Objective To compare the ratios of neuron and glia differentiated from the embryonic human neural stem cells(hNSCs) at different times in vitro. Methods The cells from hippocampus of aborted human embryo tissue(8-12 weeks after conception) were mechanically dissociated and cultured with DMEM/F 12 medium containing h-EGF,h-bFGF,h-LIF.The NSCs were induced to differentiate by 1%FBS and identified by Musashil,?-Ⅲ Tubulin,GFAP and Galc immuno-cytochemical staining at different times. Results The cell spheres were Musashil positive at the 12th hour after differentiation.On the 2nd day after differentiation,a few cells exhibited ?-Ⅲ Tubulin and GFAP immunoreactivities,but no Galc positive cells.The number of ?-Ⅲ Tubulin immuno-positive cells reached the highest on the 7(th) day and the percent was 48.2%.The number of GFAP immuno-positive cells increased from the 2nd to the 23rd day and the positive ratio reached 65.3%.A few Galc immuno-positive cells were detected with time passing.Conclusion 1% FBS may promote human NSCs to differentiate into three cell types of central nervous system,and the ratios of differentiated neuron and glia are significantly different at various times.

Vascular endothelial growth factor (VEGF) is angiogenic and neurotrophic factor. It is now known that VEGF also plays an importmant role in neurogenesis and neuroprotection in addition to angiogenesis. VEGF and VEGF receptor increase in the ischemic brain, promote vascular endothelial cell proliferation and decrease infarct volume. VEGF plays neuroprotective and neurotrophic roles by the modulation of the phosphatidylinositol3-kinase (PI3K)/Akt/nuclear factor-κB and MAPK/ERK signaling pathways. VEGF reduces ischemic neuronal apoptosis, promotes neural stem cells proliferation, migration and differentiation and improves nerve functions. In the other hands, VEGF increases permeability of blood vessel which may aggravate cerebral edema early.

Objective To study the effect of coenzymes complex combined with vitamin E on liver and kidney inju-ry induced by neonatal hyperbilirubinemia. Methods One hundred and fifty full-term neonatals with hyperbilirubinemia were chosen as observation groups, who were divided into mild, moderate and severe groups according bilirubin. Forty five healthy full-term newborns in the same period, who are either healthy or with physiological jaundice, were selected as con-trol group. Serum total bilirubin, gamma-glutamyl transferase (γ-GGT) , Malondialdehyde (MDA) and Cys-C were measured within 24 hours of hospital admission.The observation groups were randomly divided into regular and combined treatment groups. Coenzymes complex combined with vitamin E were given in addition to regular method to combined group while reg-ular group only received regular methods.All above biochemical indexes were tested in the 7th day after medication admin-istration. Results Serum MDA were higher in all observation groups (mild, moderate and severe groups) than in control group (P＜0.05);but the levels ofγ-GGT and Cys-C increased in moderate and severe groups compared with control group (P＜0.05). There were positive correlations (P＜0.05) between levels of serum total bilirubin with MDA,γ-GGT and Cys-C. Positive linear correlation were found between MDA with γ-GGT and Cys-C(P＜0.01). After early intervention,γ-GGT, Cys-C and MDA declined with drop of bilirubin level. This is more prominent and faster in a in combined treatment group than regular group (P＜0.05).Conclusion In hyperbilirubinemia newborns, lipid peroxidation activated by bilirubin may lead to damages of liver and kidney. Coenzymes combined with vitamin E have protective effect to these damages.

Objective To summarize adverse reactions of common traditional Chinese medicine injection for the treatment of cardiovascular and cerebrovascular diseases,and put forward the countermeasures.Methods Adverse reactions of common traditional Chinese medicine injection for the treatment of cardiovascular and cerebrovascular diseases were arranged,and the reasons were analyzed.Results Adverse reactions were mainly skin and cardiovascular system diseases and so on,and were related with the quality of medicinal material,preparation process,and so on.Conclusion We should strengthen every link of production,from the medicinal plant to clinical use,improve the quality of traditional Chinese medicine injection,and strengthen the supervision to reduce the incidence of adverse reactions and ensure drug safety.

Objective:To investigate the expression of phosphorylated glutamate receptor 2[p-GluR2(S880)]in oligodendrocyte precursor cells(OPCs)of mice model of hypoxic ischemic brain injury(HIBI).Methods:The HIBI model of C57BL/6 neonatal mice was established by right common carotid artery ligation and hypoxia for 90 min.The anxiety-like behavior of the mice was evaluated by elevated plus maze(EPM)and open field test(OFT).The expres-sion of p-GluR2(S880),oligodendrocyte marker 4(O4)and myelin basic protein(MBP)in brain tissue of HIBI model mice was detected by immunofluorescence staining.What's more,the expression levels of p-GluR2(S880)and MBP were detected by Western Blot.Results:Compared with sham operation group,there were significant anxiety-like behaviors 90 days after HIBI operation(P＜0.05).The expression of MBP protein decreased significantly in 14 and 28 days after HIBI operation.The expression of p-GluR2(S880)protein was up-regulated at all time points after HIBI op-eration(P＜0.05),and the number of O4 and p-GluR2(S880)double positive cells in brain tissue of HIBI group was significantly increased(P＜0.05).Conclusion:The up-regulation of p-GluR2(S880)expression in OPCs may lead to myelination disorder in HIBI model mice.

