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| 2. |
- Johansson, Björn, et al.
(författare)
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Distributed Model Predictive Consensus
- 2006
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Ingår i: Proceedings of the 17th International Symposium on Mathematical Theory of Networks and Systems. ; , s. 2438-2444
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Konferensbidrag (refereegranskat)abstract
- In this paper we consider the problem of designing a distributed control strategy such that a linear combination of the states of a number of vehicles coincide at a given time. The vehicles are described by linear difference equations and are subject to convex input constraints. It is demonstrated how primal decomposition techniques and incremental subgradient methods allow us to find a solution in which each vehicle performs individual planning of its trajectory and exchanges critical information with neighbors only. We explore various communication, computation, and control structures, and demonstrate the performance of the algorithms by numerical examples.
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| 3. |
- Johansson, Björn, et al.
(författare)
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On decentralized negotiation of optimal consensus
- 2008
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Ingår i: Automatica. - : Elsevier BV. - 0005-1098 .- 1873-2836. ; 44:4, s. 1175-1179
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Tidskriftsartikel (refereegranskat)abstract
- A consensus problem consists of finding a distributed control strategy that brings the state or output of a group of agents to a common value, a consensus point. In this paper, we propose a negotiation algorithm that computes an optimal consensus point for agents modeled as linear control systems subject to convex input constraints and linear state constraints. By primal decomposition and incremental subgradient methods, it is shown that the algorithm can be implemented such that each agent exchanges only a small amount of information per iteration with its neighbors.
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| 4. |
- Johansson, Björn, et al.
(författare)
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Subgradient methods and consensus algorithms for solving convex optimization problems
- 2008
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Ingår i: Decision and Control, 2008. CDC 2008. 47th IEEE Conference on. - : IEEE. - 9781424431236 ; , s. 4185-4190
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Konferensbidrag (refereegranskat)abstract
- In this paper we propose a subgradient method for solving coupled optimization problems in a distributed way given restrictions on the communication topology. The iterative procedure maintains local variables at each node and relies on local subgradient updates in combination with a consensus process. The local subgradient steps are applied simultaneously as opposed to the standard sequential or cyclic procedure. We study convergence properties of the proposed scheme using results from consensus theory and approximate subgradient methods. The framework is illustrated on an optimal distributed finite-time rendezvous problem.
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| 6. |
- Aminian, Behdad, et al.
(författare)
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GISOO : A virtual testbed for wireless cyber-physical systems
- 2013
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Ingår i: Industrial Electronics Society, IECON 2013 - 39th Annual Conference of the IEEE. - : IEEE. - 9781479902248 ; , s. 5588-5593
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Konferensbidrag (refereegranskat)abstract
- The increasing demand for wireless cyber-physical systems requires correct design, implementation and validation of computation, communication and control methods. Traditional simulation tools, which focus on either computation, communication or control, are insufficient when the three aspects interact. Efforts to extend the traditional tools to cover multiple domains, e.g., from simulating only control aspects to simulating both control and communication, often rely on simplistic models of a small subset of possible communication solutions. We introduce GISOO, a virtual testbed for simulation of wireless cyber-physical systems that integrates two state-of-the art simulators, Simulink and COOJA. GISOO enables users to evaluate actual embedded code for the wireless nodes in realistic cyber-physical experiments, observing the effects of both the control and communication components. In this way, a wide range of communication solutions can be evaluated without developing abstract models of their control-relevant aspects, and changes made to the networking code in simulations is guaranteed to be translated into production code without errors. A double-tank laboratory experimental setup controlled over a multi-hop relay wireless network is used to validate GISOO and demonstrate its features.
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| 7. |
- Anantharaman, Devasena, et al.
(författare)
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No causal association identified for human papillomavirus infections in lung cancer
- 2014
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Ingår i: Cancer Research. - : American Association for Cancer Research. - 0008-5472 .- 1538-7445. ; 74:13, s. 3525-3534
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Tidskriftsartikel (refereegranskat)abstract
- Human papillomavirus (HPV) infections have been implicated in lung carcinogenesis, but causal associations remain uncertain. We evaluated a potential causal role for HPV infections in lung cancer through an analysis involving serology, tumor DNA, RNA, and p16 protein expression. Association between type-specific HPV antibodies and risk of lung cancer was examined among 3,083 cases and 4,328 controls in two case-control studies (retrospective) and one nested case-control study (prospective design). Three hundred and thirty-four available tumors were subjected to pathologic evaluation and subsequent HPV genotyping following stringent conditions to detect all high-risk and two low-risk HPV types. All HPV DNA-positive tumors were further tested for the expression of p16 protein and type-specific HPV mRNA. On the basis of the consistency of the results, although HPV11 and HPV31 E6 antibodies were associated with lung cancer risk in the retrospective study, no association was observed in the prospective design. Presence of type-specific antibodies correlated poorly with the presence of the corresponding HPV DNA in the tumor. Although nearly 10% of the lung tumors were positive for any HPV DNA (7% for HPV16 DNA), none expressed the viral oncogenes. No association was observed between HPV antibodies or DNA and lung cancer survival. In conclusion, we found no supportive evidence for the hypothesized causal association between HPV infections and lung cancer. (C) 2014 AACR.
