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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.

Overexpression of lncRNA Gm15621 alleviates apoptosis and inflammation response resulting from sevoflurane treatment through inhibiting miR-133a/Sox4.

Sevoflurane is the most widely used anesthetic administered by inhalation. Exposure to sevoflurane can elicit learning deficits and abnormal cognitive disorder. In this study, we investigated the function of long noncoding RNA (lncRNA) Gm15621. Primary hippocampal neuron cells were used to analyze the function of lncRNA Gm15621 in vitro. The tunel, inflammation markers, and cell survival rates were detected to evaluate the function of lncRNA Gm15621. Dual-luciferase reporter assay was used to identify the interaction between microRNA 133a and Gm15621.

Role of autophagy in sevoflurane-induced neurotoxicity in neonatal rat hippocampal cells.

Sevoflurane has been extensively employed for induction and maintenance of general anesthesia. The effect of sevoflurane-induced apoptosis in developmental neurotoxicity has been appreciated for some time now, but the underlying mechanism of developmental neurotoxicity has not been established. The aim of our study is to evaluate the role of autophagy in sevoflurane-induced neurotoxicity through observing changes in the levels of autophagy in hippocampal neurons after exposure to sevoflurane.

Euxanthone Ameliorates Sevoflurane-Induced Neurotoxicity in Neonatal Mice.

Sevoflurane is a widely used anesthetic. A series of recent studies have shown that exposure to sevoflurane at an early stage is a risk factor for the development of learning and memory dysfunction. Euxanthone is a xanthone derivative obtained from Polygala caudata. This study was designed to investigate whether euxanthone can confer neuroprotective activities against sevoflurane-induced neurotoxicity and to determine the associated molecular mechanisms. Neonatal Sprague-Dawley (male) rats were exposed to sevoflurane with or without euxanthone treatment. The behavioral data of rats were collected at P41 (the beginning of the adult stage).

Toxicity mechanism of sevoflurane in neural stem cells of rats through DNA methylation.

The present study investigated the influence of sevoflurane on the cytotoxicity of neural stem cells of rats and deoxyribonucleic acid (DNA) methylation, and analyzed the correlation between degree of methylation and neurotoxicity of sevoflurane. Ten healthy Sprague-Dawley rats aged 6-8 weeks were randomly selected. The neural stem cells in the hippocampus of rats were isolated, followed by multiplication culture and induced differentiation. The nerve-related factors were observed and detected under a microscope. Moreover, the neural stem cells were treated with sevoflurane in different concentrations.

Both GSK-3β/CRMP2 and CDK5/CRMP2 pathways participate in the protection of dexmedetomidine against propofol-induced learning and memory impairment in neonatal rats.

Dexmedetomidine has been reported to ameliorate propofol-induced neurotoxicity in neonatal animals. However, the underlying mechanism is still undetermined. Glycogen synthase kinase-3β (GSK-3β), cycline dependent kinase-5 (CDK5) and Rho-kinase (RhoA) pathways play critical roles in neuronal development. The present study is to investigate whether GSK-3β, CDK5 and RhoA pathways are involved in the neuroprotection of dexmedetomidine. Seven-day-old (P7) Sprague-Dawley rats were anesthetized with propofol for 6 h.