Autoimmune epilepsy (AE) is a type of epilepsy mediated by autoantibodies and immune cells. The main pathogenesis of AE is that autoimmune antibodies related to AE interact with surface of nervous cell membrane antigens or intracellular antigens, which leads to the disorder of excitatory and inhibitory nervous system and causes epileptic seizures. Glutamate receptor subunit 3 peptide B antibodies (GluR3B Ab's) are one type of anti-neuron autoantibodies related to AE, and they can combine with GluR3B subunit of α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR), which causes an increase of intracellular calcium. Intracellular calcium overload further leads to dysregulation of energy metabolism in neurons or oligodendrocyte progenitor cells (OPCs). The damage of neurons or OPCs eventually trigger seizure. Here, we mainly discuss the mechanisms of GluR3B Ab's involving in the development of autoimmune epilepsy.

Based on the biomechanical simulation curve of OpenSim, an open source software of biomechanical model, a spherical exoskeleton parallel mechanism with two degrees of freedom for hip joint is proposed in this paper for the rehabilitation therapy of patients with impaired leg motor function or elderly people with walking dysfunction. Firstly, the parallel mechanism is modeled and the position inverse solution of the parallel mechanism is obtained using inverse kinematics analysis. The velocity analysis expression of the mechanism is derived by deriving the inverse kinematics solution. The model is imported into the mechanical system dynamics analysis software ADAMS and matrix processing analysis software MATLAB to carry out simulation experiments. The correctness of the velocity analysis is verified by comparing the velocity simulation results of the two methods. Then, three singular types of the mechanism are analyzed according to the obtained Jacobian matrix. According to the inverse solution of the mechanism, the reachable workspace of the mechanism is obtained by programming in MATLAB with given mechanism parameters and restriction conditions. Finally, the prototype platform is built. The experimental results show that the exoskeleton hip joint using this parallel mechanism can satisfy the requirement of rotation angle of human hip joint movement, but also can be good to assist patients with leg flexion-extension movement and adduction-abduction movement, and it is helpful to carry out corresponding rehabilitation training. It also has theoretical significance and application value for the research work of human hip exoskeleton parallel mechanism.
Biomechanical Phenomena ; Exoskeleton Device ; Hip Joint ; physiology ; Humans ; Models, Theoretical ; Movement ; Rehabilitation ; instrumentation ; Rotation ; Walking

The massive loss of oligodendrocytes caused by various pathological factors is a basic feature of many demyelinating diseases of the central nervous system (CNS). Based on a variety of studies, it is now well established that impairment of oligodendrocyte precursor cells (OPCs) to differentiate and remyelinate axons is a vital event in the failed treatment of demyelinating diseases. Recent evidence suggests that Foxg1 is essential for the proliferation of certain precursors and inhibits premature neurogenesis during brain development. To date, very little attention has been paid to the role of Foxg1 in the proliferation and differentiation of OPCs in demyelinating diseases of the CNS. Here, for the first time, we examined the effects of Foxg1 on demyelination and remyelination in the brain using a cuprizone (CPZ)-induced mouse model. In this work, 7-week-old Foxg1 conditional knockout and wild-type (WT) mice were fed a diet containing 0.2% CPZ w/w for 5 weeks, after which CPZ was withdrawn to enable remyelination. Our results demonstrated that, compared with WT mice, Foxg1-knockout mice exhibited not only alleviated demyelination but also accelerated remyelination of the demyelinated corpus callosum. Furthermore, we found that Foxg1 knockout decreased the proliferation of OPCs and accelerated their differentiation into mature oligodendrocytes both in vivo and in vitro. Wnt signaling plays a critical role in development and in a variety of diseases. GSK-3β, a key regulatory kinase in the Wnt pathway, regulates the ability of β-catenin to enter nuclei, where it activates the expression of Wnt target genes. We then used SB216763, a selective inhibitor of GSK-3β activity, to further demonstrate the regulatory mechanism by which Foxg1 affects OPCs in vitro. The results showed that SB216763 clearly inhibited the expression of GSK-3β, which abolished the effect of the proliferation and differentiation of OPCs caused by the knockdown of Foxg1. These results suggest that Foxg1 is involved in the proliferation and differentiation of OPCs through the Wnt signaling pathway. The present experimental results are some of the first to suggest that Foxg1 is a new therapeutic target for the treatment of demyelinating diseases of the CNS.