Objective: To investigate the emotional and behavioral problems among preschool children and the correlations with maternal parenting competence and family rearing environment, so as to provide a scientific basis and practical guidance for the physical and mental health development of preschool children. Methods: In June 2025, 660 preschool children aged 3-6 years old were selected from 10 kindergartens in Hefei, Anqing, and Tongling in Anhui Province by using a stratified cluster random sampling method. A questionnaire survey was conducted among all parents of preschool children using the Parent version of the Strengths and Difficulties Questionnaire, the Child Family Rearing Environment Scale, and the Chinese version of the Parenting Sense of Competence Scale. Pearson correlation analysis and multiple linear regression analysis were used to analyze the related factors of emotional and behavioral problems among preschool children. SPSS macro program Process 4.1 and Bootstrap method were used to test the mediating effect of family parenting environment between emotional and behavioral problems among preschool children and maternal parenting competence. Results: The detection rate of emotional and behavioral problems among preschool children was 20.15%. The total scores of family rearing environment and maternal parenting competence were negatively correlated with emotional and behavioral problems among preschool children ( r =-0.45,-0.79), and the total score of family rearing environment was positively correlated with the total score of maternal parenting competence ( r =0.43) (all P <0.01). Multiple linear regression showed that, after controlling whether being only child, parents educational level, registered residence location and other variables, family rearing environment, self efficacy and satisfaction were all negative predictors of emotional and behavioral problems among preschool children ( B =-0.07, -0.42, -0.42, all P <0.01). The mediation effect results showed that maternal parenting competence could positively predict the family rearing environment ( B =0.75), while maternal parenting competence and family rearing environment could both negatively predict emotional and behavioral problems among preschool children ( B =-0.49, -0.06 ) (all P <0.05). The Bootstrap sampling method test results showed that the effect value of the indirect effect of maternal parenting competence on emotional and behavioral problems through the family rearing environment was -0.04, and the effect proportion was 8.21 %. Conclusion Preschool children with a better family rearing environment and stronger maternal parenting competence are less likely to have emotional and behavioral problems, among which the family rearing environment has a mediating effect.

Objective:To investigate the expression, distribution and cellular localization of acylglycerol kinase (AGK) in liver cancer tissues, and the correlation of AGK expression with the prognosis of liver cancer patients.Methods:AGK mRNA expression data and clinical information of hepatocellular carcinoma (HCC) patients were downloaded from The Cancer Genome Atlas (TCGA) database in January 2024. The expression differences of AGK mRNA between HCC tissues and paracancerous tissues were compared, and the high and low expressions of AGK were judged by using the median expression of AGK mRNA in 369 HCC tissues as a cut-off value. A univariate logistic regression model was used to analyze the relationship between clinical pathological characteristics and high expression of AGK. The mRNA expressions in HCC tissues and paracancerous tissues of 9 datasets from the Hepatocellular Carcinoma Molecular Landscape Database (HCCDB) 2.0 were compared. The spatial distribution and cellular localization of AGK were analyzed based on multidimensional data from Bulk transcriptome sequencing (RNA-seq), single-cell sequencing and spatial RNA-seq. The expression of AGK protein in liver cancer tissues was analyzed using the Human Protein Atlas (HPA) database. Kaplan-Meier method and log-rank test were employed to compare the differences in overall survival (OS) among patients with different AGK mRNA expressions in HCCDB25 dataset of HCCDB 2.0 and HPA database. The correlation between expressions of AGK and hepatic stem cell-related markers was analyzed by using Spearman rank test based on Tumor Immune Estimation Resource (TIMER) 2.0 database.Results:Data from both the TCGA and 9 datasets of HCCDB 2.0 showed that AGK mRNA expression in HCC tissues was higher than that in paracancerous non-tumorous tissues and normal liver tissues, and the difference was statistically significant (all P < 0.001). HPA database immunohistochemical testing revealed that AGK protein was primarily localized in the cytoplasm, with positive or strong positive expression in HCC tissues and negative or weak positive expression in normal liver tissues; mass spectrometry data showed that it was upregulated in tumor samples (165 cases) compared to normal liver tissues (165 cases) ( P < 0.001). Univariate logistic regression analysis indicated that tumor family history and tumor pathological differentiation in HCC patients from TCGA database were associated with high AGK expression in tumor tissues ( P values were 0.028 and 0.050), while other factors such as