Effect of stromal cell-derived factor-1/CXCR4 axis in neural stem cell transplantation for Parkinson’s disease

Previous studies have shown that neural stem cell transplantation has the potential to treat Parkinson’s disease,but its specific mechanism of action is still unclear.Stromal cell-derived factor-1 and its receptor,chemokine receptor 4(CXCR4),are important regulators of cell migration.We speculated that the CXCR4/stromal cell-derived factor 1 axis may be involved in the therapeutic effect of neural stem cell transplantation in the treatment of Parkinson’s disease.A Parkinson’s disease rat model was injected with 6-hydroxydopamine via the right ascending nigrostriatal dopaminergic pathway,and then treated with 5μL of neural stem cell suspension(1.5×104/L)in the right substantia nigra.Rats were intraperitoneally injected once daily for 3 days with 1.25 mL/kg of the CXCR4 antagonist AMD3100 to observe changes after neural stem cell transplantation.Parkinson-like behavior in rats was detected using apomorphine-induced rotation.Immunofluorescence staining was used to determine the immunoreactivity of tyrosine hydroxylase,CXCR4,and stromal cell-derived factor-1 in the brain.Using quantitative real-time polymerase chain reaction,the mRNA expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra were measured.In addition,western blot assays were performed to analyze the protein expression of stromal cell-derived factor-1 and CXCR4.Our results demonstrated that neural stem cell transplantation noticeably reduced apomorphine-induced rotation,increased the mRNA and protein expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra,and enhanced the immunoreactivity of tyrosine hydroxylase,CXCR4,and stromal cell-derived factor-1 in the brain.Injection of AMD3100 inhibited the aforementioned effects.These findings suggest that the stromal cell-derived factor-1/CXCR4 axis may play a significant role in the therapeutic effect of neural stem cell transplantation in a rat model of Parkinson’s disease.This study was approved by the Animal Care and Use Committee of Kunming Medical University,China(approval No.SYXKK2015-0002)on April 1,2014.

新型自攻螺丝修复纵裂木柱抗压性能（英文）

目的:受压纵裂木柱缝端应力集中会引起裂缝发展和两侧木材协同工作性能下降,并削弱木柱抗压承载力。以试验和数值模拟探讨轴压和偏压作用下纵裂木柱抗压承载力的下降规律,分析自攻螺丝的修复机理,推导纵裂木柱修复临界值和最优螺丝间距。创新点:1.以自攻螺丝实现纵裂木柱抗压承载力快速有效和不影响外观的修复目标;2.以试验和数值模拟推导纵裂木柱承载力显著下降而需修复的临界值以及自攻螺丝间距的最优取值。方法:1.通过带纵缝木柱抗压试验研究纵缝及自攻螺丝对木柱承载力的影响;2.运用精细化有限元数值模拟方法,基于清样小试件木材力学测试结果,建立带纵缝木柱有限元模型;3.运用有限元模型开展参数分析,归纳整理纵缝宽度及自攻螺丝间距等主要参数对木柱承载力修复效果的影响。结论:1.纵裂木柱抗压承载力下降主要由缝端应力集中引起的裂缝开展和缝两侧木材协同工作性能下降引起;2.新型自攻螺丝垂直裂缝方向贯入可实现有效拉结,从而延缓裂缝开展和恢复木材协同工作性能;3.纵裂木柱承载力下降比率和自攻螺丝修复率均随裂缝宽度的增加而增加;4.本文中30 mm的柱中裂缝宽度可导致木柱承载力下降超过10%,因而可作为修复的临界值,而100 mm的自攻螺丝间距可基本实现100%的承载力修复,因而可作为最优螺丝间距。