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Objective To determine the efficacy and safety of trazodone in the treatment of benzodiazepine dependence. Methods Forty insomnia patients who met the Classification and Diagnostic Criteria of Mental Disorders in China Third Edition (CCMD - 3) of dependence syndrome due to benzodiazepine were involved in the study. Patients were randomly assigned to trazodone group and placebo group for 3 months. The efficacy were assessed by Withdrawal Symptoms Checklist, Hamilton Anxiety Rating Scale (HAMA) and polysomnography (PSG). Adverse events were assessed by Treatment Emergent Symptom Scale (TESS). Results The Withdrawal Symptoms Checklist of trazodone group was significantly lower after 7 d treatment than that of placebo group (P = 0.000), and HAMA score of the trazodone group was also significantly lower after 15 d treatment than that of placebo group (P = 0.000). There were no difference in Withdrawal Symptoms Checklist and HAMA of placebo group before and after treatment. Withdrawal Symptoms Checklist and HAMA of the trazodone group were decreased after treatment (P = 0.000). In comparison with placebo group, sleep parameters of the trazodone, including total sleep time (TST), sleep efficiency (SE), sleep latency (SL) and slow wave sleep (SWS) time presented improvement after 7 d treatment (P = 0.000, for all). After trazodone treatment, total sleep time, slow wave sleep time, sleep efficiency and sleep latency were improved (P = 0.000, for all). No obvious adverse reaction occurred. There were no significant differences in TESS scores between pre- and post-treatment in both groups (P > 0.05). Conclusion Trazodone is markedly effective and safe in the treatment for benzodiazepine dependence. [ABSTRACT FROM AUTHOR]

Asthma comprises one of the most common chronic inflammatory conditions, yet still lacks effective diagnostic markers and treatment targets. To gain deeper insights, we comprehensively analyzed microarray datasets of airway epithelial samples from asthmatic patients and healthy subjects in the Gene Expression Omnibus database using three machine learning algorithms. Our investigation identified a pivotal gene, STEAP4 . The expression of STEAP4 in patients with allergic asthma was found to be reduced. Furthermore, it was found to negatively correlate with the severity of the disease and was subsequently validated in asthmatic mice in this study. A ROC analysis of STEAP4 showed the AUC value was greater than 0.75. Functional enrichment analysis of STEAP4 indicated a strong correlation with IL-17, steroid hormone biosynthesis, and ferroptosis signaling pathways. Subsequently, intercellular communication analysis was performed using single-cell RNA sequencing data obtained from airway epithelial cells. The results revealed that samples exhibiting low levels of STEAP4 expression had a richer MIF signaling pathway in comparison to samples with high STEAP4 expression. Through both in vitro and in vivo experiments, we further confirmed the overexpression of STEAP4 in airway epithelial cells resulted in decreased expression of MIF, which in turn caused a decrease in the levels of the cytokines IL-33, IL-25, and IL-4; In contrast, when the STEAP4 was suppressed in airway epithelial cells, there was an upregulation of MIF expression, resulting in elevated levels of the cytokines IL-33, IL-25, and IL-4. These findings suggest that STEAP4 in the airway epithelium reduces allergic asthma Th2-type inflammatory reactions by inhibiting the MIF signaling pathway., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Qiao, Li, Liu, Duan and Jiang.)