age, gender, body mass index, alpha fetoprotein level, Child-Pugh classification, inflammation degree in paracancerous tissues, Ishak fibrosis score, pathological TNM staging, tumor clinical staging, and tumor vascular infiltration had no impact on AGK expression level in tumor tissues (all P > 0.05). One hundred and fifty-eight patients were divided into high and low KGK mRNA expression groups based on the median expression of AGK mRNA in tissues of HCCDB25 dataset, analysis showed that patients in low AGK mRNA expression group (79 cases) had better overall survival (OS) compared to the high expression group (79 cases) in tumor tissues, and the difference was statistically significant ( P = 0.038), while there was no significant difference in OS between high (79 cases) and low (79 cases) expression groups in paracancerous tissues ( P = 0.760). In HPA database, patients were divided into high and low AGK mRNA expression groups based on AGK mRNA values in liver cancer tissues corresponding to the lowest P value during OS analysis by Kaplan-Meier method; in all stages of HCC patients, low AGK mRNA expression group (279 cases) had better OS than the high expression group (76 cases), and the difference was statistically significant ( P = 0.022). The OS of high AGK mRNA expression group in patients with stages Ⅱ-Ⅲ was worse than that of low expression group, and the difference was statistically significant ( P = 0.007). The UMAP plot obtained through dimensionality reduction and cell clustering analysis based on single-cell sequencing data in HCCDB 2.0 revealed that AGK gene expression in liver cancer tissues was primarily distributed in tumor cells, NK/T cells, stromal cells, and myeloid cells. Spatial transcriptomic analysis of tissue samples from 5 HCC patients using HCCDB 2.0 online tools showed that AGK expression varied across different liver cancer tissue regions (non-tumorous tissue, paracancerous tissue, tumor junction, tumor focus, and portal vein tumor thrombus), with 3 cases showing AGK expression enrichment in tumor cells of the tumor junction, tumor focus and portal vein tumor thrombus, while lower in normal hepatocytes, stromal cells and immune cells. In 2 cases, AGK expression was more widespread. Analysis of 3 patients with significant AGK enrichment showed that in HCC samples with complete fibrous capsule, AGK was mainly localized in tumor cells of the tumor focus and junction areas, with weaker expression in paracancerous normal tissues; while in samples with incomplete capsule, high AGK expression was primarily in tumor cells of the tumor junction, tumor focus and portal vein tumor thrombus. TIMER 2.0 database assessment showed that AGK gene expression in 371 patients of TCGA database was positively correlated with the expressions of liver cancer stem cell-related marker genes, including PROM1 ( rho = 0.250), TYH1 ( rho = 0.188), CD44 ( rho = 0.268), ANPEP ( rho = 0.171), CD47 ( rho = 0.435), EPCAM ( rho = 0.246), KRT19 ( rho = 0.203), TGFB1 ( rho = 0.285), and SOX9 ( rho = 0.328) (all P < 0.001). Conclusions:AGK expression is significantly upregulated at both mRNA and protein levels in tumor tissues of HCC patients, it predominantly localizes in the tumor tissues and the cytoplasm of tumor cells within the junction areas, and its high expression closely associates with poor prognosis of patients. Its expression is positively correlated with the expression of liver cancer stem cell-related markers.

Objective:To investigate the expression, distribution and cellular localization of acylglycerol kinase (AGK) in liver cancer tissues, and the correlation of AGK expression with the prognosis of liver cancer patients.Methods:AGK mRNA expression data and clinical information of hepatocellular carcinoma (HCC) patients were downloaded from The Cancer Genome Atlas (TCGA) database in January 2024. The expression differences of AGK mRNA between HCC tissues and paracancerous tissues were compared, and the high and low expressions of AGK were judged by using the median expression of AGK mRNA in 369 HCC tissues as a cut-off value. A univariate logistic regression model was used to analyze the relationship between clinical pathological characteristics and high expression of AGK. The mRNA expressions in HCC tissues and paracancerous tissues of 9 datasets from the Hepatocellular Carcinoma Molecular Landscape Database (HCCDB) 2.0 were compared. The spatial distribution and cellular localization of AGK were analyzed based on multidimensional data from Bulk transcriptome sequencing (RNA-seq), single-cell sequencing and spatial RNA-seq. The expression of AGK protein in liver cancer tissues was analyzed using the Human Protein Atlas (HPA) database. Kaplan-Meier method and log-rank test were employed to compare the differences in overall survival (OS) among patients with different AGK mRNA expressions in HCCDB25 dataset of HCCDB 2.0 and HPA database. The correlation between expressions of AGK and hepatic stem cell-related markers was analyzed by using Spearman rank test based on Tumor Immune Estimation Resource (TIMER) 2.0 database.Results:Data from both the TCGA and 9 datasets of HCCDB 2.0 showed that AGK mRNA expression in HCC tissues was higher than that in paracancerous non-tumorous tissues and normal liver tissues, and the difference was statistically significant (all P < 0.001). HPA database immunohistochemical testing revealed that AGK protein was primarily localized in the cytoplasm, with positive or strong positive expression in HCC tissues and negative or weak positive expression in normal liver tissues; mass spectrometry data showed that it was upregulated in tumor samples (165 cases) compared to normal liver tissues (165 cases) ( P < 0.001). Univariate logistic regression analysis indicated that tumor family history and tumor pathological differentiation in HCC patients from TCGA database were associated with high AGK expression in tumor tissues ( P values were 0.028 and 0.050), while other factors such as age, gender, body mass index, alpha fetoprotein level, Child-Pugh classification, inflammation degree in paracancerous tissues, Ishak fibrosis score, pathological TNM staging, tumor clinical staging, and tumor vascular infiltration had no impact on AGK expression level in tumor tissues (all P > 0.05). One hundred and fifty-eight patients were divided into high and low KGK mRNA expression groups based on the median expression of AGK mRNA in tissues of HCCDB25 dataset, analysis showed that patients in low AGK mRNA expression group (79 cases) had better overall survival (OS) compared to the high expression group (79 cases) in tumor tissues, and the difference was statistically significant ( P = 0.038), while there was no significant difference in OS between high (79 cases) and low (79 cases) expression groups in paracancerous tissues ( P = 0.760). In HPA database, patients were divided into high and low AGK mRNA expression groups based on AGK mRNA values in liver cancer tissues corresponding to the lowest P value during OS analysis by Kaplan-Meier method; in all stages of HCC patients, low AGK mRNA expression group (279 cases) had better OS than the high expression group (76 cases), and the difference was statistically significant ( P = 0.022). The OS of high AGK mRNA expression group in patients with stages Ⅱ-Ⅲ was worse than that of low expression group, and the difference was statistically significant ( P = 0.007). The UMAP plot obtained through dimensionality reduction and cell clustering analysis based on single-cell sequencing data in HCCDB 2.0 revealed that AGK gene expression in liver cancer tissues was primarily distributed in tumor cells, NK/T cells, stromal cells, and myeloid cells. Spatial transcriptomic analysis of tissue samples from 5 HCC patients using HCCDB 2.0 online tools showed that AGK expression varied across different liver cancer tissue regions (non-tumorous tissue, paracancerous tissue, tumor junction, tumor focus, and portal vein tumor thrombus), with 3 cases showing AGK expression enrichment in tumor cells of the tumor junction, tumor focus and portal vein tumor thrombus, while lower in normal hepatocytes, stromal cells and immune cells. In 2 cases, AGK expression was more widespread. Analysis of 3 patients with significant AGK enrichment showed that in HCC samples with complete fibrous capsule, AGK was mainly localized in tumor cells of the tumor focus and junction areas, with weaker expression in paracancerous normal tissues; while in samples with incomplete capsule, high AGK expression was primarily in tumor cells of the tumor junction, tumor focus and portal vein tumor thrombus. TIMER 2.0 database assessment showed that AGK gene expression in 371 patients of TCGA database was positively correlated with the expressions of liver cancer stem cell-related marker genes, including PROM1 ( rho = 0.250), TYH1 ( rho = 0.188), CD44 ( rho = 0.268), ANPEP ( rho = 0.171), CD47 ( rho = 0.435), EPCAM ( rho = 0.246), KRT19 ( rho = 0.203), TGFB1 ( rho = 0.285), and SOX9 ( rho = 0.328) (all P < 0.001). Conclusions:AGK expression is significantly upregulated at both mRNA and protein levels in tumor tissues of HCC patients, it predominantly localizes in the tumor tissues and the cytoplasm of tumor cells within the junction areas, and its high expression closely associates with poor prognosis of patients. Its expression is positively correlated with the expression of liver cancer stem cell-related markers.

Eukaryotic organisms constantly face a wide range of internal and external factors that cause damage to their DNA. Failure to accurately and efficiently repair these DNA lesions can result in genomic instability and the development of tumors (Canela et al., 2017). Among the various forms of DNA damage, DNA double-strand breaks (DSBs) are particularly harmful. Two major pathways, non-homologous end joining (NHEJ) and homologous recombination (HR), are primarily responsible for repairing DSBs (Katsuki et al., 2020; Li and Yuan, 2021; Zhang and Gong, 2021; Xiang et al., 2023). NHEJ is an error-prone repair mechanism that simply joins the broken ends together (Blunt et al., 1995; Hartley et al., 1995). In contrast, HR is a precise repair process. It involves multiple proteins in eukaryotic cells, with the RAD51 recombinase being the key player, which is analogous to bacterial recombinase A (RecA) (Shinohara et al., 1992). The central event in HR is the formation of RAD51-single-stranded DNA (ssDNA) nucleoprotein filaments that facilitate homology search and DNA strand invasion, ultimately leading to the initiation of repair synthesis (Miné et al., 2007; Hilario et al., 2009; Ma et al., 2017).
