Objective To analyze the current state,research hotspots,and development trends of electroencephalography(EEG)applied in the field of autism spectrum disorder(ASD). Methods Relevant literature from the Web of Science core collection database from January,2014 to January,2024 were retrieved and analyzed using CiteSpace 6.2.R4. Results A total of 1 509 articles were included,with an increasing trend in publication volume over the years.The United States ranked highest in both publication volume and node centrality.The primary journals in this field were concentrated in clinical medicine,immunology and psychology.Keyword co-occurrence and clustering indicated that research primarily focused on the correlation between core symptoms of ASD and EEG indicators,differential diagnosis of ASD and its comorbidities,brain functional connectivity,and assessment of rehabilitation efficacy.Keywords bursted in the past three years mainly included artificial intelligence and machine learning. Conclusion The researches in EEG technology in the field of ASD is generally increasing.Future researches may focus on exploring the brain network mechanisms of ASD using EEG combined with multimodal neuroimaging,and machine learning technologies.

Restricted repetitive behaviors (RRBs) are the most characteristic behaviors of autism spectrum disorder. The clinical diagnosis and treatment of RRBs are extremely difficult resulting from its complex and variable etiology, highly heterogeneous clinical manifestations influenced by multiple factors (sleep quality, gastrointestinal health, age and gender), lack of precise diagnostic criteria and low effectiveness of current clinical interventions. This article mainly reviews the recent related studies on RRBs and discusses the challenges and progress in clinical diagnosis and treatment of RRBs so as to provide new ideas for future clinical diagnosis and treatment.

Objective: To investigate the effect of glycogen synthase kinase 3 β ( GSK-3 β) and its correlation with microtubule-associated protein 2 (MAP2) during cerebral hypoxia / reoxygenation (H / R) in zebrafish． Methods: The cerebral hypoxia / reoxygenation model of zebrafish was established．Healthy adult zebrafishes of the same size were divided into control group ( Control) ，hypoxia / reoxygenation group ( H / R) and hypoxia / reoxygenation + GSK-3 β inhibitor group (H / R + TDZD-8) for experiment．The brain tissues of zebrafish in each group were selected to determine the mRNA expressions of hypoxia inducible factor 1 αa and 1 αb (HiF-1αa and HIF-1 αb) at different reoxygenation time points by qRT-PCR , and the protein expression levels of HIF-1α , GSK-3 β , p-GSK-3 β (Ser 9) and MAP2 were detected by Western blot，TTC staining and TUNEL staining were used to detect cerebral infarction area and cell apoptosis ，and immunofluorescence was used to detect the distribution and expression of MAP2 in brain. Results: Compared with Control group，the mRNA levels of Hif-1αa and Hif-1 αb(P＜0. 01) and protein expression of Hif-1 α(P＜0. 01) increased in H / R group，the area of cerebral infarction (P ＜0. 01) and apoptotic cells(P ＜0. 01) increased，p-GSK-3 β ( Ser 9) / GSK-3 β ratio，MAP2 protein expression (P ＜0. 05) and immunofluorescence expression of MAP2 (P ＜0. 01 ) reduced ; Furthermore，TDZD-8 pretreatment could relieve the brain injury of H / R zebrafish by decreasing the infarct size and cell apoptosis，improving the ratio of p-GSK-3 β ( Ser 9 ) / GSK-3 β , and increasing the expression of MAP2． Conclusion Hypoxia / reoxygenation can cause brain neuron damage in zebrafish，and its mechanism may be related to inhibition of GSK-3 β phosphorylation and MAP2 expression．GSK-3 β specific inhibitor TDZD-8 can reverse the damage of brain neurons caused by hypoxia / reoxygenation by promoting the expression of P-GSK-3 β (Ser 9) and reducing MAP2 degradation.

