Post-stroke anxiety disorder （PSA） is a common psychiatric complication of stroke， which jeopardizes patients' recovery and their quality of life. Recent studies suggest that inflammation plays an important role in the pathogenesis of PSA. Therefore， this paper reviewed the related licture about the association between PSA and serum inflammatory biomarkers in order to provide references for the intervention of PSA. In this study， a comprehensive search was performed in China National knowledge Infrastructure （CNKI）， Wanfang Data， Web of Science and PubMed database to identify the well qualified literature focusing on the relationship between PSA occurrence and serum inflammatory biomarkers， and a total of 13 studies were retrieved. Analysis indicates a certain association between PSA occurrence and serum inflammatory biomarkers， and denotes that the elevation of inflammatory biomarkers may be a trigger for the disease occurrence and its progression， but the specific mechanism underlying this relationship requires further study.

Objective:To summarize the genotype and clinical phenotype of children with WWOX gene related developmental and epileptic encephalopathy (DEE).Methods:Case series studies. The clinical data of 12 children with WWOX gene related DEE who were admitted to the Neurological Department of Children′s Medical Center, Peking University First Hospital from June 2019 to December 2023 were analyzed. The children′s characteristics of gene variation, clinical phenotype, auxiliary examination results, treatment and prognosis were analyzed.Results:Among 12 children with WWOX gene related DEE, there were 7 boys and 5 girls, the age of seizure onset ranged from 10 days to 6 months (median 1.8 months). Multiple seizure types were observed, including focal seizures in 10 cases, epileptic spasms in 9 cases, tonic seizures in 4 cases, myoclonic seizures in 1 case. Among 12 cases, 9 cases had multiple seizure types. All 12 cases showed microcephaly and global developmental delay. Video electroencephalography showed slowed background activity in 6 cases, hyperarrhythmia in 6 cases, multifocal discharges in 6 cases, and focal discharges in 1 case. Epileptic spasms were detected in 8 cases, tonic seizures in 4 cases and myoclonic seizures in 1 case. Brain magnetic resonance imaging showed bilateral frontotemporal subarachnoid space widening in 5 cases, deep sulci in 3 cases, bilateral ventricular enlargement in 2 cases, callosal hypoplasia in 5 cases, and delayed white matter myelination in 3 cases. The phenotypes of 12 cases were consistent with the diagnosis of DEE, and 8 of them were diagnosed with infantile epileptic spasm syndrome. All the WWOX gene variants in 12 cases were complex heterozygous variants, including 20 variants, 11 variants and 1 large intragenic WWOX gene deletion (p.Ala149Thr, p.Arg156Ser, p.R167Tfs*8, p.Leu186Val, c.605+5G>A, p.Trp218*, p.His263Arg, p.Leu275fs*19*1, p.N285Kfs*10, p.Ser304Tyr, p.Met326Arg, loss1 exon2-8) had not been reported previously. The age of last follow-up ranged from 11 months to 5 years and 3 months. During the follow-up, 1 case died at the age of 1 year and 10 months, 2 cases were seizure-free, and 9 cases still had seizures after multiple anti-seizure medications.Conclusions:The seizure onset age of children with WWOX gene related DEE is usually less than 6 months, and some of them in neonate. The common seizure types include focal seizures and epileptic spasms. Children usually have microcephaly and global developmental delay. WWOX gene related DEE usually has drug refractory epilepsy.

Objective:To summarize the clinical features of epilepsy and (or) developmental delay associated with KCNB1 gene variants in children.Methods:A case series study was conducted on 24 children with KCNB1 gene variants associated with epilepsy and (or) developmental delay who were treated at the Children′s Medical Center of Peking University First Hospital and the Department of Neurology of Shenzhen Children′s Hospital from July 2015 to June 2024. The manifestations of seizures, electroencephalogram (EEG) and genetic test results of those children were analyzed.Results:All the KCNB1 gene variants were de novo, involving 20 different variation, including 15 missense variations, 3 frameshift variations and 2 nonsense variations. There were 7 novel variations. Among the 24 developmental and epileptic encephalopathy children, there were 14 boys and 10 girls. The last follow-up age ranged from 9 months to 13 years and 9 months. Seizures were present in 21 children (88%), with onset ranging from 1 month to 7 years, and 76% (16/21) began before 2 years of age. The seizure types included focal seizures in 15 children (71%), epileptic spasms, myoclonic seizures, and generalized tonic-clonic seizures in 6 children respectively, atypical absence seizures in 4 children, and myoclonic atonic seizures in 1 child. Seventeen children (81%) had a cluster of seizures and 5 had a history of focal status epilepticus with impaired consciousness. All 24 children had varying degrees of developmental delay, with 3 presenting solely developmental delay. EEG abnormalities were present in all the 21 children with seizures, including focal or multifocal discharges in 20 children, generalized discharges in 10 children, hypsarrhythmia in 2 children, and electrical status epilepticus during sleep in 3 children. Magnetic resonance imaging abnormalities were found in 5 of the 24 children. Among the 21 children with seizures, 57% (12/21) achieved seizure control.Conclusions:KCNB1 gene variants are predominantly de novo missense variation. Most affected children present with epilepsy, though some may exhibit only developmental delay. Epilepsy often begins before 2 years of age, with focal seizures being the most common type. About 80% of patients experience clustered seizures. Although most patients achieve seizure control, they still exhibit varying degrees of developmental delay, consistent with developmental epileptic encephalopathy.

