Listeria monocytogenes: a promising vector for tumor immunotherapy.

Cancer receives enduring international attention due to its extremely high morbidity and mortality. Immunotherapy, which is generally expected to overcome the limits of traditional treatments, serves as a promising direction for patients with recurrent or metastatic malignancies. Bacteria-based vectors such as Listeria monocytogenes take advantage of their unique characteristics, including preferential infection of host antigen presenting cells, intracellular growth within immune cells, and intercellular dissemination, to further improve the efficacy and minimize off-target effects of tailed immune treatments. Listeria monocytogenes can reshape the tumor microenvironment to bolster the anti-tumor effects both through the enhancement of T cells activity and a decrease in the frequency and population of immunosuppressive cells. Modified Listeria monocytogenes has been employed as a tool to elicit immune responses against different tumor cells. Currently, Listeria monocytogenes vaccine alone is insufficient to treat all patients effectively, which can be addressed if combined with other treatments, such as immune checkpoint inhibitors, reactivated adoptive cell therapy, and radiotherapy. This review summarizes the recent advances in the molecular mechanisms underlying the involvement of Listeria monocytogenes vaccine in anti-tumor immunity, and discusses the most concerned issues for future research.

Domino Reactions Enabling Sulfur-Mediated Gradient Interphases for High-Energy Lithium Batteries.

Silicon (Si)-based anodes are currently considered a feasible solution to improve the energy density of lithium-ion batteries owing to their sufficient specific capacity and natural abundance. However, Si-based anodes exhibit low electric conductivities and large volume changes during cycling, which could easily trigger continuous breakdown/reparation of the as-formed solid-electrolyte-interphase (SEI) layer, seriously hampering their practical application in current battery technology. To control the chemoelectrochemical instability of the conventional SEI layer, we herein propose the introduction of elemental sulfur into nonaqueous electrolytes, aiming to build a sulfur-mediated gradient interphase (SMGI) layer on Si-based anodes. The SMGI layer is generated through the domino reactions (i.e., electrochemical cascade reactions) involving the electrochemical reductions of elemental sulfur followed by nucleophilic substitutions of fluoroethylene carbonate, which endows the corresponding SEI layer with strong elasticity and chemomechanical stability and enables rapid transportation of Li+ ions. Consequently, the prototype Si||LiNi0.8Co0.1Mn0.1O2 cells attain a high-energy density of 622.2 W h kg-1 and a capacity retention of 88.8% after 100 cycles. Unlike previous attempts based on sophisticated chemical modifications of electrolyte components, this study opens a new avenue in interphase design for long-lived and high-energy rechargeable batteries.

Designer Cathode Additive for Stable Interphases on High-Energy Anodes.

Rechargeable lithium-based batteries built with high-energy anode materials (e.g., silicon-based and silicon-derivative materials) are considered a feasible solution to satisfy the stringent requirements imposed by emerging markets, including electric vehicles and grid storage, due to their higher energy density compared to contemporary lithium-ion batteries. The robustness of the solid electrolyte interphase (SEI) layer on high-energy anodes is critical to achieve long-term and stable cycling performances of the batteries. Herein, we propose a new type of designer cathode additive (DCA), i.e., an ultrathin coating layer of elemental sulfur on the cathode, for the in situ formation of a thin and robust SEI layer on various types of high-energy anodes. The DCA elemental sulfur undergoes simultaneous oxidation and reduction paths, forming lithium alkyl sulfate (R-OSO2OLi) and poly(ethylene oxide) (PEO)-like polymers on the anode surface. The as-formed R-OSO2OLi/PEO-modified SEI layer has good lithium cation (Li+) permeability to facilitate fast ion transportation across the interphases and superior elasticity to adapt to large volume changes, which is particularly effective for improving the cycling efficiency of high-energy anodes (e.g., ca. 14-35% increase in capacity retention for the silicon-carbon composite (SiC) or silicon-tin alloy (Si-Sn)||LiFePO4 cells). The present work opens a new avenue toward the practical deployment of high-energy rechargeable lithium-based batteries.

