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Titanium is a highly valued metal for its outstanding properties. Its production is costly due to its strong reactivity with oxygen, thus there are strong demands to reduce oxygen content in Ti scraps, turnings, chips, chunks, and powders for the purpose of recycling, reuse and high-quality powder production. This article reviews the current methods for reducing oxygen content (i.e. methods of deoxygenation) in Ti and its alloys, particularly metal in powder form, including Ca metal-based methods, Mg metal-based methods, electrochemical methods, and others based on remelting. Even though the details of the operations of each process vary, they share some of the same theoretical basis of relative chemical stabilities. Here we outline and evaluate these methods in terms of the fundamental principles, processing techniques, results and the pros and cons of each method. • The methods for reducing oxygen content in Ti and alloys is reviewed in this paper. • The establishment of various methods are all based on the relative thermodynamic stabilities. • The main approaches for deoxygenation include Ca metal-based, Mg metal-based, electrochemical and remelting-based methods. [ABSTRACT FROM AUTHOR]

Ovarian cancer has the highest mortality rate among all gynecological cancers with its pathogenic mechanisms largely unknown. Here, we uncovered that ovarian cancer tissues exhibit higher heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) expression than normal ovarian epithelium tissues. Increased hnRNPA2B1 level matches along with poor prognosis of ovarian cancer patients. Importantly, hnRNPA2B1 inhibition hampers growth, reduces mobility of ovarian cancer cells in vitro and hinders xenograft tumor formation in vivo. Transcriptome profiling analysis reveals that hnRNPA2B1 dictates the expression of various important genes involved in tumorigenesis and Lin-28 Homolog B (Lin28B) is down-regulated upon hnRNPA2B1 loss. hnRNPA2B1 regulates expression of Lin28B via binding to Lin28B mRNA and enhancing its stability. Furthermore, knockdown of Lin28B reduces proliferation and mobility of ovarian cancer cells and impairs tumorigenesis in vivo, whereas Lin28B overexpression promotes xenograft tumor formation. Finally, re-expression of Lin28B in hnRNPA2B1 knockdown cells results in rescued phenotypes. Collectively, our results demonstrate that hnRNPA2B1 facilitates the malignant phenotype of ovarian cancer through activating Lin28B expression. [ABSTRACT FROM AUTHOR]