Fagui Chen
Guangzhou Medical University
7 Papers
3 Citations
Fagui Chen is an academic researcher from Guangzhou Medical University. The author has contributed to research in topics: Proinflammatory cytokine & Chemistry. The author has an hindex of 1, co-authored 4 publications. Previous affiliations of Fagui Chen include Sun Yat-sen University.
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Papers
Age and Sex Distribution of Chinese Chronic Cough Patients and Their Relationship With Capsaicin Cough Sensitivity
Kefang Lai,Li Long,Fang Yi,Jiaman Tang,Zhe Chen,Fagui Chen,Jianmeng Zhou,Wen Peng,Liting Zhang,Hu Li,Wenzhi Zhan,Ruchong Chen,Wei Luo,Qiaoli Chen,Kian Fan Chung,Nanshan Zhong +15 more
TL;DR: In China, patients with chronic cough have a roughly equal sex distribution and a middle-aged predominance, irrespective of a higher cough sensitivity to capsaicin in females and older patients.
An mTOR and DNA-PK dual inhibitor CC-115 hinders non-small cell lung cancer cell growth
TL;DR: In this article , the authors evaluated CC-115's activity in different human non-small cell lung cancer (NSCLC) cells and A549 cells and found that the dual inhibitor was unable to induce significant cytotoxic and pro-apoptotic activity in the lung epithelial cells.
An mTOR and DNA-PK dual inhibitor CC-115 hinders non-small cell lung cancer cell growth
TL;DR: In this paper , the authors evaluated CC-115's activity in different human non-small cell lung cancer (NSCLC) cells and A549 cells and found that the dual inhibitor was unable to induce significant cytotoxic and pro-apoptotic activity in the lung epithelial cells.
LATE-BREAKING ABSTRACT: Inhibition of TRPA1 reduces airway inflammation and airway hyper-responsiveness in a murine model of allergic rhinitis
Zhangfu Fang,Fagui Chen,Fang Yi,Huasi Zhao,Chuqin Huang,Chenhui Li,Jiaxing Xie,Kefang Lai,Nanshan Zhong +8 more
TL;DR: TRPA1 plays an important role in driving airway inflammation and AHR in AR and may represent a promising strategy for treating AR and preventing the development of AR into asthma.
1
Non-allergic eosinophilic inflammation and airway hyperresponsiveness induced by diesel engine exhaust through activating ILCs.
Huasi Zhao,Chen Zhan,Bizhou Li,Zhangfu Fang,Mingyu Zhong,Yaowei He,Fagui Chen,Zhe Chen,Guojun Zhang,Nanshan Zhong,Kefang Lai,Ruchong Chen +11 more
TL;DR: Diesel engine exhaust induces non-allergic eosinophilic inflammation and airway hyperresponsiveness in mice through activating innate lymphoid cells (ILCs), promoting a mixed Th2/Th17 response and neutrophilic and eosinophilic inflammation.