Objective:To evaluate the relationship between methyltransferase-like 3(METTL3)-mediated RNA N6-Methyladenosine (m6A) methylation modification and silent information regulator factor 1 (SIRT1) during sevoflurane post-conditioning-induced mitigation of cognitive impairments in a mouse model of hemorrhagic shock and resuscitation(HSR).Methods:Forty clean-grade healthy male C57BL/6 mice, aged 8-10 weeks, with a body weight ranging from 22-26 g, were assigned into 5 groups ( n=8 each) using a random number table method: sham operation group, HSR group, sevoflurane post-conditioning + HSR group (SP+ HSR group), over-expression of METTL3 gene rAAV + sevoflurane post-conditioning + HSR group (METTL3+ SP+ HSR group), and over-expression of METTL3 gene rAAV negative control + sevoflurane post-conditioning + HSR group (NC+ SP+ HSR group). The HSR model was established by withdrawing 40% of the total blood volume from mice through the right carotid artery within 30 min, followed by reinfusion of the withdrawn blood over 30 min 1 h later. The SP+ HSR group underwent HSR modeling first and then inhaled sevoflurane (end-tidal concentration 2.4%) for 30 min starting from the time point immediately after blood transfusion. The Sham group and HSR group inhaled a mixture of 70% O 2 and 30% CO 2 for 30 min at the corresponding time points. In METTL3+ SP+ HSR group and NC+ SP+ HSR group, the corresponding virus 450 nl was injected into bilateral hippocampus at 4 weeks before establishing the model.Morris water maze and novel object recognition tests were conducted at 72 h after developing the model to assess the learning and memory abilities. After the end of behavioral tests, the expression of METTL3 and SIRT1 in hippocampal tissues was detected using Western blot, the expression of SIRT1 mRNA was measured using qRT-PCR, and the methylation of RNA m6A was detected using Dot blot. Results:Compared to Sham group, the escape latency was significantly prolonged at 1-6 days, the time spent in the target quadrant was shortened, the number of crossing the original platform was decreased, the novel object recognition index was decreased, the expression of METTL3 was up-regulated, the expression of SIRT1 protein and mRNA was down-regulated, and the methylation of RNA m6A was increased in HSR group( P<0.05). Compared to HSR group, the escape latency was significantly shortened at 1-6 days, the time spent in the target quadrant was prolonged, the number of crossing the original platform was increased, the novel object recognition index was increased, the expression of METTL3 was up-regulated, the expression of SIRT1 protein and mRNA was down-regulated, and the methylation of RNA m6A was increased, the novel object recognition index was increased, the expression of METTL3 was down-regulated, the expression of SIRT1 protein and mRNA was up-regulated, and the methylation of RNA m6A was decreased in SP+ HSR group( P<0.05). Compared to SP+ HSR group, the escape latency was significantly prolonged at 2-6 days, the time spent in the target quadrant was shortened, the number of crossing the original platform was decreased, the novel object recognition index was decreased, the expression of METTL3 was up-regulated, the expression of SIRT1 protein and mRNA was down-regulated, and the methylation of RNA m6A was increased in METTL3+ SP+ HSR group( P<0.05), and no significant change was found in the aforementioned indicators in NC+ SP+ HSR group ( P>0.05). Conclusions:The mechanism by which sevoflurane post-conditioning alleviates cognitive dysfunction is associated with down-regulation of METTL3 expression, reduction of RNA m6A methylation, and up-regulation of SIRT1 expression in HSR mice.

