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CLOUD COVERT he term Internet of Things (IoT) was rst introduced to the technology community in in reference to automated supply-chain management. The concept of enabling a computer to sense information without human intervention was then applied to other elds such as healthcare, home technology, environmental engineering, and transportation.With IoT implementation now becoming more widespread, we're entering the post-cloud era, in which devices will generate a lot of data at the end of the network and many applications will be deployed at the edge to process the information. Cisco Systems predicts that an estimated billion devices will connect to the Internet by . Some of the applications they run might require very short response times, some might involve private data, and some might produce huge quantities of data. Cloud computing can't support these IoT applications. Edge computing, on the other hand, can do so and will promote many new IoT applications. WHY DO WE NEED EDGE COMPUTING?Edge computing will become important for several reasons. Cloud servicesMoving all computing tasks to the cloud has been an e cient way to process data because there's more computing power in the cloud than in the devices at the network edge. However, although data-processing speeds have risen rapidly, the bandwidth of the networks that carry data to and from the cloud hasn't increased appreciably. Thus, with edge devices generating more data, the network is becoming cloud computing's bottleneck.As an example, cameras in an autonomous vehicle capture a huge amount of video data, which the system must process in real time to yield good driving decisions. If the vehicle must send the data to the cloud for processing, the response time would be too long. And a large numberThe success of the Internet of Things and rich cloud services have helped create the need for edge computing, in which data processing occurs in part at the network edge, rather than completely in the cloud. Edge computing could address concerns such as latency, mobile devices' limited battery life, bandwidth costs, security, and privacy.

Circular RNAs (circRNAs) are a class of endogendous RNAs that form a covalently closed continuous loop and exist extensively in mammalian cells. Majority of circRNAs are conserved across species and often show tissue/developmental stage-specific expression. CircRNAs were first thought to be the result of splicing error; however, subsequent research shows that circRNAs can function as microRNA (miRNA) sponges and regulate splicing and transcription. Emerging evidence shows that circRNAs possess closely associated with human diseases, especially cancers, and may serve as better biomarkers. After miRNA and long noncoding RNA (lncRNA), circRNAs are becoming a new hotspot in the field of RNA of cancer. Here, we review biogenesis and metabolism of circRNAs, their functions, and potential roles in cancer.

The recent proliferation of computing technologies, e.g., sensors, computer vision, machine learning, hardware acceleration, and the broad deployment of communication mechanisms, e.g., DSRC, C-V2X, 5G, have pushed the horizon of autonomous driving, which automates the decision and control of vehicles by leveraging the perception results based on multiple sensors. The key to the success of these autonomous systems is making a reliable decision in a real-time fashion. However, accidents and fatalities caused by early deployed autonomous vehicles arise from time to time. The real traffic environment is too complicated for the current autonomous driving computing systems to understand and handle. In this paper, we present the state-of-the-art computing systems for autonomous driving, including seven performance metrics and nine key technologies, followed by eleven challenges and opportunities to realize autonomous driving. We hope this paper will gain attention from both the computing and automotive communities and inspire more research in this direction.

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Vasculogenic mimicry (VM) gives rise to tumor neovascularization that is critical for tumor growth and metastasis. Long non-coding RNAs (lncRNAs) have been implicated in diverse and fundamental biological processes. LINC00312 is associated with lung adenocarcinoma. In this study, we found that LINC00312 induced migration, invasion and VM of lung cancer cells by direct binding to the transcription factor Y-Box Binding Protein 1 (YBX1). Moreover, we demonstrated that YBX1 is associated with different fragments within 0–2410 nt 5’region of LINC00312. In addition, LINC00312 is associated with VM in 124 lung adenocarcinoma clinical specimens. The results suggest that LINC00312 is a promising therapeutic and diagnostic target for lung adenocarcinoma.Electronic supplementary materialThe online version of this article (10.1186/s12943-018-0920-z) contains supplementary material, which is available to authorized users.

SummaryIncreasing evidence indicates that aberrant neutrophil extracellular trap (NET) formation could contribute to the pathogenesis of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Recent research has provided evidence that a novel type of ANCA autoantibody, anti-lysosomal membrane protein-2 (LAMP-2) antibody, may have a pathogenic role in AAV. We have shown previously that anti-LAMP-2 antibody-stimulated NET formation contains autoantigens and antimicrobial peptides. The current study sought to determine whether LAMP-2, as a novel antigen of ANCA, was present on NETs in AAV patients, the influence of the anti-LAMP-2 antibody on the neutrophil apoptosis rate and the role of autophagy in anti-LAMP-2 antibodyinduced NET formation. NET formation was assessed using immunofluorescence microscopy, scanning electron microscopy or live cell imaging. The neutrophil apoptosis rate was analysed using fluorescence activated cell sorting (FACS). Autophagy was detected using LC3B accumulation and transmission electron microscopy. The results showed that enhanced NET formation, which contains LAMP-2, was observed in kidney biopsies and neutrophils from AAV patients. The apoptosis rate decreased significantly in human neutrophils stimulated with anti-LAMP-2 antibody, and this effect was attenuated by the inhibitors of autophagy 3-methyladenine (3MA) and 2-morpholin-4-yl-8-phenylchromen-4-one (LY294002). The anti-LAMP-2 antibody-stimulated NET formation was unaffected by benzyloxycarbonyl-Val-Ala-Asp (OMe)-fluoromethylketone (zVAD-fmk) and necrostatin-1 (Nec-1), which are inhibitors of apoptosis and necrosis, respectively, but was inhibited by 3MA and LY294002. Moreover, the proportion of LC3BI that was converted to LC3BII increased significantly (P 5 0Á0057), and massive vacuolizations that exhibited characteristics typical of autophagy were detected in neutrophils stimulated with anti-LAMP-2 antibody. Our results provide further evidence that autophagy is involved in ANCAinduced NET formation in human neutrophils.

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