Distributed Sensor Databases for Multi-Robot Teams

In this paper we describe our implementation of a distributed sensor database that was designed to support the activities of teams of mobile robots as they explore an environment. Importantly, this approach effectively separates the process of acquiring sensor data from that of exploiting it. This allows us to develop applications where robots and human users can automatically discover and utilize sensor measurements acquired by other robots in the team. We also explain our approach to implementing distributed queries, an important capability that allows us to perform queries in a way that makes best use of the limited available communication bandwidth. Finally, we briefly describe how we have used this system to support situational awareness tasks

ABSTRACT Modular Programming Techniques for Distributed Computing Tasks

This paper describes design patterns used in developing a software platform for mobile robot teams engaged in distributed sensing and exploration tasks. The goal of the system presented is to minimize redundancy throughout the development and execution pipelines by exploring the application of a strong type system to both the collaborative development process and runtime behaviors of mobile sensor platforms. The solution we have implemented addresses both sides of this equation simultaneously by providing a system for selfdescribing inputs and outputs that facilitates code reuse among human developers and autonomous agents. This well-defined modularity allows us to treat executable code libraries as atomic elements that can be automatically shared across the network. In this fashion, we improve the performance of our development team by addressing software framework usability and the performance and capabilities of sensor networks engaged in distributed data processing. This framework adds robust design templates and greater communication flexibility onto a component system similar to TinyOS and NesC while avoiding the development effort and overhead required to field a full-fledged web services or Jini-based infrastructure. The software platform described herein has been used to field collaborative teams of UGVs and UAVs in exploration and monitoring scenarios

HDAC1,2 Knock-Out and HDACi Induced Cell Apoptosis in Imatinib-Resistant K562 Cells

Since imatinib (Glivec or Gleevec) has been used to target the BCR-ABL fusion protein, chronic myeloid leukemia (CML) has become a manageable chronic disease with long-term survival. However, 15%−20% of CML patients ultimately develop resistance to imatinib and then progress to an accelerated phase and eventually to a blast crisis, limiting treatment options and resulting in a poor survival rate. Thus, we investigated whether histone deacetylase inhibitors (HDACis) could be used as a potential anticancer therapy for imatinib-resistant CML (IR-CML) patients. By applying a noninvasive apoptosis detection sensor (NIADS), we found that panobinostat significantly enhanced cell apoptosis in K562 cells. A further investigation showed that panobinostat induced apoptosis in both K562 and imatinib-resistant K562 (IR-K562) cells mainly via H3 and H4 histone acetylation, whereas panobinostat targeted cancer stem cells (CSCs) in IR-K562 cells. Using CRISPR/Cas9 genomic editing, we found that HDAC1 and HDAC2 knockout cells significantly induced cell apoptosis, indicating that the regulation of HDAC1 and HDAC2 is extremely important in maintaining K562 cell survival. All information in this study indicates that regulating HDAC activity provides therapeutic benefits against CML and IR-CML in the clinic

Suppression of Angiogenesis by Targeting Cyclin-Dependent Kinase 7 in Human Umbilical Vein Endothelial Cells and Renal Cell Carcinoma: An In Vitro and In Vivo Study

Cancer cells rely on aberrant transcription for growth and survival. Cyclin-dependent kinases (CDKs) play critical roles in regulating gene transcription by modulating the activity of RNA polymerase II (RNAPII). THZ1, a selective covalent inhibitor of CDK7, has antitumor effects in several human cancers. In this study, we investigated the role and therapeutic potential of CDK7 in regulating the angiogenic activity of endothelial cells and human renal cell carcinoma (RCC). Our results revealed that vascular endothelial growth factor (VEGF), a critical activator of angiogenesis, upregulated the expression of CDK7 and RNAPII, and the phosphorylation of RNAPII at serine 5 and 7 in human umbilical vein endothelial cells (HUVECs), indicating the transcriptional activity of CDK7 may be involved in VEGF-activated angiogenic activity of endothelium. Furthermore, through suppressing CDK7 activity, THZ1 suppressed VEGF-activated proliferation and migration, as well as enhanced apoptosis of HUVECs. Moreover, THZ1 inhibited VEGF-activated capillary tube formation and CDK7 knockdown consistently diminished tube formation in HUVECs. Additionally, THZ1 reduced VEGF expression in human RCC cells (786-O and Caki-2), and THZ1 treatment inhibited tumor growth, vascularity, and angiogenic marker (CD31) expression in RCC xenografts. Our results demonstrated that CDK7-mediated transcription was involved in the angiogenic activity of endothelium and human RCC. THZ1 suppressed VEGF-mediated VEGFR2 downstream activation of angiogenesis, providing a new perspective for antitumor therapy in RCC patients