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Dai Shi Tian
Researcher at Huazhong University of Science and Technology
Publications - 23
Citations - 4856
Dai Shi Tian is an academic researcher from Huazhong University of Science and Technology. The author has contributed to research in topics: Microglia & Neuromyelitis optica. The author has an hindex of 12, co-authored 23 publications receiving 3289 citations.
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Journal ArticleDOI
Dysregulation of Immune Response in Patients With Coronavirus 2019 (COVID-19) in Wuhan, China.
Chuan Qin,Luoqi Zhou,Ziwei Hu,Shuo-Qi Zhang,Sheng Yang,Yu Tao,Cuihong Xie,Ke Ma,Ke Shang,Wei Wang,Dai Shi Tian +10 more
TL;DR: Investigation of NLR and lymphocyte subsets is helpful in the early screening of critical illness, diagnosis and treatment of COVID-19 and shows the novel coronavirus might mainly act on lymphocytes, especially T lymphocytes.
Journal ArticleDOI
Dual Functions of Microglia in Ischemic Stroke
Chuan Qin,Luo Qi Zhou,Xiao Tong Ma,Zi Wei Hu,Sheng Yang,Man Chen,Dale B. Bosco,Long Jun Wu,Dai Shi Tian +8 more
TL;DR: It is suggested that microglial activation is also critical for neurogenesis, angiogenesis, and synaptic remodeling, thereby promoting functional recovery after cerebral ischemia and the possible mechanisms controlling the post-ischemic activity of microglia.
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Fingolimod Protects Against Ischemic White Matter Damage by Modulating Microglia Toward M2 Polarization via STAT3 Pathway.
Chuan Qin,Wen Hui Fan,Qian Liu,Ke Shang,Madhuvika Murugan,Madhuvika Murugan,Long Jun Wu,Wei Wang,Dai Shi Tian +8 more
TL;DR: Interestingly, FTY720 could reduce cognitive decline and ameliorate the disruption of WM integrity, a potential therapeutic drug targeting brain inflammation by skewing microglia toward M2 polarization after chronic cerebral hypoperfusion.
Journal ArticleDOI
D-dimer level is associated with the severity of COVID-19.
TL;DR: Patients with severe COVID-19 have a higher level of D-dimer than those with non-severe disease, and D- dimer greater than 0.5 μg/ml is associated with severe infection in patients with CO VID-19.
Journal ArticleDOI
Chemokine CCL2-CCR2 Signaling Induces Neuronal Cell Death via STAT3 Activation and IL-1β Production after Status Epilepticus.
Dai Shi Tian,Jiyun Peng,Madhuvika Murugan,Madhuvika Murugan,Li Jie Feng,Jun-Li Liu,Ukpong B. Eyo,Ukpong B. Eyo,Li Jun Zhou,Rochelle Mogilevsky,Wei Wang,Long Jun Wu +11 more
TL;DR: It is demonstrated that CCL2–CCR2 signaling is required for monocyte infiltration, which in turn contributes to kainic acid (KA)-induced neuronal cell death, which is characteristic of epileptic brains.