Ipsilateral S2 nerve root transfer to pudendal nerve for restoration of external anal and urethral sphincter function: an anatomical study.

Patients suffer bilateral sacral plexus injuries experience severe problems with incontinence. We performed a cadaveric study to explore the anatomical feasibility of transferring ipsilateral S2 nerve root combined with a sural nerve graft to pudendal nerve for restoration of external anal and urethral sphincter function. The sacral nerve roots and pudendal nerve roots on the right side were exposed in 10 cadavers. The length from S2 nerve root origin to pudendal nerve at inferior border of piriformis was measured. The sural nerve was used as nerve graft. The diameters and nerve cross-sectional areas of S2 nerve root, pudendal nerve and sural nerve were measured and calculated, so as the number of myelinated axons of three nerves on each cadaver specimen. The length from S2 nerve root to pudendal nerve was 10.69 ± 1.67 cm. The cross-sectional areas of the three nerves were 8.57 ± 3.03 mm2 for S2, 7.02 ± 2.04 mm2 for pudendal nerve and 6.33 ± 1.61 mm2 for sural nerve. The pudendal nerve contained approximately the same number of axons (5708 ± 1143) as the sural nerve (5607 ± 1305), which was a bit less than that of the S2 nerve root (6005 ± 1479). The S2 nerve root in combination with a sural nerve graft is surgically feasible to transfer to the pudendal nerve for return of external urethral and anal sphincter function, and may be suitable for clinical application in patients suffering from incontinence following sacral plexus injuries.

Up-regulation of heat shock protein 27 inhibits apoptosis in lumbosacral nerve root avulsion-induced neurons.

Lumbosacral nerve root avulsion leads to widespread death of neurons in the anterior horn area of the injured spinal cord, which results in dysfunction in the lower extremities. Heat shock protein 27 (Hsp27) has been found to play cytoprotective roles under adverse conditions. However, the role of Hsp27 in neurons after lumbosacral nerve root avulsion is unknown. The aim of the present study was to investigate the effects and mechanism of action of Hsp27 on neurons after lumbosacral nerve root avulsion. It was found that Hsp27 expression was elevated in the anterior horn area of the injured spinal cord and the up-regulation of Hsp27 protected neurons against apoptosis after lumbosacral nerve root avulsion. In addition, Hsp27 plays an anti-apoptotic role by suppressing oxidative stress reactions. These findings indicated that Hsp27 may play a key role in resistance to lumbosacral nerve root avulsion-induced neuron apoptosis and may prove to be a potential strategy for improving prognosis after lumbosacral nerve root avulsion.

circRNA.33186 Contributes to the Pathogenesis of Osteoarthritis by Sponging miR-127-5p.

Osteoarthritis (OA), the most prevalent age-related joint disorder, is characterized by chronic inflammation, progressive articular cartilage destruction, and subchondral bone sclerosis. Accumulating evidences indicate that circular RNAs (circRNAs) play a critical role in various diseases, but the function of circRNAs in OA remains largely unknown. Here we showed that circRNA.33186 was significantly upregulated in IL-1ß)-treated chondrocytes and in cartilage tissues of a destabilized medial meniscus (DMM)-induced OA mouse model. Knockdown of circRNA.33186 increased anabolic factor (type II collagen) expression and decreased catabolic factor (MMP-13) expression. Knockdown of circRNA.33186 also promoted proliferation and inhibited apoptosis in IL-1ß-treated chondrocytes. Silencing of circRNA.33186 in vivo markedly alleviated DMM-induced OA. Mechanistic study showed that circRNA.33186 directly binds to and inhibits miR-127-5p, thereby increasing MMP-13 expression, and contributes to OA pathogenesis. Taken together, our findings demonstrated a fundamental role of circRNA.33186 in OA progression and provide a potential drug target in OA therapy.

