Epilepsy is a common neurological disease, and studies have shown that some epilepsy patients are combined with cognitive impairment. In clinical practice, it has been found that, in addition to the seizure itself, anti-seizure medications can also have a corresponding impact on the cognitive function of epilepsy patients. However, the effects of some drugs on the cognitive function of epilepsy patients are still inconclusive, and the mechanism of their influence on cognitive function in epilepsy patients is not elucidated. In recent years, some studies followed up the cognitive function of patients receiving anti-seizure medications therapy, and put forward guidance. This article focused on the research of commonly used drugs on cognitive function, the possible mechanism of drugs affecting cognitive function, the rational use of drugs in different groups of people and the prevention strategies of related cognitive dysfunction, hoping to improve emphasis on cognitive function in epilepsy patients and guide clinical practice.

Objective:To investigate the clinical characteristics and gene sequencing results of NDM, so as to provide evidence for clinical diagnosis and treatment .Methods:Clinical data of 1 child diagnosed with NDM in Hebei People's Hospital in January 2021 were retrospectively analyzed, and DNA gene sequencing was performed in the peripheral blood of the child, and relevant literatures were reviewed.Results:The child was born with a weight of 2.2kg. On the second day after birth, blood glucose significantly increased and insulin and C-peptide levels decreased. After 14 days of insulin treatment, hyperglycemia was still present, which was consistent with the diagnosis of NDM. Genetic testing indicated that there were missense mutations of newborn compound heterozygote in ABCC8 gene: c. 752G > A (p.G251E), c. 772A > G (p.R258G). The mutation of c. 772A > G in ABCC8 gene had not been reported before, and sulfonylureas were effective for the treatment of the child.Conclusion:NDM is a rare monogenic genetic disease with a lack of specificity in clinical manifestations. For children diagnosed or suspected of NDM, genetic testing should be actively carried out, which is of great significance for clinical diagnosis, treatment and prognosis.

Objective:To investigate the mediating and moderating effects of resilience on frailty and depression in the community-dwelling old adults.Methods:Totally 871 community-dwelling old adults chosen from different communities were investigated by the geriatric depression scale, Tilburg frailty indicator and 10-item Connor-Davidson resilience scale.SPSS 22.0 and AMOS 24.0 were used for data analysis, including descriptive analysis, correlation analysis, structural equation modeling and hierarchical regression analysis.Results:(1)The score of frailty (3.72±2.89)was positively correlated with the score of depression (2.63±2.57, r=0.16-0.58, P<0.01). The score of resilience(28.24±6.80) was negatively correlated with the score of frailty and depression ( r=-0.10~-0.49, both P<0.01), and frailty predicted 35% of the total variation of depression in the elderly.(2)The mediating effect of resilience was significant and the indirect effect was 0.10, accounting for 12.66% of the total variance.(3) Resilience moderated the relationship between frailty and depression ( β=-0.12, t=-4.11, R2=0.41, P<0.001). The frailty of old adults with lower resilience played a stronger predictive role in depression (simple slope=0.50, t=14.73, R2=0.01, P<0.001). Conclusion:There is a close relationship between frailty and depression in the community-dwelling older adults, and resilience plays both mediating and moderating role in the relationship.

Objective To investigate the feasibility and safety of using vasodilators in the treatment of neonates with patent ductus arteriosus (PDA) accompanied by acute heart failure and pulmonary edema. Methods The clinical data of a case of neonatal PDA accompanied by severe cardiac insufficiency and pulmonary edema in Department of Intensive Care Unit (ICU) of Hebei General Hospital, and the neonate's hemodynamic characteristics and the efficacy and adverse reactions of phentolamine, a vasodilator, in the treatment of PDA were retrospectively analyzed. Results In this neonate, on the 8th day after birth and the improvement of pulmonary hyaline membrane disease, the respiratory distress occurred again, which was related to the severe cardiac dysfunction caused by the opening of PDA. Phentolamine was given on the basis of routine treatment to reduce systemic circulatory resistance. Two hours later, the respiratory distress was relieved significantly, that was presumably related to the decline of the left to right shunt volume through the PDA. There were no adverse reactions such as blood pressure reduction and coronary insufficiency. Conclusion Neonatal PDA is easily to be complicated with severe cardiac insufficiency, and vasodilators can reduce systemic circulatory resistance, reduce left to right shunt volume through the ductus arteriosus, and reverse the acute cardiac insufficiency and pulmonary edema, the therapeutic effect of vasodilators is remarkable, safe and reliable in neonatal PDA.