Objective:To evaluate the role of silent information regulator-1 (SIRT1)/nucleotide-binding domain (NOD)-like receptor protein-3 (NLRP3) signaling pathway in sevoflurane postconditioning-induced attenuation of oxygen-glucose deprivation and restoration (OGD/R) injury in mouse hippocampal neuronal cell line (HT22) cells.Methods:The HT22 cells were seeded in a culture plate (96-well plate, 100 μl/well; 6-well plate, 2 ml/well) at the density of 5×10 4 cells/ml or in a culture dish (6 cm in diameter) and then divided into 4 groups ( n=24 each) using a random number table method: control group (Control group), OGD/R group, sevoflurane postconditioning group (SPC group), and SIRT1 small interfering RNA group (si-SIRT 1 group). In Control group, cells were cultured at 37 ℃ in normal culture atmosphere. In OGD/R group, the culture medium was replaced with glucose-free serum-free culture medium, and cells were exposed to 95% N 2+ 5% CO 2 for 4 h in an incubator at 37 ℃, and then the glucose-free serum-free culture medium was replaced with the primary culture medium, and cells were cultured for 24 h at 37 ℃ in normal culture atmosphere. In SPC group, the glucose-free serum-free culture medium was replaced with the primary cell culture medium after 4-h oxygen and glucose deprivation, the cells were put into the hypoxia incubator chamber which was filled with 2% sevoflurane immediately after start of reoxygenation, then the chamber was placed in an incubator and the cells were cultured for 1 h at 37 ℃ in normal culture atmosphere, and finally the cells were removed from the chamber and cultured for 23 h at 37 ℃ in normal culture atmosphere. In si-SIRT1 group, SIRT1 small interfering RNA 150 pmol was added at 24 h before surgery, cells were then incubated, and the other procedures were the same as those previously described in group SPC. The cell survival rate was determined using MTT assay. TUNEL assay was used to detect cell apoptosis, and the apoptosis rate was calculated. The expression of SIRT1, NLRP3, IL-1β and IL-18 mRNA was determined using polymerase chain reaction. The expression of SIRT1, NLRP3, interleukin-1beta (IL-1β) and IL-18 was detected using Western blot. Results:Compared with Control group, the cell survival rate was significantly decreased, the apoptosis rate was increased, the expression of SIRT1 protein and mRNA was down-regulated, and the expression of NLRP3, IL-1β and IL-18 protein and mRNA was up-regulated in OGD/R group ( P<0.05). Compared with OGD/R group, the cell survival rate was significantly increased, the apoptosis rate was decreased, the expression of SIRT1 protein and mRNA was up-regulated, and the expression of NLRP3, IL-1β and IL-18 protein and mRNA was down-regulated in SPC group ( P<0.05). Compared with SPC group, the cell survival rate was significantly decreased, the apoptosis rate was increased, the expression of SIRT1 protein and mRNA was down-regulated, and the expression of NLRP3, IL-1β and IL-18 protein and mRNA was up-regulated in si-SIRT1 group ( P<0.05). Conclusions:Activation of SIRT1-NLRP3 signaling pathway is involved in sevoflurane postconditioning-induced attenuation of OGD/R injury in HT22 cells.

Objective: To explore the effect of sevoflurane post-conditioning on oxygen-glucose deprivation/reoxygenation(OGD/R) damage of primary hippocampal neurons, oxidative stress and autophagy. Methods: Hippocampal neurons were cultured in uterine endometrial rats for(18±0.5) days. After 7 days, the cultured hippocampal neurons were randomly divided into three groups: normal control group(CON group), oxygen-glucose deprivation/reoxygenation(OGD/R) group and sevoflurane post-conditioning group(OGD/R+SEVO group). Primary hippocampal neurons in the CON group were cultured normally; OGD/R group was treated with oxygen-glucose deprivation for 1.5 hours and reoxygenation for 24 hours to establish oxygen and glucose deprivation/reoxygenation injury model; OGD/R+SEVO group was treated with sevoflurane for 1 hour and then reoxygenated for 23 hours. After treatments, the activity of each group of LDH was detected by colorimetric method, TUNEL staining method detected the changes of hippocampal nerve cells in each group, immunofluorescence method detected mitochondrial ROS and the expression of autophagy proteins LC3 B,and Western blot analysis detected the expression of PINK1 and Parkin. Results: Compared with CON group, the release of lactate dehydrogenase increased(P<0.01); neuronal apoptosis increased; mitochondrial ROS and the expression of autophagy marker proteins LC3 B increased(P<0.01), PINK1 and Parkin also increased in OGD/R group(P<0.001,P<0.05). Compared with OGD/R group, the release of lactate dehydrogenase was reduced(P<0.05), the apoptosis was inhibited, mitochondrial ROS and the expression of autophagy marker proteins LC3 B were reduced(P<0.05), PINK1 and Parkin protein were reduced(P<0.01,P<0.05) in OGD/R+SEVO group. Conclusion Sevoflurane post-conditioning can protect primary hippocampal neurons by reducing OGD/R-induced excessive autophagy, reducing oxidative stress, and reducing apoptosis, and its mechanism of reducing autophagy may be related to the PINK1/Parkin pathway.

