Optimizing the radiation pattern of smart antennas using genetic algorithms

This work is directed towards optimizing the radiation pattern of smart antennas using genetic algorithms. The structure of the smart antennas based on Space Division Multiple Access (SDMA) is proposed. It is composed of adaptive antennas, each of which has adjustable weight elements for amplitudes and phases of signals. The corresponding radiation pattern formula available for the utilization of numerical optimization techniques is deduced. Genetic algorithms are applied to search the best phase-amplitude weights or phase-only weights with which the optimal radiation pattern can be achieved. ^ One highlight of this work is the proposed optimal radiation pattern concept and its implementation by genetic algorithms. The results show that genetic algorithms are effective for the true Signal-Interference-Ratio (SIR) design of smart antennas. This means that not only nulls can be put in the directions of the interfering signals but also simultaneously main lobes can be formed in the directions of the desired signals. The optimal radiation pattern of a smart antenna possessing SDMA ability has been achieved. ^ The second highlight is on the weight search by genetic algorithms for the optimal radiation pattern design of antennas having more than one interfering signal. The regular criterion for determining which chromosome should be kept for the next step iteration is modified so as to improve the performance of the genetic algorithm iteration. The results show that the modified criterion can speed up and guarantee the iteration to be convergent. ^ In addition, the comparison between phase-amplitude perturbations and phase-only perturbations for the radiation pattern design of smart antennas are carried out. The effects of parameters used by the genetic algorithm on the optimal radiation pattern design are investigated. Valuable results are obtained. ^

Optimization of adaptive traffic signal control with transit signal priority at isolated intersections using parallel genetic algorithms

Optimization of adaptive traffic signal timing is one of the most complex problems in traffic control systems. This dissertation presents a new method that applies the parallel genetic algorithm (PGA) to optimize adaptive traffic signal control in the presence of transit signal priority (TSP). The method can optimize the phase plan, cycle length, and green splits at isolated intersections with consideration for the performance of both the transit and the general vehicles. Unlike the simple genetic algorithm (GA), PGA can provide better and faster solutions needed for real-time optimization of adaptive traffic signal control. ^ An important component in the proposed method involves the development of a microscopic delay estimation model that was designed specifically to optimize adaptive traffic signal with TSP. Macroscopic delay models such as the Highway Capacity Manual (HCM) delay model are unable to accurately consider the effect of phase combination and phase sequence in delay calculations. In addition, because the number of phases and the phase sequence of adaptive traffic signal may vary from cycle to cycle, the phase splits cannot be optimized when the phase sequence is also a decision variable. A "flex-phase" concept was introduced in the proposed microscopic delay estimation model to overcome these limitations. ^ The performance of PGA was first evaluated against the simple GA. The results show that PGA achieved both faster convergence and lower delay for both under- or over-saturated traffic conditions. A VISSIM simulation testbed was then developed to evaluate the performance of the proposed PGA-based adaptive traffic signal control with TSP. The simulation results show that the PGA-based optimizer for adaptive TSP outperformed the fully actuated NEMA control in all test cases. The results also show that the PGA-based optimizer was able to produce TSP timing plans that benefit the transit vehicles while minimizing the impact of TSP on the general vehicles. The VISSIM testbed developed in this research provides a powerful tool to design and evaluate different TSP strategies under both actuated and adaptive signal control. ^

Customization of the design of antenna using genetic algorithm and finite-difference time-domain technique

Antenna design is an iterative process in which structures are analyzed and changed to comply with certain performance parameters required. The classic approach starts with analyzing a "known" structure, obtaining the value of its performance parameter and changing this structure until the "target" value is achieved. This process relies on having an initial structure, which follows some known or "intuitive" patterns already familiar to the designer. The purpose of this research was to develop a method of designing UWB antennas. What is new in this proposal is that the design process is reversed: the designer will start with the target performance parameter and obtain a structure as the result of the design process. This method provided a new way to replicate and optimize existing performance parameters. The base of the method was the use of a Genetic Algorithm (GA) adapted to the format of the chromosome that will be evaluated by the Electromagnetic (EM) solver. For the electromagnetic study we used XFDTD™ program, based in the Finite-Difference Time-Domain technique. The programming portion of the method was created under the MatLab environment, which serves as the interface for converting chromosomes, file formats and transferring of data between the XFDTD™ and GA. A high level of customization had to be written into the code to work with the specific files generated by the XFDTD™ program. Two types of cost functions were evaluated; the first one seeking broadband performance within the UWB band, and the second one searching for curve replication of a reference geometry. The performance of the method was evaluated considering the speed provided by the computer resources used. Balance between accuracy, data file size and speed of execution was achieved by defining parameters in the GA code as well as changing the internal parameters of the XFDTD™ projects. The results showed that the GA produced geometries that were analyzed by the XFDTD™ program and changed following the search criteria until reaching the target value of the cost function. Results also showed how the parameters can change the search criteria and influence the running of the code to provide a variety of geometries.

Reverse Engineering of Modified Genes by Bayesian Network Analysis Defines Molecular Determinants Critical to the Development of Glioblastoma

In this study we have identified key genes that are critical in development of astrocytic tumors. Meta-analysis of microarray studies which compared normal tissue to astrocytoma revealed a set of 646 differentially expressed genes in the majority of astrocytoma. Reverse engineering of these 646 genes using Bayesian network analysis produced a gene network for each grade of astrocytoma (Grade I–IV), and ‘key genes’ within each grade were identified. Genes found to be most influential to development of the highest grade of astrocytoma, Glioblastoma multiforme were: COL4A1, EGFR, BTF3, MPP2, RAB31, CDK4, CD99, ANXA2, TOP2A, and SERBP1. All of these genes were up-regulated, except MPP2 (down regulated). These 10 genes were able to predict tumor status with 96–100% confidence when using logistic regression, cross validation, and the support vector machine analysis. Markov genes interact with NFkβ, ERK, MAPK, VEGF, growth hormone and collagen to produce a network whose top biological functions are cancer, neurological disease, and cellular movement. Three of the 10 genes - EGFR, COL4A1, and CDK4, in particular, seemed to be potential ‘hubs of activity’. Modified expression of these 10 Markov Blanket genes increases lifetime risk of developing glioblastoma compared to the normal population. The glioblastoma risk estimates were dramatically increased with joint effects of 4 or more than 4 Markov Blanket genes. Joint interaction effects of 4, 5, 6, 7, 8, 9 or 10 Markov Blanket genes produced 9, 13, 20.9, 26.7, 52.8, 53.2, 78.1 or 85.9%, respectively, increase in lifetime risk of developing glioblastoma compared to normal population. In summary, it appears that modified expression of several ‘key genes’ may be required for the development of glioblastoma. Further studies are needed to validate these ‘key genes’ as useful tools for early detection and novel therapeutic options for these tumors.