含铈硫酸氧盐储氧材料的制备及储/释氧性能研究

采用表面活性剂辅助法分别制备了铈、镧及其复合物的硫酸氧盐和掺加铜元素的硫酸氧铈,利用X射线衍射(XRD)、傅里叶红外光谱变换法(FT-IR)、BET比表面积测试法(BET)、程序升温还原法(TPR)、程序升温氧化(TPO)和氧脉冲吸附等技术手段对这些储氧材料进行了表征.结果表明,Ce2O2SO4、LaCeO2SO4的氧...     

碳源前加对低C/N城市污水的脱氮效能研究

针对合肥城市污水低C/N的水质特点和毗邻巢湖的特殊地理位置,满足尾水高质排放的要求,新建广泛应用A2/O工艺的污水处理项目,并在深度处理阶段增加反硝化生物滤池以解决出水TN不能稳定达标的问题,后置反硝化生物滤池需外加碳源,深度处理过程溶氧增高,由此产生溶氧消耗碳源。针对上述问题,通过将后置反硝化生物滤池的碳源前加至缺氧段,不仅可以在低C/N的条件下提高前置反硝化效率,还减少后期溶氧对碳源的消耗,降低污水处理成本,同时解决出水TN稳定达标的问题,出水水质达到四类水标准。     

二维C/C复合材料层叠板制备工艺及其性能的研究

研究通过浸渍—炭化法制备二维C／C复合材料层叠板的工艺参数，分析了不同基体前驱体和增密次数对材料的密度、厚度和收缩率、体积电阻率和层间剪切强度的影响，并用扫描电子显微镜进行断口分析。结果表明：选用残炭率较高的基体前驱体和适当的增密次数是制备低成本二维C／C复合材料层叠板的关键；相同纤维体积的层叠板基体炭含量越高，电阻率越小，导电性能越好；单位体积含有炭纤维越多，纤维受损几率就越大，产生结构缺陷几率越高，导致电阻率增加，导电性能下降；本实验中二维C／C复合材料层叠板制备工艺简单可行，层叠板的密度达到1．40g／cm^3以上，剪切强度为1．5MPa，断口呈脆性断裂特征。     

照相机前盖多腔模的PTC/Creo体积块快速分模技术研究

运用PTC/Creo软件的模具体积块方法,以照相机前盖多腔模布局节点中第一个参照模型作为设计的参照,分别完成其破孔分型体积块、枕位体积块与镶件体积块或分型体积块的设计,并创建体积块的组特征及其“参照”类型的阵列,成功实现了多腔模布局中其他参照模型相应体积块的设计,达到简化模具分模进程的目的。该技术演绎了模具体积块在多腔模分模设计中的功能特点与使用方法,提升了模具的设计水平,从而为快速实现多腔模布局的分模设计提供了全新的解决方案。     

纳米CaCO3增韧PVC/CPE复合材料的性能研究

研究了纳米CaCO3增韧PVC／CPE复合材料的力学性能和流变性能。结果表明，纳米CaCO3对PVC／CPE复合材料有明显的增韧作用，出现单峰最大值分布；并与CPE产生协同增韧效应。PVC／CPE复合材料的拉伸强度随纳米CaCO3和CPE的用量的增加而稍有下降。随纳米CaCO3的用量增加，PVC熔体的塑化时间延迟了5倍，凝胶速率提高了2倍，平衡粘度增加，操作范围变窄，加工难度增加。     

Arpin Regulates Migration Persistence by Interacting with Both Tankyrases and the Arp2/3 Complex

During cell migration, protrusion of the leading edge is driven by the polymerization of Arp2/3-dependent branched actin networks. Migration persistence is negatively regulated by the Arp2/3 inhibitory protein Arpin. To better understand Arpin regulation in the cell, we looked for its interacting partners and identified both Tankyrase 1 and 2 (TNKS) using a yeast two-hybrid screening and coimmunoprecipitation with full-length Arpin as bait. Arpin interacts with ankyrin repeats of TNKS through a C-terminal-binding site on its acidic tail, which overlaps with the Arp2/3-binding site. Arpin was found to dissolve the liquid–liquid phase separation of TNKS upon overexpression. To uncouple the interactions of Arpin with TNKS and Arp2/3, we introduced point mutations in the Arpin tail and attempted to rescue the increased migration persistence of the Arpin knockout cells using random plasmid integration or compensating knock-ins at the ARPIN locus. Arpin mutations impairing interactions with either Arp2/3 or TNKS were insufficient to fully abolish Arpin activity. Only the mutation that affected both interactions rendered Arpin completely inactive, suggesting the existence of two independent pathways, whereby Arpin controls the migration persistence.     

