Controlling the growth of high-activity anatase TiO2 exposed {001} facets improves greatly the adsorption and electronic and photocatalytic properties and has been attractive for various environmental and energy-related applications. In this paper, we introduced a novel approach for quantitatively measuring the percentage of exposed {001} facets in anatase TiO2 by using Raman spectroscopy. Comparing to XRD, Raman peaks originate from the vibration of molecular bonds, that is, vibrational mode Eg and A1g peaks, which are related to different crystal planes. Therefore, it provided a high sensitivity and accuracy for measuring the percentage of the exposed facets from the micro perspective of molecular bonding with less measurement errors. With the photocatalytic experiments, we found that 50% was the optimal percentage of the exposed {001} facets for the highest efficiency, which seemed more reasonable than the value of 70% obtained from XRD.

Tumor-associated macrophages (TAMs) play an essential role in metastasis. However, what enables TAMs to have a superior capacity to establish pre-metastatic microenvironment in distant organs is unclear. Here we have begun to uncover the effects of cytochrome P450 (CYP) 4A in TAMs on lung pre-metastatic niche formation and metastasis. CYP4A+ TAM infiltration was positively associated with metastasis, pre-metastatic niche formation and poor prognosis in breast cancer patients. The pharmacological inhibition of CYP4A reduced lung pre-metastatic niche formation (evidenced by a decrease in vascular endothelial growth factor receptor 1 positive (VEGFR1+) myeloid cell recruitment and pro-metastatic protein expression) and metastatic burden, accompanied with TAM polarization away from the M2 phenotype in spontaneous metastasis models of 4T1 breast cancer and B16F10 melanoma. Co-implantation of 4T1 cells with CYP4A10high macrophages promoted lung pre-metastatic niche formation and metastasis. Depletion of TAMs disrupted lung pre-metastatic niches and thereby prevented metastasis. Treatment with the CM from CYP4A10high M2 macrophages (M2) increased pre-metastatic niche formation and metastatic burden in the lungs, whereas CYP4A inhibition attenuated these effects. In vitro TAM polarization away from the M2 phenotype induced by CYP4A inhibition decreased VEGFR1+ myeloid cell migration and fibronectin expression, accompanied with downregulation of STAT3 signaling. Conversely, overexpression of CYP4A or exogenous addition of 20-hydroxyeicosatetraenoic acid promoted M2 polarization and cytokine production of macrophages and thereby enhanced migration of VEGFR1+ myeloid cells, which were reversed by siRNA or pharmacological inhibition of STAT3. Importantly, a combined blocking M2 macrophage-derived factors TGF-β, VEGF and SDF-1 abolished VEGFR1+ myeloid cell migration and fibroblast activation induced by CYP4A. In summary, CYP4A in TAMs is crucial for lung pre-metastatic niche formation and metastasis, and may serve as a potential therapeutic target in human cancer.

iRoot FS displayed in vitro biocompatibility with MC3T3-E1 cells by promoting cellular proliferation and attachment without causing cell apoptosis.