School bullying can cause severe mental health problems for both victims and perpetrators. However, the association between bullying victimization and perpetration has rarely been discussed, and no study has investigated the effects of social support, such as friendship and family support, in moderating this association. Therefore, the authors examined the moderating effects of friendship and family support on the association between bullying victimization and perpetration in adolescents. Data were obtained from the 2009 Project for the Health of Adolescents. Through multistage stratified cluster sampling, 13 junior and 10 senior high schools in southern Taiwan were selected, resulting in a representative sample of 6,445 students from grades 7 to 12. School bullying and family support were examined using the Chinese version of the School Bullying Experience Questionnaire and the Family adaptability, partnership, growth, affection, resolve instrument, respectively. Friendship support was measured using the subscale of the Taiwanese Quality of Life Questionnaire for Adolescents and adolescents’ number of friends, time spent with friends, and friend distributions. Linear regression modeling and the Johnson–Neyman technique were used to examine the moderating effects of friendship and family support on the association between bullying victimization and perpetration. For active bullying, having fun and talkative friends and friends outside school negatively moderated the intensity of the association between bullying victimization and perpetration (regression coefficients: −0.02 to −0.05), whereas, for passive bullying, only friends outside school negatively moderated the intensity of the association (regression coefficient: −0.05). By contrast, some components of friendship support positively moderated the associations. These findings suggest that higher friendship quality and having more friends outside of school attenuate the association between bullying victimization and perpetration in adolescents, thus increasing the understanding of the moderating role that social support play in such associations.

Indirubin is the active component of Dang gui Long hui Wan, a traditional Chinese herbal medicine used as therapy for chronic myelogenous leukemia (CML). In clinical studies, indirubin seldom caused major side-effects. However, the functional effect of indirubin on acute lymphoblastic leukemia (ALL) is unclear. Therefore, we investigated the effects of indirubin-3'-monoxime (I3M) on the ALL cell line JM1 and the CML cell line K562 (control). The anti-leukemia effects and mechanisms of I3M were similar on ALL and CML cells. I3M significantly and dose-dependently decreased cell viability. The G2/M cell cycle phase was arrested and the sub-G1 proportion was relatively increased. In addition, caspase-3 activation led to poly(ADP-ribose) polymerase (PARP)-1 cleavage and the progression of apoptosis. Notably, I3M induced autophagy. However, I3M had no effect on necrosis in either cell line. We specifically found that I3M only marginally affected the survival of primary mature lymphocytes, and was not cytotoxic to granulocytes. Since I3M induced apoptosis and autophagy in human lymphocytic leukemia cells and caused few side-effects in healthy lymphocytes and granulocytes, I3M may be useful for clinical anti-ALL therapy.

High mobility group AT-hook 2 (HMGA2) is an architectural transcription factor that is negatively regulated by let-7 microRNA through binding to it's 3'-untranslated region. Transgenic mice expressing Hmga2 with a truncation of its 3'-untranslated region has been shown to exhibit a myeloproliferative phenotype. To decipher the let-7-HMGA2 axis in myeloproliferative neoplasms, we employed an in vitro model supplemented with clinical correlation. Ba/F3 cells with inducible JAK2V617F expression (Ton.JAK2.V617F cells) showed upregulation of HMGA2 with concurrent let-7a repression. Ton.JAK2.V617F cells treated with a let-7a inhibitor exhibited further escalation of Hmga2 expression, while a let-7a mimic diminished the Hmga2 transcript level. Hmga2 overexpression conferred JAK2-mutated cells with a survival advantage through inhibited apoptosis. A pan-JAK inhibitor, INC424, increased the expression of let-7a, downregulated the level of Hmga2, and led to increased apoptosis in Ton.JAK2.V617F cells in a dose-dependent manner. In samples from 151 patients with myeloproliferative neoplasms, there was a modest inverse correlation between the expression levels of let-7a and HMGA2 Overexpression of HMGA2 was detected in 29 (19.2%) of the cases, and it was more commonly seen in patients with essential thrombocythemia than in those with polycythemia vera (26.9% vs 12.7%, P=0.044). Patients with upregulated HMGA2 showed an increased propensity for developing major thrombotic events, and they were more likely to harbor one of the 3 driver myeloproliferative neoplasm mutations in JAK2, MPL and CALR Our findings suggest that, in a subset of myeloproliferative neoplasm patients, the let-7-HMGA2 axis plays a prominent role in the pathogenesis of the disease that leads to unique clinical phenotypes.

Background: In this study, we examined the differential associations of various proinflammatory and anti-inflammatory cytokines with depression severity from the development of breast cancer to subsequent chemotherapy treatment. Methods: A cross-sectional study was conducted on a sample of 116 women: 29 controls without cancer, 55 patients with breast cancer who were not receiving chemotherapy, and 32 patients with breast cancer who were receiving chemotherapy. Blood samples were assayed to evaluate serum levels of the following cytokines: interferon-γ, interleukin (IL)-12 (p70), IL-1β, IL-2, tumor necrosis factor (TNF)-α, IL-4, IL-5, IL-10, IL-13, IL-6, and IL-17A. Depression severity was assessed using the Patient Health Questionnaire. Results: After adjustment for sociodemographics, consistent patterns of the association between cytokine and depression were noted in the different groups. No significant associations were observed in the controls. Inverse associations were observed between cytokines levels and depression severity in patients with breast cancer who were not receiving chemotherapy, whereas positive associations were noted in patients with breast cancer who were receiving chemotherapy. Specific differential relationships between IL-5 levels and depression severity were found between patients with breast cancer who were receiving and not receiving chemotherapy. Conclusions: Our study revealed differential relationships between cytokine levels and depression severity with the development of cancer. Immunostimulation and immunosuppression in breast cancer and cancer treatment may account for the differential responses with the development of breast cancer.

Although adolescents with attention-deficit hyperactivity disorder (ADHD) have a higher risk of suicidality and more problems related to school bullying, and quality of life (QoL) is reportedly associated with school bullying, suicide, and ADHD, no study has examined their correlation. This study examined the complex relationships between QoL, school bullying, suicide, and ADHD symptoms. A total of 203 adolescents with ADHD aged between 12 and 18 years were recruited. School bullying and QoL were examined using the Chinese version of the School Bullying Experience Questionnaire and the Taiwanese Quality of Life Questionnaire for Adolescents. Network model analysis was conducted to graphically present their relationships. We identified triangular correlations between school bullying, QoL, and suicidality, indicating possible pathways from school bullying to suicidality, and the originating or mediating roles of personal competence and psychological well-being. Furthermore, the ADHD symptoms of inattention and hyperactivity/impulsivity may differentially regulate these pathways. Longitudinal studies are warranted to confirm these findings.