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Bei Ping He

Researcher at Robarts Research Institute

Publications -  8
Citations -  581

Bei Ping He is an academic researcher from Robarts Research Institute. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Motor neuron. The author has an hindex of 6, co-authored 8 publications receiving 557 citations. Previous affiliations of Bei Ping He include University of Western Ontario.

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High Threshold for Induction of the Stress Response in Motor Neurons Is Associated with Failure to Activate HSF1

TL;DR: The results indicate that the high threshold for induction of the stress response in motor neurons stems from an impaired ability to activate the main heat shock–stress sensor, HSF1.
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Characterization of Neuronal Intermediate Filament Protein Expression in Cervical Spinal Motor Neurons in Sporadic Amyotrophic Lateral Sclerosis (ALS)

TL;DR: This paper showed that the stoichiometry of cytoskeletal protein expression in ALS spinal motor neurons is significantly altered in a pattern conducive to the formation of neurofilamentous aggregates.
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Activated microglia (BV-2) facilitation of TNF-α-mediated motor neuron death in vitro

TL;DR: It is observed a 20-fold increase in the amount of TNF-α required to kill NSC-34 cells in the absence of LPS-activated BV-2 cell supernatant, indicating that microglia secrete factor(s) that facilitate T NF-α-mediated motor neuron death in vitro.
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NMDA induces NOS 1 translocation to the cell membrane in NGF-differentiated PC 12 cells.

TL;DR: The data validate that NGF-differentiated PC12 cells may be employed as a useful in vitro model to further study the regulation of NOS1 subsequent to NMDAR activation and indicate that NMDar activation also mediates NOS 1 targeting to the membrane.
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A morphological analysis of the motor neuron degeneration and microglial reaction in acute and chronic in vivo aluminum chloride neurotoxicity.

TL;DR: It is demonstrated that microglial activation in vivo is inhibited by AlCl3 exposure, and that a correlation exists between the extent of microglia suppression and the potential for recovery, which suggests that microGlial activation is an important determinant of neuronal injury.