Objective: To investigate the change in expression of anti-senescence marker protein calmodulin (RGN) in liver tissues of rats with immune hepatic fibrosis, and to observe the effect of compound glutathione inosine injection (CGII) on it. Methods: Rat liver fibrosis model was induced by intraperitoneal injection of porcine serum, and CGII intervention was administered at the appropriate time. Rat liver tissues were stained with HE and Masson. RGN and protein expression at mRNA in liver tissues was detected by fluorescence quantitative PCR and immunohistochemistry. One-way Anova was used for measurement data. LDS test was used for two-way comparison, and pathological semi-quantitative results were analyzed by rank-sum test. Results: The relative expression of RGN mRNA and protein in liver tissue of fibrotic rats was 82.23 ± 15.21 and 12.52 ± 3.23, respectively, which were significantly lower than that of normal rats 176.39 ± 11.35 and 59.23 ± 9.13 (P < 0.01). The degree of liver fibrosis in fibrotic rats after CGII intervention was significantly lower than fibrotic rats. The relative expression of RGN mRNA and protein in the intervention group was 168.78 ± 21.31 and 46.42 ± 4.71, respectively, which were significantly higher than fibrosis and spontaneous recovery group. The difference was statistically significant (P < 0.01). The relative expression of RGN mRNA and protein in the spontaneous recovery group was 86.23 ± 17.16 and 14.34 ± 5.16, which was higher than model group. The difference was not statistically significant (P > 0.05). Conclusion The expression of RGN in liver tissue of rats with hepatic fibrosis induced by porcine serum is decreased, while the expression of RGN increases with the decrease of fibrosis after CGII intervention, suggesting that the protein may play an important role in the development of liver fibrosis.

Objective: To investigate the effect and mechanism of XTP4 gene in apoptotic hepatoblastoma HepG2 cell line. Methods: HepG2 cells were transiently transfected with small interfering RNA of XTP4 genes, plasmid pcDNA3.1/myc-His(-) A-XTP4, and hepatitis B virus X protein transactivated x gene 4 (HBX protein trans-activate gene4, XTP4) and their respective negative controls. After 48h, the overexpression and interference expression condition of XTP4 in HepG2 cells were detected by Western blot. HepG2 cells apoptosis was detected by flow cytometry. The expression levels of apoptosis-related proteins P53, Bcl-2, Bax and Caspase-3 in HepG2 cells were detected by Western blot, and Bcl-2/Bax ratio was calculated. The chemiluminescence assay was used to detect activity of caspase-3 in HepG2 cells. The measured data were presented as ( ± s), and independent sample t-test was used for comparison between the two groups. Results: HepG2 cells had successfully achieved the overexpression and interference expression of XTP4 protein. Compared with the control group, the overexpression of XTP4 in HepG2 cells had significantly decreased the number of apoptotic cells (P < 0.05), and increased Bcl-2/Bax (P < 0.05) ratio, but decreased the expression of P53 protein (P < 0.05). The protein expression of Caspase-3 and activity of caspase-3 was decreased (P < 0.05). However, interference with XTP4 expression in HepG2 cells had significantly increased the number of apoptotic cells (P < 0.05) and decreased Bcl-2/Bax (P < 0.05) ratio, but increased the expression of P53 protein (P < 0.05). The protein expression of Caspase-3 and activity of caspase-3 was increased (P<0.05). Conclusion In HepG2 apoptosis XTP4 has inhibitory effect, and its effect on inhibiting HepG2 apoptosis may be achieved by regulating the Bcl-2/Bax ratio, and the P53 protein may be involved.

Isolation rearing (IR) enhances aggressive behavior, and the central serotonin (5-hydroxytryptamine, 5-HT) system has been linked to IR-induced aggression. However, whether the alteration of central serotonin is the cause or consequence of enhanced aggression is still unknown. In the present study, using mice deficient in central serotonin Tph2 and Lmx1b, we examined the association between central serotonin and aggression with or without social isolation. We demonstrated that central serotonergic neurons are critical for the enhanced aggression after IR. 5-HT depletion in wild-type mice increased aggression. On the other hand, application of 5-HT in Lmx1b mice inhibited the enhancement of aggression under social isolation conditions. Dopamine was downregulated in Lmx1b mice. Similar to 5-HT, L-DOPA decreased aggression in Lmx1b mice. Our results link the serotoninergic system directly to aggression and this may have clinical implications for aggression-related human conditions.

