Objective To study the effects ofgranulocyte colony-stimulating factor(G-CSF) and AMD3100 on the proliferation,migration and adhesion of mesenchymal stem cells (MSCs).Methods The proliferation,migration and adhesion of MSCs were detected by MTT chromometry,transwell and adhesion test.Results When the concentration of G-CSF was 200 μg/L and AMD3100 was 0.5 mg/L,the proliferation and migration of MSCs were the strongest.When the concentration of G-CSF was 200 μg/L and AMD3100 was 0 mg/L,the adhesion of MSCs was the strongest.Conclusion The proliferation,migration,adhesion of MSCs are promoted by G-CSF,and inhibited by AMD3100.

Objective:To investigate the risk factors related to intensive care unit (ICU) readmission .Methods :A total of 2491 patients who had been transferred into Department of Critical Care Medicine of Zhongshan Hospital ,Fudan University from Nov 2008 to Dec 2011 were included .Clinical data of all the patients during their first admission to ICU were collected .All the patients were classified into non‐readmission group(Group A) and readmission group(Group B) on the basis of whether there was readmission to ICU .All the patients’ treatments were conducted under supervision of attending intensivist and in accordance with routine treatment of Department of Critical Care Medicine and related clinical guidelines .Logistic regression was performed in multivariate analyses of ICU readmission .Results:If the first admission to ICU was due to emergency ,then the chance of ICU readmission was raised(HR=4 .929 ,95% CI:1 .936‐12 .549 ,P<0 .01) .If patient underwent tracheotomy during the first ICU stay ,then the chance of ICU readmission increased (HR= 3 .395 ,95% CI:1 .622‐7 .107 , P< 0 .01) . Conclusions :Both the admission to ICU under emergency and the tracheotomy during the first ICU admission are independent risk factors for ICU readmission .

OBJECTIVETo investigate the role and mechanism of action of fibroblast growth factor-21 (FGF-21) in reducing triglyceride (TG) in the in vitro and in vivo models of nonalcoholic fatty liver disease (NAFLD).

METHODS(1) A mixture of free fatty acids was used to establish a model of steatosis in L02 cells, and the cells were treated with various concentrations of FGF-21 or fenofibrate. Twenty-four hours later, oil red O staining was performed to observe the degree of steatosis, and intracellular TG content was determined. RT-PCR and Western blot were applied to measure the mRNA and protein expression of sterol regulatory element-binding protein-1c (SREBP-1c). (2) High-fat diet was used to establish a mouse model of steatosis, and these mice were intraperitoneally injected with FGF-21 or fenofibrate. Eight weeks later, whole blood and liver samples were collected, and HE staining was performed to observe steatosis. Meanwhile, the serum levels of TG, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were measured, and TG content in the liver was also measured. One-way analysis of variance was used for comparison of data between multiple groups, and the least significant difference t-test was used for comparison between any two groups.

RESULTS(1) Compared with the control group, the model group showed significant steatosis, with significant increases in intracellular lipid droplets and TG content (t = -20.57, P < 0.01), while FGF-21 reduced the number of intracellular lipid droplets and TG content (F = 98.16, P < 0.01) in a dose-dependent manner. In addition, the model group had significantly increased mRNA and protein expression of SREBP-1c compared with the control group (t = -10.73 and -0.1006, both P < 0.01), while FGF-21 down-regulated the mRNA and protein expression of SREBP-1c (F = 161.35 and 36.72, both P < 0.01). (2) Compared with the mice in the control group, those in the model group showed significant steatosis and had significant increases in serum TG level and TG content in the liver (t = -18.84 and 15.71, both P < 0.01). FGF-21 relieved hepatic steatosis and reduced the serum TG level and TG content in the liver (t = 18.11 and 9.46, both P < 0.01). Moreover, FGF-21 reduced the serum levels of ALT and AST in NAFLD mice (t = 25.93 and 12.50, both P < 0.01).

CONCLUSIONFGF-21 can inhibit the synthesis of TG through suppressing the expression of SREBP-1c, which further confirms the potential therapeutic effect of FGF-21 in the treatment of NAFLD. This may provide new ideas for the treatment of NAFLD.

Alanine Transaminase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Cell Line ; Diet, High-Fat ; Disease Models, Animal ; Fenofibrate ; pharmacology ; Fibroblast Growth Factors ; pharmacology ; Mice ; Non-alcoholic Fatty Liver Disease ; blood ; drug therapy ; Sterol Regulatory Element Binding Protein 1 ; metabolism ; Triglycerides ; blood