ObjectiveTo explore the efficacy and mechanisms of Sini San in the treatment of depression and liver injury based on gut microbiota. MethodsThirty-two male Sprague-Dawley （SD） rats were randomly divided into a normal group， model group （M）， Sini San group （MS， 2.5 g·kg^-1）， and fluoxetine group （MF， 2 mg·kg^-1）. Except for the normal group， rats in the other three groups were subjected to chronic unpredictable mild stress （CUMS）. After 8 weeks， the open-field test and sucrose preference test were conducted. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum corticosterone （CORT）， adrenocorticotropic hormone （ACTH）， corticotropin-releasing factor （CRF）， lipopolysaccharide （LPS）， Zonulin， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， γ-aminobutyric acid （GABA） levels in the hippocampus and prefrontal cortex， and brain-derived neurotrophic factor （BDNF） levels in the hippocampus. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect hippocampal BDNF mRNA expression. Serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） levels were measured using the ultraviolet lactate dehydrogenase method. The ultrastructure of the intestinal epithelium was observed by electron microscopy， and gut microbiota in rat feces were analyzed using 16S rDNA high-throughput sequencing. ResultsCompared with the normal group， the sucrose preference of rats in the model group was significantly reduced （P0.01）， whereas it was significantly increased in the Sini San group compared with the model group （P0.05）. Compared with the normal group， hippocampal GABA protein levels and BDNF mRNA expression in the model group were significantly decreased （P0.05）， and compared with the model group， both were significantly increased in the Sini San group （P0.05， P0.01）. Compared with the normal group， serum LPS and Zonulin levels in the model group were significantly increased （P0.05， P0.01）， and compared with the model group， Zonulin levels in the Sini San group were significantly decreased （P0.05）. No obvious changes were observed in the ultrastructure of the jejunal mucosa among groups. Compared with the normal group， widened and blurred tight junctions， sparse and shortened microvilli， and mitochondrial swelling with cristae disruption in epithelial cells were observed in the ileal and colonic mucosa of the model group， which were markedly improved in the Sini San and fluoxetine groups. The results of 16S rDNA high-throughput sequencing showed that Sini San improved CUMS-induced dysbiosis of Bacteroidetes and Proteobacteria. Correlation analysis indicated that Bacteroidetes and Proteobacteria were significantly correlated with depression-related indicators， liver function， and intestinal mucosal permeability. ConclusionSini San exerts antidepressant and hepatoprotective effects by improving Bacteroidetes and Proteobacteria and inhibiting the increase in intestinal mucosal permeability in CUMS rats.

ObjectiveTo explore the efficacy and mechanisms of Sini San in the treatment of depression and liver injury based on gut microbiota. MethodsThirty-two male Sprague-Dawley （SD） rats were randomly divided into a normal group， model group （M）， Sini San group （MS， 2.5 g·kg^-1）， and fluoxetine group （MF， 2 mg·kg^-1）. Except for the normal group， rats in the other three groups were subjected to chronic unpredictable mild stress （CUMS）. After 8 weeks， the open-field test and sucrose preference test were conducted. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum corticosterone （CORT）， adrenocorticotropic hormone （ACTH）， corticotropin-releasing factor （CRF）， lipopolysaccharide （LPS）， Zonulin， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， γ-aminobutyric acid （GABA） levels in the hippocampus and prefrontal cortex， and brain-derived neurotrophic factor （BDNF） levels in the hippocampus. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect hippocampal BDNF mRNA expression. Serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） levels were measured using the ultraviolet lactate dehydrogenase method. The ultrastructure of the intestinal epithelium was observed by electron microscopy， and gut microbiota in rat feces were analyzed using 16S rDNA high-throughput sequencing. ResultsCompared with the normal group， the sucrose preference of rats in the model group was significantly reduced （P<0.01）， whereas it was significantly increased in the Sini San group compared with the model group （P<0.05）. Compared with the normal group， hippocampal GABA protein levels and BDNF mRNA expression in the model group were significantly decreased （P<0.05）， and compared with the model group， both were significantly increased in the Sini San group （P<0.05， P<0.01）. Compared with the normal group， serum LPS and Zonulin levels in the model group were significantly increased （P<0.05， P<0.01）， and compared with the model group， Zonulin levels in the Sini San group were significantly decreased （P<0.05）. No obvious changes were observed in the ultrastructure of the jejunal mucosa among groups. Compared with the normal group， widened and blurred tight junctions， sparse and shortened microvilli， and mitochondrial swelling with cristae disruption in epithelial cells were observed in the ileal and colonic mucosa of the model group， which were markedly improved in the Sini San and fluoxetine groups. The results of 16S rDNA high-throughput sequencing showed that Sini San improved CUMS-induced dysbiosis of Bacteroidetes and Proteobacteria. Correlation analysis indicated that Bacteroidetes and Proteobacteria were significantly correlated with depression-related indicators， liver function， and intestinal mucosal permeability. ConclusionSini San exerts antidepressant and hepatoprotective effects by improving Bacteroidetes and Proteobacteria and inhibiting the increase in intestinal mucosal permeability in CUMS rats.

