Objective:This study explores the relationship between emotional dysregulation, attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) symptoms using network models.Method:A total of 967 children with ADHD comorbid ODD were recruited from the outpatient department of Peking University Sixth Hospital from September 2002 to June 2022. All subjects were rated for the ADHD symptom severity using the ADHD symptom rating scale. ODD symptoms and emotional dysregulation symptoms were assessed by the Children′s Clinical Diagnostic Interview Scale, and the Conners′ Parent Symptom Questionnaire. R (version 4.2.1) packages mgm, qgraph, bnlearn, etc. were used for network analysis, and centrality indices were calculated to define central symptoms and bridge symptoms. Results:The relationship between emotional dysregulation and ODD symptoms was closer. ODD symptoms had higher strength indices, especially the items "gets annoyed or irritated by the behavior of adults"(strength=3.57) and "loses temper or gets angry with adults when does not get his or her own way"(strength=2.32). Emotional dysregulation symptoms had a higher bridge strength indices, with "temper outbursts, explosive and unpredictable behavior" (bridge strength=2.64) as the most prominent item. Bayesian network analysis showed that ADHD symptoms were at the upper of DAG, directly linked with emotional dysregulation symptoms and indirectly linked with ODD symptoms through emotional dysregulation symptoms.Conclusion:Emotional dysregulation symptoms were more closely associated with ODD symptoms than ADHD symptoms, and might potentially acted as bridge symptoms between ADHD and ODD. ADHD symptoms might drive ODD symptoms indirectly through emotional dysregulation symptoms.

Objective:This study explores the relationship between emotional dysregulation, attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) symptoms using network models.Method:A total of 967 children with ADHD comorbid ODD were recruited from the outpatient department of Peking University Sixth Hospital from September 2002 to June 2022. All subjects were rated for the ADHD symptom severity using the ADHD symptom rating scale. ODD symptoms and emotional dysregulation symptoms were assessed by the Children′s Clinical Diagnostic Interview Scale, and the Conners′ Parent Symptom Questionnaire. R (version 4.2.1) packages mgm, qgraph, bnlearn, etc. were used for network analysis, and centrality indices were calculated to define central symptoms and bridge symptoms. Results:The relationship between emotional dysregulation and ODD symptoms was closer. ODD symptoms had higher strength indices, especially the items "gets annoyed or irritated by the behavior of adults"(strength=3.57) and "loses temper or gets angry with adults when does not get his or her own way"(strength=2.32). Emotional dysregulation symptoms had a higher bridge strength indices, with "temper outbursts, explosive and unpredictable behavior" (bridge strength=2.64) as the most prominent item. Bayesian network analysis showed that ADHD symptoms were at the upper of DAG, directly linked with emotional dysregulation symptoms and indirectly linked with ODD symptoms through emotional dysregulation symptoms.Conclusion:Emotional dysregulation symptoms were more closely associated with ODD symptoms than ADHD symptoms, and might potentially acted as bridge symptoms between ADHD and ODD. ADHD symptoms might drive ODD symptoms indirectly through emotional dysregulation symptoms.

Metastasis is crucial for the mortality of non-small cell lung carcinoma (NSCLC) patients. The epithelial-mesenchymal transition (EMT) plays a critical role in regulating tumor metastasis. Glioma-associated oncogene 1 (Gli1) is aberrantly active in a series of tumor tissues. However, the molecular regulatory relationships between Gli1 and NSCLC metastasis have not yet been identified. Herein, we reported Gli1 promoted NSCLC metastasis. High Gli1 expression was associated with poor survival of NSCLC patients. Ectopic expression of Gli1 in low metastatic A549 and NCI-H460 cells enhanced their migration, invasion abilities and facilitated EMT process, whereas knock-down of Gli1 in high metastatic NCI-H1299 and NCI-H1703 cells showed an opposite effect. Notably, Gli1 overexpression accelerated the lung and liver metastasis of NSCLC in the intravenously injected metastasis model. Further research showed that Gli1 positively regulated Snail expression by binding to its promoter and enhancing its protein stability, thereby facilitating the migration, invasion and EMT of NSCLC. In addition, administration of GANT-61, a Gli1 inhibitor, obviously suppressed the metastasis of NSCLC. Collectively, our study reveals that Gli1 is a critical regulator for NSCLC metastasis and suggests that targeting Gli1 is a prospective therapy strategy for metastatic NSCLC.