An adaptive offloading framework for license plate detection in collaborative edge and cloud computing.

With the explosive growth of edge computing, huge amounts of data are being generated in billions of edge devices. It is really difficult to balance detection efficiency and detection accuracy at the same time for object detection on multiple edge devices. However, there are few studies to investigate and improve the collaboration between cloud computing and edge computing considering realistic challenges, such as limited computation capacities, network congestion and long latency. To tackle these challenges, we propose a new multi-model license plate detection hybrid methodology with the tradeoff between efficiency and accuracy to process the tasks of license plate detection at the edge nodes and the cloud server. We also design a new probability-based offloading initialization algorithm that not only obtains reasonable initial solutions but also facilitates the accuracy of license plate detection. In addition, we introduce an adaptive offloading framework by gravitational genetic searching algorithm (GGSA), which can comprehensively consider influential factors such as license plate detection time, queuing time, energy consumption, image quality, and accuracy. GGSA is helpful for Quality-of-Service (QoS) enhancement. Extensive experiments show that our proposed GGSA offloading framework exhibits good performance in collaborative edge and cloud computing of license plate detection compared with other methods. It demonstrate that when compared with traditional all tasks are executed on the cloud server (AC), the offloading effect of GGSA can be improved by 50.31%. Besides, the offloading framework has strong portability when making real-time offloading decisions.

The anti-anginal drug trimetazidine reduces neutrophil-mediated cardiac reperfusion injury.

Trimetazidine has no hemodynamic/antithrombotic actions. Hence, its anti-ischemic properties have been mostly attributed to its metabolic effects. However, this issue is not completely elucidated. We investigated whether inhibition of neutrophil activation may also contribute to its cardioprotective action. We first showed that trimetazidine inhibits neutrophil activation in vitro. We subsequently tested whether trimetazidine protects postischemic hearts from neutrophil-mediated injury. Four groups of rat hearts underwent 20 minutes of global ischemia: (1) controls, reperfused with neutrophil-enriched buffer for 5 minutes, followed by 40 minutes standard perfusate; (2) hearts from rats pretreated with trimetazidine for 1 week; (3) hearts in which 10 M trimetazidine was added to the perfusate, starting 5 minutes before ischemia and for the initial 15 minutes of reflow; (4) hearts from pretreated rats that also received trimetazidine in the perfusate. Postischemic impairment of contractile function was significantly attenuated by trimetazidine infusion (recovery of developed pressure: 68 +/- 7% versus 42 +/- 9% of baseline in controls; P < 0.05). Pretreatment alone was not effective, nor did it further improve the beneficial effects of infusion. Cardiac oxygen radical production at reflow (by electron paramagnetic resonance spectroscopy) was also reduced by trimetazidine, independently of direct scavenger effects. Thus, trimetazidine can protect postischemic hearts from neutrophil-mediated injury.