A Novel Predictor Based Framework to Improve Mobility of High Speed Teleoperated Unmanned Ground Vehicles

Teleoperated Unmanned Ground Vehicles (UGVs) have been widely used in applications when driver safety, mission eciency or mission cost is a major concern. One major challenge with teleoperating a UGV is that communication delays can significantly affect the mobility performance of the vehicle and make teleoperated driving tasks very challenging especially at high speeds. In this dissertation, a predictor based framework with predictors in a new form and a blended architecture are developed to compensate effects of delays through signal prediction, thereby improving vehicle mobility performance. The novelty of the framework is that minimal information about the governing equations of the system is required to compensate delays and, thus, the prediction is robust to modeling errors. This dissertation first investigates a model-free solution and develops a predictor that does not require information about the vehicle dynamics or human operators' motion for prediction. Compared to the existing model-free methods, neither assumptions about the particular way the vehicle moves, nor knowledge about the noise characteristics that drive the existing predictive filters are needed. Its stability and performance are studied and a predictor design procedure is presented. Secondly, a blended architecture is developed to blend the outputs of the model-free predictor with those of a steering feedforward loop that relies on minimal information about vehicle lateral response. Better prediction accuracy is observed based on open-loop virtual testing with the blended architecture compared to using either the model-free predictors or the model-based feedforward loop alone. The mobility performance of teleoperated vehicles with delays and the predictor based framework are evaluated in this dissertation with human-in-the-loop experiments using both simulated and physical vehicles in teleoperation mode. Predictor based framework is shown to provide a statistically significant improvement in vehicle mobility and drivability in the experiments performed.PHDMechanical EngineeringUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttps://deepblue.lib.umich.edu/bitstream/2027.42/146026/1/zhengys_1.pd

dp53 Restrains Ectopic Neural Stem Cell Formation in the Drosophila Brain in a Non-Apoptotic Mechanism Involving Archipelago and Cyclin E

Accumulating evidence suggests that tumor-initiating stem cells or cancer stem cells (CSCs) possibly originating from normal stem cells may be the root cause of certain malignancies. How stem cell homeostasis is impaired in tumor tissues is not well understood, although certain tumor suppressors have been implicated. In this study, we use the Drosophila neural stem cells (NSCs) called neuroblasts as a model to study this process. Loss-of-function of Numb, a key cell fate determinant with well-conserved mammalian counterparts, leads to the formation of ectopic neuroblasts and a tumor phenotype in the larval brain. Overexpression of the Drosophila tumor suppressor p53 (dp53) was able to suppress ectopic neuroblast formation caused by numb loss-of-function. This occurred in a non-apoptotic manner and was independent of Dacapo, the fly counterpart of the well-characterized mammalian p53 target p21 involved in cellular senescence. The observation that dp53 affected Edu incorporation into neuroblasts led us to test the hypothesis that dp53 acts through regulation of factors involved in cell cycle progression. Our results show that the inhibitory effect of dp53 on ectopic neuroblast formation was mediated largely through its regulation of Cyclin E (Cyc E). Overexpression of Cyc E was able to abrogate dp53′s ability to rescue numb loss-of-function phenotypes. Increasing Cyc E levels by attenuating Archipelago (Ago), a recently identified transcriptional target of dp53 and a negative regulator of Cyc E, had similar effects. Conversely, reducing Cyc E activity by overexpressing Ago blocked ectopic neuroblast formation in numb mutant. Our results reveal an intimate connection between cell cycle progression and NSC self-renewal vs. differentiation control, and indicate that p53-mediated regulation of ectopic NSC self-renewal through the Ago/Cyc E axis becomes particularly important when NSC homeostasis is perturbed as in numb loss-of-function condition. This has important clinical implications

General-Purpose Wireless Robot Interface System

Executive Summary of ME 450 F13 Team 22 Final Reporthttp://deepblue.lib.umich.edu/bitstream/2027.42/101983/1/ME450F13Project22_Photo.jpghttp://deepblue.lib.umich.edu/bitstream/2027.42/101983/2/ME450F13Project22_Summary.pd

Performance Analysis of a Model-Free Predictor for Delay Compensation in Networked Systems

One important challenge with networked systems is that communication delays can significantly deteriorate system performance. This paper considers a model-free predictor framework to compensate for communication delays and improve networked system performance, where the term model-free indicates that the predictor does not need to know the dynamic equations governing the system. Stability analysis of this predictor is available in the literature; however, ensuring stability does not guarantee a good performance. Understanding when the predictor can perform well and what its limitations are is critical, but the performance characteristics of the predictor are unknown. Hence, this paper aims to fill this gap by providing a predictor performance analysis for constant time delays. First, a frequency-domain analysis is performed for the predictor and the relationship between the predictor design parameter, time delay, and steady-state performance is revealed. Fundamental limitations of the predictor at higher frequencies are laid out. Next, this analysis is confirmed on a case study. The case study further allows for testing the transient performance of the predictor in closed-loop with the networked system, and shows that the predictor holds significant potential to alleviate the negative impact of communication delays, even if its higher frequency performance may be limited

Food restriction decreases BMR, body and organ mass, and cellular energetics, in the Chinese Bulbul (Pycnonotus sinensis)

Abstract Background Food is an important environmental factor that affects animals’ energy metabolism and food shortage has significant effects on animals’ behavior, physiology and biochemistry. However, to date few studies have focused on the thermogenesis and its effects on the body condition of birds. In this study, we examined the effects of food restriction on the body mass, basal metabolic rate (BMR) and body composition, and several physiological, biochemical and molecular markers potentially related to thermogenesis, in the Chinese Bulbul (Pycnonotus sinensis). Methods Birds in the control group were provided with food ad libitum whereas those in the food restriction group were provided with one-half of the usual quantity of food for 12 days. Oxygen consumption was measured using an open-circuit respirometry system. Mitochondrial state 4 respiration and cytochrome c oxidase (COX) activity in the liver and pectoral muscle were measured with a Clark electrode. Avian uncoupling protein (avUCP) mRNA expression was determined in pectorals muscle with quantitative Real-time PCR. Results Chinese Bulbuls in food restriction group decreased in body mass, BMR and internal organ (heart, kidneys, small intestine and total digestive tract) mass compared with the control group over the 12-day period of food restriction. Bulbuls in the food restriction group also had lower levels of state-4 respiration, COX activity in the liver and muscle, and mitochondrial avUCP gene expression in muscle compared to the control group. BMR was positively correlated with body mass, state 4 respiration in the liver and COX activity in the muscle. Conclusions Our data indicate that Chinese Bulbuls not only sustain food shortage through simple passive mechanisms, such as reducing body and organ mass and energy expenditure, but also by reducing energetic metabolism in the liver and muscle