1.Thoughts on building the early-warning system for hospital talents drainage
Chinese Journal of Hospital Administration 2009;25(5):342-343
In line with the hospital development practice in recent years,this paper discussed the early-warning system for hospital talents drainage.First of all,it points out that early-warning indicators,early-warning analysis and early-control measures are key elements of such a system.On this basis,it pinpoints key points in building this system,including organizational assurance,by-level management,dynamic tracking,fairness,bettering of HR mechanism,and reservation of potential HR resources.Therefore,this will be highly useful and practical for studying how to minimize talents drainage and maintain competitive advantages of hospitals.
2.Recent research progress on swainsonine
Haiyun QUAN ; Zhenhui REN ; Hao LU ; Shuai WANG ; Ruixu XUE ; Jianguo WANG ; Chenchen WU ; Baoyu ZHAO
Chinese Journal of Veterinary Science 2017;37(8):1633-1640
Locoweeds are presently defined as those species of the genera Oxytropis and Astragalus (family Leguminosae) that specifically contain the key toxic constituent,swainsonine.After ingesting locoweeds,livestock can develop poisoning disease characterized by chronic dysfunction of the nervous system,which causes severe economic losses to the pastoral areas.In addition,swainsonine has attracted a great attention from toxicology and medicine fields,due to its dual role of toxicity and pharmacological activity.This review not only summarizes the latest research progress of toxicity and its poisoning mechanism,pharmacological activity,source,and biosynthesis pathway of swainsonine,but also speculates the possible regulatory enzymes involved in the synthesis pathway.Moreover,the future research on swainsonine is also looked ahead,which provide references for the prevention and treatment of locoism.
3.Liraglutide ameliorates high glucose-induced oxidative stress injury in rat H9c2 cells through modulation of SIRT1
Ruixu WANG ; Xue TIAN ; Lihua ZHAO ; Qinglian LI ; Ruitian HOU ; Yu GAO ; Fengbiao JIN ; Shuying LI ; Xiaochun GE
Chinese Journal of Endocrinology and Metabolism 2023;39(7):605-610
Objective:To investigate the effect of liraglutide(LRG) on high glucose-induced oxidative stress injury in(H9c2) cardiomyocytes and its underlying mechanisms.Methods:A high glucose treatment was applied to H9c2 cells for 24 hours to establish an in vitro model of myocardial cell injury. Different concentrations of liraglutide(10, 100, 1000 nmol/L) were administered for intervention. Cell viability was evaluated using the CCK-8 assay, and changes in cell morphology were observed under an inverted microscope. After 24 hours of liraglutide(100 nmol/L) intervention following high glucose treatment, the levels of lactate dehydrogenase(LDH), superoxide dismutase(SOD), and malondialdehyde(MDA) in the cell supernatant were measured. RT-PCR and Western blotting were used to detect the mRNA and protein levels of silent information regulator factor 1(SIRT1) and forkhead box protein O1(FOXO1). Western blotting was also used to assess the acetylation level of FOXO1 protein. Small interfering RNA(siRNA) technology was employed to silence SIRT1 in H9c2 cells to confirm its role in the study. Results:Compared to the control group, the high glucose group showed decreased cell viability, cell structure damage, increased levels of LDH and MDA in the cell supernatant, decreased SOD levels, aggravated oxidative stress, decreased SIRT1 expression, and increased acetylation level of FOXO1(all P<0.05). Compared to the high glucose group, liraglutide intervention resulted in increased cell viability, improved cardiac cell morphology, reduced oxidative stress levels, increased SIRT1 expression, and decreased acetylation level of FOXO1(all P<0.05). When SIRT1 was downregulated, the protective effects of liraglutide were weakened(all P<0.05). Conclusions:Liraglutide has a protective effect against high glucose-induced oxidative stress injury in H9c2 cells, which may be associated with the upregulation of SIRT1 expression.