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本文通过数值方法求解均匀动脉中的非平稳脉动流,给出了通过测量非平稳脉动血流量确定壁面切应力的方法.作为算例,采用实测的大鼠颈总动脉流量信号,求出了均匀动脉壁面切应力波形.进一步对求得的切应力波形进行经验模态分解(EMD),得到了切应力波形的各内在模态(IMF),以及Hilbert幅值谱.从切应力波形经Hilbert-Huang变换得到的IMF和Hilbert谱图可以明显地看出切应力各频率成分的物理意义.所得结果为进一步深入研究非平稳脉动切应力与血管重建的关系提供了一种方法学基础. 相似文献
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在生长LiNbO3过程中掺进6mol%ZnO和0.2mol%Nd2O3生长了Zn:Nd:LiNbO3晶体。测试了晶体的吸收光谱,荧光光谱和抗光损伤阈值,应用简并四波混频技术研究了Zn;Nd:LiNbO3晶体的光折变效应,它的光栅形成机制是异常光生伏特效应,它的抗光损伤能力比Nd:LiNbO3晶体提高二个数量级,这是由于光电导的增强而引起的。 相似文献
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In consideration of the mechanism for shear-stress-induced Ca^2+ influx via ATP(adenosine triphosphate)-gated ion channel P2X4 in vascular endothelial cells, a modified model is proposed to describe the shear-stress-induced Ca^2+ influx. It is affected both by the Ca^2+ gradient across the cell membrane and extracellular ATP concentration on the cell surface. Meanwhile, a new static ATP release model is constructed by using published experimental data. Combining the modified intracellular calcium dynamics model with the new ATP release model, we establish a nonlinear Ca^2+ dynamic system in vascular endothelial cells. The ATP-mediated calcium response in vascular endothelial cells subjected to shear stresses is analyzed by solving the governing equations of the integrated dynamic system. Numerical results show that the shear-stress-induced calcium response predicted by the proposed model is more consistent with the experimental observations than that predicted by existing models. 相似文献
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考虑剪应力诱导血管内皮细胞钙离子内流主要取决于经由三磷酸腺苷(ATP)门控离子通道P2X4的钙离子内流这一实验事实,提出一个修正的剪应力诱导钙离子内流模型,认为钙离子内流量不仅取决于细胞膜内外钙离子浓度差,而且受细胞表面ATP浓度调节A·D2同时利用文献中公布的实验结果,建立了一个新的静态ATP分泌模型,并将其整合到修正后的钙离子内流模型中,建立了一个描述动脉内皮细胞内非线性钙离子动力学系统.求解整合后动力学系统的控制方程,可获得内皮细胞在剪应力作用下受ATP调节的钙离子响应.结果表明,与文献中其他模型比较,改进后的模型模拟的结果能更真实地反映实验事实. 相似文献
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