Objective: This study was performed to evaluate the efficacy of metformin on liver fat content (LFC) in first episode schizophrenia patients with olanzapine-induced weight gain, and the relationship between the change of LFC and the other metabolic indices. Methods: In a double-blind study, the clinically stable inpatients with first-episode schizophrenia under olanzapine monotherapy who gained more than 7% of their baseline weight were randomly assigned to two groups; one with olanzapine plus metformin (1,000 mg/day) (metformin group) and the other with olanzapine plus placebo (placebo group) for 16 weeks. All patients continued to maintain the original olanzapine dosage. LFC was measured by magnetic resonance imaging at baseline and at the end of 16 weeks, respectively. At the same time, glucose and lipid metabolism, homeostasis model assessment of insulin resistance index (HOMA-IR) were measured respectively, analyzing the correlation between the change value of LFC and other indicators. Results: Over the 16-week study period, LFC value in metformin group decreased compared with baseline. LFC change across the 16-week treatment period was −2.91% for the metformin group and 0.59% for the placebo group, with a between-group difference of −3.5% (95% confidence interval, −6.08 to −0.93; p = 0.009). Compared to baseline, in the metformin group, triglyceride and HOMA-IR reduced significantly, while high density lipoprotein cholesterol increased significantly at weeks 16. There was positive correlation between LFC changes and triglycerides, HOMA-IR changes significantly. Conclusion Metformin can significantly attenuate LFC in schizophrenia patients with olanzapine-induced weight gain. It may be related to the improvement of the part of the glucolipid metabolic indices.

Objective:To evaluate the effect of Kinesio taping on chronic nonspecific low back pain (CNLBP). Methods:The Cochrane Library, PubMed, Web of Science, CNKI, CBM, VIP, and Wanfang Data were searched for the randomized controlled trials (RCT) about the effect of Kinesio taping on CNLBP from establishment to January, 2019. The included studies were evaluated according to the method recommended by the Cochrane Collaboration. RevMan 5.3 software was used to analyze the extracted data. Results:Finally, nine RCTs involving 545 patients were included. Meta-analysis showed that the effect of Kinesio taping was significantly different in the improvement of pain compared with the non-stimulated group (MD = -0.76, 95%CI: -1.43 to -0.08, P = 0.03), the difference might be significant compared with the sham stimulation group (MD = -1.10, 95%CI: -2.22 to 0.02, P = 0.05); For improving dysfunction, the Oswestry Disability Index (ODI) scores were better in the Kinesio taping group than in the non-stimulation group (MD = -6.02, 95%CI: -8.63 to -3.41, P < 0.001) and the sham stimulation group (MD = -4.11, 95%CI: -5.82 to -2.41, P < 0.001), however, their was no significant difference in Roland Morris Disability Questionnaire (RMDQ) score between the Kinesio taping group and the non-stimulated group (MD = 0.69, 95%CI: -2.35 to 3.74, P = 0.66), and between the Kinesio taping group and the sham stimulation group (MD = -0.17, 95%CI: -1.43 to 1.08, P = 0.78). Conclusion:For the patients with CNLBP, the intervention of Kinesio taping could alleviate pain and improve function.

OBJECTIVETo investigate whether sodium valproate (VPA) directly regulates the activity of Ankyrin G(AnkG) promoter in vitro.

METHODSThe mouse AnkG promoter sequence was identified by comparing both human and mouse AnkG promoter sequences. The promoter was amplified from C57BL/6 mouse genome DNA and cloned into pGL3 Luciferase reporter vector. The Luciferase activity was detected in N2a and 293T cells and then treated with 0,0.5, and 1 mmol/L VPA for 12 h. The transcription activity of AnkG promoter in cells and the activity of VPA-treated Luciferase reporter vector in cells were detected using dual Luciferase reporter assay.

RESULTSThe AnkG promoter clone and its expression vector were successfully established, as confirmed by enzyme digestion and sequencing. The AnkG promoter showed high transcription activity in both N2a and 293T cells. The Luciferase activity was significantly induced following 0.5 mmol/L VPA treatment in both N2a and 293T cells. CONCLUSIONS VPA can up-regulate the AnkG expression via directly increasing its transcription activity. Thus, the in vivo AnkG expression may be directly regulated by the VPA at transcriptional level.

Animals ; Ankyrins ; Cell Line ; Genetic Vectors ; Humans ; Luciferases ; Mice ; Mice, Inbred C57BL ; Promoter Regions, Genetic ; Up-Regulation ; Valproic Acid