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Jimei Li

Researcher at Capital Medical University

Publications -  18
Citations -  559

Jimei Li is an academic researcher from Capital Medical University. The author has contributed to research in topics: Brain ischemia & Ischemia. The author has an hindex of 13, co-authored 18 publications receiving 477 citations. Previous affiliations of Jimei Li include Medical University of South Carolina.

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dl-3-n-Butylphthalide Prevents Neuronal Cell Death after Focal Cerebral Ischemia in Mice via the JNK Pathway

TL;DR: It is suggested that NBP protects against ischemic damage via multiple mechanisms including mitochondria associated caspase-dependent and -independent apoptotic pathways.
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Intranasal delivery of hypoxia-preconditioned bone marrow-derived mesenchymal stem cells enhanced regenerative effects after intracerebral hemorrhagic stroke in mice.

TL;DR: It is concluded that intranasal administration of BMSC is an effective treatment for ICH, and that it enhanced neuroregenerative effects and promoted neurological functional recovery after ICH.
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Acute and delayed protective effects of pharmacologically induced hypothermia in an intracerebral hemorrhage stroke model of mice

TL;DR: Data suggest that systemic injection of HPI-201 is an effective hypothermic strategy that protects the brain from ICH injury with a wide therapeutic window and the protective effect of this PIH therapy is partially mediated through the alleviation of apoptosis and neurovascular damage.
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DL-3-n-butylphthalide induced neuroprotection, regenerative repair, functional recovery and psychological benefits following traumatic brain injury in mice

TL;DR: These new findings demonstrate that NBP shows multiple therapeutic benefits after TBI, and significantly improved sensorimotor functional recovery and reduced post‐TBP depressive behavior.
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GSK-3β Inhibition Induced Neuroprotection, Regeneration, and Functional Recovery after Intracerebral Hemorrhagic Stroke:

TL;DR: The findings of this study corroborate the neuroprotective and regenerative effects of BIO and suggest that the Wnt/GSK-3β/β-catenin pathway may be explored for the treatment of acute or chronic ICH.