RNF213 inhibits migration in lung adenocarcinoma cell.

Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors, and lung adenocarcinoma (LUAD) accounts for up to 40% of NSCLC. Ring finger protein 213(RNF213) has been demonstrated to suppress several cancers, including glioblastoma and breast cancer. Nonetheless, the role of RNF213 in LUAD has not been investigated. The expression of RNF213 in LUAD tissues was analyzed by western blotting, The Cancer Genome Atlas, Genotype Tissue Expression Project, and Gene Expression Omnibus databases. Prognostic value analysis was performed through the Kaplan-Meier Plotter database. We determined the role of RNF213 in LUAD cells through cell counting kit­8 assay, migration, and invasion assay. The clinical roles of RNF213 were evaluated by immunohistochemical staining assay (IHC) and Kaplan-Meier survival analysis. RNF213 expression was reduced in LUAD, thus affecting the prognosis of LUAD. And RNF213 could suppress the migration and invasion of LUAD cells to prevent tumor development. the expression of RNF213 is positively correlated with the overall survival, providing a novel marker in the prognosis of LUAD patients.

BDNF Alleviates Microglial Inhibition and Stereotypic Behaviors in a Mouse Model of Obsessive-Compulsive Disorder.

Obsessive-compulsive disorder (OCD) is a severe mental illness characterized by obsessions and compulsions. However, its underlying mechanisms remain to be elucidated. Recent studies have suggested that neuroimmune dysregulation is involved in the pathogenesis of OCD. To investigate the role of microglia in this disorder, we established a pharmacological mouse model by using the serotonin (5-HT) 1A/1B receptor agonist RU24969 to mimic monoamine dysregulation in OCD, and we examined the morphological and functional alterations of microglia in this model. We found that RU24969 treatment led to compulsive circling behavior in mice. Strikingly, we found that the density and mobility of microglia in the prelimbic cortex were much lower in RU24969-treated mice than in control mice. Moreover, the expression of cytokines and chemokines, including BDNF, IL-1ß, IL-6, TNFα, CD80, CD86, MHC-I, and MHC-II, also decreased in RU24969-treated mice. Importantly, we found that injection of BDNF or induction of BDNF expression by trehalose completely reversed microglial dysfunction and reduced stereotypic behavior. These results indicate that microglial dysfunction is closely related to stereotypic behaviors in our mouse model of OCD and that BDNF could be an effective treatment for stereotypic behaviors.

The Occurrence of Metronidazole-Induced Encephalopathy in Cancer Patients: A Hospital-Based Retrospective Study.

BACKGROUND: Metronidazole-induced encephalopathy (MIE) is a rare but serious complication caused by metronidazole, a widely used antianaerobic drug. Previous studies prescribed MIE including dysarthria, cerebellar ataxia, and confusion after long-term use of metronidazole. Malignancy has been proposed one of the predisposing conditions for MIE. However, the occurrence of MIE in cancer patients remains unknown. METHODOLOGY: We investigated the occurrence of MIE and analyzed retrospectively by hospital-based data of 4160 cancer patients from January 2014 to December 2016. RESULTS: Findings in 793 cancer patients who underwent metronidazole therapy for anaerobic infection revealed two cases of MIE. One had renal cell carcinoma and the other had bladder urothelial carcinoma. Both of their initial presentation were cerebellar dysfunction. The occurrence of MIE was 8.6% for cases who received >30 g of cumulative dose. Hypertension was the most common comorbidity, followed by chronic renal disease and diabetes mellitus. CONCLUSION: In cancer patients, MIE should be monitored in those with genitourinary cancer, especially with renal dysfunction. Longer duration with more cumulative dose also has a greater risk of MIE. Early consideration of MIE with prompt cessation of metronidazole may result in better outcome.

Serum lipid level is not associated with symptomatic intracerebral hemorrhage after intravenous thrombolysis for acute ischemic stroke.

BACKGROUND: This study assessed whether serum lipid levels are associated with the risk of symptomatic intracerebral hemorrhage (sICH) and functional outcomes in patients with acute ischemic stroke after receiving intravenous thrombolysis. METHODS: We retrospectively analyzed consecutive ischemic stroke patients who were treated with intravenous tissue plasminogen activator between January 2007 and January 2017. Lipid levels on admission, including total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglyceride levels, as well as potential predictors of sICH were tested using univariate and multivariate analyses. RESULTS: Of the 229 enrolled patients (100 women, aged 68 ± 13 years), 14 developed sICH and 103 (45%) had favorable functional outcomes at 3 months. The patients with sICH more often had diabetes mellitus (71% vs. 26%, P = 0.01) and had more severe stroke (mean National Institutes of Health Stroke Scale [NIHSS] score of 16 vs. 13, P = 0.045). Regarding lipid subtype, total cholesterol, LDL-C, HDL-C, and triglyceride levels were not associated with sICH or functional outcomes. According to the results of multivariate analysis, the frequency of sICH was independently associated with diabetes mellitus (odds ratio [OR] = 6.04; 95% CI [1.31-27.95]; P = 0.02) and the NIHSS score (OR = 1.12; 95% CI [1.02-1.22]; P = 0.01). A higher NIHSS score was independently associated with unfavorable functional outcomes (OR = 0.86; 95% CI [0.81-0.91]; P < 0.001). CONCLUSIONS: Serum lipid levels on admission, including total cholesterol, LDL-C, HDL-C, and triglyceride levels, were not associated with sICH or 3-month functional outcomes after intravenous thrombolysis for acute ischemic stroke.