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 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.

Objective:Cardiac arrest (CA) represents a significant public health challenge, posing a substantial threat to individual health and survival. To enhance the survival rates of patients experiencing out-of-hospital cardiac arrest (OHCA), Baoan District in Shenzhen City has undertaken exploratory initiatives and practical interventions, yielding promising preliminary outcomes.Methods:1.Innovate emergency medical services by developing a "four-circle integration" system that connects to the hospital. This system encompasses the social emergency medical system, the out-of-hospital emergency medical system, the in-hospital emergency medical service system, and the intensive care treatment system. 2.Develop a comprehensive model for the construction of a social emergency medical training system, characterized by party leadership, government oversight, departmental coordination, professional guidance, technological support, and community involvement, termed the "Baonan Model." Additionally, establish evaluation criteria to assess the effectiveness of the social emergency medical training system in Baonan District; 3. Develop a cardiac arrest registration system and a social emergency medical training management system for Baonan District; 4. Enhance the proficiency in treatment techniques and the quality of cardiopulmonary resuscitation among emergency medical professionals; 5. Strengthen and advance the development of a "five-minute social rescue network" to address the critical "emergency window period." .Result:In Baonan District, 9.18% of the public is trained in emergency medical skills. The bystander CPR rate for OHCA is 26.11%, AED use is at 4.78%, the 30-day survival rate is 6.31%, and the discharge survival rate is 4.44%.Conclusion:The implementation of the aforementioned measures can substantially enhance the survival rate of patients experiencing OHCA at the time of discharge.

Objective:To investigate the characteristics of infectious pathogens in patients with refractory prostatitis,and to detect serum levels of factors related to immune inflammatory response such as macrophage inflammatory protein 1α(MIP-1α),IL-8 and cyclooxygenase-2(COX-2).Methods:A total of 87 patients with refractory chronic prostatitis who were diagnosed and treated in the Outpatient Department of Zhengzhou Ninth People's Hospital and Andrology Outpatient Department of Zhengzhou Central Hospital from October 2018 to June 2020 were selected as observation group,and 87 healthy subjects were selected as control group.Analyzed characteristics of infectious pathogens in patients with refractory prostatitis,compared serum MIP-1α,IL-8,COX-2 levels and the dif-ferent efficacy of the two groups,clinical data of the two groups of patients,serum MIP-1α,IL-8,COX-2 levels before and after treat-ment,and to analyze the correlation of the difference of serum MIP-1α,IL-8,COX-2 and the duration of the disease,the National Institutes of Health-Chronic Prostatitis Symptom Index(NIH-CPSI),maximum urinary flow rate and the relationship between serum MIP-1α,IL-8,COX-2 diffe-rence and the efficacy of patients with refractory prostatitis,and to evaluate the assessment value of serum MIP-1α,IL-8,COX-2 difference on the efficacy of patients with refractory prostatitis.Results:Bacterial infection was present in 87 specimens of prostatic fluid from patients with refractory prostatitis,and 9 patients had concomitant mycoplasma infection.From the prostatic fluid samples of 87 patients with refractory prostatitis,a total of 338 pathogenic bacteria were isolated,including 230 gram-positive bacteria,accounting for 68.05%;108 gram-negative bacteria,accounting for 31.95%;serum MIP-1α,IL-8,COX-2 levels in observation group were higher than that in control group,the difference was statistically significant(P<0.05);the course of disease,NIH-CPSI score,maximum urinary flow rate,levels of MIP-1α,IL-8,COX-2 after treatment,and the difference of MIP-1α,IL-8,COX-2 before and after treatment were compared in patients with different curative effects,and the difference was statistically signifi-cant(P<0.05);the difference between serum MIP-1α,IL-8 and COX-2 in patients with refractory prostatitis before and after treat-ment was positively correlated with disease course and NIH-CPSI score,while negatively correlated with maximum urinary flow rate(P<0.05);the differences of serum MIP-1α,IL-8 and COX-2 before and after treatment were significantly correlated with curative effect of patients with refractory prostatitis(P<0.05);AUC values of serum MIP-1α,IL-8 and COX-2 before and after treatment to evaluate the efficacy of refractory prostatitis patients were 0.856,0.819 and 0.788,respectively,and the combined AUC value was the largest,which was 0.903.Conclusion:Pathogenic bacteria in patients with refractory prostatitis are mainly gram-positive bacteria,and the serum MIP-1α,IL-8 and COX-2 are significantly increased,which are closely related to the evolution of the disease.They can be used to evaluate clinical efficacy,and provide information for subsequent treatment.

