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Wei Li

Researcher at Capital Medical University

Publications -  138
Citations -  2042

Wei Li is an academic researcher from Capital Medical University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 21, co-authored 119 publications receiving 1464 citations. Previous affiliations of Wei Li include Rutgers University & University of Medicine and Dentistry of New Jersey.

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Increasing occurrence of antimicrobial resistant hypervirulent (hypermucoviscous) Klebsiella pneumoniae isolates in China

TL;DR: Resistance to all the tested antimicrobials, except carbapenems and amikacin, was observed in a proportion of hvKP strains, 17% (5/29) of which expressed extended-spectrum β-lactamase, indicating an increasing propensity for the acquisition of antimicrobial resistance.
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Auxin signaling modules regulate maize inflorescence architecture.

TL;DR: It is suggested that auxin signaling directly controls boundary domains during axillary meristem formation and define a fundamental mechanism that regulates inflorescence architecture in one of the most widely grown crop species.
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Regulation of apoptosis by type III interferons.

TL;DR: Evidence is provided that type III IFNs, alone or in combination with other stimuli, have the potential to induce apoptosis, and it is demonstrated that the ability to trigger apoptosis is a unique intrinsic function of all IFN receptors.
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Human umbilical mesenchymal stem cells enhance the expression of neurotrophic factors and protect ataxic mice.

TL;DR: The results showed that HU-MSCs implantation significantly improved the motor skills of ataxic mice 8 weeks after application and also alleviated cerebellar atrophy and decreased the number of apoptotic cells in the therapeutic group.
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Inhibition of type I and type III interferons by a secreted glycoprotein from Yaba-like disease virus.

TL;DR: Y136 from Yaba-like disease virus is a secreted glycoprotein related to protein B18 from Vaccinia virus, a known type I IFN-binding protein and a member of the Ig superfamily that inhibits type I and type III IFNs and suggests that type IIIIFNs may be an effective treatment for some poxviral infections.