Differential Expression Profiles and Functional Predication of Circular Ribonucleic Acid in Traumatic Spinal Cord Injury of Rats.

Recent studies indicate that circular ribonucleic acids (circRNAs) are involved in a variety of human diseases. The roles of circRNAs in traumatic spinal cord injury (SCI) remain unknown, however. We performed RNA-seq to analyze the circRNA expression profile in rat spinal cord after SCI and to investigate the relevant mechanisms. In all, 150 circRNAs were significantly differentially expressed in rat spinal cord after SCI by a fold-change ≥2 and p value ≤0.05. Among these, 99 circRNAs were upregulated, while 51 were downregulated. Gene ontology, Kyoto Encyclopedia of Genes and Genomes pathway analyses, and circRNA/miocroRNA (miRNA) interaction networks were conducted to predict the potential roles of circRNAs in the process of SCI. In addition, the expression levels of six selected circRNAs were verified successfully by quantitative real-time polymerase chain reaction. Further study identified circRNA_07079 and circRNA_01282 as being associated with SCI, and they may participate in the pathophysiology of SCI through circRNA-targeted miRNA-messenger RNA axis. In summary, the results of our study revealed the expression profiles and potential functions of differentially expressed circRNAs in traumatic SCI in rats; this may provide new clues for studying the mechanisms underlying SCI and also present novel molecular targets for clinical therapy of SCI.

Silencing of circRNA.2837 Plays a Protective Role in Sciatic Nerve Injury by Sponging the miR-34 Family via Regulating Neuronal Autophagy.

Circular RNAs (circRNAs) represent a class of non-coding RNAs that are involved in transcriptional and posttranscriptional gene expression regulation and associated with different kinds of human diseases. However, the characterization and function of circular RNAs in peripheral nerve injuries remain elusive. Here, we established a rat sciatic nerve injury model and identified at least 4,942 distinct circular RNA candidates and a series of circular RNAs that were differentially expressed in injured nerve tissues compared with matched normal tissues. We characterized one frequently downregulated circular RNA, circRNA.2837, and further investigated its function in sciatic nerve injury. We found that circRNA.2837 regulated autophagy in neurons in vitro and in vivo, and downregulation of circRNA.2837 alleviated sciatic nerve injury via inducing autophagy in vivo. Mechanistically, knockdown of circRNA.2837 may protect neurons against neurological injury by acting as a sponge for members of miR-34 family. Our findings suggested that differentially expressed circular RNAs were involved in the pathogenesis of sciatic nerve injury, and circular RNAs exerted regulatory functions in sciatic nerve injury and might be used as potential targets in sciatic nerve injury therapy.

Lysophosphatidic Acid Promotes Expression and Activation of Matrix Metalloproteinase 9 (MMP9) in THP-1 Cells via Toll-Like Receptor 4/Nuclear Factor-κB (TLR4/NF-κB) Signaling Pathway.

BACKGROUND Lysophosphatidic acid (LPA) is an active compound of oxidized low-density lipoprotein that serves as an endogenous TLR4 ligand. Ligand activation of TLR4 activates nuclear factor-kappaB (NF-κB) and the transcription of NF-κB-regulated inflammatory cytokines, which are involved in the development of atherosclerosis. MMP9 is a member of the MMP family and can affect plaque stability. However, the mechanism responsible for the effect of LPA on the expression and activation of MMP9 has not been fully elucidated. In the present study we examined the effect of LPA on MMP9 expression and activity in THP-1 cells and the involvement of Toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB) signaling pathway in this effect. MATERIAL AND METHODS Human THP-1 cells were treated with 0-10 µM LPA for 4 h, or treated with 1 µM LPA for 0-8 h, and were then transfected with TLR4-specific siRNA or treated with 20 µg/ml cafestol acid phenethyl ester (CAPE, an NF-κB inhibitor). MMP9 mRNA and protein levels were measured by quantitative RT-PCR and Western blot analysis, respectively, and MMP9 activity was measured by zymography. RESULTS LPA upregulated MMP9 mRNA and protein levels and MMP9 activity in THP-1 cells in both concentration- and time-dependent manners. Transfection of cells with TLR4-siRNA-2 or treatment with CAPE significantly inhibited the upregulated MMP9 expression and activation. This inhibition was further enhanced by combining the TLR4-siRNA-2 transfection and CAPE pretreatment. CONCLUSIONS LPA can promote MMP9 expression and enhance MMP9 activity in THP-1 cells, in part via the TLR4/NF-kB signaling pathway.

