Regulation of the intermittent release of giant unilamellar vesicles under osmotic pressure

Osmotic pressure can break the fluid balance between intracellular and extracellular solutions. In hypo-osmotic solution, water molecules, which transfer into the cell and burst, are driven by the concentration difference of solute across the semi-permeable membrane. The complicated dynamic processes of intermittent bursts have been previously observed. However, the underlying physical mechanism has yet to be thoroughly explored and analyzed. Here, the intermittent release of inclusion in giant unilamellar vesicles was investigated quantitatively, applying the combination of experimental and theoretical methods in the hypo-osmotic medium. Experimentally, we adopted a highly sensitive electron multiplying charge-coupled device to acquire intermittent dynamic images. Notably, the component of the vesicle phospholipids affected the stretch velocity, and the prepared solution of vesicles adjusted the release time. Theoretically, we chose equations and numerical simulations to quantify the dynamic process in phases and explored the influences of physical parameters such as bilayer permeability and solution viscosity on the process. It was concluded that the time taken to achieve the balance of giant unilamellar vesicles was highly dependent on the molecular structure of the lipid. The pore lifetime was strongly related to the internal solution environment of giant unilamellar vesicles. The vesicles prepared in viscous solution were able to visualize long-lived pores. Furthermore, the line tension was measured quantitatively by the release velocity of inclusion, which was of the same order of magnitude as the theoretical simulation. In all, the experimental values well matched the theoretical values. Our investigation clarified the physical regulatory mechanism of intermittent pore formation and inclusion release, which provides an important reference for the development of novel technologies such as gene therapy based on transmembrane transport as well as controlled drug delivery based on liposomes.     

Mg8Sn4-xMx结构稳定性与弹性常数的第一性原理计算

利用基于密度泛函理论的CASTEP软件构建Mg₈Sn_4-xM_x(M=Al、Cu;x=0、1或2)晶体结构模型,采用第一性原理计算其晶格常数、结构稳定性和弹性常数,并分析不同量的M原子固溶于Mg₂Sn后体系的电子特性、弹性性能和本征硬度.计算结果表明,M原子能自发固溶于Mg₂Sn相,且所得Mg₈Sn_4-xM_x(x=1或2)晶体结构均可稳定存在;当2个M原子固溶于Mg₂Sn时,使其晶体结构由立方晶系转变为四方晶系.态密度分析表明,M原子固溶后体系原子存在明显轨道杂化现象,表现出较强的共价键,增加M原子固溶量不会改变各原子对态密度的贡献规律,但会提高该原子对电子对态密度的贡献度.弹性性能和本征硬度分析表明：Mg₂Sn中固溶M原子后,体系力学性能仍稳定,增加M原子固溶量,体系硬度逐渐降低,韧塑性不断提高,即M原子固溶量增加能提升体系的...     

表面活性剂单体引起的细胞膜失稳

表面活性剂常用于细胞裂解、脂质体外排与膜组分搜集等.但在临界成胶束浓度以下,它如何以单体状态与生物膜作用的机制与调控仍存在很多疑问.本文研究了表面活性剂带电性对膜失稳的影响.石英电子微天平检测发现非离子型Triton X-100产生了最显著的磷脂膜结构三维再组装.荧光显微观测表明膜表面生成了非稳的出芽微泡,在机械扰动下可发生解离.该表面活性剂溶液环境中的体外细胞也出现了活力丧失.但是,离子型CTAB与SDS却无法触发相似的膜失稳与细胞失活效应.分析认为,由于不存在后两者体系中的单体间静电排斥, Triton X-100更易高效地插入生物膜,从而诱导膜结构再组装.研究深化了表面活性剂与生物膜作用机制的理解,对表面活性剂在生物医药、膜组分萃取等领域的深化应用提供了指导与帮助.     

多聚赖氨酸诱导的负电性磷脂巨囊泡形变

利用荧光显微技术表征了多聚赖氨酸诱导的负电性磷脂巨囊泡的动力学响应行为.研究发现,多聚赖氨酸可吸附至二油酰磷脂酰胆碱和二油酰磷脂酸混合磷脂巨囊泡的表面,诱导其发生粘连、出"绳"及破裂现象.分析认为,在低盐环境中,膜形变由多聚赖氨酸吸附于二油酰磷脂酸富集区引起的膜两叶应力不对称,以及静电相互作用等因素产生.研究结果对基于聚合物-巨囊泡体系的药物输运控释、细胞形变、微控反应和基因治疗等方面的研究提供有价值的支持.     

重力场下生物膜表面的金纳米棒吸附

纳米颗粒在生物膜表面的吸附对其生物医学应用至关重要.在本研究中,采用正置与倒置石英电子微天平及耗散系数测量实验,表征了不同溶液高度的支撑膜表面金纳米棒的吸附动力学.发现金棒在重力场下产生溶液浓度不均性.长宽比增大能够提高金棒的流体力学尺寸,延缓金棒的不均再分布过程,从而维持不同溶液高度生物膜表面吸附量的一致.同时,由于浓度不均程度差异,短棒、中棒、长棒在不同溶液高度的吸附量排序关系也是变化的.在溶液底层短棒的吸附量最大,在溶液顶层中棒的吸附量最大.研究深化考察了调控纳米颗粒在生物膜表面吸附的物理因素,为纳米材料的医学应用提供了参考.