Objective: To evaluate the effect of left ventricular ejection fraction (LVEF) on clinical outcomes in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention., Methods: A total of 158 patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention between January 2005 to December 2007 were enrolled. They were divided into three groups: LVEF≤40% (n=14), LVEF 41%-55% (n=46) and LVEF>55% group (n=98). The clinical follow-up end-point was major adverse cardiac event (MACE) including death, acute myocardial infarction, stent thrombosis and stent restenosis. The clinical follow-up duration was 43.1±15.2 months. MACE occurred in 15 patients., Results: The rates of infarction site, infarction relative artery, 1-vessel disease, 2-vessel disease, hypertension, diabetes, hyperlipidemia, smoking, obesity and aspirin use were not different in three groups (P>0.05). Average CTnI, CK, CK-MB and duration of clopidogrel use were not different in three groups (P>0.05). The rate of 3-vessel disease was significantly higher in the LVEF≤40% group than that in the LVEF 41%-55% and LVEF>55% groups (P=0.0036). The rates of TIMI flow grades (Grade III) and complete revascularization were significantly higher in the LVEF 41%-55% and LVEF>55% groups than that in the LVEF≤40% group (P=0.0099, P=0.0010). The rates of Killip classification (classes II, III, IV) and average symptom-onset-to balloon-time (SOTB) were significantly lower in the LVEF 41%-55% and LVEF>55% groups than that in the LVEF≤40% group (P=0.0100, P=0.0087). The rate of drug-eluting stents was significantly lower in the LVEF≤40% group and LVEF 41%-55% group than that in LVEF>55% group (P=0.0242). Logistic regression analysis showed that LVEF was independent predictor for MACE in the follow-up period (P=0.0029). With LVEF decrease, incidence of MACE in the follow-up period significantly increased in LVEF>55% group, LVEF 41%-55% group and LVEF≤40% group (6.12% vs 8.7% vs 35.71%, P=0.0019). Incidence of total death and cardiac death in the follow-up period significantly increased in LVEF>55% group, LVEF 41%-55% group and LVEF≤40% group (1.02% vs 4.35% vs 21.43%, P=0.0090; 1.02% vs 2.17 vs 14.29%, P=0.0060)., Conclusion: In patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention, LVEF was independent predictor for MACE in the follow-up period. With LVEF decrease, incidence of MACE in the follow-up period significantly increased.

Objective: To study the effects of neuronal apoptosis under the induction of β-amyloid inflammatory supernatant., Methods: The neurons were intervened by β-amyloid-induced inflammatory supernatant at the concentration of Aβ1-42 at 125 nmol/L. And the expressions of Bcl-2, caspase-3, PARP and neuronal apoptosis were detected., Results: The caspase-3 (14.2 ± 1.8), Bcl-2 (10.6 ± 0.8) positive cells of microglia inflammatory supernatant stimulated group were significantly elevated than the control (2.2 ± 0.6, 5.0 ± 0.3, P < 0.01). Nuclear chromatin was uniform yellow-green fluorescent. And there was significant difference of neuronal apoptosis between microglia inflammatory supernatant group and Aβ1-42 directly stimulated group., Conclusion: Neuronal apoptosis is induced by caspase-3 in β-amyloid inflammatory supernatant. One of the important causes is chronic inflammatory process of activated microglia by Aβ.

Objective: To transduce the new hepatocellular carcinoma (HCC) specific antigen gene glypican3 (GPC3) into dendritic cells (DCs) and to observe the in vitro cytotoxic effect induced by the genetically modified DCs against the hepatocellular carcinoma cell line (HepG2)., Methods: This study was performed in China Medical University Shenyang, China from September 2007-February 2008. The design of the study was to modify DCs with GPC3 and to be used to activate human T cells and elicit a cell-mediated immune response against HepG2 in vitro. The GPC3 gene expression was identified by western blot and immunocytochemistry. The proliferation of responder cells and cytotoxicity against HepG2 were examined by water-soluble tetrazolium salt -1 and lactate dehydrogenase assay respectively. The interferon-y (IFN-y) secreted was detected by ELISA assay., Results: Both Western blot and immunocytochemical analysis assured the validity of GPC3 transfection. Glypican3 modified DCs were potent in inducing responder cells proliferation and IFN-y production. The cytotoxicity in the group of GPC3 transfected DCs were (38.90+/-0.95%) at the ratio of effector cells/target cells E/T:100:1, 30.83+/-1.24% at the ratio of E/T:50:1, and 23.84+/-0.65% at the ratio of E/T:10:1, respectively (which is significant compared with other groups, p<0.001). And the GPC3 modified DCs showed ability to induce high specific cytotoxicity against HepG2 in vitro., Conclusion: The effector cells stimulated with DCs that were transfected with pEF-hGPC3 plasmid could effectively lyse GPC3 expressing HepG2 cells, which suggested that those genetically engineered DCs have the potential to serve as novel vaccine for HCC.