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| 9. |
- Baglietto, Laura, et al.
(författare)
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DNA methylation changes measured in pre-diagnostic peripheral blood samples are associated with smoking and lung cancer risk
- 2017
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 140:1, s. 50-61
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Tidskriftsartikel (refereegranskat)abstract
- DNA methylation changes are associated with cigarette smoking. We used the Illumina Infinium HumanMethylation450 array to determine whether methylation in DNA from pre-diagnostic, peripheral blood samples is associated with lung cancer risk. We used a case-control study nested within the EPIC-Italy cohort and a study within the MCCS cohort as discovery sets (a total of 552 case-control pairs). We validated the top signals in 429 case-control pairs from another 3 studies. We identified six CpGs for which hypomethylation was associated with lung cancer risk: cg05575921 in the AHRR gene (p-valuepooled = 4 × 10(-17) ), cg03636183 in the F2RL3 gene (p-valuepooled = 2 × 10 (- 13) ), cg21566642 and cg05951221 in 2q37.1 (p-valuepooled = 7 × 10(-16) and 1 × 10(-11) respectively), cg06126421 in 6p21.33 (p-valuepooled = 2 × 10(-15) ) and cg23387569 in 12q14.1 (p-valuepooled = 5 × 10(-7) ). For cg05951221 and cg23387569 the strength of association was virtually identical in never and current smokers. For all these CpGs except for cg23387569, the methylation levels were different across smoking categories in controls (p-valuesheterogeneity ≤ 1.8 x10 (- 7) ), were lowest for current smokers and increased with time since quitting for former smokers. We observed a gain in discrimination between cases and controls measured by the area under the ROC curve of at least 8% (p-values ≥ 0.003) in former smokers by adding methylation at the 6 CpGs into risk prediction models including smoking status and number of pack-years. Our findings provide convincing evidence that smoking and possibly other factors lead to DNA methylation changes measurable in peripheral blood that may improve prediction of lung cancer risk.
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| 10. |
- Battram, Thomas, et al.
(författare)
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Appraising the causal relevance of DNA methylation for risk of lung cancer
- 2019
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Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 48:5, s. 1493-1504
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Tidskriftsartikel (refereegranskat)abstract
- Background: DNA methylation changes in peripheral blood have recently been identified in relation to lung cancer risk. Some of these changes have been suggested to mediate part of the effect of smoking on lung cancer. However, limitations with conventional mediation analyses mean that the causal nature of these methylation changes has yet to be fully elucidated.Methods: We first performed a meta-analysis of four epigenome-wide association studies (EWAS) of lung cancer (918 cases, 918 controls). Next, we conducted a two-sample Mendelian randomization analysis, using genetic instruments for methylation at CpG sites identified in the EWAS meta-analysis, and 29 863 cases and 55 586 controls from the TRICL-ILCCO lung cancer consortium, to appraise the possible causal role of methylation at these sites on lung cancer.Results: Sixteen CpG sites were identified from the EWAS meta-analysis [false discovery rate (FDR) < 0.05], for 14 of which we could identify genetic instruments. Mendelian randomization provided little evidence that DNA methylation in peripheral blood at the 14 CpG sites plays a causal role in lung cancer development (FDR > 0.05), including for cg05575921-AHRR where methylation is strongly associated with both smoke exposure and lung cancer risk.Conclusions: The results contrast with previous observational and mediation analysis, which have made strong claims regarding the causal role of DNA methylation. Thus, previous suggestions of a mediating role of methylation at sites identified in peripheral blood, such as cg05575921-AHRR, could be unfounded. However, this study does not preclude the possibility that differential DNA methylation at other sites is causally involved in lung cancer development, especially within lung tissue.
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