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Wei Xiao
Researcher at Shandong University
Publications - 36
Citations - 716
Wei Xiao is an academic researcher from Shandong University. The author has contributed to research in topics: COPD & Pulmonary function testing. The author has an hindex of 14, co-authored 36 publications receiving 568 citations.
Papers
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Journal ArticleDOI
The role of uPAR in epithelial-mesenchymal transition in small airway epithelium of patients with chronic obstructive pulmonary disease
TL;DR: It is proposed that increased uPAR expression in the small airway epithelium of patients with COPD participates in an active EMT process and it is demonstrated that the PI3K/Akt signaling pathway is required for uPAR-mediated EMT in HSAEpiCs.
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Management of airway mucus hypersecretion in chronic airway inflammatory disease: Chinese expert consensus (English edition)
Yongchun Shen,Shao-guang Huang,Jian Kang,Jiangtao Lin,Kefang Lai,Yongchang Sun,Wei Xiao,Lan Yang,Wanzhen Yao,Shaoxi Cai,Kewu Huang,Fuqiang Wen +11 more
TL;DR: This consensus statement describes the pathogenesis, clinical features, and the management of airway mucus hypersecretion in patients with chronic airway inflammatory diseases in the People’s Republic of China.
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A GIS-based spatial correlation analysis for ambient air pollution and AECOPD hospitalizations in Jinan, China
TL;DR: Ambient air pollution is correlated with AECOPD hospitalizations spatially, with only the PM10 concentrations at workplace showed statistical significance, with a 10 μg/m(3) increase at workplace associated with a 7% (95%CI: [3.3%, 10%]) increase of hospitalizations due to AECopD in Jinan, 2009.
Journal ArticleDOI
The effect of human antibacterial peptide LL-37 in the pathogenesis of chronic obstructive pulmonary disease.
Yuanyuan Jiang,Wei Xiao,Mao-xiang Zhu,Zhihua Yang,Xiujie Pan,Yi Zhang,Congcong Sun,Ying Xing +7 more
TL;DR: It is found that increased induced sputum levels of LL-37 in COPD patients were associated with airflow limitation, health status and exercise tolerance and the expressing intensity of LL -37 in both airway district and pulmonary alveoli area in COPd group significantly increased compared with control group.
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LL-37 secreted by epithelium promotes fibroblast collagen production: a potential mechanism of small airway remodeling in chronic obstructive pulmonary disease.
TL;DR: After cigarette smoke exposure, the increased levels of LL-37 in airway epithelium could stimulate collagen production in the underlying lung fibroblasts and may contribute to small airway remodeling in COPD.