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Your search keyword '"Wang, Yan‐Jie"' showing total 595 results
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595 results on '"Wang, Yan‐Jie"'

1. Queen: A quick, scalable, and comprehensive quantum circuit simulation for supercomputing

Author

Wang, Chuan-Chi, Lin, Yu-Cheng, Wang, Yan-Jie, Tu, Chia-Heng, and Hung, Shih-Hao

Subjects
Quantum Physics, Computer Science - Performance
Abstract

The state vector-based simulation offers a convenient approach to developing and validating quantum algorithms with noise-free results. However, limited by the absence of cache-aware implementations and unpolished circuit optimizations, the past simulators were severely constrained in performance, leading to stagnation in quantum computing. In this paper, we present an innovative quantum circuit simulation toolkit comprising gate optimization and simulation modules to address these performance challenges. For the performance, scalability, and comprehensive evaluation, we conduct a series of particular circuit benchmarks and strong scaling tests on a DGX-A100 workstation and achieve averaging 9 times speedup compared to state-of-the-art simulators, including QuEST, IBM-Aer, and NVIDIA-cuQuantum. Moreover, the critical performance metric FLOPS increases by up to a factor of 8-fold, and arithmetic intensity experiences a remarkable 96x enhancement. We believe the proposed toolkit paves the way for faster quantum circuit simulations, thereby facilitating the development of novel quantum algorithms.

Published
2024

11. Reprogramming of m6A epitranscriptome is crucial for shaping of transcriptome and proteome in response to hypoxia

Author

Wang, Yan-Jie, Yang, Bing, Lai, Qiao, Shi, Jun-Fang, Peng, Jiang-Yun, Zhang, Yin, Hu, Kai-Shun, Li, Ya-Qing, Peng, Jing-Wen, Yang, Zhi-Zhi, Li, Yao-Ting, Pan, Yue, Koeffler, H Phillip, Liao, Jian-You, and Yin, Dong

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Genetics, Human Genome, Underpinning research, 2.1 Biological and endogenous factors, Aetiology, 1.1 Normal biological development and functioning, Generic health relevance, Adenosine, Cell Line, Tumor, Chromatography, Liquid, Computational Biology, Epigenesis, Genetic, Epigenomics, Gene Expression Profiling, Gene Expression Regulation, Gene Knockdown Techniques, Gene Ontology, Humans, Hypoxia, Proteome, Proteomics, Stress, Physiological, Tandem Mass Spectrometry, Transcriptome, m(6)A epitranscriptome, trancriptome, proteome, ATP production, m6A epitranscriptome, Developmental Biology, Biochemistry and cell biology
Abstract

Hypoxia causes a series of responses supporting cells to survive in harsh environments. Substantial post-transcriptional and translational regulation during hypoxia has been observed. However, detailed regulatory mechanism in response to hypoxia is still far from complete. RNA m6A modification has been proven to govern the life cycle of RNAs. Here, we reported that total m6A level of mRNAs was decreased during hypoxia, which might be mediated by the induction of m6A eraser, ALKBH5. Meanwhile, expression levels of most YTH family members of m6A readers were systematically down-regulated. Transcriptome-wide analysis of m6A revealed a drastic reprogramming of m6A epitranscriptome during cellular hypoxia. Integration of m6A epitranscriptome with either RNA-seq based transcriptome analysis or mass spectrometry (LC-MS/MS) based proteome analysis of cells upon hypoxic stress revealed that reprogramming of m6A epitranscriptome reshaped the transcriptome and proteome, thereby supporting efficient generation of energy for adaption to hypoxia. Moreover, ATP production was blocked when silencing an m6A eraser, ALKBH5, under hypoxic condition, demonstrating that m6A pathway is an important regulator during hypoxic response. Collectively, our studies indicate that crosstalk between m6A and HIF1 pathway is essential for cellular response to hypoxia, providing insights into the underlying molecular mechanisms during hypoxia.

Published
2021

16. A Highly Damping, Crack‐Insensitive and Self‐Healable Binder for Lithium‐Sulfur Battery by Tailoring the Viscoelastic Behavior (Adv. Energy Mater. 14/2024)

Author

Si, Mengjie, primary, Jian, Xianfeng, additional, Xie, Yu, additional, Zhou, Jiahui, additional, Jian, Wei, additional, Lin, Ji, additional, Luo, Yufeng, additional, Hu, Jiayu, additional, Wang, Yan‐Jie, additional, Zhang, Dong, additional, Wang, Tiefeng, additional, Liu, Yujing, additional, Wu, Zi Liang, additional, Zheng, Si Yu, additional, and Yang, Jintao, additional

Published
2024
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25. An Inducible Nitric Oxide Synthase Dimerization Inhibitor Prevents the Progression of Osteoarthritis

Author

Shang Xian Bo, Wang Yan Jie, Cai De Chao, Ma Sai, Wang Zhe, Zhu Ya Kun, Guo Hui Hui, Wang Chen, Ma Xiao, Hu Zhong Yao, Yu Hao Ran, Zhang Ji Sen, and Cheng Wen Dan

Subjects
osteoarthritis, nitric oxide, inducible nitric oxide synthase, inhibitor, extracellular matrix, Therapeutics. Pharmacology, RM1-950
Abstract

Objective: Osteoarthritis (OA) is a degenerative joint disease. Excessive nitric oxide (NO) mediates the chondrocyte inflammatory response, apoptosis, and extracellular matrix (ECM) degradation during the occurrence and development of OA. NO in chondrocytes is mainly produced by inducible nitric oxide synthase (iNOS). The aim of this study was to design and synthesize an iNOS dimerization inhibitor and evaluate its effects on chondrocyte inflammation and articular cartilage injury in OA via in vitro and in vivo experiments.Design: The title compound 22o was designed, synthesized, and screened based on a previous study. The effects of different concentrations (5, 10, and 20 μM) of compound 22o on chondrocyte inflammatory response and ECM anabolism or catabolism were evaluated by Western blot and real-time quantitative reverse transcription-polymerase chain reaction using the rat chondrocyte model of IL-1β-induced OA. Furthermore, different doses (40 and 80 mg/kg) of compound 22o were administered by gavage to a rat OA model induced by anterior cruciate ligament transection (ACLT), and their protective effects on the articular cartilage were evaluated by histopathology and immunohistochemistry.Results: Compound 22o showed effective iNOS inhibitory activity by inhibiting the dimerization of iNOS. It inhibited the IL-1β-induced expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase 3 (MMP3) in the chondrocytes, decreased NO production, and significantly increased the expression levels of the ECM anabolic markers, aggrecan (ACAN), and collagen type II (COL2A1). Gavage with compound 22o was found to be effective in the rat OA model induced by ACLT, wherein it regulated the anabolism and catabolism and exerted a protective effect on the articular cartilage.Conclusions: Compound 22o inhibited the inflammatory response and catabolism of the chondrocytes and reduced articular cartilage injury in the rat OA model, indicating its potential as a disease-modifying OA drug.

Published
2022
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