Neonatal Exposure to Low-Dose (1.2%) Sevoflurane Increases Rats' Hippocampal Neurogenesis and Synaptic Plasticity in Later Life.

The increasing usage of general anesthetics on young children and infants has drawn extensive attention to the effects of these drugs on cognitive function later in life. Recent animal studies have revealed improvement in hippocampus-dependent performance after lower concentrations of sevoflurane exposure. However, the long-term effects of low-dose sevoflurane on the developing brain remain elusive. On postnatal day (P) 7, rats were treated with 1.2% sevoflurane (1.2% sevo group), 2.4% sevoflurane (2.4% sevo group), and air control (C group) for 6 h. On P35-40, rats' hippocampus-dependent learning and memory was tested using the Morris water maze. Cognition-related and synapse-related proteins in the hippocampus were measured using Western blotting on P35. On the same day, neurogenesis and synapse ultrastructure were evaluated using immunofluorescence and transmission electron microscopy (TEM). On P35, the rats neonatally exposed to 1.2% sevoflurane showed better behavioral results than control rats, but not in the 2.4% sevo group. Exposure to 1.2% sevoflurane increased the number of 5'-bromo-2-deoxyuridine (BrdU)-positive cells in the dentate gyrus and improved both synaptic number and ultrastructure in the hippocampus. The expression levels of BDNF, TrkB, postsynaptic density (PSD)-95, and synaptophysin in the hippocampus were also increased in the 1.2% sevo group. In contrast, no significant changes in neurogenesis or synaptic plasticity were observed between the C group and the 2.4% sevo group on P35. These results showed that exposure of the developing brain to a low concentration of sevoflurane for 6 h could promote spatial learning and memory function, along with increased hippocampal neurogenesis and synaptic plasticity, in later life.

Circular RNA Atp9b, a competing endogenous RNA, regulates the progression of osteoarthritis by targeting miR-138-5p.

Osteoarthritis (OA) is the most common joint disease and is mainly characterized by degradation of the articular cartilage. Recently, circular RNAs (circRNAs), novel noncoding RNAs with different biological functions and pathological implications, have been reported to be closely associated with various diseases. Growing evidence indicates that circRNAs act as competing endogenous RNAs (ceRNAs) that bind with microRNAs (miRNAs) and regulate their downstream functions. Here, we identified a new circRNA, circRNA_Atp9b, and further investigated its function in OA using a well-established mouse chondrocyte model. We demonstrated that circRNA_Atp9b expression was significantly up-regulated in mouse chondrocytes after stimulation with interleukin-1 beta (IL-1ß), and that knockdown of circRNA_Atp9b promoted the expression of type II collagen while inhibiting the generation of MMP13, COX-2 and IL-6. Moreover, there was a negative correlation between the expression levels of circRNA_Atp9b and microRNA (miR)-138-5p, indicating that miR-138-5p also played a role in IL-1ß-induced chondrocytes. Bioinformatics analysis predicted circRNA_Atp9b directly target miR-138-5p, which was validated by dual-luciferase assay. Further functional experiments revealed that down-regulation of miR-138-5p partly reversed the effects of circRNA_Atp9b on extracellular matrix (ECM) catabolism and inflammation. Taken together, these results suggest that circRNA_Atp9b regulates OA progression by modulating ECM catabolism and inflammation in chondrocytes via sponging miR-138-5p. Our findings provide novel insight into the regulatory mechanism of circRNA_Atp9b in OA and may contribute to establishing potential therapeutic strategies.

