Browsing by Author "Wang, Yueyang"

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    BigDataflow: A Distributed Interprocedural Dataflow Analysis Framework
    Sun, Zewen; Xu, Duanchen; Zhang, Yiyu; Qi, Yun; Wang, Yueyang; Zuo, Zhiqiang; Wang, Zhaokang; Li, Yue; Li, Xuandong; Lu, Qingda; Peng, Wenwen; Guo, Shengjian (ACM, 2023-11-30)
    Apart from forming the backbone of compiler optimization, static dataflow analysis has been widely applied in a vast variety of applications, such as bug detection, privacy analysis, program comprehension, etc. Despite its importance, performing interprocedural dataflow analysis on large-scale programs is well known to be challenging.In this paper, we propose a novel distributed analysis framework supporting the general interprocedural dataflow analysis.Inspired by large-scale graph processing, we devise a dedicated distributed worklist algorithm tailored for interprocedural dataflow analysis. We implement the algorithm and develop a distributed framework called BigDataflow running on a large-scale cluster.The experimental results validate the promising performance of BigDataflow – it can finish analyzing the program of millions lines of code in minutes. Compared with the state-of-the-art, BigDataflow achieves much more analysis efficiency.
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    Mitofusin 2 regulates neutrophil adhesive migration and the actin cytoskeleton
    Zhou, Wenqing; Hsu, Alan Y.; Wang, Yueyang; Syahirah, Ramizah; Wang, Tianqi; Jeffries, Jacob; Wang, Xu; Mohammad, Haroon; Seleem, Mohamed N.; Umulis, David; Deng, Qing (2020-09)
    Neutrophils rely on glycolysis for energy production. How mitochondria regulate neutrophil function is not fully understood. Here, we report that mitochondrial outer membrane protein Mitofusin 2 (MFN2) regulates neutrophilhomeostasis andchemotaxis in vivo. Mfn2-deficientneutrophils are released from the hematopoietic tissue, trapped in the vasculature in zebrafish embryos, and not capable of chemotaxis. Consistent with this, human neutrophil-like cells that are deficient for MFN2 fail to arrest on activated endothelium under sheer stress or perform chemotaxis on 2D surfaces. Deletion of MFN2 results in a significant reduction of neutrophil infiltration to the inflamed peritoneal cavity in mice. Mechanistically, MFN2-deficient neutrophil-like cells display disrupted mitochondria-ER interaction, heightened intracellular Ca2+ levels and elevated Rac activation after chemokine stimulation. Restoring a mitochondria-ER tether rescues the abnormal Ca2+ levels, Rac hyperactivation and chemotaxis defect resulting from MFN2 depletion. Finally, inhibition of Rac activation restores chemotaxis in MFN2-deficient neutrophils. Taken together, we have identified that MFN2 regulates neutrophil migration via maintaining the mitochondria-ER interaction to suppress Rac activation, and uncovered a previously unrecognized role of MFN2 in regulating cell migration and the actin cytoskeleton. This article has an associated First Person interview with the first authors of the paper.