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- 저자 : Zhou Jianda (검색결과 3 건)
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Xie Jianfei,Liu Min,Zhong Zhuqing,Zhang Qiuxiang,Zhou Jianda,Wang Lu,Ma Keke,Ding Siqing,Zhang Xiaohong,Sun Qian,Cheng Andy S.K. 한국간호과학회 2020 Asian Nursing Research Vol.14 No.3
Purpose: From the perspective of positive psychology, our study aimed to explore depressive symptoms and psychological well-being among Chinese nurses, as well as analyze the impacts of character strengths, self-efficacy and social support on the mental health of nurses. Methods: A cross-sectional and descriptive design using five self-reported questionnaires was used to investigate a cohort of 4238 nurses during 2018. A structural equation modeling analysis was used to verify a hypothetical model linking character strengths, self-efficacy, social support, depressive symptoms, and psychological well-being. Results: The prevalence of depression among this cohort of Chinese nurses was 58.1%. The mean scores for caring, inquisitiveness, and self-control were 19.93 (SD ¼ 2.82), 15.94 (SD ¼ 3.00), and 16.34 (SD ¼ 2.95), respectively. The hypothesized model was a good fit of the data (c2/df ¼ 1.77, p ¼ .183, root mean square error of approximation ¼ 0.04, goodness of fit index ¼ 1.00, comparative fit index ¼ 1.00, TuckereLewis index ¼ 1.00). Except for the path from self-control to depression, the other hypothetical paths investigated were statistically significant. Conclusion: Character strengths were directly and positively associated with psychological well-being. Inquisitiveness was the strongest direct protective factor for depression. In addition, character strengths indirectly alleviated depression and increased psychological well-being through mediating variables of social support and self-efficacy. This study should alert nurse managers that more attention should be paid to the character strengths and mental health of nurses. This study provides evidence for interventions based on character strengths as a management strategy to support the mental health of nurses.
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Cao, Ke,Li, Jingjing,Zhao, Yong,Wang, Qi,Zeng, Qinghai,He, Siqi,Yu, Li,Zhou, Jianda,Cao, Peiguo Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.2
miR-101 is considered to play an important role in hepatocellular carcinoma (HCC), but the underlying molecular mechanism remains to be elucidated. Here, we aimed to confirm whether Girdin is a target gene of miR-101 and determine the tumor suppressor of miR-101 through Girdin pathway. In our previous studies, we firstly found Girdin protein was overexpressed in HCC tissues, and it closely correlated to tumor size, T stage, TNM stage and Edmondson-Steiner stage of HCC patients. After specific small interfering RNA of Girdin was transfected into HepG2 and Huh7.5.1 cells, the proliferation and invasion ability of tumor cells were significantly inhibited. In this study, we further explored the detailed molecular mechanism of Girdin in HCC. Interestingly, we found that miR-101 significantly low-expressed in HCC tissues compared with that in matched normal tissues while Girdin had a relative higher expression, and miR-101 was inversely correlated with Girdin expression. In addition, after miR-101 transfection, the proliferation, migration and invasion abilities of HepG2 cells were weakened. Furthermore, we confirmed that Girdin is a direct target gene of miR-101. Finally we confirmed Talen-mediated Girdin knockout markedly suppressed cell proliferation, migration and invasion in HCC while downregulation of miR-101 significantly restored the inhibitory effect. Our findings suggested that miR-101/Girdin axis could be a potential application of HCC treatment.
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Peiguo Cao,Ke Cao,Jingjing Li,Yong Zhao,Qi Wang,Qinghai Zeng,Siqi He,Li Yu,Jianda Zhou 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.2
miR-101 is considered to play an important role in hepatocellular carcinoma (HCC), but the underlying molecular mechanism remains to be elucidated. Here, we aimed to confirm whether Girdin is a target gene of miR-101 and determine the tumor suppressor of miR-101 through Girdin pathway. In our previous studies, we firstly found Girdin protein was overexpressed in HCC tissues, and it closely correlated to tumor size, T stage, TNM stage and Edmondson-Steiner stage of HCC patients. After specific small interfering RNA of Girdin was transfected into HepG2 and Huh7.5.1 cells, the proliferation and invasion ability of tumor cells were significantly inhibited. In this study, we further explored the detailed molecular mechanism of Girdin in HCC. Interestingly, we found that miR-101 significantly low-expressed in HCC tissues compared with that in matched normal tissues while Girdin had a relative higher expression, and miR-101 was inversely correlated with Girdin expression. In addition, after miR-101 transfection, the proliferation, migration and invasion abilities of HepG2 cells were weakened. Furthermore, we confirmed that Girdin is a direct target gene of miR-101. Finally we confirmed Talen-mediated Girdin knockout markedly suppressed cell proliferation, migration and invasion in HCC while down-regulation of miR-101 significantly restored the inhibitory effect. Our findings suggested that miR-101/Girdin axis could be a potential application of HCC treatment.
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