Multicore and FPGA implementations of emotional-based agent architectures

The final publication is available at Springer via http://dx.doi.org/10.1007/s11227-014-1307-6.Control architectures based on Emotions are becoming promising solutions for the implementation of future robotic agents. The basic controllers of the architecture are the emotional processes that decide which behaviors of the robot must activate to fulfill the objectives. The number of emotional processes increases (hundreds of millions/s) with the complexity level of the application, reducing the processing capacity of the main processor to solve complex problems (millions of decisions in a given instant). However, the potential parallelism of the emotional processes permits their execution in parallel on FPGAs or Multicores, thus enabling slack computing in the main processor to tackle more complex dynamic problems. In this paper, an emotional architecture for mobile robotic agents is presented. The workload of the emotional processes is evaluated. Then, the main processor is extended with FPGA co-processors through Ethernet link. The FPGAs will be in charge of the execution of the emotional processes in parallel. Different Stratix FPGAs are compared to analyze their suitability to cope with the proposed mobile robotic agent applications. The applications are set up taking into account different environmental conditions, robot dynamics and emotional states. Moreover, the applications are run also on Multicore processors to compare their performance in relation to the FPGAs. Experimental results show that Stratix IV FPGA increases the performance in about one order of magnitude over the main processor and solves all the considered problems. Quad-Core increases the performance in 3.64 times, allowing to tackle about 89 % of the considered problems. Quad-Core has a lower cost than a Stratix IV, so more adequate solution but not for the most complex application. 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Mechanisms of MEOX1 and MEOX2 Regulation of the Cyclin Dependent Kinase Inhibitors p21CIP1/WAF1 and p16INK4a in Vascular Endothelial Cells

Senescence, the state of permanent cell cycle arrest, has been associated with endothelial cell dysfunction and atherosclerosis. The cyclin dependent kinase inhibitors p21CIP1/WAF1 and p16INK4a govern the G1/S cell cycle checkpoint and are essential for determining whether a cell enters into an arrested state. The homeodomain transcription factor MEOX2 is an important regulator of vascular cell proliferation and is a direct transcriptional activator of both p21CIP1/WAF1 and p16INK4a. MEOX1 and MEOX2 have been shown to be partially functionally redundant during development, suggesting that they regulate similar target genes in vivo. We compared the ability of MEOX1 and MEOX2 to activate p21CIP1/WAF1 and p16INK4a expression and induce endothelial cell cycle arrest. Our results demonstrate for the first time that MEOX1 regulates the MEOX2 target genes p21CIP1/WAF1 and p16INK4a. In addition, increased expression of either of the MEOX homeodomain transcription factors leads to cell cycle arrest and endothelial cell senescence. Furthermore, we show that the mechanism of transcriptional activation of these cyclin dependent kinase inhibitor genes by MEOX1 and MEOX2 is distinct. MEOX1 and MEOX2 activate p16INK4a in a DNA binding dependent manner, whereas they induce p21CIP1/WAF1 in a DNA binding independent manner

A Cyclo–dissipativity framework for power factor compensation of electrical circuits

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