Sevoflurane Affects Oxidative Stress and Alters Apoptosis Status in Children and Cultured Neural Stem Cells.

Anesthesia-induced neurotoxicity in immature animals has raised concerns about similar effects occurring in young children. Our study investigated two commonly used anesthetics-sevoflurane and propofol-for neurotoxicity in young children. Forty-seven children (aged 12-36 months) undergoing hypospadias repair surgery were randomized to receive sevoflurane (SG, n = 24) or propofol (PG, n = 23) general anesthesia. Venous blood was collected at three different times-immediately after induction, 2 h, and 3 days after surgery. The cellular portion was assessed for antioxidant defense and DNA damage, using enzyme assay kits and qRT-PCR, respectively, while serum was used to treat cultured neural stem cells (NSCs). MTT assay and TUNEL staining were performed, and the mRNA levels of antioxidant enzymes and apoptosis indicators were evaluated by qRT-PCR. Antioxidant defense and apoptosis status in the SG group were significantly higher than in the PG group at 2 h after surgery. Additionally, exposure of NSCs to postoperative serum of the SG group resulted in decreased cell density and viability, increased TUNEL-positive cells, elevated mRNA levels of antioxidant enzymes, and cleaved caspase-3 expression. Our data shows for the first time that in young children, administration of sevoflurane, but not propofol, leads to temporally increased antioxidant defense and apoptosis status as well as damage of NSCs.

The Prognostic Risk Factors of ECMO in Patients with Cardiogenic Shock: A Retrospective Cohort Analysis.

BACKGROUND: Advances in ECMO have rapidly progressed in recent years; however, the clinical mortality rate remains high. This study aimed to identify the risk factors of ECMO in patients with cardiogenic shock. METHODS: Data of patients with cardiogenic shock who received ECMO from January 2006 to August 2013 at the Affiliated Hospital of Sun Yat-Sen University were retrospectively analyzed. All patients with cardiogenic shock were divided into two groups according to whether death occurred in the hospital. The possible prognostic risk factors of ECMO were first obtained in a univariate analysis of the two groups, and the risk factors that affected the prognosis of patients who underwent ECMO were determined using a logistic regression analysis. RESULTS: This study included 94 cardiogenic shock patients who were treated with ECMO. Overall, 59 patients were successfully weaned from ECMO, which accounted for 62.7% of all patients. The multivariate analysis indicated that the independent risk factors associated with prognosis included ECMO timing (OR = 7.68; 95% CI 1.60-37.01), the occurrence of postoperative MOF (OR = 2,823.09; 95% CI 14.75-540,171.06), and the lactate level at weaning (OR = 493.17; 95% CI: 1.55-156,653.27). CONCLUSION: For patients with refractory cardiogenic shock, the early establishment of ECMO, improvement in perfusion, and the prevention of complications may improve the prognosis.

Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis.

Sevoflurane is generally considered a pro-apoptotic agent in the neonatal brain. However, recent studies have suggested that low levels of sevoflurane anesthesia may be neuroprotective and have a memory enhancing effect. The present study aimed to investigate whether sevoflurane exerts a neuroprotective effect at subclinical concentrations, with regard to oxidative state. In the current study, postnatal day 7 (P7) Sprague­Dawley rats were continuously exposed to 0.3, 1.3, or 2.3% sevoflurane for 6 h. ELISA was used to quantify the levels of superoxide dismutase, glutathione peroxidase (GSH­px) and malondialdehyde (MDA) in the plasma and the hippocampus. Terminal deoxynucleotidyl-transferase dUTP nick-end labeling staining was used to observe hippocampal neuronal apoptosis. Altered object exploration tests for recognition memory were employed to investigate long­term behavioral effects at postnatal day 28. The results demonstrated that a single 6 h exposure to a subclinical concentration (1.3%) of sevoflurane at P7 reduces MDA and GPH­px production in rats. Sevoflurane induced hippocampal apoptosis in a dose­dependent manner and altered recognition memory testing indicated no differences among the groups. Although early exposure to a subclinical concentration of sevoflurane reduced oxidative stress, it did not prevent the process of sevoflurane-induced hippocampal apoptosis. These changes did not affect subsequent recognition memory in juvenile rats.