Recombinational DNA Repair ; DNA-Binding Proteins/metabolism* ; DNA Repair ; DNA Damage ; DNA

Objective:To analyze the intellectual property risk of international cooperative scientific research involving human genetic resources, explore possible risk control measures regarding to intellectual property.Methods:By means of literature review, this paper analyzes the special attributes and strategic position of human genetic resources, reviews the policies and systems involving human genetic resources in international cooperative scientific research, identifies the intellectual property risk points, and puts forward suggestions on risk management and control from the perspective of intellectual property protection.Results:The management of human genetic resources in China is evolving quickly. However, there is still a lack of practical guidelines on intellectual property protection and development, more substantial engagement and contribution of Chinese investigators in the international collaborative research should be promoted, and the perception and awareness of the significance of human genetic resources should be enhanced.Conclusions:In the international cooperative scientific research involving human genetic resources, we should clarify the operating rules at the level of intellectual property protection, improve the substantive participation of Chinese investigators, enhance the strategic awareness and risk awareness of human genetic resources, and provide support at the level of executive management institutions.

Objective:To identify whether splenectomy for treatment of hypersplenism has any impact on development of hepatocellular carcinoma(HCC) among patients with liver cirrhosis and hepatitis.Methods:Patients who underwent splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension between January 2008 and December 2012 were included from seven hospitals in China, whereas patients receiving medication treatments for liver cirrhosis and portal hypertension (non-splenectomy) at the same time period among the seven hospitals were included as control groups. In the splenectomy group, all the patients received open or laparoscopic splenectomy with or without pericardial devascularization. In contrast, patients in the control group were treated conservatively for liver cirrhosis and portal hypertension with medicines (non-splenectomy) with no invasive treatments, such as transjugular intrahepatic portosystemic shunt, splenectomy or liver transplantation before HCC development. All the patients were routinely screened for HCC development with abdominal ultrasound, liver function and alpha-fetoprotein every 3 to 6 months. To minimize the selection bias, propensity score matching (PSM) was used to match the baseline data of patients among splenectomy versus non-splenectomy groups. The Kaplan-Meier method was used to calculate the overall survival and cumulative incidence of HCC development, and the Log-rank test was used to compare the survival or disease rates between the two groups. Univariate and Cox proportional hazard regression models were used to analyze the potential risk factors associated with development of HCC.Results:A total of 871 patients with liver cirrhosis and hypertension were included synchronously from 7 tertiary hospitals. Among them, 407 patients had a history of splenectomy for hypersplenism (splenectomy group), whereas 464 patients who received medical treatment but not splenectomy (non-splenectomy group). After PSM,233 pairs of patients were matched in adjusted cohorts. The cumulative incidence of HCC diagnosis at 1,3,5 and 7 years were 1%,6%,7% and 15% in the splenectomy group, which was significantly lower than 1%,6%,15% and 23% in the non-splenectomy group ( HR=0.53,95% CI:0.31 to 0.91, P=0.028). On multivariable analysis, splenectomy was independently associated with decreased risk of HCC development ( HR=0.55, 95%CI:0.32 to 0.95, P=0.031). The cumulative survival rates of all the patients at 1,3,5,and 7 years were 100%,97%,91%,86% in the splenectomy group,which was similar with that of 100%,97%,92%,84% in the non-splenectomy group ( P=0.899). In total,49 patients (12.0%) among splenectomy group and 75 patients (16.2%) in non-splenectomy group developed HCC during the study period, respectively. Compared to patients in non-splenectomy group, patients who developed HCC after splenectomy were unlikely to receive curative resection for HCC (12.2% vs. 33.3%,χ2=7.029, P=0.008). Conclusion:Splenectomy for treatment of hypersplenism may decrease the risk of HCC development among patients with liver cirrhosis and portal hypertension.