Objective To investigate the effect of Yiqi Jiedu Recipe(YQ)on the proliferation,migration,and invasion of nasopharyngeal carcinoma cells,and to explore its mechanisms of action on proliferation,migration,and invasion through the TGF-β1/SMAD3 signaling pathway.Methods(1)The 5-8F cells were divided into four groups:solvent control group,YQ 0.5 mg·mL-1 group,YQ 1.0 mg·mL-1 group,and 5-fluorouracil 2 μg·mL-1 group.Cell proliferation was monitored using real-time cell analysis(RTCA).Wound healing experiment was conducted to assess cell migration.After 24 hours of drug intervention,transwell assay was employed to measure cell invasion.The protein expression levels of β-catenin,E-cadherin,N-cadherin,TGF-β1,and SMAD3 in the cells were evaluated using the Western Blot method.(2)The 5-8F cells were divided into five groups:solvent control group,TGF-β1 10 ng·mL-1 group,TGF-β1 10 ng·mL-1+YQ 1.0 mg·mL-1 group,YQ 1.0 mg·mL-1 group,and LY3200882 10 μmol·L-1 group.Cell proliferation was monitored using RTCA.Wound healing experiment was conducted to assess cell migration.After 24 hours of drug intervention,transwell assay was employed to measure cell invasion.The protein expression levels of β-catenin,E-cadherin,N-cadherin,TGF-β1,and SMAD3 in the cells were evaluated using Western Blot.(3)The nude mice were randomly assigned into the model group,YQ group,and 5-fluorouracil group.Subcutaneous injection of 5-8F cell suspension was performed to establish the xenograft nude mouse model of nasopharyngeal carcinoma.After the tumors reached a certain size,the 5-fluorouracil group received intraperitoneal injection of 5-Fu once every 2 days,while the other groups were orally administered corresponding drugs once a day for three consecutive weeks.Tumor volume was measured every 3 days.Western Blot was conducted to assess the protein expression levels of β-catenin,E-cadherin,and N-cadherin in the tissues of each group.Results Compared with the solvent control group,the proliferation curves of 5-8F cells in the YQ(0.5 mg·mL-1,1.0 mg·mL-1)groups showed a decrease.The migration and invasion abilities of the cells were both reduced(P＜0.05,P＜0.01).Additionally,the expression of E-cadherin protein significantly increased(P＜0.01),while the protein expression of β-catenin,N-cadherin,TGF-β1,and SMAD3 all decreased(P＜0.05,P＜0.01).Compared with the model group,the transplanted tumor volume of nasopharyngeal carcinoma in the YQ group significantly decreased(P＜0.05).Furthermore,the protein expression of β-catenin and N-cadherin in the transplanted tissues of the YQ group was significantly downregulated(P＜0.05,P＜0.01),while the expression of E-cadherin protein was significantly upregulated(P＜0.01).After the addition of the activator and inhibitor of TGF-β1 signaling pathway,compared with the YQ 1.0 mg·mL-1 group,the TGF-β1 10 ng·mL-1+YQ 1.0 mg·mL-1 group showed a significant increase in the expression of TGF-β1,SMAD3,β-catenin,and N-cadherin proteins(P＜0.05,P＜0.01)and obvious enhancement of the abilities of cell proliferation,migration,and invasion(P＜0.01).Conclusion Yiqi Jiedu Recipe can inhibit the proliferation,migration,and invasion by regulating the TGF-β1/SMAD3 signaling pathway.

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.

Autism spectrum disorder (ASD) is a multifactorial disease, with social difficulties and repetitive behaviors as its core symptoms. With the improvement of diagnostic methods, the detection rate of ASD is increasing year by year.Cognitive flexibility impairment is very obvious in most autistic patients.More and more studies have shown that cognitive flexibility impairment is related to the occurrence and development of core symptoms. However, the mechanism of cognitive flexibility impairment in autism remains unclear. The frontal lobe plays an important role in advanced cognition, and its complete development is related to cognitive function. Recent studies have shown that frontal lobe dysfunction is closely related to cognitive flexibility deficits in autistic patients, and the abnormal changes in the frontal lobe, the associated default mode network dysfunction and frontal striatal circuit defects may be the important mechanisms of cognitive flexibility impairment. Based on the recent clinical and basic studies on cognitive flexibility in autism, this article reviews the mechanisms of frontal lobe and related circuits involved in the impairment of cognitive flexibility in autism.

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.