Lithium Treatment Prevents Apoptosis in Neonatal Rat Hippocampus Resulting from Sevoflurane Exposure.

We aimed to observe the therapeutic effects of lithium on inhalational anesthetic sevoflurane-induced apoptosis in immature brain hippocampus. From postnatal day 5 (P5) to P28, male Sprague-Dawley pups were intraperitoneally injected with lithium chloride or 0.9 % sodium chloride. On P7 after the injection, pups were exposed to 2.3 % sevoflurane or air for 6 h. Brain tissues were harvested 12 h and 3 weeks after exposure. Cleaved caspase-3, nNOS protein, GSK-3ß,p-GSK-3ß were assessed by Western blot, and histopathological changes were assessed using Nissl stain and TUNEL stain. From P28, we used the eight-arm radial maze test and step-through test to evaluate the influence of sevoflurane exposure on the learning and memory of juvenile rats. The results showed that neonatal sevoflurane exposure induced caspase-3 activation and histopathological changes in hippocampus can be attenuated by lithium chloride. Sevoflurane increased GSK-3ß activity while pretreatment of lithium decreased GSK-3ß activity. Moreover, sevoflurane showed possibly slight but temporal influence on the spatial learning and the memory of juvenile rats, and chronic use of lithium chloride might have the therapeutic effect. Our current study suggests that lithium attenuates sevoflurane induced neonatal hippocampual damage by GSK-3ß pathway and might improve learning and memory deficits in rats after neonatal exposure.

Propofol Protects Against H2O2-Induced Oxidative Injury in Differentiated PC12 Cells via Inhibition of Ca(2+)-Dependent NADPH Oxidase.

Propofol (2,6-diisopropylphenol) is a widely used general anesthetic with anti-oxidant activities. This study aims to investigate protective capacity of propofol against hydrogen peroxide (H2O2)-induced oxidative injury in neural cells and whether the anti-oxidative effects of propofol occur through a mechanism involving the modulation of NADPH oxidase (NOX) in a manner of calcium-dependent. The rat differentiated PC12 cell was subjected to H2O2 exposure for 24 h to mimic a neuronal in vitro model of oxidative injury. Our data demonstrated that pretreatment of PC12 cells with propofol significantly reversed the H2O2-induced decrease in cell viability, prevented H2O2-induced morphological changes, and reduced the ratio of apoptotic cells. We further found that propofol attenuated the accumulation of malondialdehyde (biomarker of oxidative stress), counteracted the overexpression of NOX core subunit gp91(phox) (NOX2) as well as the NOX activity following H2O2 exposure in PC12 cells. In addition, blocking of L-type Ca(2+) channels with nimodipine reduced H2O2-induced overexpression of NOX2 and caspase-3 activation in PC12 cells. Moreover, NOX inhibitor apocynin alone or plus propofol neither induces a significant downregulation of NOX activity nor increases cell viability compared with propofol alone in the PC12 cells exposed to H2O2. These results demonstrate that the protective effects of propofol against oxidative injury in PC12 cells are mediated, at least in part, through inhibition of Ca(2+)-dependent NADPH oxidase.

Cerebral ischemia during surgery: an overview.

