ObjectiveTo explore the role of neuroimaging features monitored by functional near-infrared spectroscopy （fNIRS） in postoperative delirium （POD） in elderly patients undergoing joint replacement during perioperative period， and to provide a basis for early clinical prediction. MethodsA total of 105 elderly patients who underwent joint replacement under general anesthesia were included. The Mini-Mental State Examination （MMSE） scale was used to evaluate the patient's cognition one day before the operation. Before the start of the surgery， fNIRS was used to monitor the changes of cerebral blood oxygen saturation when the patient performed the task state. The 3-minute delirium diagnostic scale （3D-CAM scale） was used to evaluate the occurrence of POD at 24， 48 and 72 h after operation. Brain network analysis was performed and Logistic regression analysis was used to explore the relationship between fNIRS monitoring data and POD in elderly patients undergoing joint replacement surgery during preoperative task state. The receiver operating characteristic curve （ROC curve） was constructed to evaluate the diagnostic efficacy， and the Hosmer-Lemeshow goodness-of-fit test was used to test the goodness of fit of the model. ResultsAmong 105 patients， 100 cases were effectively analyzed， of which 20 cases （20%） had POD. Brain network analysis showed that the r value of functional connectivity correlation coefficient in POD group （0.069±0.118） was lower than that in non-POD group （0.073±0.084）. The low channel connectivity of right primary somatosensory cortex-right primary motor cortex （RS1-RM1） and left anterior pole-right Broca's triangle （LFP-RBA44） was an important factor affecting the occurrence of POD （P < 0.05）. Based on this result， the area under the ROC curve was 0.797 and 0.784， respectively. The results of Hosmer-Lemeshow goodness-of-fit test showed that the model fitted well （all P>0.5）. ConclusionThe neuroimaging features extracted from the cerebral oxygen saturation data monitored by fNIRS are significantly correlated with the risk of POD in elderly patients undergoing joint replacement during perioperative period. Among them， the low connectivity of preoperative RS1-RM1 and LFP-RBA44 brain network channels is an important influencing factor of POD occurrence. Predicting the occurrence of POD based on fNIRS is conducive to the early intervention and risk reduction of perioperative complications， improving medical quality and promoting precision medical practice.

Objective To evaluate the application of different anesthetic drugs—remimazolam(RM)and propofol(PPF)—in anesthesia for pediatric adenoidectomy and tonsillectomy and its effect on emergence agitation.Methods A total of 120 children undergoing elective adenoidectomy and tonsillectomy under general anesthesia in Xinhua Hospital,Huainan Xinhua Medical Group between December 2022 and August 2024 were enrolled.With a random number table,they were assigned to a PPF group receiving PPF and remifentanil and a RM group receiving RM and remifentanil,with 60 cases in each group.The primary and secondary outcome indicators of the two groups were compared.The primary outcome indicator was the incidence of emergence agitation.Secondary outcome indicators included anesthesia-related parameters,changes in mean arterial pressure(MAP)and heart rate(HR)at different time points during surgery,changes in pediatric anesthesia emergence delirium(PAED)scores at different time points after recovery,changes in Ramsay sedation scores and Face,Legs,Activity,Cry,Consolability(FLACC)pain scores at 2,4,12,and 24 hours after surgery,incidence of negative postoperative behavioral changes(NPOBCs)at 7 and 14 days,and adverse events during anesthesia.Results The incidence rate of emergence agitation was lower in the RM group than that of the PPF group(5.00%vs.18.33%,P<0.05).The RM group also demonstrated significantly shorter anesthesia time,extubation time,wake-up time,and postanesthesia care unit(PACU)than those in the PPF group(P<0.05).HR and MAP in the RM group were higher than those in the PPF group at 3 min after induction,at the time of tracheal intubation,during tonsillectomy,and at the end of surgery,with the difference being statistically significant(P<0.05).The PAED scores at different time points after recovery,Ramsay sedation scores and FLACC scores at 2,4 and 12 hours after surgery,the incidence of NPOBCs at 7 days after surgery,and the incidence of adverse reactions during anesthesia were lower in the RM group than those in the PPF group,with the difference being statistically significant(P<0.05).Conclusion RM improves the anesthesia effect and recovery quality of children undergoing adenoidectomy and tonsillectomy,relieves the severity of emergence agitation,reduces the incidence of agitation,and demonstrates good safety.