Objective To explore the association between the ZNF804A gene genetic variation poly-morphism rs1344706 and brain structure and function in patients with schizophrenia. Methods Literature search was conducted in Pubmed and other databases,the processes were performed in strict accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines,then the Comprehensive Meta-Analysis software was used for meta-analysis. Results Schizophrenia patients with rs1344706 risk al-lele had lager gray matter in the amount of brain regions including frontal lobe (z＝3.445,P＝0.001),tempo-ral lobe (z＝2.140,P＝0.032) and other brain regions; healthy controls with the risk allele had smaller gray matter and regional activity in the frontal lobe ( gray matter: z＝－2.008, P＝0.045, regional activity: z＝－4.036,P＜0.01) and other regions. Sensitivity analysis was stable,but publication bias existed in a few ana-lyses of indexes. Conclusion The risk allele in ZNF804A gene rs1344706 has positive effects on the brain structure in patients with schizophrenia,but negative effects on the brain structure and function in the healthy individuals.

PURPOSE: Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) has been implicated as an oncogene in the development and progression of osteosarcoma. This study aims to explore the mechanism of NEAT1 in osteosarcoma. MATERIALS AND METHODS: Expressions of NEAT1 and miR-194 in osteosarcoma tissues and cells were detected by quantitative real-time PCR. The effects of NEAT1 knockdown or miR-194 overexpression on cell proliferation, invasion, and apoptosis were determined by 3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromide (MTT) assay, transwell invasive assay, and flow cytometry analysis, respectively. Luciferase reporter assay was performed to observe the possible interaction between NEAT1 and miR-194. RESULTS: NEAT1 was upregulated and miR-194 was downregulated in osteosarcoma tissues and cells. Knockdown of NEAT1 or overexpression of miR-194 suppressed proliferation and invasion and induced apoptosis of osteosarcoma cells in vitro. Luciferase reporter assay validated that NEAT1 could interact with miR-194 and negatively modulated its expression. Furthermore, inhibition of miR-194 reversed the suppression of proliferation and invasion and the promotion of apoptosis induced by NEAT1 depletion in osteosarcoma cells. CONCLUSION: Knockdown of NEAT1 suppressed proliferation and invasion and induced apoptosis in osteosarcoma cells by inhibiting miR-194 expression.
Apoptosis* ; Carcinogenesis ; Cell Proliferation ; Flow Cytometry ; In Vitro Techniques ; Luciferases ; Oncogenes ; Osteosarcoma* ; Real-Time Polymerase Chain Reaction ; RNA, Long Noncoding*

AIM: To evaluate the effect of GYY4137, a novel hydrogen sulfide (H2S) donor, on cytosolic lipid decomposition in mouse primary steatosis hepatocytes.METHODS: Oleic acid (OA) was used to induce hepatic steatosis model in vitro.The C57BL/6 mouse primary hepatocytes isolated and cultured by 2-step in situ perfusion were divided into 4 groups: the cells in control group were incubated with normal medium for 54 h;the cells in model group were incubated with OA at 1.2 mmol/L for 48 h followed by serum-free phenol red-free RPMI-1640 for 6 h;the cells in H2S group or DL-propar-gylglycine (PAG;an inhibitor of cystathione γ-lysase, inhibiting H2S synthesis) group were incubated with OA at 1.2 mmol/L for 48 h followed by serum-free phenol red-free RPMI-1640 which contained 1 mmol/L GYY4137 or 200 μmol/L PAG for 6 h.The glycerin release and the protein expression of hormone-sensitive lipase (HSL) in the cells were mea-sured.RESULTS: Compared with model group, the glycerin release and the protein expression of phosphorylated HSL (p-HSL) in H2S group decreased significantly, while those increased significantly in PAG group.CONCLUSION: In steatosis hepatocytes, exogenous H2S possibly decreases cytosolic lipid decomposition by decreasing the protein level of p-HSL.