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Bo Hu
Researcher at Wuhan University
Publications - 43
Citations - 776
Bo Hu is an academic researcher from Wuhan University. The author has contributed to research in topics: Medicine & Myocardial infarction. The author has an hindex of 8, co-authored 36 publications receiving 519 citations.
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Journal ArticleDOI
Suspected myocardial injury in patients with COVID-19: Evidence from front-line clinical observation in Wuhan, China.
Qing Deng,Bo Hu,Yao Zhang,Hao Wang,Xiaoyang Zhou,Wei Hu,Yuting Cheng,Jie Yan,Haiqin Ping,Qing Zhou +9 more
TL;DR: The clinical evidence in this study suggested that myocardial injury is more likely related to systemic consequences rather than direct damage by the 2019 novel coronavirus.
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Extracorporeal Membrane Oxygenation for Coronavirus Disease 2019-Induced Acute Respiratory Distress Syndrome: A Multicenter Descriptive Study.
Xiao Yang,Shuhan Cai,Yun Luo,Fangfang Zhu,Ming Hu,Yan Zhao,Ruiqiang Zheng,Xuyan Li,Bo Hu,Zhiyong Peng +9 more
TL;DR: Extracorporeal membrane oxygenation might be an effective salvage treatment for patients with severe acute respiratory syndrome coronavirus 2 pneumonia associated with severe Acute respiratory distress syndrome.
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[Corrigendum] HMGB1 participates in LPS‑induced acute lung injury by activating the AIM2 inflammasome in macrophages and inducing polarization of M1 macrophages via TLR2, TLR4, and RAGE/NF‑κB signaling pathways.
TL;DR: The first two authors on the paper, Jing Wang and Ruiting Li, should have been credited with joint first author status and the affiliation addresses should have appeared as follows.
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HMGB1 participates in LPS‑induced acute lung injury by activating the AIM2 inflammasome in macrophages and inducing polarization of M1 macrophages via TLR2, TLR4, and RAGE/NF‑κB signaling pathways Corrigendum in /10.3892/ijmm.2020.4530
TL;DR: Results indicated that HMGB1 could participate in the pathogenesis of ALI by activating the AIM2 inflammasome in macrophages, as well as inducing polarization of M1 macrophage through TLR2, TLR4 and RAGE/NF-κB signaling pathways.
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GTS-21 Reduces Inflammation in Acute Lung Injury by Regulating M1 Polarization and Function of Alveolar Macrophages.
TL;DR: The GTS-21 substantially ameliorates LPS-induced ALI, and is predominantly associated with the inhibition of pulmonary AM M1 polarization and alteration in AM function.