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SmartTots and IARS News, Press Releases and Events

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SmartTots – Perspectives from the Front Lines

Millions of children undergo surgery annually. Recent studies suggest there may be reason for concern. This video, featuring Dr. Dean Andropoulos, Dr. Peter Davis, and Dr. Caleb Ing, provides a summary as to why research is needed and the type that is needed.

SmartTots to Help Make Anesthetics and Sedatives Safer for Children

Dr. Janet Woodcock, director of the Center for Drug Evaluation and Research at the Food and Drug Administration, and Dr. Michael Roizen, of the International Anesthesia Research Society, unveil a new partnership that aims to make anesthesia safer for children.

Pediatric Anesthesia Questions and Myths-Mayo Clinic

Dr. Randall Flick at Mayo Clinic “debunks myths” and answers common questions raised by parents in regard to anesthesia.

Effects of embryonic propofol exposure on axonal growth and locomotor activity in zebrafish

Prenatal propofol exposure induced neurotoxicity in the developing brains and led to persistent learning deficits in the offspring. Our goal was to use zebrafish to explore whether the decline in learning and memory was correlated with inhibition of neuronal growth after propofol exposure. Zebrafish embryos at 6 hours postfertilization (hpf) were exposed to control or 1, 2 or 4 μg/mL propofol until 48 hpf. Spontaneous locomotor activity and swimming behavior in response to dark‐to‐light photoperiod stimulation were studied in zebrafish larvae at 6 days postfertilization (dpf).

Inhibition of the electron transport chain in propofol induced neurotoxicity in zebrafish embryos

Fetal and neonatal exposure to propofol can lead to neuronal death and long-term neurobehavioral deficiencies in both rodents and nonhuman primates. Zebrafish embryo, which is fertilized ex-utero, has provided us a new model species to study the effects of general anesthetics on developing brain. Inhibited electron transport chain leads to mitochondrial dysfunction and insufficient energy production. The aim of this study was to dissect the role of electron transport chain in propofol-induced neurotoxicity.

NR2B receptor- and calpain-mediated KCC2 cleavage resulted in cognitive deficiency exposure to isoflurane

During brain development, volatile anesthetic can rapidly interfere with physiologic patterns of dendritic development and synaptogenesis and impair the formation of precise neuronal circuits. KCC2 plays vital roles in spine development and synaptogenesis through its Cl- transport function and structural interactions with the spine cytoskeleton protein 4.1 N. The aim of this study was to dissect the mechanism of volatile anesthetics, which impair dendritic development and synaptogenesis via mediation of KCC2 cleavage.

Dexmedetomidine Alleviates Neurogenesis Damage Following Neonatal Midazolam Exposure in Rats through JNK and P38 MAPK Pathways

Midazolam, a widely used anesthetic, inhibits proliferation of neural stem cells (NSCs) and induces neuroapoptosis in neonates. Dexmedetomidine, an effective auxiliary medicine in clinical anesthesia, protects the developing brain against volatile anesthetic-induced neuroapoptosis. Whether dexmedetomidine protects against neurogenesis damage induced by midazolam remains unknown. This study aims to clarify the protective effect of dexmedetomidine on midazolam-induced neurogenesis damage and explore its potential mechanism.