Campus bullying and associated factors among college and middle school students in Tibet / 中国学校卫生

Objective@#To understand campus bullying in colleges and middle schools in Tibet, and to analyze related influencing factors, so as to provide reliable basis and reference for formulating targeted intervention measures.@*Methods@#A stratified cluster sampling method was used to investigate the status and influencing factors of being bullied by questionnaire among 3 875 college and middle school students in Ngari, Qamdo, Lhasa, Nagqu and Xigaze of Tibet, from September to November 2019. Chi-square test and Logistic regression method were used for data analysis.@*Results@#The report rate of campus bullying among college and middle school students in Tibet was 5.50%; 4.35% for girls and 6.76% for boys；8.81% for college students, 1.64% for senior high school students and 5.94% for junior high school students. The results of multivariate Logistic regression analysis showed that smoking ( OR =1.71), Internet addiction ( OR =3.82), depression ( OR =3.84), obesity ( OR =2.02), single parent family ( OR = 1.67 ) and reorganized family ( OR =3.74) were positively correlated with campus bullying ( P <0.05). Girls ( OR =0.66) and senior high school ( OR =0.28) were negatively correlated with campus bullying ( P <0.05).@*Conclusion@#Campus bullying is related to campus environment, family type, behaviors and life styles, etc. Efforts should be committed to build a caring campus culture and a good family moral education environment, in order to reduce the incidence of campus bullying and associated adverse effects.

AKAP95 promotes cell cycle progression via interactions with cyclin E and low molecular weight cyclin E.

AKAP95 in lung cancer tissues showed higher expression than in paracancerous tissues. AKAP95 can bind with cyclin D and cyclin E during G1/S cell cycle transition, but its molecular mechanisms remain unclear. To identify the mechanism of AKAP95 in cell cycle progression, we performed AKAP95 transfection and silencing in A549 cells, examined AKAP95, cyclin E1 and cyclin E2 expression, and the interactions of AKAP95 with cyclins E1 and E2. Results showed that over-expression of AKAP95 promoted cell growth and AKAP95 bound cyclin E1 and E2, low molecular weight cyclin E1 (LWM-E1) and LWM-E2. Additionally AKAP95 bound cyclin E1 and LMW-E2 in the nucleus during G1/S transition, bound LMW-E1 during G1, S and G2/M, and bound cyclin E2 mainly on the nuclear membrane during interphase. Cyclin E2 and LMW-E2 were also detected. AKAP95 over-expression increased cyclin E1 and LMW-E2 expression but decreased cyclin E2 levels. Unlike cyclin E1 and LMW-E2 that were nuclear located during the G1, S and G1/S phases, cyclin E2 and LMW-E1 were expressed in all cell cycle phases, with cyclin E2 present in the cytoplasm and nuclear membrane, with traces in the nucleus. LMW-E1 was present in both the cytoplasm and nucleus. The 20 kDa form of LMW-E1 showed only cytoplasmic expression, while the 40 kDa form was nuclear expressed. The expression of AKAP95, cyclin E1, LMW-E1 and -E2, might be regulated by cAMP. We conclude that AKAP95 might promote cell cycle progression by interacting with cyclin E1 and LMW-E2. LMW-E2, but not cyclin E2, might be involved in G1/S transition. The binding of AKAP95 and LMW-E1 was found throughout cell cycle.

Expression of AKAP95, Cx43, CyclinE1 and CyclinD1 in esophageal cancer and their association with the clinical and pathological parameters.

OBJECTIVE: To investigate correlations among A-kinase anchor protein95 (AKAP95), Connexin43 (Cx43), CyclinE1 and CyclinD1 in esophageal squamous cell cancer tissues, and their relationship with clinical and pathological parameters. METHODS: The protein levels of AKAP95, Cx43, CyclinE1 and CyclinD1 in 54 cases of esophageal squamous cell cancer tissues were determined by immunohistochemistry. RESULTS: The expression of AKAP95, CyclinE1 and CyclinD1 in esophageal squamous cell cancer tissues (53.70%, 88.89%, 72.22%, respectively) was significantly increased when compared to pericarcinoma tissues (20.00%, P < 0.05; 6.67%, P < 0.01; and 20.00%, P < 0.05; respectively). By contrast, Cx43 expression in esophageal squamous cell cancer tissues (22.22%) was lower than that in pericarcinoma tissues (60.00%, P < 0.05). The expression of AKAP95, Cx43, CyclinE1 and CyclinD1 in the tissues of esophageal squamous cell carcinoma was unrelated to lymph node metastasis and the degree of differentiation. The expression of Cx43, CyclinE1, CyclinD1 in the tissues of esophageal squamous cell carcinoma was significantly correlated with AKAP95, respectively (P < 0.05). CONCLUSION: Expression levels of AKAP95, CyclinE1 and CyclinD1 were higher, and that of Cx43 lower in esophageal squamous cell carcinoma tissues as compared pericarcinoma tissues, which suggests their importance in the incidence and development of esophageal squamous cell carcinoma. The expression of Cx43, CyclinE1, CyclinD1 in the tissues of esophageal squamous cell carcinoma was correlated with AKAP95, respectively. The expression of AKAP95, Cx43, CyclinE1 and CyclinD1 in the tissues of esophageal squamous cell carcinoma was unrelated to the degree of differentiation and lymph node metastasis.

Synergistic effects of AKAP95, Cyclin D1, Cyclin E1, and Cx43 in the development of rectal cancer.

OBJECTIVE: To explore the expression of A-kinase anchor protein 95 (AKAP95), Cyclin D1, Cyclin E1, and Connexin43 (Cx43) in rectal cancer tissues and assess the associations between each of the proteins and pathological parameters, as well as their inter-relationships. METHODS: AKAP95, Cyclin D1, Cyclin E1, and Cx43 protein expression rates were evaluated by immunohistochemistry in 50 rectal cancer specimens and 16 pericarcinoma tissues. RESULTS: The positive rates of AKAP95, Cyclin E1, and Cyclin D1 proteins were 54.00 vs. 18.75%, 62.00 vs. 6.25%, and 72.00 vs. 31.25% in rectal cancer specimens and pericarcinoma tissues, respectively, representing statistically significant differences (P < 0.05). The positive rate of Cx43 protein expression in rectal cancer tissues was 44.00% and 62.50% in pericarcinoma tissues, and the difference between them was not significant (P > 0.05). No significant associations were found between protein expression of AKAP95, Cyclin E1, Cyclin D1, and Cx43, and the degree of differentiation, histological type, and lymph node metastasis of rectal cancer (P > 0.05). However, significant correlations were obtained between the expression rates of AKAP95 and Cyclin E1, Cyclin E1 and Cyclin D1, Cyclin E1 and Cx43 protein, and Cyclin D1 and Cx43, respectively (P < 0.05). CONCLUSION: AKAP95, Cyclin E1, and Cyclin D1 protein expression rates were significantly higher in rectal cancer tissues compared with pericarcinoma samples, suggesting an association between these proteins and the development and progression of rectal cancer. In addition, the significant correlations between the proteins (AKAP95 and Cyclin E1, Cyclin E1 and Cyclin D1, Cyclin E1 and Cx43 protein, and Cyclin D1 and Cx43) indicate the possible synergistic effects of these factors in the development and progression of rectal cancer.