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Tianwen Lai

Researcher at Zhejiang University

Publications -  45
Citations -  1153

Tianwen Lai is an academic researcher from Zhejiang University. The author has contributed to research in topics: Medicine & Inflammation. The author has an hindex of 17, co-authored 36 publications receiving 795 citations. Previous affiliations of Tianwen Lai include Guangdong Medical College.

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Activation of MTOR in pulmonary epithelium promotes LPS-induced acute lung injury.

TL;DR: Results demonstrate that activation of MTOR in the epithelium promotes LPS-induced ALI, likely through downregulation of autophagy and the subsequent activation of NFKB, and may represent a novel therapeutic strategy for preventing ALI induced by certain bacteria.
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Long-term efficacy and safety of omalizumab in patients with persistent uncontrolled allergic asthma: a systematic review and meta-analysis.

TL;DR: It was indicated that omalizumab use for at least 52 weeks in patients with persistent uncontrolled allergic asthma was accompanied by an acceptable safety profile, but it lacked effect on the asthma exacerbations.
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YKL-40 is correlated with FEV1 and the asthma control test (ACT) in asthmatic patients: influence of treatment

TL;DR: YKL-40 was reduced in the serum of asthmatic patients after appropriate treatment, and the levels correlated with improvements in %FEV1 and ACT, and high levels of serum YKL40 may be refractory to current asthma treatments.
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MTOR Suppresses Cigarette Smoke-Induced Epithelial Cell Death and Airway Inflammation in Chronic Obstructive Pulmonary Disease.

TL;DR: It is demonstrated that MTOR suppresses CS-induced inflammation and emphysema—likely through modulation of autophagy, apoptosis, and necroptosis—and thus suggest that activation of MTOR may represent a novel therapeutic strategy for COPD.
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Effectiveness and safety of PD-1/PD-L1 inhibitors in the treatment of solid tumors: a systematic review and meta-analysis.

TL;DR: PD-1 inhibitors are more effective for improving the PFS, OS, and ORR of cancer patients with little toxicity, despite having little effect on increasing of the DCR.