News and EventsSmartTots and IARS News, Press Releases and Events
SmartTots: Building Community and Advocating for Important Research
SmartTots pediatric anesthetic neurotoxicity thought leaders discuss the current status of the field and provide insights into the future of the research. View on YouTube.
Pediatric Anesthetic Neurotoxicity: Finding Ways to Move Forward
Pediatric anesthetic neurotoxicity investigators discuss the state of the research and identify compelling ways to move the field forward. View on YouTube.
Pediatric Anesthetic Neurotoxicity: Designing the Proper Study
Pediatric anesthetic neurotoxicity thought leaders ponder the feasibility of designing and conducting studies that successfully isolate the effects of anesthetics from the effects of the procedure or patient’s underlying condition. View on YouTube.
Pediatric Anesthetic Neurotoxicity: The Pre-Clinical Journey
Pediatric anesthetic neurotoxicity researchers discuss how pre-clinical studies are providing insight into the mechanisms of neurotoxicity, and the impact on the future of clinical studies. View on YouTube.
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.
Sevoflurane diminishes neurogenesis and promotes ferroptosis in embryonic prefrontal cortex via inhibiting nuclear factor-erythroid 2-related factor 2 expression.
Objective: Prenatal sevoflurane exposure may pose neurotoxicity to embryonic brain development and lead to cognitive dysfunction in offspring, but the underlying mechanism is still unclear. We aimed to investigate whether sevoflurane could cause neurogenesis abnormality and ferroptosis in embryonic prefrontal cortex (PFC) and to identify the role of nuclear factor-erythroid 2-related factor 2 (Nrf2) in the sevoflurane-related neurotoxicity.
Neonatal anesthesia, while often essential for surgeries or imaging procedures, is accompanied by significant risks to redox balance in the brain due to the relatively weak antioxidant system in children. Oxidative stress is characterized by concentrations of reactive oxygen species (ROS) that are elevated beyond what can be accommodated by the antioxidant defense system. In neonatal anesthesia, this has been proposed to be a contributing factor to some of the negative consequences (e.g., learning deficits and behavioral abnormalities) that are associated with early anesthetic exposure.
LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497-5p to upregulate NLRX1.
Long non-coding RNA (lncRNA) small nucleolar RNA host gene 12 (SNHG12) has been reported to participate in the regulation of various nervous system disorders. Bupivacaine (BV), a commonly used local anesthetic, could generate neurotoxicity in neurons. This work intended to investigate the role and specific mechanism of SNHG12 in BV-induced neurotoxicity.
Downregulation of HOTAIR reduces neuronal pyroptosis by targeting miR-455-3p/NLRP1 axis in propofol-treated neurons in vitro.
Propofol is one of the most common intravenous anesthetics which may cause neuronal cell death in young mice. HOX transcript antisense RNA (HOTAIR) was abnormally expressed in neurodegenerative diseases. However, the effect of HOTAIR on propofol-induced pyroptosis of neurons and related mechanisms are still unknown. In this study, propofol treatment significantly reduced neuronal the viability of neurons, and promoted the expression of inflammation-related factors.
Aim: Ketamine is an anesthetic adjunct widely applied in the clinic that can induce hippocampal neurodegeneration in the brain. MicroRNAs (miRNAs) have been shown to be related to the regulation of ketamine-mediated neurotoxicity. This investigation aimed to determine the function of miR-384-5p in ketamine-induced neurotoxicity.
Identification of microRNA/target gene in the dentate gyrus of 7 day old mice following isoflurane exposure.
Studies on rodents and nonhuman primates suggest that exposure to anesthetics, particularly in the young brain, is associated with neuronal apoptosis as well as hippocampal‑dependent cognitive dysfunction. Disruption of the development of dentate gyrus may play an important role in anesthetics‑induced neurotoxicity.