N-doped pinecone-based carbon with a hierarchical porous pie-like structure: a long-cycle-life anode material for potassium-ion batteries.

Pinecone-based biomass carbon (PC) is a potential anode material for potassium-ion batteries because it is abundant, cheap, renewable, and easy to obtain. However, because of inferior kinetics and the effects of volume expansion due to the large radius of the K+ ion, it does not meet commercial performance requirements. In this study, nitrogen-doped PC (NPC) was prepared by carbonization in molten ZnCl2 with urea as a nitrogen source. A strategy based on synergistic effects between N doping and ZnCl2 molten salt was used to produce a hierarchically porous pie-like NPC with abundant defects and active sites and an enlarged interlayer distance-properties that enhance K+ adsorption, promote K+ intercalation/diffusion, and reduce the effects of volume expansion. This NPC exhibited a high reversible capacity (283 mA h g-1 at 50 mA g-1) and superior rate performance and cyclic stability (110 mA h g-1 after 1000 cycles at 5 A g-1), demonstrating its potential for use in potassium-ion batteries.

Boron-Doped Pine-Cone Carbon With 3D Interconnected Porosity for Use as an Anode for Potassium-Ion Batteries With Long Life Cycle.

Potassium-ion batteries (KIBs) have received widespread attention as an alternative to lithium-ion batteries because of their low cost and abundance of potassium. However, the poor kinetic performance and severe volume changes during charging/discharging due to the large radius of potassium leading to low capacity and rapid decay. Therefore, development of anode materials with sufficient space and active sites for potassium ion deintercalation and desorption is necessary to ensure structural stability and good electrochemical activity. This study prepared boron-doped pine-cone carbon (BZPC) with 3D interconnected hierarchical porous in ZnCl2 molten-salt by calcination under high temperature. The hierarchical porous structure promoted the penetration of the electrolyte, improved charge-carrier diffusion, alleviated volume changes during cycling, and increased the number of micropores available for adsorbing potassium ions. In addition, due to B doping, the BZPC material possessed abundant defects and active centers, and a wide interlayer distance, which enhanced the adsorption of K ions and promoted their intercalation and diffusion. When used as the anode of a KIB, BZPC provided a high reversible capacity (223.8 mAh g-1 at 50 mA g-1), excellent rate performance, and cycling stability (115.9 mAh g-1 after 2000 cycles at 1 A g-1).

Macrovascular Endothelial Cells Enhance the Motility of Liver Cancer Cells by Up-regulation of MMP-3, Activation of Integrin/FAK Signaling Pathway and Induction of Non-classical Epithelial-mesenchymal Transition.

Background: Liver cancer with portal vein tumor thrombus (PVTT) indicates a serious prognosis. The molecular mechanism of PVTT formation is not totally clarified, the invasion of blood vessels by liver cancer cells is the key step and portal vein endothelial cells plays critical role. Methods: Conditioned medium (CM) of human umbilical vein endothelial cells (HUVEC) were used to culture liver cancer cells and prostate cancer cells for cell motility and viability analysis for the purpose of simulating the role of macrovascular endothelial cells in the development of liver cancer. Results: HUVEC-CM caused long spindle-shaped changes in liver cancer cells; the invasion and migration ability of Bel-7402 and MHCC-LM3 (cultured in HUVEC-CM) increased significantly. Integrins/FAK (focal adhesion kinase) signaling pathway was activated and MMP-3 was up-regulated. However, classical epithelial-mesenchymal transition (EMT) did not involve. HUVEC-CM caused a decrease of cell population in G1- and S-phase of Bel-7402, it also caused an accumulation of cell population in G1 phase and a decrease of cell population in S-phase of MHCC-LM3, MHCC-97L and DU-145. HUVEC-CM promotes apoptosis of Bel-7402 and MHCC-97L and the nude mouse tumorigenic experiment did not find that the HUVEC-CM increase the tumorigenic ability of liver cancer cells. Conclusion: HUVEC may provide an easy-to-adhere roadbed for liver cancer cells invasion of blood vessels by altering extracellular matrix (ECM), activating integrins/FAK pathway and inducing non-classical EMT. The effect of HUVEC-CM on cell viability was cancer cell type dependent. It is a meaningful glance at the mechsanism of PVTT.

MRC-5 Cancer-associated Fibroblasts Influence Production of Cancer Stem Cell Markers and Inflammation-associated Cell Surface Molecules, in Liver Cancer Cell Lines.

Background: Current opinion suggests that expansion of cancer stem cells (CSCs) and activation of pro-tumoral inflammation cascade correlate with cancer progression. Materials and methods: We explored the possible contributions of MRC-5 cancer-associated fibroblasts to the expression profiles of CSC markers and inflammation-associated cell surface molecules. The liver cancer cell lines Bel-7402, SMMC-7721, MHCC-LM3, and HepG2 cultured in conditioned medium (CM) from MRC-5 served as test groups, whereas the liver cancer cell lines cultured in normal medium served as control groups. Results: Flow cytometry revealed that the proportions of CD90+ cells were significantly higher in MHCC-LM3-(MRC-5)-CM and HepG2-(MRC-5)-CM cells, and moderately higher in Bel-7402-(MRC-5)-CM and SMMC-7721-(MRC-5)-CM cells, than in controls. The CD90+/CD45- proportions were elevated in Bel-7402-(MRC-5)-CM and MHCC-LM3-(MRC-5)-CM cells, but reduced in HepG2-(MRC-5)-CM and SMMC-7721-(MRC-5)-CM cells, as compared to controls. Western blotting indicated that Nanog was downregulated in MHCC-LM3-(MRC-5)-CM and HepG2-(MRC-5)-CM cells, compared to controls; that POU5F1 (OCT4/3) was downregulated in MHCC-LM3-(MRC-5)-CM, but upregulated in Bel-7402-(MRC-5)-CM and HepG2-(MRC-5)-CM cells, compared to controls, and that CK19 was upregulated in Bel-7402-(MRC-5)-CM and MHCC-LM3-(MRC-5)-CM cells, compared to controls. Proportions of cells expressing Toll-like receptor-1+ (TLR1) and TLR4 were significantly higher in MHCC-LM3-(MRC-5)-CM cells, and moderately higher in HepG2-(MRC-5)-CM cells, than controls. However, the TLR1+ and TLR4+ proportions were lower in Bel-7402-(MRC-5)-CM and SMMC-7721-(MRC-5)-CM cells than controls. Proportions of CD25+ cells were reduced in HepG2-(MRC-5)-CM and SMMC-7721-(MRC-5)-CM cells, but elevated in MHCC-LM3-(MRC-5)-CM and Bel-7402-(MRC-5)-CM cells, compared to controls. Proportion of CD61+ cells was higher in liver cancer cells cultured in MRC-5-CM than in controls. Proportion of CD14+ cells was lower in HCC cells cultured in MRC-5-CM than in controls. Conclusion: MRC-5 extensively affected the production of CSC markers and inflammation-associated cell surface molecules. Tumor-targeting molecular therapies should consider these findings.