Objective:To summarize the clinical phenotypes and genetic variations of children with epilepsy related to CLCN4 gene mutations. Methods:A retrospective analysis was conducted on 9 children with epilepsy who were diagnosed with CLCN4 gene mutations through whole-exome sequencing of family members. These children were treated at the Department of Pediatrics, Peking University First Hospital from December 2016 to March 2024. Their clinical manifestations, electroencephalogram, cranial imaging characteristics, and treatment follow-up were reviewed. Results:Among the 9 children, 6 were male and 3 were female. All cases involved de novo mutations. Three cases carried the c.823G>A/p.V275M variant, 2 cases carried the c.2152C>T/ p.R718W variant, 1 case carried the c.1630G>A/pG544R variant, and 1 case carried the c.2167C>T/ p.R723W variant. Two cases carried the unreported new variant c.848G>T/p.S283I and c.818G>A/ p.G273E. The onset age of epilepsy ranged from 55 days to 10 years, with a median onset age of 14 months. Seven out of 9 children had epilepsy onset before the age of 2 years. The types of seizures varied: 8 had focal seizures, 1 had generalized tonic-clonic seizures, 2 had myoclonic seizures, 1 had epileptic spasms, and 1 had atypical absence seizures. Three children experienced multiple types of seizures. All 9 children exhibited developmental delays to varying degrees: 8 had global developmental delay and 1 had cognitive developmental delay. Developmental delays were observed in 7 children before the onset of epilepsy. Clinically, 1 child was diagnosed with infantile epileptic spasms syndrome, 7 with unclassified developmental and epileptic encephalopathy, and 1 with focal epilepsy with developmental delay. At the last follow-up, the age of the children ranged from 2 years and 5 months to 13 years and 9 months. Seizures had been controlled in 3 children for a duration of 4 to 12 months. Conclusions:De novo variants are common in CLCN4 variants. Most seizures onset in infancy, seizure types are various, and focal seizures are common. Most of them have developmental delay and drug-resistant epilepsy, and some of them have developmental delay before seizure onset, which is consistent with the characteristics of developmental and epileptic encephalopathy.

Objective: Excessive daytime sleepiness (EDS) and insomnia symptoms are common in patients with major depressive disorder (MDD), which might lead to a poor prognosis and an increased risk of depression relapse. The current study aimed to investigate the prevalence, and sociodemographic and clinical correlates of EDS and insomnia symptoms among adolescents with MDD. Methods: The sample of this cross-sectional study included 297 adolescents (mean age=15.26 years; range=12–18 years; 218 females) with MDD recruited from three general and four psychiatric hospitals in five cities (Hefei, Bengbu, Fuyang, Suzhou, and Ma’anshan) in Anhui Province, China between January and August, 2021. EDS and insomnia symptoms, and clinical severity of depressive symptoms were assessed using Epworth sleepiness scale, Insomnia Severity Index, and Clinical Global Impression-Severity. Results: The prevalence of EDS and insomnia symptoms in adolescents with MDD was 39.7% and 38.0%, respectively. Binary logistic regression analyses showed that EDS symptoms were significantly associated with higher body mass index (odds ratio [OR]=1.097, 95% confidence interval [CI]=1.027–1.172), more severe depressive symptoms (OR=1.313, 95% CI=1.028–1.679), and selective serotonin reuptake inhibitors use (OR=2.078, 95% CI=1.199–3.601). And insomnia symptoms were positively associated with female sex (OR=1.955, 95% CI=1.052–3.633), suicide attempts (OR=1.765, 95% CI=1.037–3.005), more severe depressive symptoms (OR=2.031, 95% CI=1.523–2.709), and negatively associated with antipsychotics use (OR=0.433, 95% CI=0.196–0.952). Conclusion EDS and insomnia symptoms are common among adolescents with MDD. Considering their negative effects on the clinical prognosis, regular screening and clinical managements should be developed for this patient population.