Objective: To investigate the effect of sirtuin 2(SIRT2) on the proliferation and migration of cardiac fibroblasts(CFs)in C57BL/6 mice under angiotensin II(Ang Ⅱ) stimulation. Methods : The hearts were taken from 1 to 2 days C57BL/6 milk mice. After cutting and digesting, CFs were extracted by different adhesion centrifugation. After CFs attachment, the cells were cultured under control medium and Ang Ⅱ(100 nmol/L) medium and treated using OE-SIRT2 plasmid to overexpression the SIRT2 gene. RT-qPCR was used to detect mRNA expression of SIRT2 proliferating cell nuclear antigen(PCNA), periostin(POSTN)and type Ⅰ collagen procollagen A1(Col1A1), Western blot assay was used to measure the protein expression levels of SIRT2, PCNA, POSTN and Col1A1, CCK-8 assay and EdU assay were used to evaluate CFs proliferation rate, Transwell experiment was used to assess CFs migration activity. Results: Compared with control group, Ang Ⅱ stimulation led to down-regulation of SIRT2 expression in CFs, increased collagen expression, and promoted CFs proliferation and migration. The expression of SIRT2 was up regulated in CFs treated with OE-SIRT2 plasmid under Ang Ⅱ stimulation, Col1A1, POSTN and PCNA expression was down regulated, and CFs proliferation and migration ability decreased. Conclusion Overexpression of SIRT2 can inhibit the proliferation and migration of CFs under Ang Ⅱ stimulation, indicating that SIRT2 may be a key regulatory point in the onset and progression of cardiac fibrosis.

Objective:To evaluate the role of microglial hypoxia-inducible factor-3α (HIF-3α) in cognitive impairment after hemorrhagic shock and resuscitation(HSR) and the relationship with neuronal ferroptosis in mice.Methods:Twenty-four specific pathogen-free healthy male C57BL/6 mice, aged 10 weeks, weighing 25-30 g, were divided into 3 groups ( n=8 each) using a random number table method: sham operation group (Sham group), HSR group, and HSR+ ferroptosis inhibitor (ferrostatin-1) group (HSR+ Fer-1 group). Sixteen C57BL/6 mice and 16 HIF-3α flox/flox: Cx3crl Cre (HIF-3α CKO) mice were selected and assigned to 2 groups ( n=8 each) using a random number table method: sham operation group (WT-Sham group, HIF-3α CKO-Sham group) and HSR group (WT-HSR group, HIF-3α CKO-HSR group). To establish the HSR model, 40% of the total blood volume was withdrawn at a steady rate via the right carotid artery within 30 min and 1 h later reinfused through the jugular vein over a period of 30 min. Ferrostatin-1 10 mg/kg was nasally administered once mice recovered after HSR in HSR+ Fer-1 group. The cognitive function was evaluated by the novel object recognition test at 72 h after developing the model. The hippocampal tissues were collected under deep anesthesia after evaluation for determination of the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1) in the ipsilateral hippocampi (by Western blot) and expression of microglial HIF-3α and GPX4 and FTH1 in neurons in the hippocampal CA3 region (by immunofluorescence staining) and for examination of the ultrastructure of mitochondria in hippocampal neurons (with a transmission electron microscope). Results:Compared to Sham group, the cognitive and discrimination indexes were significantly decreased, and the expression of GPX4 and FTH1 was down-regulated in HSR group ( P<0.05). Compared to HSR group, the cognitive and discrimination indexes were significantly increased, and the expression of GPX4 and FTH1 in the hippocampi was up-regulated in HSR+ Fer-1 group ( P<0.05). Compared to WT-Sham group, the cognitive and discrimination indexes were significantly decreased, and the expression of microglial HIF-3α in the hippocampal CA3 region was up-regulated, and the expression of neuronal GPX4 and FTH1 was down-regulated in WT-HSR group ( P<0.05), and no statistically significant change was found in the aforementioned parameters in HIF-3α CKO-Sham group ( P>0.05). Compared to WT-HSR group, the cognitive and discrimination indexes were significantly increased, and the expression of microglial HIF-3α in the hippocampal CA3 region was down-regulated, the expression of GPX4 and FTH1 was up-regulated ( P<0.05), and mitochondrial damage in the neurons was significantly attenuated in HIF-3α CKO-HSR group. Conclusions:Microglial HIF-3α-mediated ferroptosis in hippocampal neurons is involved in cognitive impairment following HSR in mice.

