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1.
J Nurs Manag ; 27(6): 1285-1293, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31144776

RESUMO

AIM: This study aims to identify the role that spiritual climate has in reducing burnout and intentions to leave amongst clinical nurses. BACKGROUND: Both shortages and the high turnover of nurses are challenging problems worldwide. Enhancing the spiritual climate amongst nurses can enhance teamwork, organisational commitment and job satisfaction and can play a role in reducing burnout and turnover intention. METHODS: A total of 207 clinical nurses working at a tertiary university hospital were included in this cross-sectional, single-site study. Independent-samples t test and ANOVA, Pearson correlation analysis and hierarchical regression analysis were used to explore the relationships amongst related factors. RESULTS: Most clinical departments showed a moderate spiritual climate (60.24 ± 0.82) with high job burnout (33.62 ± 0.28) and turnover intention (2.37 ± 0.57). A good spiritual climate was correlated with high job satisfaction (r = 0.412, p < 0.01), low burnout and turnover intention (r = -0.423, p < 0.01 and r = -0.292, p < 0.01, respectively). Spiritual climate could also indirectly influence nurses' job burnout and turnover intention (R2  = 10.31%). CONCLUSIONS: Different departments have different spiritual climates. The findings from this study indicate that spiritual climate may impact nursing burnout and turnover. IMPLICATIONS FOR NURSING MANAGEMENT: Using a spiritual climate scale provides health care decision-makers with clear information about staff spirituality well-being. Interventions to improve spiritual climate can benefit teamwork in clinical departments.


Assuntos
Esgotamento Profissional/complicações , Satisfação no Emprego , Cultura Organizacional , Espiritualidade , Adulto , Atitude do Pessoal de Saúde , Esgotamento Profissional/psicologia , China , Estudos Transversais , Feminino , Humanos , Intenção , Masculino , Pessoa de Meia-Idade , Reorganização de Recursos Humanos/tendências , Inquéritos e Questionários , Local de Trabalho/psicologia , Local de Trabalho/normas
2.
Metabolism ; 79: 10-23, 2018 02.
Artigo em Inglês | MEDLINE | ID: mdl-29080813

RESUMO

OBJECTIVE: Growth hormone stimulates growth by increasing insulin-like growth factor 1 expression and secretion. In the presence of insufficient nutrients, GH increases, whereas IGF-1 expression becomes severely suppressed, leading to GH resistance. This study aimed to explore the effect of arginine (Arg) on GH resistance during malnutrition and to describe its underlying mechanism. METHODS: C57BL/6J mice were injected intraperitoneally with Arg for 1h or subjected to caloric restriction with Arg supplement in drinking water for 18days. HepG2 cells were exposed to different Arg concentrations for 24h. Signaling pathway agonists/inhibitors, siRNA, and overexpression plasmids were used to investigate the underlying molecular mechanism. Liver-specific toll-like receptor (TLR4) knockout mice were utilized to clarify the role of TLR4 in Arg-induced IGF-I expression and secretion. RESULTS: Arg inhibited the TLR4 downstream pathway by binding to TLR4 and consequently activated Janus kinase 2/signal transducer and activator of transcription 5 signaling pathway. As a result, IGF-1 transcription and secretion increased. Arg activity was absent in liver-specific TLR4 knockout mice and was greatly suppressed in liver with overexpressed TLR4, suggesting that hepatic TLR4 was required and sufficient to induce GH resistance. By contrast, the mammalian target of rapamycin pathway was unnecessary for Arg activity. Arg not only significantly increased IGF-1 expression and secretion under acute fasting and chronic CR conditions but also attenuated body weight loss. CONCLUSIONS: Our results demonstrate a previously unappreciated pathway involving Arg that reverses GH resistance and alleviates malnutrition-induced growth restriction through the inhibition of TLR4-mediated inflammatory pathway.


Assuntos
Arginina/farmacologia , Hormônio do Crescimento/metabolismo , Inflamação/metabolismo , Receptor 4 Toll-Like/antagonistas & inibidores , Animais , Humanos , Fator de Crescimento Insulin-Like I/metabolismo , Janus Quinase 2/biossíntese , Janus Quinase 2/genética , Masculino , Desnutrição/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Transporte Proteico , RNA Interferente Pequeno/metabolismo , Fator de Transcrição STAT5/biossíntese , Fator de Transcrição STAT5/genética , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/genética
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