Objective:To explore the independent influencing factors of patients with spontaneous rupture hemorrhage of primary liver cancer (PLC).Methods:A retrospective cohort study was conducted. The clinical data of 128 patients with PLC spontaneous rupture hemorrhage in Ningxia Medical University General Hospital from January 2017 to March 2022 were analyzed, including 108 males and 20 females, aged (53.4±10.6) years. According to different treatment, 128 patients were divided into liver resection group (LR, n=28), interventional group [ n=39, transcatheter arterial chemoembolization (TACE) and transcatheter arterial embolization (TAE)], and conservative group ( n=61). Univariate and multivariate Cox regression was performed to analyze prognostic factors. The LR and TACE groups were subdivided into LR (aLR, n=15), TACE/TAE (aTACE, n=33) and LR+ TACE ( n=19) groups. Kaplan-Meier analysis was performed, and the survival rate was compared by log-rank test. Results:The median survival time of LR group and TACE group was 23 months and 21 months, respectively, with no statistical significance ( P>0.05). The median survival time (38 months) in LR+ TACE group was significantly longer than that in aLR group (10 months) and aTACE group (9 months), and the difference was statistically significant ( P<0.05). Univariate analysis showed that Barcelona Clinical Liver Cancer (BCLC)staging, tumor length ≥10.0 cm, vascular invasion, α-fetoprotein ≥400 μg/L, total bilirubin, prothrombin time and treatment affected overall survival of PLC spontaneous rupture hemorrhage patients (all P<0.05). Multivariate analysis showed that BCLC staging, tumor length ≥10.0 cm, Child-Pugh grade and treatment were independent influencing factors for overall survival of PLC spontaneous rupture hemorrhage patients (all P<0.05). Conclusion:BCLC stage, tumor length ≥10.0 cm, Child-Pugh grade and treatment method are independent predictors of overall survival in patients with spontaneous rupture of PLC. LR combined with TACE therapy can improve the survival and prognosis of patients with spontaneous rupture of primary liver cancer.

Objective To observe the effect of group biofeedback in patients with residual schiz-ophrenia(RS).Methods A total of 127 patients with RS were selected as study objects,and ran-domly divided into control group(n=63)and observation group(n=64).The control group re-ceived routine nursing,and the observation group received group biofeedback based on the control group.The Positive and Negative Symptom Scale(PANSS),Personal and Social Performance Scale(PSP)and Self-awareness Inventory(SAI)Questionnaire(treatment compliance)scores were com-pared between the two groups.Results After 12 weeks of intervention,the score of the positive symptoms,the score of negative symptoms and the total score of PANSS in the observation group were significantly lower than those in the control group(P＜0.05).The number of patients with PSP scores greater than 70 to 100 and greater than 30 to 70 in the observation group was significantly more than those in the control group,and the number of patients with PSP score of 0 to 30 was significantly less than that in the control group(P＜0.05).The SAI score of the observation group after interven-tion was significantly higher than that before intervention and control group,and the number of com-pleted biofeedback therapy in the observation group was significantly more than that in the control group(P＜0.05).Conclusion Group biofeedback can promote symptom relief and improve treat-ment compliance in patients with RS.

Objective To observe the effect of group biofeedback in patients with residual schiz-ophrenia(RS).Methods A total of 127 patients with RS were selected as study objects,and ran-domly divided into control group(n=63)and observation group(n=64).The control group re-ceived routine nursing,and the observation group received group biofeedback based on the control group.The Positive and Negative Symptom Scale(PANSS),Personal and Social Performance Scale(PSP)and Self-awareness Inventory(SAI)Questionnaire(treatment compliance)scores were com-pared between the two groups.Results After 12 weeks of intervention,the score of the positive symptoms,the score of negative symptoms and the total score of PANSS in the observation group were significantly lower than those in the control group(P＜0.05).The number of patients with PSP scores greater than 70 to 100 and greater than 30 to 70 in the observation group was significantly more than those in the control group,and the number of patients with PSP score of 0 to 30 was significantly less than that in the control group(P＜0.05).The SAI score of the observation group after interven-tion was significantly higher than that before intervention and control group,and the number of com-pleted biofeedback therapy in the observation group was significantly more than that in the control group(P＜0.05).Conclusion Group biofeedback can promote symptom relief and improve treat-ment compliance in patients with RS.

Background: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic β-cell senescence. However, targets and effective agents for preventing stearic acid-induced β-cell senescence are still lacking. Although melatonin administration can protect β-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse β-cells and elucidated the possible role of microRNAs in this process. Methods: β-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated β-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked β-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. Results: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR- 8114 expression in both mouse islets and β-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced β-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected β-cells. Conclusion These data demonstrate that melatonin protects against stearic acid-induced β-cell senescence by inhibiting miR-146a- 5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced β-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.