Autism spectrum disorder(ASD) is a neurodevelopmental disorder, and social impairment was one of the core symptoms of ASD, which can seriously affects the social life of patients.The pathogenesis of social impairment in ASD is unclear and it may involves many brain abnormalities.The related theories and hypotheses are numerous and there is no unified conclusion. Studies have shown that the cerebellum has extensive connections with brain networks and is involved in the regulation of social cognition, but its role in ASD has not been fully emphasized.The structural and functional abnormalities of the cerebellar-cortex (CC) loop in ASD patients can lead to language communication disorders, empathy disorders, difficulties in interpreting social cues, abnormal social reward processing and emotional regulation disorders, which are closely related to ASD social impairment. Noninvasive brain stimulation of the superficial cerebellum can improve the abnormal CC circuit in ASD patients, and the cerebellum can be considered as a target for the treatment of social disorders in ASD in the future.Based on the clinical and basic researches on social impairment in ASD in recent years, this article reviews the relevant manifestations of disorders which cerebellar and CC circuit involved, aiming to promote the development of related research in the future.

As the incidence of autism rises annually,its unknown pathogenesis makes it challenging to treat the varied repetitive and stereotyped behaviors that characterize its core symptoms.The striatum is an important brain region for the control of locomotor behaviors,featuring a unique mosaic structure,complex neural origin,and finely regulated developmental process that is highly susceptible to genetic and environmental influences.Both clinical and basic studies have indicated that abnormal development of the striatal nuclei may contribute to the pathogenesis of these repetitive stereotyped behaviors in autism.Clinical imaging data have primarily identified gross anatomical variations in the stratum(e.g.,its general outline),but lack the resolution necessary to detect the cellular and subcellular alterations within the region.By introducing the abnormalities in the spatiotemporal development of the striatum and their links to the characteristic behaviors of autism,this review aims to advance our understanding of the role of the striatum in autism pathogenesis and to inform future animal studies and clinical research.

Autism spectrum disorder(ASD) is a neurodevelopmental disorder, and social impairment was one of the core symptoms of ASD, which can seriously affects the social life of patients.The pathogenesis of social impairment in ASD is unclear and it may involves many brain abnormalities.The related theories and hypotheses are numerous and there is no unified conclusion. Studies have shown that the cerebellum has extensive connections with brain networks and is involved in the regulation of social cognition, but its role in ASD has not been fully emphasized.The structural and functional abnormalities of the cerebellar-cortex (CC) loop in ASD patients can lead to language communication disorders, empathy disorders, difficulties in interpreting social cues, abnormal social reward processing and emotional regulation disorders, which are closely related to ASD social impairment. Noninvasive brain stimulation of the superficial cerebellum can improve the abnormal CC circuit in ASD patients, and the cerebellum can be considered as a target for the treatment of social disorders in ASD in the future.Based on the clinical and basic researches on social impairment in ASD in recent years, this article reviews the relevant manifestations of disorders which cerebellar and CC circuit involved, aiming to promote the development of related research in the future.

