In this work, a facile route using a simple solvothermal reaction and sequential calcinations to synthesize porous R-Fe 2 O 3 flower-like nanostructures without employing templates or matrices for self-assembly is presented. The flower-like nanostructures are composed of nanosheets with a thickness of about 20 nm, which are characterized by field-emission scanning electron microscopy (FESEM). Influencing factors such as the dosage of reactants and the solvents are systematically investigated. A possible formation mechanism for the flower-like nanostructure is proposed. A BET test shows that the product is porous and has a large surface area. The electrochemical, magnetic, and photocatalytic properties of the as-obtained R-Fe 2 O 3 3D nanostructure are systematically investigated. The result shows that these properties are greatly affected by the porous structure.

No abstract

Background Lipid metabolism reprogramming is a hallmark for tumor which contributes to tumorigenesis and progression, but the commonality and difference of lipid metabolism among pan-cancer is not fully investigated. Increasing evidences suggest that the alterations in tumor metabolism, including metabolite abundance and accumulation of metabolic products, lead to local immunosuppression in the tumor microenvironment. An integrated analysis of lipid metabolism in cancers from different tissues using multiple omics data may provide novel insight into the understanding of tumorigenesis and progression. Results Through systematic analysis of the multiple omics data from TCGA, we found that the most-widely altered lipid metabolism pathways in pan-cancer are fatty acid metabolism, arachidonic acid metabolism, cholesterol metabolism and PPAR signaling. Gene expression profiles of fatty acid metabolism show commonalities across pan-cancer, while the alteration in cholesterol metabolism and arachidonic acid metabolism differ with tissue origin, suggesting tissue specific lipid metabolism features in different tumor types. An integrated analysis of gene expression, DNA methylation and mutations revealed factors that regulate gene expression, including the differentially methylated sites and mutations of the lipid genes, as well as mutation and differential expression of the up-stream transcription factors for the lipid metabolism pathways. Correlation analysis of the proportion of immune cells in the tumor microenvironment and the expression of lipid metabolism genes revealed immune-related differentially expressed lipid metabolic genes, indicating the potential crosstalk between lipid metabolism and immune response. Genes related to lipid metabolism and immune response that are associated with poor prognosis were discovered including HMGCS2, GPX2 and CD36, which may provide clues for tumor biomarkers or therapeutic targets. Conclusions Our study provides an integrated analysis of lipid metabolism in pan-cancer, highlights the perturbation of key metabolism processes in tumorigenesis and clarificates the regulation mechanism of abnormal lipid metabolism and effects of lipid metabolism on tumor immune microenvironment. This study also provides new clues for biomarkers or therapeutic targets of lipid metabolism in tumors. Electronic supplementary material The online version of this article (10.1186/s12859-019-2734-4) contains supplementary material, which is available to authorized users.