Search

Manipulation of cell–cell interactions via cell surface engineering has potential biomedical applications in tissue engineering and cell therapy. However, manipulation of the comprehensive and multiple intercellular interactions remains a challenge and missing elements. Herein, utilizing a DNA triangular prism (TP) and a branched polymer (BP) as functional modules, we fabricate tunable DNA scaffold networks on the cell surface. The responsiveness of cell–cell recognition, aggregation and dissociation could be modulated by aptamer‐functionalized DNA scaffold networks with high accuracy and specificity. By regulating the DNA scaffold networks coated on the cell surface, controlled intercellular molecular transportation is achieved. Our tunable network provides a simple and extendible strategy which addresses a current need in cell surface engineering to precisely manipulate cell–cell interactions and shows promise as a general tool for controllable cell behavior. [ABSTRACT FROM AUTHOR]

Although Ru(bpy)32+‐doped silica nanoparticles have been widely explored as the labelling tags for electrochemiluminescence (ECL) sensing different targets, the poor electrical conductive properties of the silica nano‐matrix greatly limit their ECL sensitivity. Therefore, a novel scheme to overcome this drawback on Ru(bpy)32+‐doped silica nanoparticles ECL is desirable. Here, a new scheme for this purpose was developed based on electrochemically depositing a nanoscale chitosan hydrogel layer on the carbon nanotube (CNT) surface to form chitosan hydrogel shell@CNT core nanocomposites. In this case, the nanoscale chitosan hydrogel layer only formed on the CNT surface due to the superior electrocatalytic effect of CNT on H+ reduction compared with the basic glass carbon electrode. Due to both the superhydrophilic properties and polyelectrolyte features of nanoscale chitosan hydrogel on the CNT surface, chemical affinity as well as the electric conductivity between Ru(bpy)32+‐doped silica nanoparticles and CNT were obviously enhanced, and then the ECL effectivity of Ru(bpy)32+ inside silica nanoparticles was improved. Furthermore, based on the discriminative interaction of these Ru(bpy)32+‐doped silica nanoparticles towards both the ssDNA probes and the ssDNA probe/miRNA complex, as well as the specific adsorption effect of these nanoparticles on the nanoscale chitosan shell@Nafion/CNT core‐modified glass carbon electrode, a highly sensitive ECL method for miRNA determination was developed and successfully used to detect miRNA in human serum samples. [ABSTRACT FROM AUTHOR]

Nitrogen-(N) and sulfur-(S) codoped carbon dots (N/S-CDs) are facilely developed by a one-pot hydrothermal process from thiourea and o-phenylenediamine as carbon precursors. The as-fabricated N/S-CDs reveal a high quantum yield of 26% and a large Stokes shift up to 106 nm under the excitation of 450 nm with good water dispersibility as well as antiphotobleaching. With addition of Fe3+, fluorescence quenching happens with a good linearity within 0.3–70 μM and a low detection limit of 0.19 μM. However, the quenched fluorescence could be rapidly recovered with the addition of monohydrogen phosphate ([HPO4]2–) due to formation of the stable complex [Fe-(HPO4)]+ by a competitive reaction between the N/S-CDs-Fe3+ complex and [HPO4]2–, a good linearity is in the range of 0.3–60 μM with a low detection limit of 0.27 μM. Thus, a significant "on–off–on" fluorescence response is performed with obvious color change from yellow-dark brown-yellow. In addition, the practical application and the confocal microscopic images all suggest that the N/S-CDs could target both Fe3+ and [HPO4]2– in living cells, implying that the N/S-CDs possess the diverse applications for Fe3+ and [HPO4]2– recognitions in biomedical fields. [ABSTRACT FROM AUTHOR]

The effects of superplasticizer agent and retarder on the apparent viscosity, thixotropy and rheological properties of 3D printing building mortars at different shear rates were investigated. The results show that when the amount of superplasticizer agent is increased, the apparent viscosity is almost unchanged, the thixotropy will first decrease and then tend to be unchanged, the plastic viscosity will decrease first and then increase, and the yield stress will gradually decrease; the retarder will increase the apparent viscosity of the 3D printing building mortar and increase the yield stress of the slurry. When the amount is higher, the thixotropy of the mortar will increase. The rheological properties of 3D printing mortar can be improved by adding appropriate superplasticizer and retarder, which can meet the printing requirements. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is the most common cause of death, environmental factors, such as arsenic, playing an important role in the progress of CVD. Vascular endothelial dysfunction (VED) is a crucial early feature for CVD, inorganic arsenic (iAs) can induce autophagy in various cells. However, the role of endothelial autophagy has rarely been studied in VED triggered by arsenic. Total of one hundred and twenty healthy male C57BL/6J mice weighing 18–22 g were randomly divided into an arsenic-exposure group and a control group for 3, 6, 9, and 12 weeks. The results showed that, independent of the exposure period, autophagy markers of p-ATG16L1 levels and Beclin 1 contents in the aortic arch endothelium increased significantly compared with those of the corresponding control group. And different exposure duration decreased NO contents in the serum significantly. Combined with the histological changes that endothelial injury aggravated gradually with the increasing exposure period, suggesting that under exposure to iAs over 9 weeks, VED was remarkably induced, and consistant high levels of endothelial autophagy may play an important role. Additionally, levels of p-AMPKα/AMPKα increased significantly and p-mTORC1/mTORC1 levels decreased remarkably in the aortic arch endothelium. Then, a NaAsO 2 -induced-VED in vitro model was used to explore the mechanism of arsenic-induced endothelial autophagy. Similarly, p-AMPKα/AMPKα level significantly increased, and p-mTORC1/mTORC1 level remarkably decreased induced by 30 μmol/L NaAsO 2 in HUAECs. Further, an AMPK inhibitor (Compound C) pre-treatment prior to arsenic exposure reversed the increased autophagy level, and alleviated the endothelial dysfunction in HUVECs, as shown by the significant increase in the intracellular NO content and the cell vitality. Mechanistically, we revealed that AMPKα is active in autophagy of endothelial cells in arsenic-induced VED by regulating mTORC1/p70S6K/ULK1. The present study provide a new promising target for prevention and control arsenic-associated CVD. • NaAsO 2 upregulates autophagy in aortic endothelium, inducing endothelial dysfunction. • AMPKα pathways activate in endothelial cells during the process of autophagy. • AMPKα activates autophagy by regulating mTOR \ p70S6K \ ULK1. • AMPKα is a new promising target against arsenic-induced vascular diseases. [ABSTRACT FROM AUTHOR]

Byline: Yimin Zhang, Xiangdong He, Qiaoling Liu, Bangchun Wen Techniques from the perturbation method, the reliability-based design theory and optimisation techniques are employed to present a practical and effective method for the reliability-based optimisation of automobile components. The theoretical formulae for reliability-based optimisation are obtained. The most probable point perturbation method (MPPPM) and reliability-based optimisation theory are employed to develop the reliability-based optimal design of automobile components. Two examples are used to illustrate the reliability-based optimisation formulation and demonstrate the method. The accuracy of the approach proposed is evaluated by comparing their results to that obtained from Monte Carlo simulations (MCS).