Objective To compare the adherent cells derived from human placenta,umbilical cord blood and bone marrow,and provide laboratory data for clinical application of mesenchymal stem cells.Methods Adherent cells were isolated from human placenta tissues by enzyme digestion,and mononuclear cells(MNC) were isolated from umbilical cord blood(UCB) by 60g/L HES and density gradient centrifugation and MNC were isolated from bone marrow(BM) by density gradient centrifugation,and then these cells were cultured in vitro.Their biological characteristics were studied and compared.Results The adherent cells cultured from human placenta and umbilical cord blood had disparate shape in vitro respectively.And they had some differences in growth and shape from those derived from bone marrow.The adherent cells derived from the three tissues all expressed CD106 and CD44 in immunohistochemistry staining.Conclusion The adherent cells derived from human placenta and umbilical cord blood have the basic features of mesenchymal stem cells.

Mock circulatory system (MCS) is an experimental platform for simulating hemodynamic performance of human circulatory system, and has been widely used in in-vitro hemodynamic performance evaluation of passive devices such as ventricular assist devices (VADs), artificial valves, as well as hemodynamic responses of mock circulation loop. MCSs are capable of simulating various physiological conditions, including health, exercise, and heart failure, by adjusting drive element of heart simulator and lumped-parameter element of vasculature components. Since 1 960 s, the research and development target of MSCs has evolved from meeting the basic performance evaluation requirement of VADs and mechanical valve to mimicking local hemodynamic characteristics in vital organs. This review summarizes the design principles, system construction of MCSs as well as its research progress and future prospects.

ObjectiveTo observe the effect of Hedysari Radix polysaccharide （HRP） on the Janus kinase 2 （JAK2）/signal transducer and activator of transcription protein 3 （STAT3） signaling pathway in diabetic nephropathy db/db mice. MethodFifty db/db mice were randomly divided into model group， irbesartan group （irbesartan suspension， 22.75 mg·kg^-1）， and high-， medium-， and low-dose HRP groups （HRP suspension， 200， 100， 50 mg·kg^-1） according to the body weight， with 10 mice in each group. Another 10 C57BL/6 mice were assigned to the normal group. The mice were treated with corresponding drugs by gavage， while those in the normal group and the model group received distilled water at 5 mL·kg^-1. The mice in the six groups were administered once a day by gavage for 12 consecutive weeks. The uric acid （UA）， triglycerides （TG）， and total cholesterol （TC） were detected. Periodic acid-Schiff （PAS） staining and Masson staining were used to observe the pathological changes in kidney tissues. Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were used to detect the protein and mRNA expression levels of JAK2， STAT3， suppressor of cytokine signaling 3 （SOCS3）， and tumor necrosis factor-α （TNF-α） in the kidney. ResultAfter 12 weeks of treatment， compared with the normal group， the model group showed significant pathological ultrastructural changes in kidney tissues and increased UA， TG， and TC levels （P<0.01）. Compared with the model group， the high- and medium-dose HRP groups and the irbesartan group showed improvement in pathological ultrastructure of kidney tissues and reduced UA， TG， and TC levels （P<0.05， P<0.01）. Compared with the normal group， the model group showed a decrease in SOCS3 protein and mRNA expression levels and an increase in JAK2， STAT3， and TNF-α protein and mRNA expression levels （P<0.01）. Compared with the model group， the high- and medium-dose HRP groups and the irbesartan group showed an increase in SOCS3 protein and mRNA expression levels and a decrease in JAK2， STAT3， and TNF-α protein and mRNA expression levels （P<0.05， P<0.01）. ConclusionHRP can alleviate renal damage in diabetic nephropathy to a certain extent， and its mechanism may be related to the inhibition of the activation of the JAK2/STAT3 signaling pathway.