Plectin Downregulation Inhibits Migration and Suppresses Epithelial Mesenchymal Transformation of Hepatocellular Carcinoma Cells via ERK1/2 Signaling

Plectin, as a cytoskeleton-related protein, is involved in various physiological and pathological processes of many cell types. Studies have found that plectin affects cancer cell invasion and metastasis, but the exact mechanism is not fully understood. In this study, we aim to investigate the role of plectin in the migration of hepatocellular carcinoma (HCC) cells and explore its relevant molecular mechanism. Herein, we found that the expression of plectin in HCC tissue and cells was significantly increased compared with normal liver tissue and cells. After downregulation of plectin, the migration ability of HCC cells was significantly lower than that of the control group. Moreover, the expression of E-cadherin was upregulated and the expression of N-cadherin and vimentin was downregulated, suggesting that plectin downregulation suppresses epithelial mesenchymal transformation (EMT) of HCC cells. Mechanically, we found that plectin downregulation repressed the extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation. Activation of ERK1/2 recovered the plectin downregulation-inhibited migration and EMT of HCC cells. Taken together, our results demonstrate that downregulation of plectin inhibits HCC cell migration and EMT through ERK1/2 signaling, which provides a novel prognostic biomarker and potential therapeutic target for HCC.     

Cleavage of the Perlecan-Semaphorin 3A-Plexin A1-Neuropilin-1 (PSPN) Complex by Matrix Metalloproteinase 7/Matrilysin Triggers Prostate Cancer Cell Dyscohesion and Migration

The Perlecan-Semaphorin 3A-Plexin A1-Neuropilin-1 (PSPN) Complex at the cell surface of prostate cancer (PCa) cells influences cell–cell cohesion and dyscohesion. We investigated matrix metalloproteinase-7/matrilysin (MMP-7)’s ability to digest components of the PSPN Complex in bone metastatic PCa cells using in silico analyses and in vitro experiments. Results demonstrated that in addition to the heparan sulfate proteoglycan, perlecan, all components of the PSPN Complex were degraded by MMP-7. To investigate the functional consequences of PSPN Complex cleavage, we developed a preformed microtumor model to examine initiation of cell dispersion after MMP-7 digestion. We found that while perlecan fully decorated with glycosaminoglycan limited dispersion of PCa microtumors, MMP-7 initiated rapid dyscohesion and migration even with perlecan present. Additionally, we found that a bioactive peptide (PLN4) found in perlecan domain IV in a region subject to digestion by MMP-7 further enhanced cell dispersion along with MMP-7. We found that digestion of the PSPN Complex with MMP-7 destabilized cell–cell junctions in microtumors evidenced by loss of co-registration of E-cadherin and F-actin. We conclude that MMP-7 plays a key functional role in PCa cell transition from a cohesive, indolent phenotype to a dyscohesive, migratory phenotype favoring production of circulating tumor cells and metastasis to bone.     

Sinulariolide Suppresses Human Hepatocellular Carcinoma Cell Migration and Invasion by Inhibiting Matrix Metalloproteinase-2/-9 through MAPKs and PI3K/Akt Signaling Pathways

Sinulariolide is an active compound isolated from the cultured soft coral Sinularia flexibilis. In this study, we investigate the migration and invasion effects of sinulariolide in hepatocellular carcinoma cell HA22T. Sinulariolide inhibited the migration and invasion effects of hepatocellular carcinoma cells in a concentration-dependent manner. The results of zymography assay showed that sinulariolide suppressed the activities of matrix metalloproteinase (MMP)-2 and MMP-9. Moreover, protein levels of MMP-2, MMP-9, and urokinase-type plasminogen activator (uPA) were reduced by sinulariolide in a concentration-dependent manner. Sinulariolide also exerted an inhibitory effect on phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), phosphatidylinositol 3-kinase (PI3K), Akt, Focal adhesion kinase (FAK), growth factor receptor-bound protein 2 (GRB2). Taken together, these results demonstrated that sinulariolide could inhibit hepatocellular carcinoma cell migration and invasion and alter HA22T cell metastasis by reduction of MMP-2, MMP-9, and uPA expression through the suppression of MAPKs, PI3K/Akt, and the FAK/GRB2 signaling pathway. These findings suggest that sinulariolide merits further evaluation as a chemotherapeutic agent for human hepatocellular carcinoma.