ABSTRACT
Discharge against medical advice (DAMA) conflicts with the purpose of disease treatment in children. Some research has shown that there are high proportions of extremely preterm infants and infants with asphyxia or congenital malformation in neonates with DAMA. This suggests that the sustainable development of neonatology needs cooperation and co-development with obstetrics, neonatal surgery, and radiology to reduce the rate of DAMA. With reference to the current status of research in both China and other countries, this article reviews the causes for DAMA and the strategies for reducing the rate of DAMA, in order to provide a theoretical basis for effectively reducing the rate of DAMA from the neonatal intensive care unit, improving treatment outcomes of the neonates, and increasing hospitals' comprehensive benefits.
Subject(s)
Humans , Infant, Newborn , Ethics, Medical , Health Services Needs and Demand , Insurance, Health , Intensive Care Units, Neonatal , Patient Discharge , Prenatal Care , Treatment RefusalABSTRACT
OBJECTIVE: To isolate and purify 2α, 3α, 24-trihydroxy-12-alkene-28-ursolic acid from the roots of Actinidia eriantha Benth, establish its determination method, and compare the contents in different extracted parts and samples from different sources. METHODS: An HPLC-PDA method was established for the content determination. The contents of 2α, 3α, 24-trihydroxy-12-alkene-28-ursolic acid in the roots of Actinidia eriantha Benth from five different sources and different extracted parts were determined by standard curve method. RESULTS: The content of 2α, 3α, 24-trihydroxy-12-alkene-28-ursolic acid was higher in the samples from Shouning county of Fuzhou city and Yunhe county of Lishui city while lower in those from Yongjia county of Wenzhou city and Lishui city. And in different extracted parts, the content was the highest in dichloromethane part, lower in ethanol part, and the lowest in methanol part. CONCLUSION: The method is stable and accurate with good reproducibility and can be used for the determination of 2α, 3α, 24-trihydroxy-12-alkene-28-ursolic acid in the roots of Actinidia eriantha Benth. The content of 2α, 3α, 24-trihydroxy-12-al-kene-28-ursolic acid is different in Actinidia eriantha Benth samples from different sources, which is the highest in dichloromethane part.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of insulin-like growth factor-1 (IGF-1), which can promote cell differentiation and inhibit cell apoptosis, on hyperoxia-induced apoptosis in A549 cells and its anti-apoptotic mechanism.</p><p><b>METHODS</b>A549 cells were sub-cultured, exposed to hyperoxic conditions and were then treated with different concentrations of IGF-1 (1, 10, and 100 ng/mL) for 48 hours. Cell viability was measured by MTT assay. Cell apoptosis was evaluated by Annexin V-FITC/PI double-staining flow cytometry. Expression levels of Bax and Bcl-2 were measured by flow cytometry.</p><p><b>RESULTS</b>The middle-dose and high-dose IGF-1 intervention groups had higher cell viabilities than the hyperoxic exposure group [(64±3)% and (88±4)% vs (51±3)%; P<0.05]. Compared with the air control group, the hyperoxic exposure group had a significantly higher apoptotic rate [(38.3±5.4)% vs (2.4±0.9)%; P<0.05], a significantly lower expression level of Bcl-2 [(72±5)% vs (91±4)%; P<0.05], and a significantly higher expression level of Bax [(54±6)% vs (3±2)%; P<0.05]. Compared with the hyperoxic exposure group, the low-dose, middle-dose, and high-dose IGF-1 intervention groups had significantly lower apoptotic rates [(16.1±4.7)%, (9.2±2.8)%, and (6.9±2.5)% vs (38.3±5.4)%; P<0.05], significantly higher expression level of Bcl-2 [(79±4)%, (94±4)%, and (100±5)% vs (72±5)%; P<0.05], and significantly lower expression level of Bax [(26±4)%, （5±2)%, and (4±2)% vs (54±6)%; P<0.05].</p><p><b>CONCLUSIONS</b>Hyperoxia significantly inhibits proliferation and promotes apoptosis in A549 cells. IGF-1 may promote cell proliferation and inhibit hyperoxia-induced apoptosis in A549 cells by regulating the expression of Bcl-2 and Bax.</p>