718 research outputs found

    Applications of Intelligent Vision in Low-Cost Mobile Robots

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    With the development of intelligent information technology, we have entered an era of 5G and AI. Mobile robots embody both of these technologies, and as such play an important role in future developments. However, the development of perception vision in consumer-grade low-cost mobile robots is still in its infancies. With the popularity of edge computing technology in the future, high-performance vision perception algorithms are expected to be deployed on low-power edge computing chips. Within the context of low-cost mobile robotic solutions, a robot intelligent vision system is studied and developed in this thesis. The thesis proposes and designs the overall framework of the higher-level intelligent vision system. The core system includes automatic robot navigation and obstacle object detection. The core algorithm deployments are implemented through a low-power embedded platform. The thesis analyzes and investigates deep learning neural network algorithms for obstacle object detection in intelligent vision systems. By comparing a variety of open source object detection neural networks on high performance hardware platforms, combining the constraints of hardware platform, a suitable neural network algorithm is selected. The thesis combines the characteristics and constraints of the low-power hardware platform to further optimize the selected neural network. It introduces the minimize mean square error (MMSE) and the moving average minmax algorithms in the quantization process to reduce the accuracy loss of the quantized model. The results show that the optimized neural network achieves a 20-fold improvement in inference performance on the RK3399PRO hardware platform compared to the original network. The thesis concludes with the application of the above modules and systems to a higher-level intelligent vision system for a low-cost disinfection robot, and further optimization is done for the hardware platform. The test results show that while achieving the basic service functions, the robot can accurately identify the obstacles ahead and locate and navigate in real time, which greatly enhances the perception function of the low-cost mobile robot

    Critical Molecular Pathways in Cancer Stem Cells of Chronic Myeloid Leukemia: A Dissertation

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    Chronic myeloid leukemia (CML) is a disease characterized by the expansion of granulocytic cells. The BCR-ABL tyrosine kinase inhibitor imatinib, the frontline treatment for Ph+ leukemias, can induce complete hematologic and cytogenetic response in most chronic phase CML patients. Despite the remarkable initial clinic effects, it is now recognized that imatinib will unlikely cure patients because a small cell population containing leukemic stem cells (LSCs) with self-renewal capacity is insensitive to tyrosine kinase inhibitors. In Chapter I, I briefly review the BCR-ABL kinase and its related signaling pathways. BCR-ABL kinase activates several signaling pathways including MAPK, STAT, and JNK/SAPK. BCR-ABL also mediates kinase-independent pathways through SRC family kinases. I will also discuss pathways involving β-catenin, hedgehog, FoxO and Alox5 are critical to the regulation of self-renewal and differentiation in LSC of CML. As detailed in Chapter II, I describe our work evaluating the effects of omacetaxine, a novel CML drug inducing cell apoptosis by inhibition of protein synthesis, on self-renewal and differentiation of LSCs and BCR-ABL-induced CML and acute lymphoblastic leukemia (B-ALL) in mice. We found that treatment with omacetaxine decreased the number of LSCs and prolonged the survival of mice with CML or B-ALL. In chapter III, I describe that Alox5 is an essential gene in the function of LSCs and CML development. We show evidence that Alox5 affects differentiation, cell division, and survival of long-term LSCs. Treatment of CML mice with a 5-LO inhibitor also impaired the function of LSCs similarly and prolonged survival. In chapter IV, I present evidence of our work showing a further dissection the Alox5 pathway by comparing the gene expression profiles of wild type and Alox5-/- LSCs. We show that Msr1 deletion causes acceleration of CML development. We also show that Msr1 affects CML development by regulating the PI3K-AKT pathway and β-catenin. Taken together, these results demonstrate that some pathways including Alox5 and Msr1 play an important role in regulating the self-renewal and differentiation of LSC. More efforts should be put into developing the novel strategies that may effectively target LSCs and thus cure CML
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