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Abstract-Geographic routing has been considered as an attractive approach for resource-constrained wireless sensor networks (WSNs) since it exploits local location information instead of global topology information to route data. However, this routing approach often suffers from the routing hole (i.e., an area free of nodes in the direction closer to destination) in various environments such as buildings and obstacles during data delivery, resulting in route failure. Currently, existing geographic routing protocols tend to walk along only one side of the routing holes to recover the route, thus achieving suboptimal network performance such as longer delivery delay and lower delivery ratio. Furthermore, these protocols cannot guarantee that all packets are delivered in an energy-efficient manner once encountering routing holes. In this paper, we focus on addressing these issues and propose an energy-aware dual-path geographic routing (EDGR) protocol for better route recovery from routing holes. EDGR adaptively utilizes the location information, residual energy, and the characteristics of energy consumption to make routing decisions, and dynamically exploits two node-disjoint anchor lists, passing through two sides of the routing holes, to shift routing path for load balance. Moreover, we extend EDGR into three-dimensional (3D) sensor networks to provide energy-aware routing for routing hole detour. Simulation results demonstrate that EDGR exhibits higher energy efficiency, and has moderate performance improvements on network lifetime, packet delivery ratio, and delivery delay, compared to other geographic routing protocols in WSNs over a variety of communication scenarios passing through routing holes. The proposed EDGR is much applicable to resource-constrained WSNs with routing holes.

Tumor-initiating cells (TICs) maintain heterogeneity within tumors and seed metastases at distant sites, contributing to therapeutic resistance and disease recurrence. In colorectal cancer (CRC), strategy that effectively eradicates TICs and is of potential value for clinical use still remains in need. Methods : The anti-tumorigenic activity of a small-molecule inhibitor of KDM6 histone demethylases named GSK-J4 in CRC was evaluated by in vitro assays and in vivo imaging of xenografted tumors. Sphere formation, flow cytometry analysis of cell surface markers and intestinal organoid formation were performed to examine the impact of GSK-J4 on TIC properties. Transcriptome analysis and global profiling of H3K27ac, H3K27me3, and KDM6A levels by ChIP-seq were conducted to elucidate how KDM6 inhibition reshapes epigenetic landscape and thereby eliminating TICs. Results : GSK-J4 alleviated the malignant phenotypes of CRC cells in vitro and in vivo , sensitized them to chemotherapeutic treatment, and strongly repressed TIC properties and stemness-associated gene signatures in these cells. Mechanistically, KDM6 inhibition induced global enhancer reprogramming with a preferential impact on super-enhancer-associated genes, including some key genes that control stemness in CRC such as ID1 . Besides, expression of both Kdm6a and Kdm6b was more abundant in mouse intestinal crypt when compared with upper villus and inhibition of their activities blocked intestinal organoid formation. Finally, we unveiled the power of KDM6B in predicting both the overall survival outcome and recurrence of CRC patients. Conclusions : Our study provides a novel rational strategy to eradicate TICs through reshaping epigenetic landscape in CRC, which might also be beneficial for optimizing current therapeutics.

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