Inhibitory neuron map of sevoflurane induced neurotoxicity model in young primates.

Introduction: Sevoflurane, one of the most commonly used anesthetic agents in children, may induce neuronal dysfunction and cognitive impairment. Exposure to sevoflurane might induce an imbalance between neural excitation and inhibition which could be a mechanism behind anesthesia-induced cognitive and affective dysfunctions. However, the underlying mechanisms remain unclear.

Effects of Sevoflurane Anesthesia on Cerebral Lipid Metabolism in the Aged Brain of Marmosets and Mice.

Objective: In the lipid-rich brain, lipids performed signaling processes associated with the control system of the cell cycle, stress, and inflammatory reactions, as well as maintained brain and cellular homeostasis. The effects of general anesthesia on brain impairment in the elderly were controversial and complex. The study sought to evaluate the effect of lipid metabolism in the brain of aged marmosets and mice under long-term exposure to sevoflurane.

The Effect of Sevoflurane Anesthesia on the Biomarkers of Neural Injury in the Prefrontal Cortex of Aged Marmosets.

Background: Surgery under general anesthesia leads to neural injury, especially in older patients. Sevoflurane anesthesia without surgery for 2 h does not induce neural injury, however, whether prolonger sevoflurane anesthesia without surgery has the same consequence is still unknown.

Methods: In the present study, aged marmosets were exposed to a clinical concentration of sevoflurane (1.

Identification of Prefrontal Cortex and Amygdala Expressed Genes Associated With Sevoflurane Anesthesia on Non-human Primate.

Clinical trials and animal studies have indicated that long-term use or multiple administrations of anesthesia may lead to fine motor impairment in the developing brain. Most studies on anesthesia-induced neurotoxicity have focused on the hippocampus and prefrontal cortex (PFC); however, the role of other vital encephalic regions, such as the amygdala, is still unclear. Herein, we focused on sevoflurane, the most commonly used volatile anesthetic in infants, and performed a transcriptional analysis of the PFC and amygdala of macaques after multiple exposures to the anesthetic by RNA sequencing.

Epitranscriptomic Analysis of N6-methyladenosine in Infant Rhesus Macaques after Multiple Sevoflurane Anesthesia.

Clinical investigations to date have proposed the possibility that exposure to anesthetics is associated with neurodevelopmental deficits. Sevoflurane is the most commonly used general anesthetic in pediatric patients. Animal studies have demonstrated that multiple exposures to sevoflurane during the postnatal period resulted in neuropathological brain changes and long-term cognitive deficits.

Sevoflurane impairs m6A-mediated mRNA translation and leads to fine motor and cognitive deficits.

Clinical surgical practices have found that children who undergo multiple anesthesia may have an increased risk of deficiencies in cognition and fine motor control. Here, we report that YT521-B homology domain family 1 (YTHDF1), a critical reader protein for N6-methyladenosine-modified mRNA, was significantly downregulated in the prefrontal cortex of young mice after multiple sevoflurane anesthesia exposures. Importantly, sevoflurane led to a decrease in protein synthesis in mouse cortical neurons that was fully rescued by YTHDF1, suggesting that anesthesia may affect early brain development by affecting m6A-dependent mRNA translation.

Fine particles in surgical smoke affect embryonic cardiomyocyte differentiation through oxidative stress and mitophagy.

Surgical smoke is widespread in operating rooms, and fine particles are the main toxic components. However, the effect of fine particles in surgical smoke on embryonic development has not yet been studied. This study evaluated the effect of fine particles in surgical smoke on embryonic development and compared it with that of atmospheric fine particles.

Dusp4 Contributes to Anesthesia Neurotoxicity via Mediated Neural Differentiation in Primates.

Background: Children who are exposed to anesthesia multiple times may undergo cognitive impairment during development. The underlying mechanism has been revealed as anesthesia-induced cognitive deficiency in young rodents and monkeys. However, the molecular mechanism of sevoflurane-induced neural development toxicity is unclear.

Role of Parkin-mediated mitophagy in glucocorticoid-induced cardiomyocyte maturation.

Glucocorticoids can promote cardiomyocyte maturation. However, the mechanism underlying glucocorticoid-mediated cardiomyocyte maturation is still unclear. Mitophagy plays a key role in cardiomyocyte maturation.