Abstract: To investigate the role and mechanism of mitochondrial permeability transition pore(MPTP) in the damage of hippocampal neurons in SD rats induced by exposure for 6 hours to sevoflurane. Methods: The hippocampal neurons of primary cultured SD rats and fetal rats were randomly divided into control group(Con group), cyclosporin A group(CsA group, 0.1,0.5,1 μmol/L), 3% sevoflurane exposure for 6 h Group(Sevo group), cyclosporin A pretreatment+3% sevoflurane 6 h group(Sevo+CsA group, 0.1, 0.5, 1 μmol/L). CCK-8 kit was used to detect cell activity, TUNEL staining was used to detect neuron apoptosis, JC-1 kit was used to detect mitochondrial membrane potential, Calcein AM was used to detect MPTP opening degree, and Western blot was used to detect proteins expression of brain-derived neurotrophic factor(BDNF), postsynaptic compact protein(PSD-95), Snaptophysin, Snapsin-1, and Cyclophilin D(CypD). Results: Compared with Con group, the cell viability of Sevo group was significantly reduced(P<0.05), the apoptosis rate of neurons increased(P<0.01),the expression of synapse proteins decreased(P<0.05), the mitochondrial membrane potential decreased(P<0.01), the opening degree of MPTP increased(P<0.01), and the expression of CypD protein increased(P<0.01). Cyclosporin A, a specific inhibitor of MPTP opening, could reduce hippocampal neuron apoptosis and synaptic damage caused by sevoflurane exposure, maintain mitochondrial membrane potential, and inhibit MPTP opening and CypD protein expression. Conclusion Prolonged exposure to sevoflurane can cause damage to hippocampal neurons in SD rats. The mechanism is related to the promotion of CypD-mediated MPTP opening.

Objective    Though investigating the causes of untreated congenital heart disease among children aged 3–14 years in Panzhihua city, to provide the basis for formulating intervention measures in the next step. Methods    A survey was conducted on the children aged 3 to 14 years in Panzhihua city from March 2015 to December 2017. The causes of untreated congenital heart disease were analyzed. Results     Of 148 children with untreated congenital heart diseases, 82 were found to have congenital heart disease or heart murmur before screening. Among them, 59 parents (71.95%) thought that hospitalization was expensive; 42 parents (53.84%) thought that their children were asymptomatic and did not need treatment. Doctors suggested that 13 children (15.85%) be observed. Sixty-six patients of congenital heart disease were found for the first time in this screening, with an average age of 7.11±1.23 years. The patients in the rural population (n=44, 81.82%) were significantly more than the patients in the urban (n=12, 18.18%, P<0.01). Atrial septal defect ranked the first among the diseases, and 45 (68.18%) children did not regularly participate in child health care after birth. Conclusion    Most families with untreated congenital heart disease in Panzhihua city think that the cost of treatment is high and there is no need for treatment. And most of them do not participate in child health care regularly. Atrial septal defect ranks first among the diseases. Free screening and treatment of congenital heart disease is of great significance in Panzhihua city.