Objective:To identify whether splenectomy for treatment of hypersplenism has any impact on development of hepatocellular carcinoma(HCC) among patients with liver cirrhosis and hepatitis.Methods:Patients who underwent splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension between January 2008 and December 2012 were included from seven hospitals in China, whereas patients receiving medication treatments for liver cirrhosis and portal hypertension (non-splenectomy) at the same time period among the seven hospitals were included as control groups. In the splenectomy group, all the patients received open or laparoscopic splenectomy with or without pericardial devascularization. In contrast, patients in the control group were treated conservatively for liver cirrhosis and portal hypertension with medicines (non-splenectomy) with no invasive treatments, such as transjugular intrahepatic portosystemic shunt, splenectomy or liver transplantation before HCC development. All the patients were routinely screened for HCC development with abdominal ultrasound, liver function and alpha-fetoprotein every 3 to 6 months. To minimize the selection bias, propensity score matching (PSM) was used to match the baseline data of patients among splenectomy versus non-splenectomy groups. The Kaplan-Meier method was used to calculate the overall survival and cumulative incidence of HCC development, and the Log-rank test was used to compare the survival or disease rates between the two groups. Univariate and Cox proportional hazard regression models were used to analyze the potential risk factors associated with development of HCC.Results:A total of 871 patients with liver cirrhosis and hypertension were included synchronously from 7 tertiary hospitals. Among them, 407 patients had a history of splenectomy for hypersplenism (splenectomy group), whereas 464 patients who received medical treatment but not splenectomy (non-splenectomy group). After PSM,233 pairs of patients were matched in adjusted cohorts. The cumulative incidence of HCC diagnosis at 1,3,5 and 7 years were 1%,6%,7% and 15% in the splenectomy group, which was significantly lower than 1%,6%,15% and 23% in the non-splenectomy group ( HR=0.53,95% CI:0.31 to 0.91, P=0.028). On multivariable analysis, splenectomy was independently associated with decreased risk of HCC development ( HR=0.55, 95%CI:0.32 to 0.95, P=0.031). The cumulative survival rates of all the patients at 1,3,5,and 7 years were 100%,97%,91%,86% in the splenectomy group,which was similar with that of 100%,97%,92%,84% in the non-splenectomy group ( P=0.899). In total,49 patients (12.0%) among splenectomy group and 75 patients (16.2%) in non-splenectomy group developed HCC during the study period, respectively. Compared to patients in non-splenectomy group, patients who developed HCC after splenectomy were unlikely to receive curative resection for HCC (12.2% vs. 33.3%,χ2=7.029, P=0.008). Conclusion:Splenectomy for treatment of hypersplenism may decrease the risk of HCC development among patients with liver cirrhosis and portal hypertension.

Objective To observe the effect of scalp nerve block ( SNB ) with ropivacaine hydrochloride at different time points on pain management after craniotomy. Methods Ninety patients undergoing craniotomy were randomly divided into 3 groups:group A, SNB conducted before surgery;group B, SNB conducted after surgery;group C, SNB conducted both before and after surgery, with 0. 5% of ropivacaine hydrochloride in each group. All patients received the same general anesthesia and diclofenac sodium were administered rectally as rescue analgesics. Sites and duration of surgeries, end-tidal sevoflurane concentration during incision, HR and SBP levels during the course of surgery and postoperative period, the VAS scores, GCS and Ramsay scores at 0. 5, 2, 4, 6, 12, 24, 48 h postoperatively, time of the first rescue appication analgesics and total consumption of rescue analgesics, the adverse effects, awareness under anesthesia were analyzed respectively, as well as local anesthesia relevant adverse events and time of wound healing. Results The end-tidal sevoflurane concentration was significantly decreased in group B (3. 19±0. 36)% as compared with group A (1. 81±0. 24)% and C (1. 77±0. 33)% (P<0. 05);The VAS scores of group A (3. 77±2. 27, 4. 20±2. 09) at 2 and 4 h were higher than those in group B (2. 77±1. 98, 3. 20±2. 20) and C (2. 97±1. 77,2. 27±1. 93) (P<0. 05), while at other time points the differences were not significant (P>0. 05);Compared with group A (600 mg), the consumption of rescue analgesics of group B (300 mg) and C (250 mg) were statistically lower (P<0. 05);Vital signs, GCS, Ramsay scores, time of the first rescue analgesics postoperatively used, and time of wound healing among the three groups were not various significantly (P>0. 05);The relevant side effects were not different statistically, and there were no patients suffering from obvious awareness under anesthesia, pruritus, respiratory depression or local anesthesia relevant adverse effects. Conclusion SNB conducted before surgery can decrease the consumption of sevoflurane during incision, but has limited analgesic effects postoperatively. SNB conducted after surgery may provide transitional analgesia for neurosurgical patients undergoing craniotomy, while SNB conducted both before and after surgery does not show significantly longer analgesic time in postoperative pain management.