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3D object detection is important for various indoor applications to understand the environment. Previous voting-based methods voted on the center of each seed point, which may suffer from errors from background points or adjacent objects. And the size-fixed feature grouping module is unsuitable for indoor objects with variable sizes. In this paper, we propose a Size Adaptive Clustering method for 3D object detection in point clouds . First, we present a super-voting module to divide seed points into foreground and background points and perform enhanced voting on the foreground seeds. To create a good match for the feature clustering area and the size of an object, we design a size-adaptive clustering module to infer a clustering radius based on the seed-to-vote displacement offset. Finally, because indoor objects are highly related to spatial room layouts, a position-aware module is used to calculate aware weights among objects and enhance the features of occluded objects. Experiments show that our method outperforms VoteNet by a large margin on ScanNet V2 (mAP@0.250 +8.3%, mAP@0.50 +14.2%) and SUN RGB-D (mAP@0.250 +3.5%, mAP@0.50 +13.6%). The proposed method can detect indoor objects with variable sizes in high accuracy, and perform robustly in case of occluded objects. The code of 3DSAC will be available at github-3DSAC.

Spinal cord injury (SCI) can lead to varying degrees of sensory and motor dysfunction. Salvianolic acid B (Sal-B) is the dominating bioactive constituent of Danshen, which has been reported to alleviate liver fibrosis and exert neuroprotective effects. But, the influence of Sal-B in SCI remains mysterious. The research planned to delve the protective function of Sal-B in hydrogen peroxide (H2O2)-caused PC-12 cell injury. H2O2-caused PC-12 cells injury model was built, CCK-8, Transwell and flow cytometry experiments were enforced to assess cell proliferation, migration and apoptosis. The microRNA (miR)-26a plasmid and the matching control were transfected into PC-12 cells, subsequently, the influence of miR-26a inhibition in H2O2-corrupted PC-12 cells was evaluated. The cell growth-correlated factors and PI3K/AKT and MEK/ERK pathways were assayed through western blot assay. Results corroborated that Sal-B eased H2O2-evoked injury in PC-12 cells. Ascended miR-26a was monitored in Sal-B and H2O2-exposed cells. MiR-26a inhibition annulled the protective action of Sal-B in H2O2-corrupted cells. The protective function of Sal-B was enabled through activating PI3K/AKT and MEK/ERK pathways. These findings delineated that Sal-B protected PC-12 cells against H2O2-caused injury through ascending miR-26a via initiating PI3K/AKT and MEK/ERK pathways.HighlightsH2O2 causes PC-12 cell injury;Sal-B eases H2O2-caused PC-12 cell injury;Sal-B protects PC-12 cells against H2O2-caused injury via elevating miR-26a;Sal-B activates AKT and MEK/ERK pathways via modulating miR-26a.

Introduction Osteoblasts and osteoclasts are cells of osteoblastic origin, and are vital in homeostasis of the skeleton. miRs are important for functioning, survival and differentiation of osteoclasts. It has been reported previously that miR-23b-3p is involved in osteoporosis and in regulation of differentiation of osteoblasts. It is also involved in the process of bone formation. However, the role of miR-23b-3p in differentiation of osteoclasts remains unexplored. Material and methods CSF-1 and ODF induced osteoclasts were used for the study. RNA isolation was done from TIB-71 cells. TRAP staining was done for TRAP-positive osteoclast formation. PIT assay for bone resorption was performed. For in vivo studies osteoclast-specific miR-23b-3p transgenic mice were developed. Results The levels of miR-23b-3p were upregulated in bone marrow monocytes during osteoclastogenesis with colony stimulating factor-1 and osteoclast differentiation factor induction, which suggests that miR-23b-3p plays a crucial role in differentiation of osteoclasts. Over-expression of miR-23b-3p in bone marrow monocytes leads to osteoclastogenesis, whereas the inhibition ameliorates it. We further studied the function of miR-23b-3p via PI3K/AKT targeting the PTEN pathway. In vivo, osteoclast-specific miR-23b-3p transgenic mice showed suppressed PTEN and elevated osteoclast activity, and the mice showed decreased bone mineral density. Conclusions The results suggest that miR-23b-3p regulates the differentiation of osteoclasts by targeting PTEN through the PI3K/AKT cascade.

With the substantial increase of vehicles on road, driving safety and transportation efficiency have become increasingly concerned focus from drivers, passengers, and governments. Wireless networks constructed by vehicles and infrastructures provide abundant information to share for the sake of both enhanced safety and network efficiency. This paper presents the systematic research to enhance the vehicle safety by wireless communication, in the aspects of information acquisition through vehicle sensing, vehicle-to-vehicle (V2V) routing protocol for the highly dynamic vehicle network, vehicle-to-infrastructure (V2I) routing protocol for a tradeoff in real-time performance and load balance, and hardware implementation of V2V system with on-road test. Simulations and experimental result validate the feasibility of the algorithms and communication system.

Introduction: Osteoblasts and osteoclasts are cells of osteoblastic origin, and are vital in homeostasis of the skeleton. miRs are important for functioning, survival and differentiation of osteoclasts. It has been reported previously that miR-23b-3p is involved in osteoporosis and in regulation of differentiation of osteoblasts. It is also involved in the process of bone formation. However, the role of miR-23b-3p in differentiation of osteoclasts remains unexplored. Material and methods: CSF-1 and ODF induced osteoclasts were used for the study. RNA isolation was done from TIB-71 cells. TRAP staining was done for TRAP-positive osteoclast formation. PIT assay for bone resorption was performed. For in vivo studies osteoclast-specific miR-23b-3p transgenic mice were developed. Results: The levels of miR-23b-3p were upregulated in bone marrow monocytes during osteoclastogenesis with colony stimulating factor-1 and osteoclast differentiation factor induction, which suggests that miR-23b-3p plays a crucial role in differentiation of osteoclasts. Over-expression of miR23b-3p in bone marrow monocytes leads to osteoclastogenesis, whereas the inhibition ameliorates it. We further studied the function of miR-23b-3p via PI3K/AKT targeting the PTEN pathway. In vivo, osteoclast-specific miR23b-3p transgenic mice showed suppressed PTEN and elevated osteoclast activity, and the mice showed decreased bone mineral density. Conclusions: The results suggest that miR-23b-3p regulates the differentiation of osteoclasts by targeting PTEN through the PI3K/AKT cascade. [ABSTRACT FROM AUTHOR]