Objective To evaluate the treatment effect of combination of dexmedetomidine and droperidol on emergence agitation during general anesthesia recovery period in the elderly undergoing thoracotomy. Methods Sixty patients with severe emergence agitation during general anesthesia recovery period undergoing thoracotomy for esophageal cancer or pulmonary lobectomy, aged 66-75 years, falling into ASA physical status Ⅱ or Ⅲ, were divided into three groups, 20 patients in each according to table of random number: group droperidol (group F) and group dexmedetomidine (group D) and group dexmedetomidine combining droperidol (group DF). In group F, 0.06 mg/kg droperidol was administrated via central vein. In group D, 1 μg/kg dexmedetomidine was pumped via central vein in 10 min, followed by continuous infusion of dexmedetomidine in 0.2 μg·kg-1·h-1 for 1 h. While in group DF, 0.03 mg/kg droperidol was administrated via central vein and 0.5 μg/kg dexmedetomidine was pumped via central vein in 10 min, then followed by continuous infusion of dexmedetomidine in 0.2 μg·kg-1·h-1 for 1 h. The agitation scores and the Ramsay scores were collected after the beginning of anti-agitation. Arterial blood partial pressure of carbon dioxide was tested. Postoperative complications including nausea and vomiting were recorded. Results Compared with group D, the agitation scores at 5, 10, 15 and 20 min in group DF were lower (P ＜ 0.05). Comparing with group F, the agitation scores at 60, 90 and 120 min in group DF were lower (P ＜ 0.05). The incidence of over-sedation in group DF and in group D was less than that in group F (P ＜ 0.05). PaCO2 was unaltered in all the groups after treatment. The incidence of nausea, vomiting, bradycardia, hypertension, hypotension and respiration depression and long QT interval between the groups were comparable. Conclusion Combination of dexmedetomidine and droperidol is effective and safe in the treatment of agitation during sevoflurane general anesthesia recovery period in the elderly undergoing thoracotomy.

Objective To evalute the role of phosphatidylinositol 3?kinase(PI3K)∕serine?threo?nine kinase(Akt)∕endothelial nitric oxide synthase(eNOS)signaling pathway in sevoflurane postcondi?tioning?induced attenuation of brain injury in a rat model of hemorrhagic shock and resuscitation(HSR). Methods Seventy?two pathogen?free healthy adult male Sprague?Dawleg rats, weighing 300-350 g, were divided into 4 groups(n=18 each)using a random number table: sham operation group(group S), group HSR, sevoflurane postconditioning group(group SP)and sevoflurane postconditioning plus PI3K∕Akt signaling pathway specific inhibitor wortmannin group(group SP+WT). Hemorrhagic shock was in?duced by withdrawing blood(40% of the total blood volume)from the right common carotid artery over an interval of 30 min, and 1 h later the animals were resuscitated with infusion of the shed blood via the left jugular vein over 30 min. In group SP+WT, wortmannin 0.6 mg∕kg was administrated via the jugular vein at 30 min before establishment of the model. In SP and SP+WT groups, 2.4% sevoflurane was inhaled for 30 min starting from the onset of infusion of the shed blood. At 10 min before withdrawing blood(T0), im?mediately after the end of withdrawing blood(T1), at 30 min and 1 h after the end of withdrawing blood (T2,3)and immediately after infusion of the shed blood(T4), blood samples from the common carotid ar?tery were collected for blood gas analysis, the blood lactate concentration was recorded, and mean arterial pressure was simultaneously recorded. At 24 h after infusion of the shed blood, 6 rats were randomly select?ed from each group and sacrificed, and their brains were immediately removed for determination of cerebral infarct volume(by TTC staining), expression of hippocampal caspase?3(by immuno?histochemistry), and expression of Akt, phosphorylated Akt(p?Akt)and eNOS(by Western blot). The ratio of p?Akt∕Akt was calculated. Results Compared with group S, the mean arterial pressure was significantly decreased and the blood lactate concentration was increased at T1?3, the cerebral infarct volume was increased, and the expression of caspase?3 was up?regulated in the other three groups, and the ratio of p?Akt∕Akt was sig?nificantly increased, and eNOS expression was up?regulated in group SP(P<0.05). Compared with group HSR, the cerebral infarct volume was significantly decreased, the expression of caspase?3 was down?regula?ted, the ratio of p?Akt∕Akt was increased, and eNOS expression was up?regulated in group SP(P<0.05). Compared with group SP, the cerebral infarct volume was significantly increased, the expression of caspase?3 was up?regulated, the ratio of p?Akt∕Akt was decreased, and eNOS expression was down?regula?ted in group SP+WT(P<0.05). Conclusion PI3K∕Akt∕eNOS signaling pathway activation mediates sevoflurane postconditioning?induced attenuation of brain injury in a rat model of HSR.