Objective:To evaluate the role of microglial hypoxia-inducible factor-3α (HIF-3α) in cognitive impairment after hemorrhagic shock and resuscitation(HSR) and the relationship with neuronal ferroptosis in mice.Methods:Twenty-four specific pathogen-free healthy male C57BL/6 mice, aged 10 weeks, weighing 25-30 g, were divided into 3 groups ( n=8 each) using a random number table method: sham operation group (Sham group), HSR group, and HSR+ ferroptosis inhibitor (ferrostatin-1) group (HSR+ Fer-1 group). Sixteen C57BL/6 mice and 16 HIF-3α flox/flox: Cx3crl Cre (HIF-3α CKO) mice were selected and assigned to 2 groups ( n=8 each) using a random number table method: sham operation group (WT-Sham group, HIF-3α CKO-Sham group) and HSR group (WT-HSR group, HIF-3α CKO-HSR group). To establish the HSR model, 40% of the total blood volume was withdrawn at a steady rate via the right carotid artery within 30 min and 1 h later reinfused through the jugular vein over a period of 30 min. Ferrostatin-1 10 mg/kg was nasally administered once mice recovered after HSR in HSR+ Fer-1 group. The cognitive function was evaluated by the novel object recognition test at 72 h after developing the model. The hippocampal tissues were collected under deep anesthesia after evaluation for determination of the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1) in the ipsilateral hippocampi (by Western blot) and expression of microglial HIF-3α and GPX4 and FTH1 in neurons in the hippocampal CA3 region (by immunofluorescence staining) and for examination of the ultrastructure of mitochondria in hippocampal neurons (with a transmission electron microscope). Results:Compared to Sham group, the cognitive and discrimination indexes were significantly decreased, and the expression of GPX4 and FTH1 was down-regulated in HSR group ( P<0.05). Compared to HSR group, the cognitive and discrimination indexes were significantly increased, and the expression of GPX4 and FTH1 in the hippocampi was up-regulated in HSR+ Fer-1 group ( P<0.05). Compared to WT-Sham group, the cognitive and discrimination indexes were significantly decreased, and the expression of microglial HIF-3α in the hippocampal CA3 region was up-regulated, and the expression of neuronal GPX4 and FTH1 was down-regulated in WT-HSR group ( P<0.05), and no statistically significant change was found in the aforementioned parameters in HIF-3α CKO-Sham group ( P>0.05). Compared to WT-HSR group, the cognitive and discrimination indexes were significantly increased, and the expression of microglial HIF-3α in the hippocampal CA3 region was down-regulated, the expression of GPX4 and FTH1 was up-regulated ( P<0.05), and mitochondrial damage in the neurons was significantly attenuated in HIF-3α CKO-HSR group. Conclusions:Microglial HIF-3α-mediated ferroptosis in hippocampal neurons is involved in cognitive impairment following HSR in mice.

As the incidence of autism rises annually,its unknown pathogenesis makes it challenging to treat the varied repetitive and stereotyped behaviors that characterize its core symptoms.The striatum is an important brain region for the control of locomotor behaviors,featuring a unique mosaic structure,complex neural origin,and finely regulated developmental process that is highly susceptible to genetic and environmental influences.Both clinical and basic studies have indicated that abnormal development of the striatal nuclei may contribute to the pathogenesis of these repetitive stereotyped behaviors in autism.Clinical imaging data have primarily identified gross anatomical variations in the stratum(e.g.,its general outline),but lack the resolution necessary to detect the cellular and subcellular alterations within the region.By introducing the abnormalities in the spatiotemporal development of the striatum and their links to the characteristic behaviors of autism,this review aims to advance our understanding of the role of the striatum in autism pathogenesis and to inform future animal studies and clinical research.

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.