Engineered Si sandwich electrode: Si nanoparticles/graphite sheet hybrid on ni foam for next-generation high-performance lithium-ion batteries.

Si-based electrodes for lithium ion batteries typically exhibit high specific capacity but poor cycling performance. A possible strategy to improve the cycling performance is to design a novel electrode nanostructure. Here we report the design and fabrication of Ni/Si-nanoparticles/graphite clothing hybrid electrodes with a sandwich structure. An efficient dip-coating of Si-NPs combined with carbon deposition was adopted to synthesize the unique architecture, where the Si-NPs are sandwiched between the Ni matrix and the graphite clothing. This material architecture offers many critical features that are desirable for high-performance Si-based electrodes, including efficient ion diffusion, high conductivity, and structure durability, thus ensuring the electrode with outstanding electrochemical performance (reversible capacity of 1800 mA h g(-1) at 2 A g(-1) after 500 cycles). In addition, the hybrid anode does not require any polymeric binder and conductive additives and holds great potential for application in Li-ion batteries.

Notch1 signaling regulates the proliferation and self-renewal of human dental follicle cells by modulating the G1/S phase transition and telomerase activity.

Multipotent human dental follicle cells (HDFCs) have been intensively studied in periodontal regeneration research, yet the role of Notch1 in HDFCs has not been fully understood. The aim of the current study is to explore the role of Notch1 signaling in HDFCs self-renewal and proliferation. HDFCs were obtained from the extracted wisdom teeth from adolescent patients. Regulation of Notch1 signaling in the HDFCs was achieved by overexpressing the exogenous intracellular domain of Notch1 (ICN1) or silencing Notch1 by shRNA. The regulatory effects of Notch1 on HDFC proliferation, cell cycle distribution and the expression of cell cycle regulators were investigated through various molecular technologies, including plasmid construction, retrovirus preparation and infection, qRT-PCR, western blot, RBP-Jk luciferase reporter and cell proliferation assay. Our data clearly show that constitutively activation of Notch1 stimulates the HDFCs proliferation while inhibition of the Notch1 suppresses their proliferation in vitro. In addition, the HDFCs proliferation is associated with the increased expression of cell cycle regulators, e.g. cyclin D1, cyclin D2, cyclin D3, cyclin E1, CDK2, CDK4, CDK6, and SKP2 and the decreased expression of p27 (kip1). Moreover, our data show that the G1/S phase transition (indicating proliferation) and telomerase activity (indicating self-renewal) can be enhanced by overexpression of ICN1 but halted by inhibition of Notch1. Together, the current study provides evidence for the first time that Notch1 signaling regulates the proliferation and self-renewal capacity of HDFCs through modulation of the G1/S phase transition and the telomerase activity.