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5. Weakly-supervised Part-Attention and Mentored Networks for Vehicle Re-Identification

Author

Tang, Lisha, Wang, Yi, and Chau, Lap-Pui

Subjects
Computer Science - Computer Vision and Pattern Recognition
Abstract

Vehicle re-identification (Re-ID) aims to retrieve images with the same vehicle ID across different cameras. Current part-level feature learning methods typically detect vehicle parts via uniform division, outside tools, or attention modeling. However, such part features often require expensive additional annotations and cause sub-optimal performance in case of unreliable part mask predictions. In this paper, we propose a weakly-supervised Part-Attention Network (PANet) and Part-Mentored Network (PMNet) for Vehicle Re-ID. Firstly, PANet localizes vehicle parts via part-relevant channel recalibration and cluster-based mask generation without vehicle part supervisory information. Secondly, PMNet leverages teacher-student guided learning to distill vehicle part-specific features from PANet and performs multi-scale global-part feature extraction. During inference, PMNet can adaptively extract discriminative part features without part localization by PANet, preventing unstable part mask predictions. We address this Re-ID issue as a multi-task problem and adopt Homoscedastic Uncertainty to learn the optimal weighing of ID losses. Experiments are conducted on two public benchmarks, showing that our approach outperforms recent methods, which require no extra annotations by an average increase of 3.0% in CMC@5 on VehicleID and over 1.4% in mAP on VeRi776. Moreover, our method can extend to the occluded vehicle Re-ID task and exhibits good generalization ability., Comment: This work has been submitted to the IEEE for possible publication. Copyright may be transferred without notice, after which this version may no longer be accessible

Published
2021

39. Mutant NPM1-Regulated FTO-Mediated m6A Demethylation Promotes Leukemic Cell Survival via PDGFRB/ERK Signaling Axis

Author

Xiao, Qiaoling, Lei, Li, Ren, Jun, Peng, Meixi, Jing, Yipei, Jiang, Xueke, Huang, Junpeng, Tao, Yonghong, Lin, Can, Yang, Jing, Sun, Minghui, Tang, Lisha, Wei, Xingyu, Yang, Zailin, and Zhang, Ling

Subjects
Cancer Research, Oncology, N6-methyladenosine, hemic and lymphatic diseases, nucleophosmin 1, PDGFRB, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, acute myeloid leukemia, FTO, ERK cascade, RC254-282
Abstract

Acute myeloid leukemia (AML) with nucleophosmin 1 (NPM1) mutations exhibits distinct biological and clinical features, accounting for approximately one-third of AML. Recently, the N6-methyladenosine (m6A) RNA modification has emerged as a new epigenetic modification to contribute to tumorigenesis and development. However, there is limited knowledge on the role of m6A modifications in NPM1-mutated AML. In this study, the decreased m6A level was first detected and high expression of fat mass and obesity-associated protein (FTO) was responsible for the m6A suppression in NPM1-mutated AML. FTO upregulation was partially induced by NPM1 mutation type A (NPM1-mA) through impeding the proteasome pathway. Importantly, FTO promoted leukemic cell survival by facilitating cell cycle and inhibiting cell apoptosis. Mechanistic investigations demonstrated that FTO depended on its m6A RNA demethylase activity to activate PDGFRB/ERK signaling axis. Our findings indicate that FTO-mediated m6A demethylation plays an oncogenic role in NPM1-mutated AML and provide a new layer of epigenetic insight for future treatments of this distinctly leukemic entity.

Published
2022

41. Application of Neuroimaging for the Prediction of Hemorrhagic Transformation after Intravenous Thrombolysis in Acute Ischemic Stroke.

Author

Yang, Miaomiao, Tang, Lisha, Hu, Zhiping, and Tang, Xiangqi

Subjects
*ISCHEMIC stroke, *TISSUE plasminogen activator, *STROKE patients, *CEREBROVASCULAR disease, *BRAIN imaging, *STROKE, *THROMBOLYTIC therapy
Abstract

Background: Ischemic stroke is a common cerebrovascular disease with high morbidity, disability, and mortality worldwide. Currently, recombinant tissue plasminogen activator is the main intravenous thrombolysis agent for the treatment of acute ischemic stroke within 4.5 h after onset. Hemorrhagic transformation (HT) is the most serious complication of intravenous thrombolysis, which can significantly aggravate clinical poor prognosis. Therefore, it is important to early predict the risk of post-thrombolysis HT in patients with acute ischemic stroke. Summary: Recently, several studies have reported that neuroimaging techniques have potential value in predicting HT after intravenous thrombolysis in patients with acute ischemic stroke. The corresponding neuroimaging parameters may be effective predictors of HT after intravenous thrombolysis. In this review, we summarized and discussed the application of neuroimaging techniques and related parameters in predicting HT after intravenous thrombolysis. Key Messages: Recognizing and understanding the predictive performance of neuroimaging parameters for HT may help assess the risk of HT after intravenous thrombolysis in patients with acute ischemic stroke and make an appropriate treatment decision. [ABSTRACT FROM AUTHOR]

Published
2023
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49. Mutant NPM1-Regulated FTO-Mediated m6A Demethylation Promotes Leukemic Cell Survival via PDGFRB/ERK Signaling Axis.

Author

Xiao, Qiaoling, Lei, Li, Ren, Jun, Peng, Meixi, Jing, Yipei, Jiang, Xueke, Huang, Junpeng, Tao, Yonghong, Lin, Can, Yang, Jing, Sun, Minghui, Tang, Lisha, Wei, Xingyu, Yang, Zailin, and Zhang, Ling

Subjects
CELL survival, ACUTE myeloid leukemia, DEMETHYLATION, RNA modification & restriction, ADIPOSE tissues
Abstract

Acute myeloid leukemia (AML) with nucleophosmin 1 (NPM1) mutations exhibits distinct biological and clinical features, accounting for approximately one-third of AML. Recently, the N 6-methyladenosine (m6A) RNA modification has emerged as a new epigenetic modification to contribute to tumorigenesis and development. However, there is limited knowledge on the role of m6A modifications in NPM1-mutated AML. In this study, the decreased m6A level was first detected and high expression of fat mass and obesity-associated protein (FTO) was responsible for the m6A suppression in NPM1-mutated AML. FTO upregulation was partially induced by NPM1 mutation type A (NPM1-mA) through impeding the proteasome pathway. Importantly, FTO promoted leukemic cell survival by facilitating cell cycle and inhibiting cell apoptosis. Mechanistic investigations demonstrated that FTO depended on its m6A RNA demethylase activity to activate PDGFRB/ERK signaling axis. Our findings indicate that FTO-mediated m6A demethylation plays an oncogenic role in NPM1-mutated AML and provide a new layer of epigenetic insight for future treatments of this distinctly leukemic entity. [ABSTRACT FROM AUTHOR]

Published
2022
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50. Controllable Self-Assembly of SERS Hotspots in Liquid Environment

Author

Zhang, De, primary, Tang, Lisha, additional, Chen, Jie, additional, Tang, Zhexiang, additional, Liang, Pei, additional, Huang, Youyi, additional, Cao, Minhui, additional, Zou, Mingqiang, additional, Ni, Dejiang, additional, Chen, Jinlei, additional, Yu, Zhi, additional, and Jin, Shangzhong, additional

Published
2021
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