Objective:To investigate the application value of preoperative clinical and magnetic resonance imaging (MRI) targetoid enhancement combined with alpha-fetoprotein in evaluating the expression of cytokeratin 19 (CK19) in patients undergoing radical resection for single hepatocellular carcinoma (HCC) without macrovascular invasion.Methods:The retrospective cohort study was conducted. The clinicopathological data of 220 patients who underwent radical resection for single HCC without macrovascular invasion in the General Hospital of Ningxia Medical University from January 2016 to December 2020 were collected. There were 171 males and 49 females, aged (56±11)years. Of the 220 patients, 52 cases showed positive CK19 expression, while 168 cases showed negative CK19 expression. Observation indicators: (1) MRI and immunohistochemical staining results of patients with different status of CK19 expression; (2) comparison of clinical features of patients with different status of CK19 expression; (3) comparison of MRI features in patients with different status of CK19 expression; (4) analysis of influencing factors for CK19 expression in patients and predictive value. The normality of continuous variables was tested using the Shapiro-Wilk test. Measurement data with normal distribution were expressed as Mean± SD, and comparison between groups was conducted using the t test. Measurement data with skewed distribution were expressed as M( Q1, Q3), and comparison between groups was conducted using the Mann-Whitney U test. Count data were expressed as absolute numbers and (or) percentages, and comparison between groups was conducted using the chi-square test. Comparison of ordinal data was analyzed by the non-parameter rank sum test. The relevant clinical and imaging features with P<0.05 were included in the binary Logistic regression model. The receiver operating characteristic (ROC) curve was drawn and the area under curve (AUC) was used to evaluate the predictive efficiency of the model. Results:(1) MRI and immunohistochemical staining results of patients with different status of CK19 expre-ssion. Results of MRI examination in patients with positive CK19 expression showed the tumors with low-signal intensity on plain T1-weighted imaging, annular high enhancement in the arterial phase, clear boundaries in the portal venous phase, central enhance-ment in the delayed phase and targetoid high signals on diffusion-weighted imaging (DWI). Immuno-histochemical staining revealed a positive CK19 expression. Results of MRI examination in patients with negative CK19 expression showed the tumors with low-signal intensity on plain T1-weighted imaging, non-annular high enhancement in the arterial phase, unclear boundaries in the portal venous phase, low signals compared with peripheral liver tissue in the delayed phase and uniform high signals on DWI. Immunohistochemical staining revealed a negative CK19 expression. (2) Clinical features of patients with different status of CK19 expression. The neutrophil count and cases with alpha-fetoprotein (AFP) ≥400 μg/L were 3.07(2.21,4.41)×10 9/L and 26 in patients with positive CK19 expression, versus 2.72(2.05, 3.51)×10 9/L and 48 in patients with negative CK19 expression, showing significant differences between them ( Z=?2.06, χ2=8.17, P<0.05). (3) Compari-son of MRI features in patients with different status of CK19 expression. Cases with tumor diameter ≥ 5 cm and cases with tumor showing targetoid enhancement were 34 and 22 in patients with positive CK19 expression, versus 82 and 24 in patients with negative CK19 expression, showing significant differences between them ( χ2=4.38, 18.86, P<0.05). (4) Analysis of influencing factors for CK19 expression in patients and predictive value. Results of multivariate analysis showed that AFP ≥ 400 μg/L and targetoid enhance-ment were independent risk factors for positive CK19 expression in HCC patients [ odds ratio=2.09, 3.23, 95% confidence interval ( CI) as 1.06?4.13, 1.49?6.99, P<0.05]. Results of ROC curve analysis showed that the AUC of targetoid enhancement for predicting positive CK19 expression was 0.64 (95% CI as 0.57?0.71), with the sensitivity and specificity as 42.31% and 85.71%. The AUC of AFP ≥400 μg/L for predicting positive CK19 expression was 0.61 (95% CI as 0.53?0.68), with the sensitivity and specificity as 51.00% and 71.43%. The AUC of targetoid enhancement combined with AFP ≥400 μg/L for predicting positive CK19 expression was 0.69 (95% CI as 0.61?0.77), with the sensitivity and specificity as 67.31% and 63.10%, respectively. Conclusions:Targetoid enhancement and AFP ≥400 μg/L are independent risk factors for positive CK19 expression in patients with single HCC without macrovascular invasion. Their combination has clinical value for preoperative evaluation of CK19 expression.