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Cheng Wang

Researcher at National Center for Toxicological Research

Publications -  60
Citations -  3689

Cheng Wang is an academic researcher from National Center for Toxicological Research. The author has contributed to research in topics: Neurotoxicity & Anesthetic. The author has an hindex of 27, co-authored 60 publications receiving 3271 citations. Previous affiliations of Cheng Wang include Food and Drug Administration & University of Texas Health Science Center at San Antonio.

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Ketamine-induced neuronal cell death in the perinatal rhesus monkey.

TL;DR: Ketamine increased N-methyl-D-aspartate (NMDA) receptor NR1 subunit messenger RNA in the frontal cortex where enhanced cell death was apparent and a shorter duration of ketamine anesthesia did not result in neuronal cell death in the 5-day-old monkey.
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Ketamine anesthesia during the first week of life can cause long-lasting cognitive deficits in rhesus monkeys

TL;DR: It is demonstrated that a single 24-h episode of ketamine anesthesia, occurring during a sensitive period of brain development, results in very long-lasting deficits in brain function in primates and provides proof-of-concept that general anesthesia during critical periods of brainDevelopment can result in subsequent functional deficits.
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Prolonged exposure to ketamine increases neurodegeneration in the developing monkey brain

TL;DR: Data show that treatment with ketamine up to 3 h is without adverse effects as determined by nerve cell death, and the threshold duration below which no neurotoxicity would be expected is somewhere between 3 and 9 h.
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Potential Neurotoxicity of Ketamine in the Developing Rat Brain

TL;DR: It is demonstrated that ketamine administration results in a dose-related and exposure-time dependent increase in neuronal cell death during development and ketamine-induced cell death appears to be apoptotic in nature and closely associated with enhanced NMDA receptor subunit mRNA expression.
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The role of the N-methyl-D-aspartate receptor in ketamine-induced apoptosis in rat forebrain culture.

TL;DR: The data suggest that NR1 antisense offers neuroprotection from apoptosis in vitro, and that upregulation of the NR1 following ketamine administration is, at least, partially responsible for the observed apoptosis.