with TP53 alterations likely play an important and underestimated role in a proportion of patients with MPM, which warrants further exploration.
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