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1.
Geriatr Nurs ; 42(4): 843-849, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34090229

RESUMO

Many terminally ill older adults depend on family members to make medical decisions in China. Many family members find it difficult to make do-not-resuscitate (DNR) decisions in emergency departments (ED). Currently, factors that affect DNR decision making by family members for older adults needing emergency care have not been well studied. This qualitative inquiry explores factors influencing DNR decision-making among family members of terminally ill older adults in ED. Semi-structured in-depth interviews were conducted for a 12-family member of terminally ill older adults at ED in China. Results of the conventional content analysis showed that family members made DNR decisions based on a wide of reasons: (a) subjective perception of family members, (b) conditions of the terminally ill older adults, (c) external environmental factors, and (d) internal family factors. The findings of this study expand our knowledge and understanding of factors influencing DNR decision-making by family members of terminally ill older adults in ED.


Assuntos
Ordens quanto à Conduta (Ética Médica) , Doente Terminal , Idoso , China , Tomada de Decisões , Serviço Hospitalar de Emergência , Família , Humanos
2.
World J Emerg Med ; 11(4): 231-237, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33014219

RESUMO

BACKGROUND: Consenting to do-not-resuscitate (DNR) orders is an important and complex medical decision-making process in the treatment of patients at the end-of-life in emergency departments (EDs). The DNR decision in EDs has not been extensively studied, especially in the Chinese mainland. METHODS: This retrospective chart study of all deceased patients in the ED of a university hospital was conducted from January 2017 to December 2019. The patients with out-of-hospital cardiac arrest were excluded. RESULTS: There were 214 patients' deaths in the ED in the three years. Among them, 132 patients were included in this study, whereas 82 with out-of-hospital cardiac arrest were excluded. There were 99 (75.0%) patients' deaths after a DNR order medical decision, 64 (64.6%) patients signed the orders within 24 hours of the ED admission, 68 (68.7%) patients died within 24 hours after signing it, and 97 (98.0%) patients had DNR signed by the family surrogates. Multivariate analysis showed that four independent factors influenced the family surrogates' decisions to sign the DNR orders: lack of referral (odds ratio [OR] 0.157, 95% confidence interval [CI] 0.047-0.529, P=0.003), ED length of stay (ED LOS) ≥72 hours (OR 5.889, 95% CI 1.290-26.885, P=0.022), acute myocardial infarction (AMI) (OR 0.017, 95% CI 0.001-0.279, P=0.004), and tracheal intubation (OR 0.028, 95% CI 0.007-0.120, P<0.001). CONCLUSIONS: In the Chinese mainland, the proportion of patients consenting for DNR order is lower than that of developed countries. The decision to sign DNR orders is mainly affected by referral, ED LOS, AMI, and trachea intubation.

4.
J Ethnopharmacol ; 147(2): 509-16, 2013 May 20.
Artigo em Inglês | MEDLINE | ID: mdl-23545455

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Panax ginseng is a well-known traditional Chinese medicine and has been used for treatment of various diseases for more than four thousand years in Asia. Ginseng saponins or ginsenosides, the active constituents are reported to possess antidiabetic activity, but their antihyperglycemic mechanisms are not fully elucidated. In the present study, the mechanisms of action of ginsenoside Re were investigated in vitro models. MATERIALS AND METHODS: 3T3-L1 cells were chosen as the model to investigate the molecular mechanisms of action of ginsenoside Re. Influence of ginsenoside Re on the adipogenesis was examined by determining TG levels in 3T3-L1 adipocytes by the method of TG oxidation enzyme. Glucose uptake in 3T3-L1 cells stimulated by insulin in the absence or presence of ginsenoside Re were quantified by measuring (3)H-2-deoxy-d-glucose levels. Cytokine proteins released into the medium including adiponectin and TNF-α were tested using respective ELISA kits. In addition, real time RT-PCR was conducted to investigate the expression changes of PPAR-γ and its responsive genes, ap2, adiponectin, IRS-1, GLUT4 and TNF-α. And western blot analysis was performed to determine the translocation of GLUT4. Finally, effects of ginsenoside Re on NO production in 3T3-L1 adipocytes and in macrophages were investigated through measurement of nitrite concentration by Griess reagent. RESULTS: Ginsenoside Re induced adipogenesis of 3T3-L1 adipocytes by accumulating TG, increased glucose uptake and up-regulated PPAR-γ2, IRS-1, ap2 and adiponectin genes expressions. Meanwhile, Re also increased production and release of adiponectin. Although having no effects on GLUT4 gene expression, Re facilitated GLUT4 protein translocation to the membranes. In addition, Re inhibited the expression and release of TNF-α. Finally, Re did not show inhibitory effects on NO production both in 3T3-L1 cells stimulated by LPS, TNF-α and IFN-γ and in LPS-stimulated mouse peritoneal macrophages. CONCLUSIONS: Ginsenoside Re exhibited the action of reducing insulin resistance through activation of PPAR-γ pathway by directly increasing the expressions of PPAR-γ2 and its responsive genes, adiponectin, IRS-1, ap2, inhibiting TNF-α production and facilitating the translocation of GLUT4 to promote glucose uptake and disposal in 3T3-L1 adipocytes.


Assuntos
Ginsenosídeos/farmacologia , Resistência à Insulina , PPAR gama/genética , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Células 3T3-L1 , Adipogenia/efeitos dos fármacos , Adiponectina/genética , Adiponectina/metabolismo , Animais , Células Cultivadas , Proteínas de Ligação a Ácido Graxo/genética , Regulação da Expressão Gênica/efeitos dos fármacos , Glucose/metabolismo , Transportador de Glucose Tipo 4/genética , Proteínas Substratos do Receptor de Insulina/genética , Macrófagos Peritoneais/efeitos dos fármacos , Macrófagos Peritoneais/metabolismo , Masculino , Camundongos , Óxido Nítrico/metabolismo , Fator de Necrose Tumoral alfa/genética
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