Cerebral ischemia is the pathophysiological condition in which the oxygenated cerebral blood flow is less than what is needed to meet cerebral metabolic demand. It is one of the most debilitating complications in the perioperative period and has serious clinical sequelae. The monitoring and prevention of intraoperative cerebral ischemia are crucial because an anesthetized patient in the operating room cannot be neurologically assessed. In this paper, we provide an overview of the definition, etiology, risk factors, and prevention of cerebral ischemia during surgery.

Propofol-induced rhabdomyolysis: a case report.

OBJECTIVE: To report a case of propofol-induced rhabdomyolysis. In this case, widespread myolysis was detected after induction of anesthesia. CASE SUMMARY: A 54-year-old female patient was scheduled for a hysterectomy. Beginning shortly after the induction of anesthesia with propofol, several episodes of ventricular fibrillation occurred. Despite intensive care, the patient failed to recover. During most episodes of ventricular fibrillation, marked hyperthermia or hyperkalemia were not observed. Unexplained, widespread myolysis affecting both skeletal and cardiac muscle was observed at autopsy. DISCUSSION: In this patient, the evidence for rhabdomyolysis is robust. Clinical characteristics are similar to those observed in propofol infusion syndrome. The absence of a body temperature over 40 °C precludes the possibility of malignant hyperthermia. Widespread rhabdomyolysis locations cannot be explained by precordial electric shocks. Propofol is the only drug used in this case that has been reported to induce rhabodomyolysis. CONCLUSIONS: Signs of propofol-induced rhabdomyolysis may be different from those of malignant hyperthermia. Even a regular induction dose of propofol for adults could possibly trigger rhabdomyolysis similar to what is observed in children diagnosed with propofol infusion syndrome. Though rare, care should still be taken when administering propofol.

Risk factors for hypothermia in patients under general anesthesia: Is there a drawback of laminar airflow operating rooms? A prospective cohort study.

INTRODUCTION: The aim of this study was to estimate the prevalence and risk factors of hypothermia under general anesthesia in a large domestic hospital. METHOD: All of the consecutive 1840 patients who underwent scheduled surgery between August and December 2013 were admitted to the study. The nasopharyngeal temperature was measured, and the following variables were also recorded: sex, age, type of surgery, duration of anesthesia, active warming devices and type of operating room. Univariate and multiple regression binary logistic analyses with odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to assess the relationship between each clinical risk factor and hypothermia. RESULTS: The prevalence of hypothermia under general anesthesia was 25.7%. In the univariate analysis, the risk factors of hypothermia were age, the duration of anesthesia, the type of operating room and the type of surgery. Sex was not included. In the multiple logistic regression analysis, the significant risk factors of hypothermia were advanced age, laminar airflow operating rooms and general surgeries. CONCLUSION: Intraoperative hypothermia is still common and should therefore receive serious attention. Advanced age, the use of a laminar airflow operating room and general surgeries are high risk factors of hypothermia.

Sevoflurane-induced down-regulation of hippocampal oxytocin and arginine vasopressin impairs juvenile social behavioral abilities.

Cumulative evidence indicates that early childhood anesthesia can alter a child's future behavioral performance. Animal researchers have found that sevoflurane, the most commonly used anesthetic for children, can produce damage in the neonatal brains of rodents. To further investigate this phenomenon, we focused on the influence of sevoflurane anesthesia on the development of juvenile social behavioral abilities and the pro-social proteins oxytocin (OT) and arginine vasopressin (AVP) in the neonatal hippocampus. A single 6-h sevoflurane exposure for postnatal day 5 mice resulted in decreased OT and AVP messenger RNA (mRNA) and protein levels in the hippocampus. OT and AVP proteins became sparsely distributed in the dorsal hippocampus after the exposure to sevoflurane. Compared with the air-treated group, mice in the sevoflurane-treated group showed signs of impairment in social recognition memory formation and social discrimination ability. Sevoflurane anesthesia reduces OT and AVP activities in the neonatal hippocampus and impairs social recognition memory formation and social discrimination ability in juvenile mice.