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Wide-area distributed computing environment is the main platform for storing large amounts of data and conducting wide-area computing. Tasks and data are jointly scheduled among multiple computing platforms to improve system efficiency. However, large network latency and limited bandwidth in wide-area networks may cause a large delay in scheduling information and data migration, which brings low task execution efficiency and a long time waiting for data. Traditional works mainly focus on allocating tasks based on data locality or distributing data replications, but optimizing task allocation or data placement alone is insufficient from a global perspective. To mitigate the impact of large network latency and limited bandwidth on system performance, joint online optimization of task rescheduling and data redistribution is proposed in this study. The task allocation and data placement can be adjusted collaboratively during the system running process through the task stealing and backfilling mechanism and the data replication placement mechanism. The experimental results indicate that compared with the state-of-the-art method, the proposed method improves the system throughput and computing resource utilization by 20.67% and 20.26% respectively, and can significantly reduce the global data migration costs. &nbsp

Atrazine (2-chloro-4-ethytlamino-6-isopropylamine-1,3,5-triazine, ATR) is widely used as a broad-spectrum herbicide. Animal studies have demonstrated that ATR exposure can cause cell death in dopaminergic neurons. The molecular mechanisms underlying ATR-induced neuronal cell death, however, are unknown. In this study, we investigated the autophagy and apoptosis induced by ATR in dopaminergic neurons in vivo. Wistar rats were administered with ATR at doses of 10, 50 and 100 mg/kg body weight by oral gavage for three months. In terms of histopathology, the expression of autophagy- and apoptosis-related genes as well as proteins related to the Beclin-1/B-cell lymphoma 2 (Bcl-2) autophagy and apoptosis pathways were examined in the rat nigrostriatal dopaminergic system. We observed degenerative micromorphology indicative of neuronal apoptosis and mitochondrial autophagy by electron microscopy in ATR-exposed rat striatum. The rat ventral mesencephalon in the ATR-exposed groups also showed increased expression of Beclin-1, LC3-II, Bax and Caspase-9, and decreased expression of tyrosine hydroxylase (TH), Bcl-xl and Bcl-2. These findings indicate that ATR may induce autophagy- and apoptosis-related changes in doparminergic neurons. Furthermore, this induction may be regulated by the Beclin-1 and Bcl-2 autophagy and apoptosis pathways, and this may help to better understand the mechanism underlying the neurotoxicity of ATR.