Multiple sevoflurane exposures don't disturb the T-cell receptor repertoire in infant rhesus monkeys' thymus.

Aims: Multiple surgical procedures and anesthesia increase the risk of the development in children. However, the influence of such exposures on the developing childhood immunity organs is rarely reported.

Materials And Methods: High-throughput sequencing of T-cell receptor (TCR) repertoires (TCRseq) from rhesus monkeys' thymus was performed to investigate whether anesthetics could induce de novo antigen recognition via TCR or TCR development impairments.

Multiple sevoflurane exposures during pregnancy inhibit neuronal migration by upregulating prostaglandin D2 synthase.

Background: The second trimester is a period of neurogenesis and neuronal migration, which may be affected by exposure to anesthetics. Studies have suggested that multiple anesthetic exposures may have a significant impact on neuronal migration.

Methods: Pregnant C57BL/6 mice at embryonic day 14.

The role of long non-coding RNA SNHG12 in neuroprotection following cerebral ischemic injury.

As one of the major causes of mortality and disability worldwide, ischemic stroke has never been received enough attention. Following ischemia/reperfusion injury, long non-coding RNAs have been extensively found to be involved into inflammatory responses, microvascular endothelial cell death, and angiogenesis in the brain. The small nucleolar RNA host gene 12 was found to be significantly increased following transient middle cerebral artery occlusion.

Disrupted folate metabolism with anesthesia leads to myelination deficits mediated by epigenetic regulation of ERMN.

Background: Exposure to anesthetics during early life may impair cognitive functions. However, the underlying mechanisms remain largely unknown. We set out to determine effects of sevoflurane anesthesia on folate metabolism and myelination in young non-human primates, mice and children.

Fundamentals of fetal toxicity relevant to sevoflurane exposures during pregnancy.

Over the last three decades, advances in medical and surgical techniques have proven life saving and life-improving for young children. Consequently, early and repeated exposure to general anesthetics in childhood has increased. However, accumulating evidence suggests that general anesthetics may be neurotoxic in children.

Mesenchymal stromal cells attenuate sevoflurane-induced apoptosis in human neuroglioma H4 cells.

Background: Inhalation of sevoflurane can induce neuronal apoptosis, cognitive impairment and abnormal behaviors. Bone marrow mesenchymal stem cells (MSCs) can secret neurotrophic factors and cytokines to protect from oxidative stress-related neuronal apoptosis. However, whether MSCs can protect from sevoflurane-induced neuronal apoptosis and the potential mechanisms are unclear.

Surface Modified with a Host Defense Peptide-Mimicking β-Peptide Polymer Kills Bacteria on Contact with High Efficacy.

Methicillin-resistant Staphylococcus aureus (MRSA) has been one of the major nosocomial pathogens to cause frequent and serious infections that are associated with various biomedical surfaces. This study demonstrated that surface modified with host defense peptide-mimicking β-peptide polymer, has surprisingly high bactericidal activities against Escherichia coli ( E. coli) and MRSA.

Nrf2 Activation Induced by Sirt1 Ameliorates Acute Lung Injury After Intestinal Ischemia/Reperfusion Through NOX4-Mediated Gene Regulation.

Background/aims: Nuclear erythroid 2-related factor-2 (Nrf2) is a major stress-response transcription factor that has been implicated in regulating ischemic angiogenesis. We investigated the effects of Nrf2 in regulating revascularization and modulating acute lung injury.

Methods: The expression of Nrf2 and sirtuin1 (Sirt1) was assessed in lung tissue by western blotting and immunofluorescence staining after intestinal ischemia/reperfusion (IIR) in Nrf2-/- and wild-type (WT) mice.

Lidocaine inhibits the proliferation of lung cancer by regulating the expression of GOLT1A.

Objectives: Lidocaine is the most commonly used local anaesthetic in clinical and can inhibit proliferation, suppress invasion and migration and induce apoptosis in human lung adenocarcinoma (LAD) cells. However, its specific downstream molecular mechanism is unclear.

Materials And Methods: LAD cell lines, A549 and H1299 cells, were treated with lidocaine.