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Bai Lu

Researcher at Tsinghua University

Publications -  151
Citations -  31805

Bai Lu is an academic researcher from Tsinghua University. The author has contributed to research in topics: Neurotrophic factors & Long-term potentiation. The author has an hindex of 80, co-authored 144 publications receiving 29387 citations. Previous affiliations of Bai Lu include McGovern Institute for Brain Research & Roche Institute of Molecular Biology.

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The BDNF val66met polymorphism affects activity-dependent secretion of BDNF and human memory and hippocampal function

TL;DR: A role is demonstrated for BDNF and its val/met polymorphism in human memory and hippocampal function and it is suggested val/ met exerts these effects by impacting intracellular trafficking and activity-dependent secretion of BDNF.
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SHED: Stem cells from human exfoliated deciduous teeth

TL;DR: It is shown that a naturally exfoliated human organ contains a population of stem cells that are completely different from previously identified stem cells, which may be an unexpected unique resource for stem-cell therapies including autologous stem- cell transplantation and tissue engineering.
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The yin and yang of neurotrophin action

TL;DR: The proteolytic cleavage of proneurotrophins represents a mechanism that controls the direction of action of neurotrophins and has profound implications for the understanding of the role of neurotrophic molecules in a wide range of cellular processes.
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Direct current stimulation promotes BDNF-dependent synaptic plasticity: potential implications for motor learning.

TL;DR: It is demonstrated in mouse M1 slices that DCS induces a long-lasting synaptic potentiation (DCS-LTP), which is polarity specific, NMDA receptor dependent, and requires coupling of DCS with repetitive low-frequency synaptic activation (LFS).
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Regulation of synaptic responses to high-frequency stimulation and LTP by neurotrophins in the hippocampus

TL;DR: The results suggest that BDNF may regulate LTP in developing and adult hippocampus by enhancing synaptic responses to tetanic stimulation, and a TrkB–IgG fusion protein, which scavenges endogenous BDNF11, reduced the synaptic responses in adult hippocampus as well as the magnitude of LTP.