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SmartTots and IARS News, Press Releases and EventsSmartTots – 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 Induces Hippocampal Neuronal Apoptosis by Altering the Level of Neuropeptide Y in Neonatal Rats.
Numerous studies have shown that the inhaled general anesthetic sevoflurane imposes toxicity on the central nervous system during the developmental period but the underlying mechanisms remain unclear. Neuropeptide Y (NPY) was reported to have important neuroprotective effects, which can attenuate neuronal loss under pathological conditions. However, the effects of NPY on sevoflurane-induced hippocampal neuronal apoptosis have not been investigated.
Compound Porcine Cerebroside and Ganglioside Injection (CPCGI) Attenuates Sevoflurane-Induced Nerve Cell Injury by Regulating the Phosphorylation of p38 MAP Kinase (p38MAPK)/Nuclear Factor kappa B (NF-κB) Pathway.
Compound porcine cerebroside and ganglioside injection (CPCGI) has been widely applied in clinical practice in China to treat functional confusion caused by brain diseases. Sevoflurane, a frequently-used inhalational anesthetic, was discovered to have neurotoxicity that can cause neurological damage in patients. The present study was performed to investigate the protective effect of CPCGI on sevoflurane-induced nerve damage and to reveal the neuroprotective mechanisms of CPCGI.
Maternal Treadmill Exercise Reduces the Neurotoxicity of Prenatal Sevoflurane Exposure in Rats via Activation of p300 Histone Acetyltransferase.
Repeated or prolonged use of general anesthetics in pregnant women may disturb the neurodevelopment of infants. Compelling evidence indicates that maternal exercise during pregnancy has positive effects on the cognitive function of offspring. We previously confirmed the preventive potential of maternal treadmill training for cognitive deficits induced by in utero exposure to sevoflurane in rat pups. However, the underlying mechanism(s) needed further clarification.
Regions of the basal ganglia and primary olfactory system are most sensitive to neurodegeneration after extended sevoflurane anesthesia in the perinatal rat.
Extended general anesthesia early in life is neurotoxic in multiple species. However, little is known about the temporal progression of neurodegeneration after general anesthesia. It is also unknown if a reduction in natural cell death, or an increase in cell creation, occurs as a form of compensation after perinatal anesthesia exposure.
LncRNA LINC00641 Sponges miR-497-5p to Ameliorate Neural Injury Induced by Anesthesia via Up-Regulating BDNF.
Ketamine, which is widely used in anesthesia, can induce cortical neurotoxicity in patients. This study aims to investigate the effects of long non-coding RNA LINC00641 on the ketamine-induced neural injury.
An appropriate level of autophagy reduces emulsified isoflurane-induced apoptosis in fetal neural stem cells.
Autophagy plays essential roles in cell survival. However, the functions and regulation of the autophagy-related proteins Atg5, LC3B, and Beclin 1 during anesthetic-induced developmental neurotoxicity remain unclear. This study aimed to understand the autophagy pathways and mechanisms that affect neurotoxicity, induced by the anesthetic emulsified isoflurane, in rat fetal neural stem cells.