基于柔性多羧酸配体H3TCOPM构筑的Co(Ⅱ)配合物的合成与结构

以三苯甲烷-4,4’,4"-三羧酸（H₃TCOPM）为主配体,以含氮二齿配体4,4’-bipyridine（4,4’-bipy）为辅助配体,与Co（NO₃）₂·6H₂O通过溶剂热反应得到了2个配位聚合物{[Co₂（α-OH-TCOPM）（OH）（H₂O）₄]·DMF}_n（1）（α-OH-H₃TCOPM=三苯甲醇-4,4’,4"-三羧酸）和{[Co₃（α-OH-TCOPM）₂（4,4’-bipy）₃（H₂O）₆]·2H₂O}_n（2）。晶体结构分析表明,配合物1为四边形的二维层状结构,而配合物2为二维网状结构。采用红外光谱、粉末X射线衍射对配合物进行了表征,用热重分析仪研究了其热稳定性。     

一种可移动超分辨成像系统的制备及其性质研究

基于浸没透镜设计了一种超分辨成像系统,利用SU-8光刻胶和直径为4.87 m的微球实现纳米级别的超分辨成像。介绍微球成像放大率的求解方法,并通过软件模拟了超分辨成像系统的焦距。通过改变SU-8胶的厚度（从3.4 m到0）,系统的放大率也随之改变（放大率从1.6x到2.6x）。实验表明:SU-8胶的厚度对微球放大率有直接影响,通过该系统可以在普通光学显微镜下观察到蓝光光碟条纹。     

A mathematical model for ATP-mediated calcium dynamics in vascular endothelial cells induced by fluid shear stress

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.     

基于柔性多羧酸配体H3TCOPM构筑的Co(Ⅱ)配合物的合成与结构

以三苯甲烷-4,4′,4″-三羧酸(H_3TCOPM)为主配体,以含氮二齿配体4,4′-bipyridine(4,4′-bipy)为辅助配体,与Co(NO_3)_2·6H_2O通过溶剂热反应得到了2个配位聚合物{[Co_2(α-OH-TCOPM)(OH)(H_2O)_4]·DMF}_n(1)(α-OH-H_3TCOPM=三苯甲醇-4,4′,4″-三羧酸)和{[Co_3(α-OH-TCOPM)_2(4,4′-bipy)_3(H_2O)_6]·2H_2O}_n(2)。晶体结构分析表明,配合物1为四边形的二维层状结构,而配合物2为二维网状结构。采用红外光谱、粉末X射线衍射对配合物进行了表征,用热重分析仪研究了其热稳定性。     

一种剪应力作用下ATP调节的血管内皮细胞内钙离子动力学数学模型

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P2X4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．