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430 results on '"Meng, Dawei"'

35. A Study of Human Flesh Search Based on SIR Flooding on Scale-Free Networks

Author

Meng, Dawei, Zhang, Lei, Cheng, Long, Hutchison, David, editor, Kanade, Takeo, editor, Kittler, Josef, editor, Kleinberg, Jon M., editor, Mattern, Friedemann, editor, Mitchell, John C., editor, Naor, Moni, editor, Nierstrasz, Oscar, editor, Pandu Rangan, C., editor, Steffen, Bernhard, editor, Sudan, Madhu, editor, Terzopoulos, Demetri, editor, Tygar, Doug, editor, Vardi, Moshe Y., editor, Weikum, Gerhard, editor, Tan, Ying, editor, Shi, Yuhui, editor, and Mo, Hongwei, editor

Published
2013
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45. Calculation of faults between core laminations and prediction of axial damage depth of large motors

Author

Jinhui Liu, Wang Xiaohui, Meng Dawei, and Mengmeng Ai

Subjects
010302 applied physics, Core (optical fiber), Materials science, Mechanics of Materials, Mechanical Engineering, 0103 physical sciences, Geometry, Hardware_PERFORMANCEANDRELIABILITY, Electrical and Electronic Engineering, Condensed Matter Physics, 01 natural sciences, Electronic, Optical and Magnetic Materials
Abstract

A method to analytically calculate the parameters of the fault area between core laminations are proposed and the dynamic trend of the fault development is predicted to comprehensively and accurately obtain the fault degree and damage level of short-circuits between the core laminations of large motors. Considering the influences of frequency and magnetic flux on the axial skin depth of the core and of the eddy current loss on the insulation resistance between the laminations and reviewing the laminations of the stator core tooth as the research object, based on the Maxwell equations and equivalent circuit theory, analytic expressions of active power and induced voltage in the fault area between the laminations are derived; the influence of the number of fault laminations on the electrical parameters in the fault area is quantitatively analyzed; the actual fault development process of the short-circuit faults between the laminations are obtained; and the correctness and effectiveness of the proposed method are verified via numerical simulations and the experiment of faults between core laminations. The sequence of induced voltage changing with the number of fault laminations is selected as the grey sequence to establish the grey prediction model (GM (1,1)). The development curve of the damage depth of the faults between core laminations along the axial direction is illustrated by calculating the sequence data. The results show that the error between the predicted value of the damage depth of the short-circuit fault herein and the experimental value is less than 7%. This method can be used in engineering practices.

Published
2021

46. A molecular brake that modulates spliceosome pausing at detained introns contributes to neurodegeneration.

Author

Meng, Dawei, Zheng, Qian, Zhang, Xue, Piao, Xuejiao, Luo, Li, and Jia, Yichang

Abstract

Emerging evidence suggests that intron-detaining transcripts (IDTs) are a nucleus-detained and polyadenylated mRNA pool for cell to quickly and effectively respond to environmental stimuli and stress. However, the underlying mechanisms of detained intron (DI) splicing are still largely unknown. Here, we suggest that post-transcriptional DI splicing is paused at the Bact state, an active spliceosome but not catalytically primed, which depends on Smad Nuclear Interacting Protein 1 (SNIP1) and RNPS1 (a serine-rich RNA binding protein) interaction. RNPS1 and Bact components preferentially dock at DIs and the RNPS1 docking is sufficient to trigger spliceosome pausing. Haploinsufficiency of Snip1 attenuates neurodegeneration and globally rescues IDT accumulation caused by a previously reported mutant U2 snRNA, a basal spliceosomal component. Snip1 conditional knockout in the cerebellum decreases DI splicing efficiency and causes neurodegeneration. Therefore, we suggest that SNIP1 and RNPS1 form a molecular brake to promote spliceosome pausing, and that its misregulation contributes to neurodegeneration. [ABSTRACT FROM AUTHOR]

Published
2023
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