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RISS 인기검색어
- 검색키워드
- 저자 : Anduaga, Javier (검색결과 3 건)
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Association Between Burnout and Intention to Emigrate in Peruvian health-care Workers
Anduaga-Beramendi, Alexander,Beas, Renato,Maticorena-Quevedo, Jesus,Mayta-Tristan, Percy Occupational Safety and Health Research Institute 2019 Safety and health at work Vol.10 No.1
Background: Emigration of health-care workers is a problem within global health systems which affects many countries, including Peru. Several factors have caused health-care workers to emigrate, including burnout syndrome (BS). This study aims to identify the association between BS and its dimensions with the intention of physicians and nurses to emigrate from Peru in 2014. Methods: A cross-sectional study, based on a secondary analysis of the National Survey of Health Users (ENSUSALUD - 2014) was conducted. Sampling was probabilistic, considering the 24 departments of Peru. We include the questionnaire for physicians and nurses, accounting for 5062 workers. BS was measured by the Maslach Burnout Inventory-Human Services Survey. Adjusted odds ratio (OR) was calculated using multiple logistic regression. Results: Of the study population, 44.1% were physicians, 37.7% males, and 23.1% were working in Lima. It was found that 2.8% [95% confidence interval (CI): 2.19-3.45] of health-care workers had BS. The overall prevalence of intention to emigrate among health-care workers was 7.4% (95% CI: 6.36-8.40). Association was found between BS and intention to emigrate in Peruvian health-care workers (OR = 2.15; 95% CI: 1.05-4.40). Emotional exhaustion was the BS dimension most associated with intention to emigrate (OR = 1.80; 95% CI: 1.16-2.78). Conclusion: Physicians and nurses from Peru who suffered from BS were more likely to have intention to emigrate. Policies should be established to reduce BS as a strategy to control "brain drain" from health-care workers of Peru.
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Association Between Burnout and Intention to Emigrate in Peruvian health-care Workers
Alexander Anduaga-Beramendi,Renato Beas,Jesus Maticorena-Quevedo,Percy Mayta-Tristán 한국산업안전보건공단 산업안전보건연구원 2019 Safety and health at work Vol.10 No.1
Background: Emigration of health-care workers is a problem within global health systems which affects many countries, including Peru. Several factors have caused health-care workers to emigrate, including burnout syndrome (BS). This study aims to identify the association between BS and its dimensions with the intention of physicians and nurses to emigrate from Peru in 2014. Methods: A cross-sectional study, based on a secondary analysis of the National Survey of Health Users (ENSUSALUD - 2014) was conducted. Sampling was probabilistic, considering the 24 departments of Peru. We include the questionnaire for physicians and nurses, accounting for 5062 workers. BS was measured by the Maslach Burnout Inventory-Human Services Survey. Adjusted odds ratio (OR) was calculated using multiple logistic regression. Results: Of the study population, 44.1% were physicians, 37.7% males, and 23.1% were working in Lima. It was found that 2.8% [95% confidence interval (CI): 2.19e3.45] of health-care workers had BS. The overall prevalence of intention to emigrate among health-care workers was 7.4% (95% CI: 6.36e8.40). Association was found between BS and intention to emigrate in Peruvian health-care workers (OR ¼ 2.15; 95% CI: 1.05e4.40). Emotional exhaustion was the BS dimension most associated with intention to emigrate (OR ¼ 1.80; 95% CI: 1.16e2.78). Conclusion: Physicians and nurses from Peru who suffered from BS were more likely to have intention to emigrate. Policies should be established to reduce BS as a strategy to control “brain drain” from healthcare workers of Peru.
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Cho, Jun-Ho,Kim, Goo-Young,Pan, Chi-Jiunn,Anduaga, Javier,Choi, Eui-Ju,Mansfield, Brian C.,Chou, Janice Y. Public Library of Science 2017 PLoS genetics Vol.13 No.5
<▼1><P>A deficiency in glucose-6-phosphatase-α (G6Pase-α) in glycogen storage disease type Ia (GSD-Ia) leads to impaired glucose homeostasis and metabolic manifestations including hepatomegaly caused by increased glycogen and neutral fat accumulation. A recent report showed that G6Pase-α deficiency causes impairment in autophagy, a recycling process important for cellular metabolism. However, the molecular mechanism underlying defective autophagy is unclear. Here we show that in mice, liver-specific knockout of G6Pase-α (L-<I>G6pc</I>-/-) leads to downregulation of sirtuin 1 (SIRT1) signaling that activates autophagy via deacetylation of autophagy-related (ATG) proteins and forkhead box O (FoxO) family of transcriptional factors which transactivate autophagy genes. Consistently, defective autophagy in G6Pase-α-deficient liver is characterized by attenuated expressions of autophagy components, increased acetylation of ATG5 and ATG7, decreased conjugation of ATG5 and ATG12, and reduced autophagic flux. We further show that hepatic G6Pase-α deficiency results in activation of carbohydrate response element-binding protein, a lipogenic transcription factor, increased expression of peroxisome proliferator-activated receptor-γ (PPAR-γ), a lipid regulator, and suppressed expression of PPAR-α, a master regulator of fatty acid β-oxidation, all contributing to hepatic steatosis and downregulation of SIRT1 expression. An adenovirus vector-mediated increase in hepatic SIRT1 expression corrects autophagy defects but does not rectify metabolic abnormalities associated with G6Pase-α deficiency. Importantly, a recombinant adeno-associated virus (rAAV) vector-mediated restoration of hepatic G6Pase-α expression corrects metabolic abnormalities, restores SIRT1-FoxO signaling, and normalizes defective autophagy. Taken together, these data show that hepatic G6Pase-α deficiency-mediated down-regulation of SIRT1 signaling underlies defective hepatic autophagy in GSD-Ia.</P></▼1><▼2><P><B>Author summary</B></P><P>GSD-Ia is an autosomal recessive metabolic disorder caused by a deficiency in G6Pase-α, a key enzyme in maintaining blood glucose levels between meals. Despite strong compliance to dietary therapies, GSD-Ia patients continue manifesting metabolic aberrations including excessive accumulation of glycogen and lipid in the liver. Recently, G6Pase-α deficiency has been linked to impairment in autophagy, a recycling process essential for cellular homeostasis. However, the underlying mechanism is unclear. In this study, we show that hepatic G6Pase-α deficiency alters the activity and/or expression of several lipid regulators, leading to hepatic steatosis and reduced expression of SIRT1, an enzyme that regulates the activity of many proteins via deacetylation. The impaired SIRT1 signaling increases the acetylation of ATG proteins critical for autophagic vesicle elongation, and reduces the activity of FoxO factors that can induce autophagy genes. Consistently, the G6Pase-α-deficient liver exhibits autophagy impairment characterized by attenuated expression of many autophagy components, defective autophagic vesicle elongation, impaired autophagosome formation, and reduced autophagy flux. Importantly, SIRT1 overexpression in G6Pase-α-deficient liver corrects autophagy deficiency. Finally, restoration of hepatic G6Pase-α expression corrects metabolic abnormalities, restores SIRT1-FoxO signaling, and normalizes defective autophagy. Collectively, hepatic G6Pase-α deficiency-mediated down-regulation of SIRT1 signaling underlies defective hepatic autophagy in GSD-Ia.</P></▼2>
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