No abstract

A facile method was developed to synthesize ultrafine Ni–Co alloy nanoparticles embedded into 3D porous graphitic carbon, an excellent electrode material for supercapacitors.

Large-scale fabrication of nanostructured Cu3SbSe4 and its Sn-doped sample Cu3Sb0.98Sn0.02Se4 through a low-temperature co-precipitation route is reported. The effects of hot-pressing temperatures, time and Sn doping on the thermoelectric properties of Cu3SbSe4 are explored. The maximum figure of merit ZTmax obtained here reaches 0.62 for the un-doped Cu3SbSe4, which is three times as large as that of Cu3SbSe4 synthesized by the fusion method. Due to the ameliorated power factor by optimized carrier concentration and the reduced lattice thermal conductivity by enhanced phonon scattering at grain interfaces, Sn doping leads to an improvement of thermoelectric performance as compared to Cu3SbSe4. The maximum ZT for Cu3Sb0.98Sn0.02Se4 is 1.05 in this work, which is 50% larger than the largest value reported.

CoNi alloy nanoparticles incorporated into S,N-doped carbon structure was obtained by pyrolysis treatment of 2D S,N-containing Co/Ni MOFs nanosheets, as electrode material exhibiting high supercapacitor performance.

The shedding of airway epithelial cells and loss of epithelial functional homeostasis are major pathological characteristics of asthma; however, the mechanism underlying these pathologies remains obscure. Our previous work showed that there were three variation sites in 5 0 flanking region of integrin b4 in asthma patients, which was correlated with decreased expression of integrin b4 in peripheral leukocytes. Integrin b4 is an important structural adhesion molecule on airway epithelia to keep the structural adhesion of epithelial cells. In this work, we further demonstrated that integrin b4 expression was downregulated in airway epithelia of asthma patients. To probe the relationship between imbalanced expression of integrin b4 and dysfunction of the airway epithelial cells in asthma, integrin b4 was silenced in human bronchial epithelium cells (16HBE14O) by integrin b4 small-interfering RNA lentivirus vector. Upon silencing of integrin b4, 16HBE14O cells showed reduced proliferation and wound repair. Most cells were shown to be arrested in G1 phase after integrin b4 silencing, and increased apoptosis was induced in the integrin b4-silenced cells. In summary, our results provided compelling evidence that integrin b4 was involved in the structural integrity and functional homeostasis of airway epithelial cells. It is likely that downregulation of integrin b4 on asthma airway epithelia contributes to the structural disruption and dysfunction of airway epithelial cells.

No abstract

Integrin beta 4 (ITGB4) is a structural adhesion molecule which engages in maintaining the integrity of airway epithelial cells. Its specific cytomembrane structural feature strongly indicates that ITGB4 may engage in many signaling pathways and physiologic processes. However, in addition to adhesion, the specific biologic significance of ITGB4 in airway epithelial cells is almost unknown. In this article, we investigated the expression and functional properties of ITGB4 in airway epithelial cells in vivo and in vitro. Human bronchial epithelial cell line (16HBE14O-cells) and primary rat tracheal epithelial cells (RTE cells) were used to determine ITGB4 expression under ozone tress or mechanical damage, respectively. An ovalbumin (OVA)-challenged asthma model was used to investigate ITGB4 expression after antigen exposure in vivo. In addition, an ITGB4 overexpression vector and ITGB4 silence virus vector were constructed and transfected into RTE cells. Then, wound repair ability and anti-oxidation capacity was evaluated. Our results demonstrated that, on the edge of mechanically wounded cell areas, ITGB4 expression was increased after mechanical injury. After ozone stress, upregulation expression of ITGB4 was also detected. In the OVA-challenged asthma model, ITGB4 expression was decreased on airway epithelial cells accompanying with structural disruption and damage of anti-oxidation capacity. Besides, our study revealed that upregulation of ITGB4 promotes wound repair ability and anti-oxidative ability, while such abilities were blocked when ITGB4 was silenced. Taken together, these results showed that ITGB4 was a new interesting molecule involved in the regulation of wound repair and anti-oxidation processes for airway epithelial cells.

No abstract